PMID- 39387403
OWN - NLM
STAT- Publisher
LR  - 20241010
IS  - 1744-8298 (Electronic)
IS  - 1479-6678 (Linking)
DP  - 2024 Oct 10
TI  - Methotrexate, blood pressure and arterial function in rheumatoid arthritis: study 
      protocol.
PG  - 1-13
LID - 10.1080/14796678.2024.2411167 [doi]
AB  - This article discusses the rationale and design of the study "Methotrexate, blood 
      pressure, and arterial function in rheumatoid arthritis". The recognition that 
      immune activation and excess inflammation favor atherosclerosis has stimulated a 
      significant body of research not only to identify new drugs targeting these 
      pathways but also to repurpose (reposition) existing immunomodulatory medications 
      as atheroprotective agents. Observational studies in patients with rheumatoid 
      arthritis have reported that treatment with methotrexate, a traditional 
      disease-modifying antirheumatic drug, is associated with a significantly lower 
      risk of cardiovascular morbidity and mortality when compared with other 
      disease-modifying antirheumatic drugs. One potential mechanism accounting for the 
      reduced cardiovascular risk associated with methotrexate is the lowering effect 
      on arterial blood pressure. However, such effect has only been observed in 
      cross-sectional and observational studies. Given the established role of 
      hypertension as a leading cardiovascular risk factor, these observations justify 
      an intervention comparison study, the focus of this article, investigating the 
      temporal effects of methotrexate on blood pressure and various surrogate markers 
      of atherosclerosis in patients with rheumatoid arthritis. The results of this 
      study might lead to the repurposing of methotrexate for cardiovascular prevention 
      in patients with and without autoimmune disorders.Clinical Trial Registration: 
      NCT03254589 (ClinicalTrials.gov).
FAU - Mangoni, Arduino A
AU  - Mangoni AA
AUID- ORCID: 0000-0001-8699-1412
AD  - College of Medicine & Public Health, Flinders Health & Medical Research 
      Institute, Flinders University, Adelaide, Australia.
AD  - Department of Clinical Pharmacology, Finders Medical Centre, Southern Adelaide 
      Local Health Network, Adelaide, Australia.
FAU - Wiese, Michael D
AU  - Wiese MD
AUID- ORCID: 0000-0002-3255-9242
AD  - Centre for Pharmaceutical Innovation, Clinical & Health Sciences, University of 
      South Australia, Adelaide, Australia.
FAU - Woodman, Richard J
AU  - Woodman RJ
AUID- ORCID: 0000-0002-4094-1222
AD  - Centre for Epidemiology & Biostatistics, College of Medicine & Public Health, 
      Flinders University, Adelaide, Australia.
FAU - Sotgia, Salvatore
AU  - Sotgia S
AUID- ORCID: 0000-0002-3717-3437
AD  - Department of Biomedical Sciences, University of Sassari, Sassari, Italy.
FAU - Zinellu, Angelo
AU  - Zinellu A
AUID- ORCID: 0000-0002-8396-0968
AD  - Department of Biomedical Sciences, University of Sassari, Sassari, Italy.
FAU - Carru, Ciriaco
AU  - Carru C
AUID- ORCID: 0000-0002-6985-4907
AD  - Department of Biomedical Sciences, University of Sassari, Sassari, Italy.
AD  - Medical Oncology Unit, University Hospital (AOUSS), Sassari, Italy.
FAU - Hulin, Julie-Ann
AU  - Hulin JA
AUID- ORCID: 0000-0003-4886-0416
AD  - College of Medicine & Public Health, Flinders Health & Medical Research 
      Institute, Flinders University, Adelaide, Australia.
FAU - Shanahan, E Michael
AU  - Shanahan EM
AUID- ORCID: 0000-0001-8309-3289
AD  - College of Medicine & Public Health, Flinders Health & Medical Research 
      Institute, Flinders University, Adelaide, Australia.
AD  - Department of Rheumatology, Flinders Medical Centre, Southern Adelaide Local 
      Health Network, Adelaide, Australia.
FAU - Tommasi, Sara
AU  - Tommasi S
AUID- ORCID: 0000-0002-9449-2602
AD  - College of Medicine & Public Health, Flinders Health & Medical Research 
      Institute, Flinders University, Adelaide, Australia.
AD  - Department of Clinical Pharmacology, Finders Medical Centre, Southern Adelaide 
      Local Health Network, Adelaide, Australia.
LA  - eng
SI  - ClinicalTrials.gov/NCT03254589
PT  - Journal Article
DEP - 20241010
PL  - England
TA  - Future Cardiol
JT  - Future cardiology
JID - 101239345
SB  - IM
OAB - This article describes a research study looking at the effects of a 
      well-established antirheumatic drug, methotrexate, on blood pressure and blood 
      vessels in patients with rheumatoid arthritis, a disabling condition affecting 
      the joints as well as other organs and tissues. Methotrexate is commonly used in 
      rheumatoid arthritis, given its ability to suppress inflammation and the 
      activation of the immune system. However, excessive inflammation and immune 
      activation are linked to atherosclerosis, a condition characterised by the 
      build-up of plaques in blood vessels and the development of clots. Therefore, 
      methotrexate might also be helpful in combating atherosclerosis because of its 
      ability to suppress inflammation and immune system activation. We have previously 
      observed that patients with rheumatoid arthritis receiving methotrexate have 
      lower blood pressure when compared with patients receiving other antirheumatic 
      drugs. However, in this study we could not prove that methotrexate directly 
      reduces blood pressure. Given that high blood pressure is well known to damage 
      the blood vessels and promote atherosclerosis and its devastating manifestations, 
      for example, heart attack and stroke, this article will discuss a new study that 
      compares blood pressure for individuals assigned to different treatments to 
      assess whether methotrexate can lower blood pressure over time and exert 
      additional beneficial effects on blood vessels in patients with rheumatoid 
      arthritis. The results of this study will be helpful in determining whether 
      methotrexate can be routinely used to combat atherosclerosis and consequently 
      reduce the risk of heart attack and stroke in patients with rheumatoid arthritis 
      and, potentially, other patient groups.
OABL- eng
OTO - NOTNLM
OT  - active
OT  - arthritis
OT  - atherosclerosis
OT  - blood inflammation
OT  - drug repositioning
OT  - immunity
OT  - methotrexate
OT  - pressure
OT  - preventive medicine
OT  - rheumatoid
OT  - stiffness
EDAT- 2024/10/13 21:10
MHDA- 2024/10/13 21:10
CRDT- 2024/10/10 07:23
PHST- 2024/10/13 21:10 [medline]
PHST- 2024/10/13 21:10 [pubmed]
PHST- 2024/10/10 07:23 [entrez]
AID - 10.1080/14796678.2024.2411167 [doi]
PST - aheadofprint
SO  - Future Cardiol. 2024 Oct 10:1-13. doi: 10.1080/14796678.2024.2411167.

PMID- 39391127
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20241012
IS  - 2772-8293 (Electronic)
IS  - 2772-8293 (Linking)
VI  - 3
IP  - 4
DP  - 2024 Nov
TI  - Incidence of cardiovascular events in a population-based Danish cohort with 
      atopic dermatitis.
PG  - 100338
LID - 10.1016/j.jacig.2024.100338 [doi]
LID - 100338
AB  - BACKGROUND: The risk of cardiovascular disease in atopic dermatitis (AD) is not 
      well established. OBJECTIVES: Our aims were to evaluate the incidence rate (IR) 
      of venous thromboembolism (VTE) in patients with AD in a population-based cohort 
      study and to assess atherosclerotic cardiovascular disease (ASCVD) risk factors 
      and incidence of malignancies, major adverse cardiovascular events (MACE), and 
      VTE in patients with AD and rheumatoid arthritis (RA) in a nested cohort 
      analysis. METHODS: Data from individuals age 12 years or older (nested cohort 
      age ≥ 18 years) from January 1, 2000, to December 31, 2018, were extracted from 
      the Danish National Patient Registry. Patients with AD were age- and sex-matched 
      with 10 healthy controls. ASCVD risk factors included age 65 years or older and 
      history of smoking, coronary artery disease, stroke, deep vein thrombosis (DVT), 
      pulmonary embolism (PE), and malignancy. RESULTS: The population-based cohort 
      comprised 190,751 patients (17,341 patients with AD and 173,410 healthy 
      controls). The IRs per 100 patient-years were comparable between the AD cohort 
      and healthy controls for VTE (0.14 [95% CI = 0.12-0.16] vs 0.11 [95% CI = 
      0.11-0.12]), DVT (0.08 [95% CI = 0.06-0.09] vs 0.06 [95% CI = 0.06-0.07]), and PE 
      (0.06 [95% CI = 0.05-0.08] vs 0.05 [95% CI = 0.05-0.05]). The IR for VTE was 
      higher in the AD cohort age 65 years or older (0.71 [95% CI = 0.56-0.90]) than in 
      the age-matched controls (0.50 [95% CI = 0.46-0.54]). ASCVD risk factors were 
      more frequent in the patients with RA than in the patients with AD. The IRs for 
      malignancies and MACE were higher with specific ASCVD risk factors. CONCLUSIONS: 
      The IRs of cardiovascular events were comparable between the AD cohort and 
      general population. The risk of VTE, malignancy, or MACE was higher with specific 
      ASCVD risk factors, underscoring the need for patient monitoring.
CI  - © 2024 Published by Elsevier Inc. on behalf of the American Academy of Allergy, 
      Asthma & Immunology.
FAU - Egeberg, Alexander
AU  - Egeberg A
AD  - Bispebjerg University Hospital, University of Copenhagen, Copenhagen, Denmark.
AD  - Department of Clinical Medicine, Faculty of Health and Medical Sciences, 
      University of Copenhagen, Copenhagen, Denmark.
FAU - Wollenberg, Andreas
AU  - Wollenberg A
AD  - Ludwig Maximilian University, Munich, Germany.
AD  - University of Augsburg, Augsburg, Germany.
FAU - Bieber, Thomas
AU  - Bieber T
AD  - Christine Kühne - Center for Allergy Research and Education (CK-CARE), Medicine 
      Campus, Davos, Switzerland.
FAU - Lemeshow, Adina R
AU  - Lemeshow AR
AD  - Pfizer Inc, New York, NY.
FAU - Vyas, Shefali
AU  - Vyas S
AD  - Pfizer Inc, New York, NY.
LA  - eng
PT  - Journal Article
DEP - 20240901
PL  - United States
TA  - J Allergy Clin Immunol Glob
JT  - The journal of allergy and clinical immunology. Global
JID - 9918453488706676
PMC - PMC11466631
OTO - NOTNLM
OT  - Atherosclerotic cardiovascular disease
OT  - Denmark
OT  - Janus kinase inhibitor
OT  - atopic dermatitis
OT  - deep vein thrombosis
OT  - major adverse cardiovascular event
OT  - malignancies
OT  - pulmonary embolism
OT  - rheumatoid arthritis
OT  - venous thromboembolism
COIS- This study was funded by 10.13039/100004319Pfizer Inc. Disclosure of potential 
      conflicts of interest: A. Egeberg has received research funding from Pfizer Inc, 
      AbbVie, Almirall, 10.13039/100002491Bristol-Myers Squibb, 
      10.13039/100008349Boehringer Ingelheim, 10.13039/100004312Eli Lilly and Company, 
      Novartis, Janssen, the Danish National Psoriasis Foundation, the Simon Spies 
      Foundation, and the Kgl Hofbundtmager Aage Bang Foundation, as well as honoraria 
      for serving as a consultant and/or speaker from Pfizer, AbbVie, Amgen, Almirall, 
      Bristol-Myers Squibb, Boehringer Ingelheim, Dermavant, Eli Lilly and Company, 
      Galápagos NV, Galderma, Horizon Therapeutics, Janssen, LEO Pharma, McNeil 
      Consumer Healthcare, Mylan, Novartis, Samsung Bioepis Co, Ltd, Sun 
      Pharmaceuticals, UCB, Union Therapeutics, and Zuellig Pharma, Ltd. A. Wollenberg 
      is an advisor, speaker, or investigator for Pfizer, Aileens, Almirall, 
      Beiersdorf, Bioderma, Bristol-Myers Squibb, Chugai, Eli Lilly and Company, 
      Galápagos, Galderma, GSK, Hans Karrer, Hexal, Janssen, LEO Pharma, L’Oreal, 
      Maruho, MedImmune, Novartis, Pierre Fabre, Regeneron, Sanofi-Genzyme, Santen, and 
      UCB. T. Bieber is a lecturer and/or consultant for Pfizer Inc, AbbVie, Almirall, 
      AnaptysBio, Arena Pharmaceuticals, Asana Biosciences, BioVerSys, Boehringer 
      Ingelheim, Daiichi Sankyo, Dermavant Roivant, Eli Lilly and Company, 
      Galápagos/MorphoSys, Galderma, Glenmark, GSK, Incyte, Kymab, LEO Pharma, 
      L´Oréal/La Roche Posay, Menlo Therapeutics, Novartis, RAPT Therapeutics (FLX 
      Bio), Sanofi Regeneron, UCB, and Vectans Pharma and an investigator for AFYX 
      (DermTreat). A. R. Lemeshow is an employee and shareholder in Pfizer Inc. S. Vyas 
      was an employee and shareholder in Pfizer Inc at the time of the study.
EDAT- 2024/10/11 06:23
MHDA- 2024/10/11 06:24
PMCR- 2024/09/01
CRDT- 2024/10/11 04:16
PHST- 2024/03/22 00:00 [received]
PHST- 2024/07/03 00:00 [revised]
PHST- 2024/08/06 00:00 [accepted]
PHST- 2024/10/11 06:24 [medline]
PHST- 2024/10/11 06:23 [pubmed]
PHST- 2024/10/11 04:16 [entrez]
PHST- 2024/09/01 00:00 [pmc-release]
AID - S2772-8293(24)00134-6 [pii]
AID - 100338 [pii]
AID - 10.1016/j.jacig.2024.100338 [doi]
PST - epublish
SO  - J Allergy Clin Immunol Glob. 2024 Sep 1;3(4):100338. doi: 
      10.1016/j.jacig.2024.100338. eCollection 2024 Nov.

PMID- 39347795
OWN - NLM
STAT- Publisher
LR  - 20240930
IS  - 1861-0692 (Electronic)
IS  - 1861-0684 (Linking)
DP  - 2024 Sep 30
TI  - Subclinical left ventricular dysfunction in rheumatoid arthritis: findings from 
      the prospective Porto-RA cohort.
LID - 10.1007/s00392-024-02548-6 [doi]
AB  - AIM: Patients with rheumatoid arthritis (RA) have an increased risk of cardiac 
      dysfunction and heart failure (HF) due to a pro-inflammatory state. Detecting 
      cardiac dysfunction in RA is challenging as these patients often present 
      preserved ejection fraction (EF) but may have subclinical ventricular 
      dysfunction. Echocardiographic strain analysis is a promising tool for early 
      detection of subclinical left ventricular systolic dysfunction (LVSD). This study 
      assesses the prognostic role of strain analysis in RA. METHODS AND RESULTS: 
      Prospective study of 277 RA patients without known heart disease and preserved 
      EF, categorized by left ventricular global longitudinal strain (GLS): normal GLS 
      (≤ - 18%) vs. subclinical LVSD (> - 18%). Primary outcome was a composite of 
      myocardial infarction, HF hospitalization, stroke, or cardiovascular death 
      (MACE). Mean age was 57 years, 79% female. Although mean GLS was within normal 
      (- 20 ± 3%), subclinical LVSD was observed in 24% of patients (n = 67) and was 
      positively correlated with older age (OR 1.54 per 10 years; p < 0.001) and 
      comorbid conditions, such as dyslipidemia (OR 2.27; p = 0.004), obesity (OR 2.29; 
      p = 0.015), and chronic kidney disease (OR 8.39; p = 0.012). Subclinical LVSD was 
      independently associated with a 3.9-fold higher risk of MACE (p = 0.003) and a 
      3.4-fold higher risk of HF hospitalization/cardiovascular death (p = 0.041). A 
      GLS threshold of > - 18.5% provided optimal sensitivity (78%) and specificity 
      (74%) in identifying patients at elevated MACE risk (AUC = 0.78; p < 0.001). 
      CONCLUSION: Subclinical LVSD, identified by reduced GLS, was strongly associated 
      with adverse cardiovascular events in RA. Whether these findings have therapeutic 
      implications is worth exploring in clinical trials.
CI  - © 2024. The Author(s).
FAU - Alexandre, André
AU  - Alexandre A
AUID- ORCID: 0000-0003-2465-2217
AD  - Department of Cardiology, Unidade Local de Saúde de Santo António, Largo Do Prof. 
      Abel Salazar, 4099-001, Porto, Portugal. andrealexandre_1@msn.com.
AD  - ICBAS-School of Medicine and Biomedical Sciences, University of Porto, 4050-313, 
      Porto, Portugal. andrealexandre_1@msn.com.
FAU - Sá-Couto, David
AU  - Sá-Couto D
AD  - Department of Cardiology, Unidade Local de Saúde de Santo António, Largo Do Prof. 
      Abel Salazar, 4099-001, Porto, Portugal.
AD  - ICBAS-School of Medicine and Biomedical Sciences, University of Porto, 4050-313, 
      Porto, Portugal.
FAU - Brandão, Mariana
AU  - Brandão M
AD  - ICBAS-School of Medicine and Biomedical Sciences, University of Porto, 4050-313, 
      Porto, Portugal.
AD  - Clinical Immunology Unit, Unidade Local de Saúde de Santo António, 4099-001, 
      Porto, Portugal.
AD  - Autoimmunity and Neurosciences Group, UMIB-Unit for Multidisciplinary Research in 
      Biomedicine, ICBAS-School of Medicine and Biomedical Sciences, University of 
      Porto, 4050-313, Porto, Portugal.
FAU - Cabral, Sofia
AU  - Cabral S
AD  - Department of Cardiology, Unidade Local de Saúde de Santo António, Largo Do Prof. 
      Abel Salazar, 4099-001, Porto, Portugal.
AD  - ICBAS-School of Medicine and Biomedical Sciences, University of Porto, 4050-313, 
      Porto, Portugal.
FAU - Fonseca, Tomás
AU  - Fonseca T
AD  - ICBAS-School of Medicine and Biomedical Sciences, University of Porto, 4050-313, 
      Porto, Portugal.
AD  - Clinical Immunology Unit, Unidade Local de Saúde de Santo António, 4099-001, 
      Porto, Portugal.
AD  - Autoimmunity and Neurosciences Group, UMIB-Unit for Multidisciplinary Research in 
      Biomedicine, ICBAS-School of Medicine and Biomedical Sciences, University of 
      Porto, 4050-313, Porto, Portugal.
FAU - Costa, Rita Quelhas
AU  - Costa RQ
AD  - Department of Internal Medicine, Unidade Local de Saúde de Entre Douro E Vouga, 
      Aveiro, Portugal.
FAU - Marinho, António
AU  - Marinho A
AD  - ICBAS-School of Medicine and Biomedical Sciences, University of Porto, 4050-313, 
      Porto, Portugal.
AD  - Clinical Immunology Unit, Unidade Local de Saúde de Santo António, 4099-001, 
      Porto, Portugal.
AD  - Autoimmunity and Neurosciences Group, UMIB-Unit for Multidisciplinary Research in 
      Biomedicine, ICBAS-School of Medicine and Biomedical Sciences, University of 
      Porto, 4050-313, Porto, Portugal.
FAU - Vasconcelos, Carlos
AU  - Vasconcelos C
AD  - Clinical Immunology Unit, Unidade Local de Saúde de Santo António, 4099-001, 
      Porto, Portugal.
AD  - Autoimmunity and Neurosciences Group, UMIB-Unit for Multidisciplinary Research in 
      Biomedicine, ICBAS-School of Medicine and Biomedical Sciences, University of 
      Porto, 4050-313, Porto, Portugal.
FAU - Ferreira, Betânia
AU  - Ferreira B
AD  - Autoimmunity and Neurosciences Group, UMIB-Unit for Multidisciplinary Research in 
      Biomedicine, ICBAS-School of Medicine and Biomedical Sciences, University of 
      Porto, 4050-313, Porto, Portugal.
AD  - Hospital da Luz Arrábida, Vila Nova de Gaia, Portugal.
FAU - Ferreira, João Pedro
AU  - Ferreira JP
AD  - Université de Lorraine, INSERM, Centre d'Investigations Cliniques Plurithématique 
      1433, CHRU de Nancy, Inserm U1116 F-CRIN INI-CRCT (Cardiovascular and Renal 
      Clinical Trialists), Nancy, France.
AD  - Department of Surgery and Physiology, Faculty of Medicine of the University of 
      Porto, Porto, Portugal.
FAU - Rodrigues, Patrícia
AU  - Rodrigues P
AD  - Department of Cardiology, Unidade Local de Saúde de Santo António, Largo Do Prof. 
      Abel Salazar, 4099-001, Porto, Portugal.
AD  - ICBAS-School of Medicine and Biomedical Sciences, University of Porto, 4050-313, 
      Porto, Portugal.
AD  - Cardiovascular Research Group, UMIB-Unit for Multidisciplinary Research in 
      Biomedicine, ICBAS-School of Medicine and Biomedical Sciences, University of 
      Porto, 4050-313, Porto, Portugal.
LA  - eng
PT  - Journal Article
DEP - 20240930
PL  - Germany
TA  - Clin Res Cardiol
JT  - Clinical research in cardiology : official journal of the German Cardiac Society
JID - 101264123
SB  - IM
OTO - NOTNLM
OT  - Heart failure
OT  - Left ventricular global longitudinal strain
OT  - Major adverse cardiovascular events
OT  - Rheumatoid arthritis
OT  - Subclinical cardiac dysfunction
EDAT- 2024/09/30 12:46
MHDA- 2024/09/30 12:46
CRDT- 2024/09/30 11:02
PHST- 2024/06/22 00:00 [received]
PHST- 2024/09/16 00:00 [accepted]
PHST- 2024/09/30 12:46 [medline]
PHST- 2024/09/30 12:46 [pubmed]
PHST- 2024/09/30 11:02 [entrez]
AID - 10.1007/s00392-024-02548-6 [pii]
AID - 10.1007/s00392-024-02548-6 [doi]
PST - aheadofprint
SO  - Clin Res Cardiol. 2024 Sep 30. doi: 10.1007/s00392-024-02548-6.

PMID- 39292496
OWN - NLM
STAT- Publisher
LR  - 20240921
IS  - 2380-6591 (Electronic)
IS  - 2380-6583 (Print)
DP  - 2024 Sep 18
TI  - Exploring the Link Between Genetic Predictors of Cardiovascular Disease and 
      Psoriasis.
LID - 10.1001/jamacardio.2024.2859 [doi]
LID - e242859
AB  - IMPORTANCE: The epidemiological link between immune-mediated diseases (IMIDs) and 
      cardiovascular disease has often been attributed to systemic inflammation. 
      However, the direction of causality and the biological mechanisms linking 
      cardiovascular disease with IMIDs are incompletely understood. Given the robust 
      epidemiological association and the growing body of supportive mechanistic 
      evidence, psoriasis is an exemplary IMID model for exploring this relationship. 
      OBJECTIVE: To assess the bidirectional relationships between genetic predictors 
      of psoriasis and the 2 major forms of cardiovascular disease, coronary artery 
      disease (CAD) and stroke, and to evaluate the association between genetic 
      predictors of cardiovascular disease with 9 other IMIDs. DESIGN, SETTING, AND 
      PARTICIPANTS: This was a genetic association study using mendelian randomization 
      (MR), a powerful genetic tool to help distinguish causation from associations 
      observed in epidemiological studies, to provide supportive evidence for causality 
      between traits. The study conducted 2-sample MR analyses using summary-level data 
      from large-scale genome-wide association meta-analysis studies (GWAS) for each 
      trait. The analysis focused on individuals of European descent from GWAS 
      meta-analyses, involving CAD, stroke, psoriasis, and 9 other IMIDs. Data were 
      analyzed from January 2023 to May 2024. EXPOSURES: Genetic predictors of CAD, 
      stroke, psoriasis, and 9 other IMIDs. MAIN OUTCOMES AND MEASURES: The primary 
      outcomes were the associations of genetic predictors of CAD and stroke with the 
      risk of psoriasis and 9 other IMIDs, determined using inverse-variance weighted 
      (IVW) MR estimates. RESULTS: This study included 181 249 cases and 1 165 690 
      controls with CAD, 110 182 cases and 1 503 898 controls with stroke, 36 466 cases 
      and 458 078 controls with psoriasis, for a total of approximately 3 400 000 
      individuals, and 9 other IMIDs. In contrast to previous assumptions, genetic 
      predictors of psoriasis were found to have no association with CAD or stroke. In 
      the reverse direction, genetic predictors of both CAD (MR estimate IVW odds ratio 
      [OR], 1.07; 95% CI, 1.04-1.10; P = .003) and stroke (IVW OR, 1.22; 95% CI, 
      1.05-1.41; P = .01) were found to have risk-increasing associations with 
      psoriasis. Adjusting for stroke rendered the associations of genetically 
      predicted CAD with psoriasis risk nonsignificant (and vice versa), suggesting 
      that a shared effect underlying genetic risk for CAD and stroke associates with 
      increased psoriasis risk. No risk-increasing associations were observed for 
      genetic predictors of cardiovascular disease with other common IMIDs, including 
      rheumatoid arthritis and inflammatory bowel disease. CONCLUSIONS AND RELEVANCE: 
      Findings of this mendelian randomization study indicate that genetic predictors 
      of cardiovascular disease were associated with increased psoriasis risk with no 
      reciprocal effect or association with other IMIDs. Elucidating mechanisms 
      underpinning this association could lead to novel therapeutic approaches in both 
      diseases.
FAU - Ramessur, Ravi
AU  - Ramessur R
AD  - St John's Institute of Dermatology, School of Basic & Medical Biosciences, 
      Faculty of Life Sciences & Medicine, King's College London, London, United 
      Kingdom.
FAU - Saklatvala, Jake
AU  - Saklatvala J
AD  - Department of Medical and Molecular Genetics, School of Basic & Medical 
      Biosciences, King's College London, London, United Kingdom.
FAU - Budu-Aggrey, Ashley
AU  - Budu-Aggrey A
AD  - MRC Integrative Epidemiology Unit at University of Bristol, Bristol, United 
      Kingdom.
AD  - Population Health Sciences, Bristol Medical School, Bristol, United Kingdom.
FAU - Ostaszewski, Marek
AU  - Ostaszewski M
AD  - Luxembourg Centre for Systems Biomedicine, University of Luxembourg, 
      Esch-sur-Alzette, Luxembourg.
FAU - Möbus, Lena
AU  - Möbus L
AD  - Finnish Hub for Development and Validation of Integrated Approaches, Faculty of 
      Medicine and Health Technology, Tampere University, Tampere, Finland.
FAU - Greco, Dario
AU  - Greco D
AD  - Finnish Hub for Development and Validation of Integrated Approaches, Faculty of 
      Medicine and Health Technology, Tampere University, Tampere, Finland.
AD  - Division of Pharmaceutical Biosciences, Faculty of Pharmacy, University of 
      Helsinki, Helsinki, Uusimaa, Finland.
FAU - Ndlovu, Matladi
AU  - Ndlovu M
AD  - Department of Immunology Research, UCB, Brussels, Belgium.
FAU - Mahil, Satveer K
AU  - Mahil SK
AD  - St John's Institute of Dermatology, School of Basic & Medical Biosciences, 
      Faculty of Life Sciences & Medicine, King's College London, London, United 
      Kingdom.
FAU - Barker, Jonathan N
AU  - Barker JN
AD  - St John's Institute of Dermatology, School of Basic & Medical Biosciences, 
      Faculty of Life Sciences & Medicine, King's College London, London, United 
      Kingdom.
FAU - Brown, Sara
AU  - Brown S
AD  - Centre for Genomic and Experimental Medicine, University of Edinburgh, Edinburgh, 
      Scotland, United Kingdom.
AD  - Department of Dermatology, NHS Lothian, Edinburgh, Scotland, United Kingdom.
FAU - Paternoster, Lavinia
AU  - Paternoster L
AD  - MRC Integrative Epidemiology Unit at University of Bristol, Bristol, United 
      Kingdom.
AD  - Population Health Sciences, Bristol Medical School, Bristol, United Kingdom.
AD  - NIHR Bristol Biomedical Research Centre, University Hospitals Bristol and Weston 
      NHS Foundation Trust and University of Bristol, Bristol, United Kingdom.
FAU - Dand, Nick
AU  - Dand N
AD  - Department of Medical and Molecular Genetics, School of Basic & Medical 
      Biosciences, King's College London, London, United Kingdom.
FAU - Simpson, Michael A
AU  - Simpson MA
AD  - Department of Medical and Molecular Genetics, School of Basic & Medical 
      Biosciences, King's College London, London, United Kingdom.
FAU - Smith, Catherine H
AU  - Smith CH
AD  - St John's Institute of Dermatology, School of Basic & Medical Biosciences, 
      Faculty of Life Sciences & Medicine, King's College London, London, United 
      Kingdom.
LA  - eng
PT  - Journal Article
DEP - 20240918
PL  - United States
TA  - JAMA Cardiol
JT  - JAMA cardiology
JID - 101676033
SB  - IM
CIN - doi: 10.1001/jamacardio.2024.2868
PMC - PMC11411451
COIS- Conflict of Interest Disclosures: Dr Ndlovu reported receiving an employee salary 
      from UCB BioPharma Employee and nonfinancial support from European Federation of 
      Pharmaceutical Industries and Associations (EFPIA) Innovative Medicines 
      Initiative (IMI) Biomarkers in Atopic Dermatitis and Psoriasis (BIOMAP) in-kind 
      contribution during the conduct of the study Dr Barker reported receiving 
      advisory board/speaker fees and/or received research funding from AbbVie, 
      Almirall, Amgen, Anaptys-Bio, Boehringer-Ingelheim, Bristol Myers Squibb, Johnson 
      & Johnson, Lilly, Novartis, Samsung, Sandoz, Sun Pharma, and UCB BioPharma. Dr 
      Brown reported receiving grants from EC-IMI BIOMAP, Wellcome Trust Senior 
      Research Fellowship, Medical Research Council, British Skin Foundation, Rosetrees 
      Trust, Stoneygates Trust, Charles Wolfson Charitable Trust, and European Lead 
      Factory outside the submitted work. Dr Paternoster reported receiving grants from 
      IMI during the conduct of the study. Dr Smith reported receiving grants from 
      IMI-EU academic industry consortium with multiple partners, the Psoriasis 
      Association, the National Institute for Health Care and Research, AstraZeneca, 
      and Boehringer Ingelheim outside the submitted work. No other disclosures were 
      reported.
EDAT- 2024/09/18 12:52
MHDA- 2024/09/18 12:52
PMCR- 2024/09/18
CRDT- 2024/09/18 11:43
PHST- 2024/09/18 12:52 [medline]
PHST- 2024/09/18 12:52 [pubmed]
PHST- 2024/09/18 11:43 [entrez]
PHST- 2024/09/18 00:00 [pmc-release]
AID - 2823895 [pii]
AID - hoi240051 [pii]
AID - 10.1001/jamacardio.2024.2859 [doi]
PST - aheadofprint
SO  - JAMA Cardiol. 2024 Sep 18:e242859. doi: 10.1001/jamacardio.2024.2859.

PMID- 39270774
OWN - NLM
STAT- Publisher
LR  - 20240913
IS  - 1532-6500 (Electronic)
IS  - 1058-2746 (Linking)
DP  - 2024 Sep 11
TI  - Revision Shoulder Arthroplasty: Predictors of Subsequent Revision Surgery and 
      Economic Burden amongst Medicare Beneficiaries.
LID - S1058-2746(24)00626-8 [pii]
LID - 10.1016/j.jse.2024.07.033 [doi]
AB  - BACKGROUND: Revision shoulder arthroplasty continues to add an increasing burden 
      on patients and the healthcare system. This study aimed to delineate long-term 
      shoulder arthroplasty revision incidence, quantify associated Medicare spending, 
      and identify relevant predictors of both revision and spending. METHODS: The 
      complete 2016-2022(Q3) Medicare fee-for-service inpatient and outpatient claims 
      data was analyzed. Patients receiving a primary total shoulder arthroplasty for 
      osteoarthritis, rotator cuff pathology, or inflammatory arthropathy were included 
      and subsequent ipsilateral revision surgeries were identified. The time to 
      revision was modeled using the Prentice, Williams, and Peterson Gap Time Model. 
      Medicare spending within 90 days post-discharge was modeled using a generalized 
      linear model. The analysis was subdivided by index procedure type: anatomic total 
      shoulder arthroplasty (TSA) and reverse shoulder arthroplasty (RSA). RESULTS: A 
      total of 82,949 primary TSAs and 172,524 RSAs were identified. Compared to index 
      TSA cases, index RSA cases had a lower first revision rate in an observation 
      window of nearly 7 years (1.9% vs. 3.5%, p<0.001), but a higher rate of second 
      (11.4% vs. 4.9%, p<0.001) as well as third revision (13.8% vs. 13.8%, p=0.449). 
      TSA spending was significantly lower than RSA spending for the index procedure 
      ($21,531 vs. $23,267, p<0.001), first ($23,096 vs. $26,414, p<0.001), and second 
      ($25,060 vs. $29,983, p<0.001) revision. There was no statistically significant 
      difference in third revision between TSA and RSA groups ($31,313 vs. $30,829, 
      p=0.860). Age, sex, race, and rheumatoid arthritis were among the top predictors 
      of revisions. Top predictors of Medicare spending included having a 
      non-osteoarthritis surgical indication, a hospital stay of three or more days, a 
      discharge to a setting other than home, malnutrition, dementia, stroke, major 
      kidney diseases, and being operated on in a teaching hospital. CONCLUSION: 
      Compared with TSA, RSA was associated with a lower first revision rate, but a 
      higher subsequent revision rate. An index RSA procedure was also associated with 
      higher initial Medicare spending as well as subsequent revision surgery spending 
      compared with an index TSA procedure. Demographics and comorbid medical 
      conditions were among the top predictors of revisions, while procedure-related 
      factors predicted Medicare spending.
CI  - Copyright © 2024. Published by Elsevier Inc.
CN  - Avant-Garde Health and Codman Shoulder Society Value-Based Care Group
FAU - Khan, Adam Z
AU  - Khan AZ
AD  - Department of Orthopaedic Surgery, Southern California Permanente Medical Group, 
      Panorama City, CA, USA. Electronic address: adamzkhan12@gmail.com.
FAU - Liu, Harry H
AU  - Liu HH
AD  - Avant-garde Health, Boston, MA, USA.
FAU - Costouros, John G
AU  - Costouros JG
AD  - Institute for Joint Restoration and Research, California Shoulder Center, Menlo 
      Park, CA.
FAU - Best, Matthew J
AU  - Best MJ
AD  - Department of Orthopaedic Surgery, Johns Hopkins Hospital, Johns Hopkins 
      University School of Medicine, Baltimore, MD, USA.
FAU - Fedorka, Catherine J
AU  - Fedorka CJ
AD  - Cooper Bone and Joint Institute, Cooper University Hospital, Camden, NJ, USA.
FAU - Sanders, Brett
AU  - Sanders B
AD  - Center for Sports Medicine and Orthopaedics, Chattanooga, TN, USA.
FAU - Abboud, Joseph A
AU  - Abboud JA
AD  - Rothman Institute, Thomas Jefferson University Hospital, Philadelphia, PA, USA.
FAU - Warner, Jon J P
AU  - Warner JJP
AD  - Department of Orthopaedic Surgery, Harvard Medical School, Boston Shoulder 
      Institute, Massachusetts General Hospital, Boston, MA, USA.
FAU - Fares, Mohamad Y
AU  - Fares MY
AD  - Rothman Institute, Thomas Jefferson University Hospital, Philadelphia, PA, USA.
FAU - Kirsch, Jacob M
AU  - Kirsch JM
AD  - Department of Orthopaedic Surgery, New England Baptist Hospital, Tufts University 
      School of Medicine, Boston, MA, USA.
FAU - Simon, Jason E
AU  - Simon JE
AD  - Department of Orthopaedic Surgery, Massachusetts General 
      Hospital/Newton-Wellesley Hospital, Boston, MA, USA.
FAU - O'Donnell, Evan A
AU  - O'Donnell EA
AD  - Department of Orthopaedic Surgery, Harvard Medical School, Boston Shoulder 
      Institute, Massachusetts General Hospital, Boston, MA, USA.
FAU - Woodmass, Jarret
AU  - Woodmass J
AD  - Pan Am Clinic, Winnipeg, MB, Canada.
FAU - Armstrong, April D
AU  - Armstrong AD
AD  - Department of Orthopaedics and Rehabilitation, Bone and Joint Institute, Penn 
      State Milton S. Hershey Medical Center, Hershey, PA, USA.
FAU - Zhang, Xiaoran
AU  - Zhang X
AD  - Avant-garde Health, Boston, MA, USA.
FAU - Beck da Silva Etges, Ana Paula
AU  - Beck da Silva Etges AP
AD  - Avant-garde Health, Boston, MA, USA.
FAU - Jones, Porter
AU  - Jones P
AD  - Avant-garde Health, Boston, MA, USA.
FAU - Haas, Derek A
AU  - Haas DA
AD  - Avant-garde Health, Boston, MA, USA.
FAU - Gottschalk, Michael B
AU  - Gottschalk MB
AD  - Department of Orthopaedic Surgery, Emory University, Atlanta, GA, USA.
LA  - eng
PT  - Journal Article
DEP - 20240911
PL  - United States
TA  - J Shoulder Elbow Surg
JT  - Journal of shoulder and elbow surgery
JID - 9206499
SB  - IM
OTO - NOTNLM
OT  - Cost Analysis
OT  - Medicare Spending
OT  - Reverse Shoulder Arthroplasty
OT  - Revision Shoulder Arthroplasty
OT  - Risk Factor Analysis
OT  - Total Shoulder Arthroplasty
EDAT- 2024/09/14 10:42
MHDA- 2024/09/14 10:42
CRDT- 2024/09/13 19:25
PHST- 2023/12/16 00:00 [received]
PHST- 2024/07/22 00:00 [revised]
PHST- 2024/07/25 00:00 [accepted]
PHST- 2024/09/14 10:42 [medline]
PHST- 2024/09/14 10:42 [pubmed]
PHST- 2024/09/13 19:25 [entrez]
AID - S1058-2746(24)00626-8 [pii]
AID - 10.1016/j.jse.2024.07.033 [doi]
PST - aheadofprint
SO  - J Shoulder Elbow Surg. 2024 Sep 11:S1058-2746(24)00626-8. doi: 
      10.1016/j.jse.2024.07.033.

PMID- 39239402
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240910
IS  - 0915-5287 (Print)
IS  - 2187-5626 (Electronic)
IS  - 0915-5287 (Linking)
VI  - 36
IP  - 9
DP  - 2024 Sep
TI  - Influence of caregiver understanding of their capability to perform activities of 
      daily living, disease comprehension, and attitudes on occupational low back pain: 
      a cross-sectional study.
PG  - 577-582
LID - 10.1589/jpts.36.577 [doi]
AB  - [Purpose] The aim in this study was to evaluate the impact of caregiver 
      understanding of their ability to perform activities of daily living (ADLs), 
      movement abilities, diseases, and attitudes on the prevalence of occupational low 
      back pain. [Participants and Methods] A cross-sectional survey was conducted of 
      caregivers of older adults living in residential care facilities. Of the 150 
      questionnaires distributed, 71 were valid. The survey collected data on 
      demographics, low back pain status using a numerical rating scale, and 
      familiarity with ten ADLs and five diseases (stroke, rheumatoid arthritis, 
      fractures, Parkinson's disease, and dementia). [Results] In this study, 52% of 
      the participants reported lower back pain. Significant factors included an 
      understanding of repositioning in ADLs, familiarity with stroke and rheumatoid 
      arthritis, and attitudes toward using patients' residual functions. Participants 
      with limited knowledge of repositioning and stroke, a better understanding of 
      rheumatoid arthritis, and those who did not consider residual function were more 
      prone to lower back pain. [Conclusion] Our findings highlight the importance of 
      enhancing caregiver education on ADL movements and disease specifics, 
      particularly stroke and rheumatoid arthritis, and promoting the use of patients' 
      residual capabilities. Improved training and information sharing among caregivers 
      may reduce the risk of occupational low back pain.
CI  - 2024©by the Society of Physical Therapy Science. Published by IPEC Inc.
FAU - Yokoyama, Daiki
AU  - Yokoyama D
AD  - Department of Physical Therapy, Ota College of Medical Technology: 1373 
      Higashinagaoka-cho, Ota-shi, Gunma 373-0812, Japan.
AD  - Department of Rehabilitation Sciences, Gunma University Graduate School of Health 
      Sciences, Japan.
FAU - Tamura, Shuntaro
AU  - Tamura S
AD  - Department of Physical Therapy, Ota College of Medical Technology: 1373 
      Higashinagaoka-cho, Ota-shi, Gunma 373-0812, Japan.
FAU - Fujisaki, Kazuki
AU  - Fujisaki K
AD  - Department of Physical Therapy, Ota College of Medical Technology: 1373 
      Higashinagaoka-cho, Ota-shi, Gunma 373-0812, Japan.
FAU - Mitsuyama, Kenichiro
AU  - Mitsuyama K
AD  - Department of Rehabilitation, Long-term Care Health Facility Yamazakura, Japan.
FAU - Sato, Tomohiko
AU  - Sato T
AD  - Department of Physical Therapy, Ota College of Medical Technology: 1373 
      Higashinagaoka-cho, Ota-shi, Gunma 373-0812, Japan.
FAU - Kobayashi, Kazura
AU  - Kobayashi K
AD  - Department of Occupational Therapy, Ota College of Medical Technology, Japan.
FAU - Otani, Tomohiro
AU  - Otani T
AD  - Department of Physical Therapy, Ota College of Medical Technology: 1373 
      Higashinagaoka-cho, Ota-shi, Gunma 373-0812, Japan.
LA  - eng
PT  - Journal Article
DEP - 20240905
PL  - Japan
TA  - J Phys Ther Sci
JT  - Journal of physical therapy science
JID - 9105359
PMC - PMC11374168
OTO - NOTNLM
OT  - Capability activity of daily living (ADL)
OT  - Caregivers
OT  - Occupational low back pain
COIS- There are no conflicts of interest to disclose in this study.
EDAT- 2024/09/06 06:42
MHDA- 2024/09/06 06:43
PMCR- 2024/09/01
CRDT- 2024/09/06 04:36
PHST- 2024/05/29 00:00 [received]
PHST- 2024/06/16 00:00 [accepted]
PHST- 2024/09/06 06:43 [medline]
PHST- 2024/09/06 06:42 [pubmed]
PHST- 2024/09/06 04:36 [entrez]
PHST- 2024/09/01 00:00 [pmc-release]
AID - 2024-062 [pii]
AID - 10.1589/jpts.36.577 [doi]
PST - ppublish
SO  - J Phys Ther Sci. 2024 Sep;36(9):577-582. doi: 10.1589/jpts.36.577. Epub 2024 Sep 
      5.

PMID- 39206075
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240901
IS  - 2050-0904 (Print)
IS  - 2050-0904 (Electronic)
IS  - 2050-0904 (Linking)
VI  - 12
IP  - 9
DP  - 2024 Sep
TI  - Emergence of acute quadriparesis in a young patient following myocardial 
      infarction. A case report.
PG  - e9366
LID - 10.1002/ccr3.9366 [doi]
LID - e9366
AB  - Cerebrovascular events are closely related to cardiac events. Chronic 
      inflammatory diseases, such as rheumatoid arthritis (RA), increase the risk of 
      cardiovascular and cerebrovascular stroke. The link between RA, myocardial 
      infarction, and resulting neurological issues highlights the case's complexity, 
      stressing the need for a comprehensive, interdisciplinary medical approach.
CI  - © 2024 The Author(s). Clinical Case Reports published by John Wiley & Sons Ltd.
FAU - Daneshyar, Sajjad
AU  - Daneshyar S
AUID- ORCID: 0000-0002-7553-3843
AD  - Department of Neurology, School of Medicine Hamadan University of Medical 
      Sciences Hamadan Iran.
FAU - Khazaei, Mojtaba
AU  - Khazaei M
AD  - Department of Neurology, School of Medicine Hamadan University of Medical 
      Sciences Hamadan Iran.
FAU - Nazifi, Mozhgan
AU  - Nazifi M
AD  - Department of Neurology, School of Medicine Hamadan University of Medical 
      Sciences Hamadan Iran.
LA  - eng
PT  - Case Reports
PT  - Journal Article
DEP - 20240827
PL  - England
TA  - Clin Case Rep
JT  - Clinical case reports
JID - 101620385
PMC - PMC11348400
OTO - NOTNLM
OT  - arthritis rheumatoid
OT  - myocardial infarction
OT  - risk factors
OT  - stroke
COIS- The authors declare no conflict of interest.
EDAT- 2024/08/31 09:52
MHDA- 2024/08/31 09:53
PMCR- 2024/08/27
CRDT- 2024/08/29 04:13
PHST- 2023/12/29 00:00 [received]
PHST- 2024/08/05 00:00 [revised]
PHST- 2024/08/13 00:00 [accepted]
PHST- 2024/08/31 09:53 [medline]
PHST- 2024/08/31 09:52 [pubmed]
PHST- 2024/08/29 04:13 [entrez]
PHST- 2024/08/27 00:00 [pmc-release]
AID - CCR39366 [pii]
AID - 10.1002/ccr3.9366 [doi]
PST - epublish
SO  - Clin Case Rep. 2024 Aug 27;12(9):e9366. doi: 10.1002/ccr3.9366. eCollection 2024 
      Sep.

PMID- 39171836
OWN - NLM
STAT- MEDLINE
DCOM- 20241104
LR  - 20241104
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Print)
IS  - 1462-0324 (Linking)
VI  - 63
IP  - 11
DP  - 2024 Nov 1
TI  - Rheumatoid arthritis and the risk of ischaemic stroke after diagnosis of atrial 
      fibrillation: a Norwegian nationwide register study.
PG  - 2997-3005
LID - 10.1093/rheumatology/keae458 [doi]
AB  - OBJECTIVES: RA patients have an increased risk for cardiovascular diseases, 
      including atrial fibrillation (AF), but the impact of RA on ischaemic stroke risk 
      in the context of AF remains unknown. We explored whether the risk of ischaemic 
      stroke after diagnosis of AF is further increased among patients with RA compared 
      with non-RA patients. METHODS: In the nationwide Norwegian Cardio-Rheuma 
      Register, we evaluated cumulative incidence and hazard rate of ischaemic stroke 
      after the first AF diagnosis (2750 individuals with RA and 158 879 without RA 
      between 2010 and 2017) by using a competing risk model with a 3-month delayed 
      entry. RESULTS: The 5-year unadjusted cumulative incidence of ischaemic stroke 
      was 7.3% (95% CI: 5.9-8.7%) for patients with RA and 5.0% (95% CI: 4.9-5.2%) for 
      patients without RA. Unadjusted univariate analyses indicated that AF patients 
      with RA had a HR of 1.36 (95% CI: 1.13, 1.62) for ischaemic stroke compared with 
      those without RA. Sex- and age-adjusted HR for ischaemic stroke in RA patients 
      with AF was 1.25 (95% CI: 1.05, 1.50), and the effect size remained unchanged 
      after adjustment for diabetes, hypertension, atherosclerotic cardiovascular 
      disease and oral anticoagulant (OAC) treatment. RA patients were less likely to 
      receive OAC treatment than non-RA patients (adjusted odds ratio 0.88, 95% CI: 
      0.80, 0.97). CONCLUSION: RA patients diagnosed with AF are at a further increased 
      risk for stroke compared with non-RA patients with AF, and less likely to receive 
      OAC treatment, emphasizing the need to improve stroke prevention in AF patients 
      with RA.
CI  - © The Author(s) 2024. Published by Oxford University Press on behalf of the 
      British Society for Rheumatology.
FAU - Kerola, Anne M
AU  - Kerola AM
AUID- ORCID: 0000-0003-2257-3291
AD  - Department of Rheumatology, Inflammation Center, Helsinki University Hospital and 
      University of Helsinki, Helsinki, Finland.
AD  - Department of Internal Medicine, Päijät-Häme Central Hospital, Lahti, Finland.
FAU - Ikdahl, Eirik
AU  - Ikdahl E
AD  - Department of Rheumatology, REMEDY-Centre for Treatment of Rheumatic and 
      Musculoskeletal Diseases, Diakonhjemmet Hospital, Oslo, Norway.
FAU - Engebretsen, Ingrid
AU  - Engebretsen I
AUID- ORCID: 0000-0001-9608-6731
AD  - Department of Health and Life science, Oslo Economics, Oslo, Norway.
FAU - Bugge, Christoffer
AU  - Bugge C
AUID- ORCID: 0000-0002-0766-2870
AD  - Department of Health and Life science, Oslo Economics, Oslo, Norway.
FAU - Semb, Anne Grete
AU  - Semb AG
AUID- ORCID: 0000-0003-2730-2853
AD  - Preventive Cardio-Rheuma Clinic, Section for Research and Innovation, 
      REMEDY-Centre for Treatment of Rheumatic and Musculoskeletal Diseases, 
      Diakonhjemmet Hospital, Oslo, Norway.
LA  - eng
GR  - Olav Thon's Foundation/
GR  - The Research Council of Norway/
GR  - FOREUM Foundation for Research in Rheumatology/
GR  - Women's College Hospital/
PT  - Journal Article
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
SB  - IM
MH  - Humans
MH  - *Atrial Fibrillation/epidemiology/complications
MH  - Norway/epidemiology
MH  - Female
MH  - Male
MH  - *Ischemic Stroke/epidemiology/etiology
MH  - *Registries
MH  - Aged
MH  - Middle Aged
MH  - *Arthritis, Rheumatoid/complications/epidemiology
MH  - Incidence
MH  - Risk Factors
MH  - Aged, 80 and over
MH  - Adult
PMC - PMC11534115
OTO - NOTNLM
OT  - RA
OT  - atrial fibrillation
OT  - competing risks
OT  - ischaemic stroke
OT  - registry study
EDAT- 2024/08/22 12:44
MHDA- 2024/11/04 22:24
PMCR- 2024/08/22
CRDT- 2024/08/22 08:33
PHST- 2024/04/05 00:00 [received]
PHST- 2024/07/26 00:00 [accepted]
PHST- 2024/11/04 22:24 [medline]
PHST- 2024/08/22 12:44 [pubmed]
PHST- 2024/08/22 08:33 [entrez]
PHST- 2024/08/22 00:00 [pmc-release]
AID - 7738813 [pii]
AID - keae458 [pii]
AID - 10.1093/rheumatology/keae458 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2024 Nov 1;63(11):2997-3005. doi: 
      10.1093/rheumatology/keae458.

PMID- 39116084
OWN - NLM
STAT- MEDLINE
DCOM- 20240808
LR  - 20240810
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 19
IP  - 8
DP  - 2024
TI  - Mortality and major adverse cardiovascular events after glucagon-like peptide-1 
      receptor agonist initiation in patients with immune-mediated inflammatory 
      diseases and type 2 diabetes: A population-based study.
PG  - e0308533
LID - 10.1371/journal.pone.0308533 [doi]
LID - e0308533
AB  - OBJECTIVE: To assess the risk of all-cause mortality and major adverse 
      cardiovascular events (MACE) in patients with immune-mediated inflammatory 
      diseases (IMIDs) and type 2 diabetes newly initiating glucagon-like peptide-1 
      receptor agonists (GLP-1-RAs) versus dipeptidyl peptidase-4 inhibitors (DPP-4is). 
      METHODS: We performed a population-based cohort study using administrative health 
      data from British Columbia. Patients with an IMID (i.e., rheumatoid arthritis, 
      psoriatic disease, ankylosing spondylitis, inflammatory bowel disease, or a 
      systemic autoimmune rheumatic disease) and type 2 diabetes who newly initiated a 
      GLP-1-RA or DPP-4i between January 1, 2010, and December 31, 2021 were identified 
      using ICD-9/10 codes. The primary outcome was all-cause mortality. Secondary 
      outcomes included MACE and its components (i.e., cardiovascular death, myocardial 
      infarction, and ischemic stroke). Cox proportional hazard regressions were used 
      with propensity score overlap weighting. The analysis was repeated in age- and 
      sex-matched adults without IMIDs. RESULTS: We identified 10,855 adults with IMIDs 
      and type 2 diabetes who newly initiated a GLP-1-RA or DPP-4i. All-cause mortality 
      rate was lower among initiators of GLP-1-RAs compared to initiators of DPP-4is, 
      with a weighted hazard ratio (HR) of 0.48 (95% confidence interval [CI], 
      0.31-0.75) and rate difference (RD) of -9.4 (95% CI, -16.0 to -2.7) per 1000 
      person-years. Rate of MACE was also lower with GLP-1-RA exposure (HR 0.66 
      [0.50-0.88], RD -10.5 [-20.4 to -0.8]). Effect sizes were similar in adults 
      without IMIDs. CONCLUSION: In patients with IMIDs and type 2 diabetes, GLP-1-RA 
      exposure is associated with a lower risk of all-cause mortality and MACE compared 
      to a cardioneutral active comparator.
CI  - Copyright: © 2024 Karacabeyli et al. This is an open access article distributed 
      under the terms of the Creative Commons Attribution License, which permits 
      unrestricted use, distribution, and reproduction in any medium, provided the 
      original author and source are credited.
FAU - Karacabeyli, Derin
AU  - Karacabeyli D
AUID- ORCID: 0000-0002-6597-0302
AD  - Division of Rheumatology, Department of Medicine, University of British Columbia, 
      Vancouver, British Columbia, Canada.
AD  - Arthritis Research Canada, Vancouver, British Columbia, Canada.
FAU - Lacaille, Diane
AU  - Lacaille D
AD  - Division of Rheumatology, Department of Medicine, University of British Columbia, 
      Vancouver, British Columbia, Canada.
AD  - Arthritis Research Canada, Vancouver, British Columbia, Canada.
FAU - Lu, Na
AU  - Lu N
AD  - Arthritis Research Canada, Vancouver, British Columbia, Canada.
FAU - McCormick, Natalie
AU  - McCormick N
AUID- ORCID: 0000-0002-4147-8348
AD  - Arthritis Research Canada, Vancouver, British Columbia, Canada.
AD  - Division of Rheumatology, Allergy, and Immunology, Department of Medicine, 
      Massachusetts General Hospital and Harvard Medical School, Boston, MA, United 
      States of America.
FAU - Xie, Hui
AU  - Xie H
AD  - Arthritis Research Canada, Vancouver, British Columbia, Canada.
AD  - Faculty of Health Sciences, Simon Fraser University, Burnaby, British Columbia, 
      Canada.
FAU - Choi, Hyon K
AU  - Choi HK
AD  - Arthritis Research Canada, Vancouver, British Columbia, Canada.
AD  - Division of Rheumatology, Allergy, and Immunology, Department of Medicine, 
      Massachusetts General Hospital and Harvard Medical School, Boston, MA, United 
      States of America.
FAU - Aviña-Zubieta, J Antonio
AU  - Aviña-Zubieta JA
AUID- ORCID: 0000-0001-5526-663X
AD  - Division of Rheumatology, Department of Medicine, University of British Columbia, 
      Vancouver, British Columbia, Canada.
AD  - Arthritis Research Canada, Vancouver, British Columbia, Canada.
LA  - eng
PT  - Journal Article
DEP - 20240808
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Glucagon-Like Peptide-1 Receptor)
RN  - 0 (Dipeptidyl-Peptidase IV Inhibitors)
RN  - 0 (Hypoglycemic Agents)
SB  - IM
MH  - Humans
MH  - *Diabetes Mellitus, Type 2/drug therapy/complications/mortality
MH  - Female
MH  - Male
MH  - *Glucagon-Like Peptide-1 Receptor/agonists
MH  - Middle Aged
MH  - Aged
MH  - *Cardiovascular Diseases/mortality
MH  - Dipeptidyl-Peptidase IV Inhibitors/therapeutic use/adverse effects
MH  - Adult
MH  - Inflammation
MH  - Cohort Studies
MH  - Hypoglycemic Agents/therapeutic use/adverse effects
MH  - British Columbia/epidemiology
MH  - Proportional Hazards Models
PMC - PMC11309412
COIS- The authors have declared that no competing interests exist. HKC reports research 
      support from Horizon and consulting fees from ANI and LG Chem outside of the 
      submitted work. HKC has participated on an advisory board for Shanton, unrelated 
      to the submitted work.
EDAT- 2024/08/08 18:42
MHDA- 2024/08/08 18:43
PMCR- 2024/08/08
CRDT- 2024/08/08 13:34
PHST- 2024/03/22 00:00 [received]
PHST- 2024/07/24 00:00 [accepted]
PHST- 2024/08/08 18:43 [medline]
PHST- 2024/08/08 18:42 [pubmed]
PHST- 2024/08/08 13:34 [entrez]
PHST- 2024/08/08 00:00 [pmc-release]
AID - PONE-D-24-11342 [pii]
AID - 10.1371/journal.pone.0308533 [doi]
PST - epublish
SO  - PLoS One. 2024 Aug 8;19(8):e0308533. doi: 10.1371/journal.pone.0308533. 
      eCollection 2024.

PMID- 39113098
OWN - NLM
STAT- MEDLINE
DCOM- 20240808
LR  - 20240809
IS  - 1757-6512 (Electronic)
IS  - 1757-6512 (Linking)
VI  - 15
IP  - 1
DP  - 2024 Aug 7
TI  - Therapeutic potential of adipose-derived stem cell extracellular vesicles: from 
      inflammation regulation to tissue repair.
PG  - 249
LID - 10.1186/s13287-024-03863-5 [doi]
LID - 249
AB  - Inflammation is a key pathological feature of many diseases, disrupting normal 
      tissue structure and resulting in irreversible damage. Despite the need for 
      effective inflammation control, current treatments, including stem cell 
      therapies, remain insufficient. Recently, extracellular vesicles secreted by 
      adipose-derived stem cells (ADSC-EVs) have garnered attention for their 
      significant anti-inflammatory properties. As carriers of bioactive substances, 
      these vesicles have demonstrated potent capabilities in modulating inflammation 
      and promoting tissue repair in conditions such as rheumatoid arthritis, 
      osteoarthritis, diabetes, cardiovascular diseases, stroke, and wound healing. 
      Consequently, ADSC-EVs are emerging as promising alternatives to conventional 
      ADSC-based therapies, offering advantages such as reduced risk of immune 
      rejection, enhanced stability, and ease of storage and handling. However, the 
      specific mechanisms by which ADSC-EVs regulate inflammation under pathological 
      conditions are not fully understood. This review discusses the role of ADSC-EVs 
      in inflammation control, their impact on disease prognosis, and their potential 
      to promote tissue repair. Additionally, it provides insights into future clinical 
      research focused on ADSC-EV therapies for inflammatory diseases, which overcome 
      some limitations associated with cell-based therapies.
CI  - © 2024. The Author(s).
FAU - Zhou, Bohuai
AU  - Zhou B
AD  - State Key Laboratory of Oral Diseases & National Clinical Research Center for 
      Oral Diseases & Engineering Research Center of Oral Translational Medicine, 
      Ministry of Education & National Engineering Laboratory for Oral Regenerative 
      Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, 
      610041, China.
AD  - Department of Oral and Maxillofacial Surgery, West China Hospital of Stomatology, 
      Sichuan University, Chengdu, 610041, China.
FAU - Chen, Qiuyu
AU  - Chen Q
AD  - State Key Laboratory of Oral Diseases & National Clinical Research Center for 
      Oral Diseases & Engineering Research Center of Oral Translational Medicine, 
      Ministry of Education & National Engineering Laboratory for Oral Regenerative 
      Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, 
      610041, China.
AD  - Department of Oral and Maxillofacial Surgery, West China Hospital of Stomatology, 
      Sichuan University, Chengdu, 610041, China.
FAU - Zhang, Qiuwen
AU  - Zhang Q
AD  - The Affiliated Stomatological Hospital Southwest Medical University, Luzhou, 
      646000, China.
FAU - Tian, Weidong
AU  - Tian W
AD  - State Key Laboratory of Oral Diseases & National Clinical Research Center for 
      Oral Diseases & Engineering Research Center of Oral Translational Medicine, 
      Ministry of Education & National Engineering Laboratory for Oral Regenerative 
      Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, 
      610041, China.
AD  - Department of Oral and Maxillofacial Surgery, West China Hospital of Stomatology, 
      Sichuan University, Chengdu, 610041, China.
FAU - Chen, Tian
AU  - Chen T
AD  - State Key Laboratory of Oral Diseases & National Clinical Research Center for 
      Oral Diseases & Engineering Research Center of Oral Translational Medicine, 
      Ministry of Education & National Engineering Laboratory for Oral Regenerative 
      Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, 
      610041, China. 907064309@qq.com.
AD  - Department of Orthodontics, West China Hospital of Stomatology, Sichuan 
      University, Chengdu, 610041, China. 907064309@qq.com.
FAU - Liu, Zhi
AU  - Liu Z
AD  - State Key Laboratory of Oral Diseases & National Clinical Research Center for 
      Oral Diseases & Engineering Research Center of Oral Translational Medicine, 
      Ministry of Education & National Engineering Laboratory for Oral Regenerative 
      Medicine, West China Hospital of Stomatology, Sichuan University, Chengdu, 
      610041, China. zliu830@163.com.
LA  - eng
GR  - 82100959/National Natural Science Foundation of China/
PT  - Journal Article
PT  - Review
DEP - 20240807
PL  - England
TA  - Stem Cell Res Ther
JT  - Stem cell research & therapy
JID - 101527581
SB  - IM
MH  - Humans
MH  - *Extracellular Vesicles/metabolism
MH  - *Inflammation/therapy/metabolism/pathology
MH  - *Adipose Tissue/cytology/metabolism
MH  - Animals
MH  - Stem Cells/metabolism/cytology
MH  - Wound Healing
PMC - PMC11304935
OTO - NOTNLM
OT  - Adipose-derived stem cell
OT  - Cell-free therapy
OT  - Extracellular vesicles
OT  - Inflammation control
OT  - Tissue repair
COIS- The authors declare no competing interest.
EDAT- 2024/08/08 00:42
MHDA- 2024/08/08 06:42
PMCR- 2024/08/07
CRDT- 2024/08/07 23:46
PHST- 2024/03/30 00:00 [received]
PHST- 2024/07/27 00:00 [accepted]
PHST- 2024/08/08 06:42 [medline]
PHST- 2024/08/08 00:42 [pubmed]
PHST- 2024/08/07 23:46 [entrez]
PHST- 2024/08/07 00:00 [pmc-release]
AID - 10.1186/s13287-024-03863-5 [pii]
AID - 3863 [pii]
AID - 10.1186/s13287-024-03863-5 [doi]
PST - epublish
SO  - Stem Cell Res Ther. 2024 Aug 7;15(1):249. doi: 10.1186/s13287-024-03863-5.

PMID- 39077648
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240731
IS  - 2153-8174 (Electronic)
IS  - 2153-8174 (Print)
IS  - 1530-6550 (Linking)
VI  - 25
IP  - 1
DP  - 2024 Jan
TI  - Prediction of Major Adverse Cardiovascular Events by Triglyceride Glucose Index 
      in Predominantly Male Patients with Rheumatoid Arthritis.
PG  - 28
LID - 10.31083/j.rcm2501028 [doi]
LID - 28
AB  - BACKGROUND: Rheumatoid arthritis (RA) is a systemic and chronic autoimmune 
      disease that is characterized by persistent joint inflammation. RA patients 
      experience a considerably increased risk of cardiovascular-related morbidity and 
      mortality. The current study investigated the association between triglyceride 
      glucose (TyG) index and major adverse cardiovascular events (MACEs) in a 
      predominantly male cohort of RA patients. METHODS: A total of 1613 RA patients 
      (81.53% male) were selected from the Kailuan study. The TyG index was calculated 
      as the logarithmic product of fasting blood triglyceride and fasting blood 
      glucose divided by two. MACEs were defined as the composite of non-fatal 
      myocardial infarctions and non-fatal strokes. Cox proportional hazards analysis 
      was performed to study the association between the TyG index and MACEs. RESULTS: 
      A total of 59 MACEs occurred during the median follow-up time of 5.32 years. 
      Following adjustment for age and gender, analysis by multivariable Cox 
      proportional hazards (model 1) showed that an elevated TyG index was associated 
      with an increased risk of MACEs (quartile 2, hazard ratio (HR): 2.741, 95% 
      confidence interval (CI): 1.220-6.157, p = 0.015; quartile 4, HR: 2.521, 95% CI: 
      1.074-5.917, p = 0.034). After adjustment for other variables, Cox proportional 
      hazards analysis (model 2) showed that an elevated TyG index was independently 
      associated with an increased risk of MACEs (quartile 2, HR: 2.348, 95% CI: 
      1.009-5.465, p = 0.048). In addition, subgroup analysis showed a higher TyG index 
      was significantly linked to an increased risk of MACEs in patients aged more than 
      65 years (quartile 2, HR: 6.048, 95% CI: 1.311-27.908, p = 0.021; quartile 4, HR: 
      12.074, 95% CI: 1.438-101.358, p = 0.022). CONCLUSIONS: The TyG index was 
      associated with an increased risk of MACEs in a predominantly male cohort of RA 
      patients. This index may be helpful for the prediction of MACEs in male patients 
      with RA. CLINICAL TRIAL REGISTRATION: Registration number in the Chinese clinical 
      trial registry: ChiCTR-TNRC-11001489.
CI  - Copyright: © 2024 The Author(s). Published by IMR Press.
FAU - Zhang, Jiawei
AU  - Zhang J
AD  - Department of Rehabilitation Medicine, Kailuan Tangjiazhuang Hospital, 063000 
      Tangshan, Hebei, China.
FAU - Hou, Qiqi
AU  - Hou Q
AD  - Hebei Medical University, 050017 Shijiazhuang, Hebei, China.
FAU - Han, Quanle
AU  - Han Q
AD  - Department of Cardiology, Tangshan Gongren Hospital, 063000 Tangshan, Hebei, 
      China.
FAU - Peng, Xu
AU  - Peng X
AD  - Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität 
      Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.
FAU - Cao, Hongxia
AU  - Cao H
AD  - Catheterization Unit, Tangshan Gongren Hospital, 063000 Tangshan, Hebei, China.
FAU - Wu, Shouling
AU  - Wu S
AD  - Department of Cardiology, Kailuan General Hospital, 063000 Tangshan, Hebei, 
      China.
AD  - School of Clinical Medicine, North China University of Science and Technology, 
      063000 Tangshan, Hebei, China.
FAU - Li, Kangbo
AU  - Li K
AD  - Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität 
      Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.
AD  - School of Clinical Medicine, North China University of Science and Technology, 
      063000 Tangshan, Hebei, China.
LA  - eng
PT  - Journal Article
DEP - 20240115
PL  - Singapore
TA  - Rev Cardiovasc Med
JT  - Reviews in cardiovascular medicine
JID - 100960007
PMC - PMC11262396
OTO - NOTNLM
OT  - cardiovascular disease
OT  - myocardial infarction
OT  - rheumatoid arthritis
OT  - stroke
OT  - triglyceride glucose index
COIS- The authors declare no conflict of interest.
EDAT- 2024/07/30 06:42
MHDA- 2024/07/30 06:43
PMCR- 2024/01/15
CRDT- 2024/07/30 05:09
PHST- 2023/08/01 00:00 [received]
PHST- 2023/09/01 00:00 [revised]
PHST- 2023/09/15 00:00 [accepted]
PHST- 2024/07/30 06:43 [medline]
PHST- 2024/07/30 06:42 [pubmed]
PHST- 2024/07/30 05:09 [entrez]
PHST- 2024/01/15 00:00 [pmc-release]
AID - S1530-6550(23)01149-3 [pii]
AID - 10.31083/j.rcm2501028 [doi]
PST - epublish
SO  - Rev Cardiovasc Med. 2024 Jan 15;25(1):28. doi: 10.31083/j.rcm2501028. eCollection 
      2024 Jan.

PMID- 39059285
OWN - NLM
STAT- MEDLINE
DCOM- 20240808
LR  - 20240808
IS  - 1872-6968 (Electronic)
IS  - 0303-8467 (Linking)
VI  - 244
DP  - 2024 Sep
TI  - Causal association between rheumatoid arthritis and risk of stroke: A Mendelian 
      randomization study.
PG  - 108465
LID - S0303-8467(24)00352-4 [pii]
LID - 10.1016/j.clineuro.2024.108465 [doi]
AB  - BACKGROUND: Active rheumatoid arthritis (RA) may damage vascular endothelial 
      cells, thereby increasing the likelihood of adverse cardiovascular events. 
      However, it is not yet clearly established whether RA also increases the risk of 
      adverse cerebrovascular events, particularly stroke. OBJECTIVE: This study was 
      designed to evaluate the likelihood of a causal association between RA and 
      stroke. METHOD: A two-sample Mendelian randomization (MR) analysis was performed 
      using the inverse variance-weighted (IVW) average, weighted median, and MR-Egger 
      regression methods. The analysis utilized publicly available summary statistics 
      datasets from Genome-wide association studies (GWAS) meta-analyses for RA in 
      individuals of European descent (total n = 484,598; case = 5427, control = 
      479,171) as the exposure cohort, and from GWAS meta-analyses for "vascular/heart 
      problems diagnosed by doctor: stroke" in individuals included in the UK Biobank 
      (total n = 461,880; case = 7055, control = 454,825, MRC-IEU consortium) as the 
      outcome cohort. RESULTS: Eight single-nucleotide polymorphisms with genome-wide 
      significance were selected from the GWASs on RA as the instrumental variables. 
      The results of the MR-Egger and weighted median analyses showed no causal 
      association between RA and stroke (OR = 1.081, 95 % CI [0.943-1.240], P = 0.304) 
      vs. OR = 1.079, 95 % CI [0.988-1.179], P = 0.091), respectively. However, the 
      inverse variance-weighted (IVW) analysis results revealed a causal association 
      between RA and stroke (OR = 1.115, 95 % CI [1.040-1.194], P = 0.002). Cochran's Q 
      test and MR-Egger regression revealed no evidence of heterogeneity and horizontal 
      pleiotropy. CONCLUSION: The MR analysis results indicated that rheumatoid 
      arthritis (RA) may be causally associated with an increased risk of stroke.
CI  - Copyright © 2024 Elsevier B.V. All rights reserved.
FAU - Qiang, Fuyong
AU  - Qiang F
AD  - Department of Rheumatism and Immunology, The First Affiliated Hospital of Wannan 
      Medical College, No. 2, Zheshan West Road, Jinghu District, Wuhu, Anhui 
      241001, China.
FAU - Xuan, Dan
AU  - Xuan D
AD  - Department of Rheumatism and Immunology, The First Affiliated Hospital of Wannan 
      Medical College, No. 2, Zheshan West Road, Jinghu District, Wuhu, Anhui 
      241001, China.
FAU - Li, Zhi
AU  - Li Z
AD  - Department of Rheumatism and Immunology, The First Affiliated Hospital of Wannan 
      Medical College, No. 2, Zheshan West Road, Jinghu District, Wuhu, Anhui 
      241001, China.
FAU - Chen, Lanfang
AU  - Chen L
AD  - Department of Rheumatism and Immunology, The First Affiliated Hospital of Wannan 
      Medical College, No. 2, Zheshan West Road, Jinghu District, Wuhu, Anhui 
      241001, China.
FAU - Wang, Li
AU  - Wang L
AD  - Department of Rheumatism and Immunology, The First Affiliated Hospital of Wannan 
      Medical College, No. 2, Zheshan West Road, Jinghu District, Wuhu, Anhui 
      241001, China.
FAU - Sheng, Jun
AU  - Sheng J
AD  - Department of Rheumatism and Immunology, The First Affiliated Hospital of Wannan 
      Medical College, No. 2, Zheshan West Road, Jinghu District, Wuhu, Anhui 
      241001, China. Electronic address: 476319700@qq.com.
LA  - eng
PT  - Journal Article
DEP - 20240721
PL  - Netherlands
TA  - Clin Neurol Neurosurg
JT  - Clinical neurology and neurosurgery
JID - 7502039
SB  - IM
MH  - Humans
MH  - *Arthritis, Rheumatoid/genetics/complications
MH  - *Mendelian Randomization Analysis
MH  - *Stroke/genetics/epidemiology
MH  - *Genome-Wide Association Study
MH  - *Polymorphism, Single Nucleotide/genetics
MH  - Risk Factors
MH  - Genetic Predisposition to Disease/genetics
OTO - NOTNLM
OT  - Mendelian randomization
OT  - Rheumatoid arthritis
OT  - Stroke
COIS- Conflict of interest The authors declare that they have no conflict of interest.
EDAT- 2024/07/27 10:42
MHDA- 2024/08/09 00:42
CRDT- 2024/07/26 18:09
PHST- 2024/07/04 00:00 [received]
PHST- 2024/07/20 00:00 [accepted]
PHST- 2024/08/09 00:42 [medline]
PHST- 2024/07/27 10:42 [pubmed]
PHST- 2024/07/26 18:09 [entrez]
AID - S0303-8467(24)00352-4 [pii]
AID - 10.1016/j.clineuro.2024.108465 [doi]
PST - ppublish
SO  - Clin Neurol Neurosurg. 2024 Sep;244:108465. doi: 10.1016/j.clineuro.2024.108465. 
      Epub 2024 Jul 21.

PMID- 39045492
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240725
IS  - 1178-2390 (Print)
IS  - 1178-2390 (Electronic)
IS  - 1178-2390 (Linking)
VI  - 17
DP  - 2024
TI  - Incidence Rate of Cardiovascular Events in Rheumatoid Arthritis: An Observational 
      Cohort Study in Saudi Arabia.
PG  - 3357-3370
LID - 10.2147/JMDH.S459555 [doi]
AB  - PURPOSE: Rheumatoid arthritis (RA) doubles the morbidity of cardiovascular 
      disease (CVD) and leads to a 50% increase in mortality compared to the general 
      population. This study aims to estimate the CVD incidence among RA patients in 
      Saudi Arabia (SA), vital for assessing CVD burdens within this group. PATIENTS 
      AND METHODS: This retrospective study took place at two centers in the Eastern 
      Province of SA, including all adult RA patients who visited the rheumatology 
      clinic from 2016 to 2021 and were prescribed disease-modifying antirheumatic 
      drugs (DMARDs). CVD incidence was determined by the diagnosis of ischemic heart 
      disease (IHD), stroke/transient ischemic attack (TIA), venous thromboembolism 
      (VTE), heart failure (HF), and arrhythmia post-RA diagnosis. Additional data 
      collected included demographics, CVD risk factors, comorbidities, RA-related 
      factors, and medication usage. RESULTS: The study comprised 651 patients, 80.5% 
      of whom were females with an average age of 51. The overall CVD incidence was 
      11.2 per 1000 person-years, with males experiencing five times more incidents 
      than females. The prevalence of CVD risk factors included 18.7% with 
      hypertension, 7.8% with hyperlipidemia, 18.9% with diabetes, and 42.9% with 
      obesity. Significant predictors of CVD were male gender and RA duration, with 
      adjusted odds ratios (aOR) of 3.17 (95% CI 1.10 to 9.14, P=0.033) and 64.81 (95% 
      CI 3.68 to 1140.6, P=0.004), respectively. CONCLUSION: This unique study from SA 
      examined the CVD incidence in RA patients, identifying long disease duration and 
      male gender as significant predictors. Effective reduction of CVD risk in RA 
      patients requires aggressive management of modifiable risk factors and regular 
      risk assessments.
CI  - © 2024 AlGhalawin et al.
FAU - AlGhalawin, Laila Saleh
AU  - AlGhalawin LS
AD  - Pharmaceutical Care Affairs, Dammam Medical Complex, Eastern Health Cluster, 
      Dammam, Saudi Arabia.
FAU - Alomar, Mukhtar
AU  - Alomar M
AD  - Pharmaceutical Care Affairs, Dammam Medical Complex, Eastern Health Cluster, 
      Dammam, Saudi Arabia.
FAU - Al Bassam, Shahad
AU  - Al Bassam S
AD  - Department of Pharmacy Practice, College of Clinical Pharmacy, Imam Abdulrahman 
      Bin Faisal University, Dammam, Saudi Arabia.
FAU - AlHamdan, Aqeelah Abdullah
AU  - AlHamdan AA
AD  - Pharmacy Department, Al-Mana General Hospital, Dammam, Saudi Arabia.
FAU - Anan, Hadeel
AU  - Anan H
AD  - Pharmaceutical Care and Formulary Management Affairs, Eastern Health Cluster, 
      Dammam, Saudi Arabia.
FAU - Altaweel, Marwah
AU  - Altaweel M
AD  - Pharmaceutical Care Affairs, Saud AlBabtain Cardiac Center, Eastern Health 
      Cluster, Dammam, Saudi Arabia.
FAU - Alomran, Zainab Abbas
AU  - Alomran ZA
AD  - Department of Pharmacy Practice, College of Clinical Pharmacy, King Faisal 
      University, Al-Ahsa, Saudi Arabia.
FAU - Al Khamis, Reem
AU  - Al Khamis R
AD  - Independent Researcher, Dammam, Saudi Arabia.
FAU - Alqatri, Asma Ibrahim
AU  - Alqatri AI
AD  - Pharmacy Department, Saudi German Hospital, Dammam, Saudi Arabia.
FAU - Alamoudi, Marwan M
AU  - Alamoudi MM
AD  - Rheumatology Department, Dammam Medical Complex, Eastern Health Cluster, Dammam, 
      Saudi Arabia.
FAU - Alamer, Ahmad
AU  - Alamer A
AD  - Department of Clinical Pharmacy, College of Pharmacy, Prince Sattam Bin Abdulaziz 
      University, Alkharj, Saudi Arabia.
LA  - eng
PT  - Journal Article
DEP - 20240712
PL  - New Zealand
TA  - J Multidiscip Healthc
JT  - Journal of multidisciplinary healthcare
JID - 101512691
PMC - PMC11264283
OTO - NOTNLM
OT  - anti-rheumatic
OT  - arrhythmia
OT  - autoimmune arthritis
OT  - cardio-rheumatology
OT  - cardiovascular
COIS- The authors report no conflicts of interest in this work.
EDAT- 2024/07/24 06:41
MHDA- 2024/07/24 06:42
PMCR- 2024/07/12
CRDT- 2024/07/24 04:25
PHST- 2024/02/21 00:00 [received]
PHST- 2024/06/12 00:00 [accepted]
PHST- 2024/07/24 06:42 [medline]
PHST- 2024/07/24 06:41 [pubmed]
PHST- 2024/07/24 04:25 [entrez]
PHST- 2024/07/12 00:00 [pmc-release]
AID - 459555 [pii]
AID - 10.2147/JMDH.S459555 [doi]
PST - epublish
SO  - J Multidiscip Healthc. 2024 Jul 12;17:3357-3370. doi: 10.2147/JMDH.S459555. 
      eCollection 2024.

PMID- 39043615
OWN - NLM
STAT- MEDLINE
DCOM- 20240723
LR  - 20240726
IS  - 2056-5933 (Electronic)
IS  - 2056-5933 (Linking)
VI  - 10
IP  - 3
DP  - 2024 Jul 23
TI  - Biological use influences the impact of inflammation on risk of major adverse 
      cardiovascular events in rheumatoid arthritis.
LID - 10.1136/rmdopen-2024-004546 [doi]
LID - e004546
AB  - OBJECTIVES: Chronic inflammation promotes cardiovascular risk in rheumatoid 
      arthritis (RA). Biological disease-modifying antirheumatic drugs (bDMARDs) 
      improve disease activity and cardiovascular disease outcomes. We explored whether 
      bDMARDs influence the impact of disease activity and inflammatory markers on 
      long-term cardiovascular risk in RA. METHODS: We studied 4370 participants 
      without cardiovascular disease in a 10-country observational cohort of patients 
      with RA. Endpoints were (1) major adverse cardiovascular events (MACE) 
      encompassing myocardial infarction, stroke and cardiovascular death; and (2) any 
      ischaemic cardiovascular events (iCVE) including MACE plus revascularisation, 
      angina, transient ischaemic attack and peripheral arterial disease. RESULTS: Over 
      26 534 patient-years, 239 MACE and 362 iCVE occurred. The interaction between 
      28-joint Disease Activity Score with C-reactive protein (DAS28-CRP) and bDMARD 
      use was significant for MACE (p=0.017), suggesting the effect of DAS28-CRP on 
      MACE risk differed among bDMARD users (n=515) and non-users (n=3855). DAS28-CRP 
      (per unit increase) is associated with MACE risk in bDMARD non-users (HR 1.21 
      (95% CI 1.07 to 1.37)) but not users (HR 0.69 (95% CI 0.40 to 1.20)). The 
      interaction between CRP (per log unit increase) and bDMARD use was also 
      significant for MACE (p=0.011). CRP associated with MACE risk in bDMARD non-users 
      (HR 1.16 (95% CI 1.04 to 1.30)), but not users (HR 0.65 (95% CI 0.36 to 1.17)). 
      No interaction was observed between bDMARD use and DAS28-CRP (p=0.167) or CRP 
      (p=0.237) for iCVE risk. CONCLUSIONS: RA activity and inflammatory markers 
      associated with risk of MACE in bDMARD non-users but not users suggesting the 
      possibility of biological-specific benefits locally on arterial wall 
      independently of effects on systemic inflammation.
CI  - © Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No 
      commercial re-use. See rights and permissions. Published by BMJ.
FAU - Karpouzas, George Athanasios
AU  - Karpouzas GA
AUID- ORCID: 0000-0003-1065-1563
AD  - Internal Medicine - Rheumatology, The Lundquist Institute, Torrance, California, 
      USA gkarpouzas@lundquist.org.
AD  - Rheumatology, Harbor-UCLA Medical Center, Torrance, California, USA.
FAU - Ormseth, Sarah R
AU  - Ormseth SR
AD  - The Lundquist Institute, Torrance, California, USA.
FAU - van Riel, Piet Leonardus Cornelis Maria
AU  - van Riel PLCM
AD  - IQ Healthcare, Radboud University, Nijmegen, Gelderland, Netherlands.
AD  - Rheumatology, Bernhoven Hospital Location Oss, Oss, Noord-Brabant, Netherlands.
FAU - Gonzalez-Gay, Miguel A
AU  - Gonzalez-Gay MA
AUID- ORCID: 0000-0002-7924-7406
AD  - Rheumatology, Hospital Universitario Marques de Valdecilla, Santander, Cantabria, 
      Spain.
AD  - IIS-Fundacion Jimenez Diaz, Madrid, Spain.
FAU - Corrales, Alfonso
AU  - Corrales A
AD  - Hospital Universitario Marques de Valdecilla, Santander, Cantabria, Spain.
FAU - Rantapää-Dahlqvist, Solbritt
AU  - Rantapää-Dahlqvist S
AUID- ORCID: 0000-0001-8259-3863
AD  - Department of Public Health and Clinical Medicine/Rheumatology, Umea Universitet, 
      Umea, Sweden.
FAU - Sfikakis, Petros P
AU  - Sfikakis PP
AD  - First Dept. of Propedeutic Medicine, University of Athens, Athens, Attica, 
      Greece.
FAU - Dessein, Patrick
AU  - Dessein P
AD  - School of Physiology, University of the Witwatersrand Johannesburg, Johannesburg, 
      South Africa.
FAU - Tsang, Linda
AU  - Tsang L
AD  - Vrije Universiteit Brussel, Brussel, Belgium.
FAU - Hitchon, Carol
AU  - Hitchon C
AD  - Rheumatology, University of Manitoba, Winnipeg, Manitoba, Canada.
FAU - El-Gabalawy, Hani
AU  - El-Gabalawy H
AD  - Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, 
      Canada.
FAU - Pascual-Ramos, Virginia
AU  - Pascual-Ramos V
AUID- ORCID: 0000-0002-7368-498X
AD  - Immunology and Rheumatology, Instituto Nacional de Ciencias Medicas y Nutricion 
      Salvador Zubiran, Mexico City, Mexico City, Mexico.
FAU - Contreras-Yáñez, Irazú
AU  - Contreras-Yáñez I
AD  - Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Medicas 
      y Nutricion Salvador Zubiran, Ciudad de Mexico, Mexico.
FAU - Colunga-Pedraza, Iris J
AU  - Colunga-Pedraza IJ
AUID- ORCID: 0000-0002-2786-5843
AD  - Rheumatology, Hospital Universitario Dr José Eleuterio González, Monterrey, Nuevo 
      León, Mexico.
FAU - Galarza-Delgado, Dionicio Angel
AU  - Galarza-Delgado DA
AUID- ORCID: 0000-0001-9714-2109
AD  - Rheumatology, Hospital Universitario Dr Jose Eleuterio Gonzalez, Monterrey, Nuevo 
      León, Mexico.
FAU - Azpiri-Lopez, Jose Ramon
AU  - Azpiri-Lopez JR
AD  - Hospital Universitario Dr José Eleuterio González, Monterrey, Nuevo León, Mexico.
FAU - Semb, Anne Grete
AU  - Semb AG
AUID- ORCID: 0000-0003-2730-2853
AD  - Rheumatology and Research, Diakonhjemmet Hospital, Oslo, Norway.
FAU - Misra, Durga Prasanna
AU  - Misra DP
AUID- ORCID: 0000-0002-5035-7396
AD  - Clinical Immunology and Rheumatology, Sanjay Gandhi Post Graduate Institute of 
      Medical Sciences, Lucknow, Uttar Pradesh, India.
FAU - Hauge, Ellen-Margrethe
AU  - Hauge EM
AD  - Department of Joint and Connective Tissue Diseases, Aarhus Universitetshospital, 
      Aarhus, Denmark.
AD  - Department of Clinical Medicine, Aarhus Universitet, Aarhus, Midtjylland, 
      Denmark.
FAU - Kitas, George
AU  - Kitas G
AD  - Department of Rheumatology, The Dudley Group NHS Foundation Trust, Dudley, West 
      Midlands, UK.
LA  - eng
PT  - Journal Article
PT  - Observational Study
DEP - 20240723
PL  - England
TA  - RMD Open
JT  - RMD open
JID - 101662038
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biomarkers)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Humans
MH  - *Arthritis, Rheumatoid/complications/drug therapy
MH  - Male
MH  - Female
MH  - Middle Aged
MH  - *Antirheumatic Agents/therapeutic use/adverse effects
MH  - *Cardiovascular Diseases/etiology/epidemiology/mortality
MH  - *Inflammation
MH  - Aged
MH  - Biomarkers
MH  - C-Reactive Protein/metabolism/analysis
MH  - Risk Factors
MH  - Severity of Illness Index
PMC - PMC11268070
OTO - NOTNLM
OT  - Arthritis, Rheumatoid
OT  - Biological Therapy
OT  - Cardiovascular Diseases
OT  - Inflammation
COIS- Competing interests: None declared.
EDAT- 2024/07/24 00:42
MHDA- 2024/07/24 00:43
PMCR- 2024/07/23
CRDT- 2024/07/23 22:33
PHST- 2024/05/16 00:00 [received]
PHST- 2024/07/05 00:00 [accepted]
PHST- 2024/07/24 00:43 [medline]
PHST- 2024/07/24 00:42 [pubmed]
PHST- 2024/07/23 22:33 [entrez]
PHST- 2024/07/23 00:00 [pmc-release]
AID - rmdopen-2024-004546 [pii]
AID - 10.1136/rmdopen-2024-004546 [doi]
PST - epublish
SO  - RMD Open. 2024 Jul 23;10(3):e004546. doi: 10.1136/rmdopen-2024-004546.

PMID- 39003659
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240822
IS  - 2193-8261 (Print)
IS  - 2193-6544 (Electronic)
IS  - 2193-6544 (Linking)
VI  - 13
IP  - 3
DP  - 2024 Sep
TI  - Prevalence of Tendon Rupture and Tendinopathies Among Patients with 
      Atherosclerotic Cardiovascular Disease Derived From United States Administrative 
      Claims Data.
PG  - 575-591
LID - 10.1007/s40119-024-00374-5 [doi]
AB  - INTRODUCTION: The prevalence of tendon rupture and tendinopathies (TRT) has not 
      been determined in a large population of patients with atherosclerotic 
      cardiovascular disease (ASCVD). We investigated TRT prevalence among patients 
      with ASCVD and in the general population, using data from the Symphony Health 
      Integrated Dataverse, a large US medical and pharmacy claims database. METHODS: 
      This retrospective, observational study included patients aged ≥ 19 years from 
      the claims database during the identification period (January 2019 to December 
      2020) and 12 months of continuous enrollment. The primary outcome was evidence of 
      TRT in the 12 months following the index date (first ASCVD diagnosis in the ASCVD 
      cohort; first claim in the claims database in the overall population). Diagnostic 
      codes (ICD-10 and/or CPT) were used to define ASCVD and TRT diagnosis. RESULTS: 
      The ASCVD cohort and overall population included 5,589,273 and 61,715,843 
      patients, respectively. In the ASCVD cohort, use of medications with a potential 
      or known association with TRT was identified in 67.9% (statins), 17.7% 
      (corticosteroids), and 16.7% (fluoroquinolones) of patients. Bempedoic acid use 
      was reported in 1556 (< 0.1%) patients. TRT prevalence during 12-month follow-up 
      was 3.4% (ASCVD cohort) and 1.9% (overall population). Among patients with ASCVD, 
      83.5% experienced TRT in only one region of the body. Factors most associated 
      with TRT in the ASCVD cohort were increasing age, most notably in those aged 
      45-‍64 years (odds ratio [OR] 2.19; 95% confidence interval [CI] 2.07-2.32), 
      obesity (OR 1.51; 95% CI 1.50-1.53), and rheumatoid arthritis (OR 1.47; 95% CI 
      1.45-1.79). Use of statins or bempedoic acid was not associated with increased 
      TRT risk. CONCLUSION: Patients with ASCVD may have greater risk of TRT than the 
      general population, which may be driven by an increased prevalence of 
      comorbidities and use of medications with a potential or known association with 
      TRT.
CI  - © 2024. The Author(s).
FAU - Gillard, Kristin K
AU  - Gillard KK
AUID- ORCID: 0000-0003-3342-2878
AD  - Esperion Therapeutics Inc., Ann Arbor, MI, USA. kristin.mariek@gmail.com.
AD  - , 245 Lindero Avenue, Long Beach, CA, 90803, USA. kristin.mariek@gmail.com.
FAU - Bloedon, LeAnne
AU  - Bloedon L
AD  - Esperion Therapeutics Inc., Ann Arbor, MI, USA.
FAU - Grady-Benson, John C
AU  - Grady-Benson JC
AD  - Orthopedic Associates of Hartford PC, Hartford, CT, USA.
AD  - Department of Orthopedic Surgery, The Bone and Joint Institute at Hartford 
      HealthCare, Hartford, CT, USA.
FAU - Edwards, Alison
AU  - Edwards A
AD  - Symphony Health, ICON Plc Company, Blue Bell, PA, USA.
FAU - Fahy, Sean
AU  - Fahy S
AD  - Symphony Health, ICON Plc Company, Blue Bell, PA, USA.
FAU - Sasiela, William J
AU  - Sasiela WJ
AD  - Esperion Therapeutics Inc., Ann Arbor, MI, USA.
FAU - Louie, Michael J
AU  - Louie MJ
AD  - Esperion Therapeutics Inc., Ann Arbor, MI, USA.
FAU - Thompson, Paul D
AU  - Thompson PD
AD  - Cardiovascular Institute, Hartford HealthCare, Hartford, CT, USA.
LA  - eng
PT  - Journal Article
DEP - 20240714
PL  - England
TA  - Cardiol Ther
JT  - Cardiology and therapy
JID - 101634495
PMC - PMC11333683
OAB - Patients with atherosclerosis, the main cause of heart attacks, strokes, and 
      peripheral vascular disease, typically require several drugs to control the 
      disease. Some of the drugs used to treat atherosclerosis have been linked to a 
      higher occurrence of tendon tears (or ruptures) or swelling/inflammation of the 
      tendons (tendinopathies). However, there may be other factors present in these 
      patients that increase the risk of tendon injuries that are not related to these 
      drugs. This study used the medical records of over 5.5 million patients with 
      atherosclerosis and over 63 million patients reflecting the general population in 
      the United States to determine the prevalence of tendon injury. Additionally, the 
      researchers looked at other factors that might be related to a higher risk of 
      tendon injury in each group. Over a 12-month period, tendon injuries occurred in 
      3.4% of patients with atherosclerosis and 1.8% of patients in the general 
      population. In patients with atherosclerosis, factors such as being obese, older 
      (45–64 years), or having rheumatoid arthritis were also linked to an increased 
      risk of tendon injuries. There was no association seen between statin or 
      bempedoic acid use and tendon injuries. These results may help healthcare 
      providers to determine the underlying risk of tendon injuries and guide treatment 
      of this patient population.
OABL- eng
OTO - NOTNLM
OT  - ASCVD
OT  - Medical claims database
OT  - Risk factors
OT  - Statins
OT  - Tendinopathies
OT  - Tendon rupture
COIS- Paul D. Thompson is on the Study Executive Committee for the CLEAR Outcomes 
      study, funded by Esperion Therapeutics, Inc. He receives research support to his 
      institution from Esperion and Novartis, has consulted for Esperion and Amgen, and 
      owns stock in AbbVie, Abbott Labs, CVS, General Electric, Johnson & Johnson, 
      Medtronic, Sarepta, and Shockwave Medical. LeAnne Bloedon is an employee of 
      Esperion Therapeutics, Inc. Michael J. Louie and Kristin K. Gillard were 
      employees of Esperion Therapeutics, Inc. at the time of the study, and are now 
      employees of UroGen Pharma and Bristol Myers Squibb, respectively. Alison Edwards 
      and Sean Fahy are employees of Symphony Health. John C. Grady-Benson has no 
      relevant conflicts of interest to declare. William J. Sasiela is a current 
      consultant for, and former employee of, Esperion Therapeutics, Inc. and may own 
      stock and/or stock options.
EDAT- 2024/07/14 12:45
MHDA- 2024/07/14 12:46
PMCR- 2024/07/14
CRDT- 2024/07/14 11:03
PHST- 2024/03/04 00:00 [received]
PHST- 2024/06/06 00:00 [accepted]
PHST- 2024/07/14 12:46 [medline]
PHST- 2024/07/14 12:45 [pubmed]
PHST- 2024/07/14 11:03 [entrez]
PHST- 2024/07/14 00:00 [pmc-release]
AID - 10.1007/s40119-024-00374-5 [pii]
AID - 374 [pii]
AID - 10.1007/s40119-024-00374-5 [doi]
PST - ppublish
SO  - Cardiol Ther. 2024 Sep;13(3):575-591. doi: 10.1007/s40119-024-00374-5. Epub 2024 
      Jul 14.

PMID- 38965838
OWN - NLM
STAT- Publisher
LR  - 20240705
IS  - 2005-6443 (Print)
IS  - 2005-6443 (Linking)
DP  - 2024 Jul 5
TI  - Association between Breakfast Consumption Frequency and Chronic Inflammation in 
      Korean Adult Males: Korea National Health and Nutrition Examination Survey 
      2016-2018.
LID - 10.4082/kjfm.23.0151 [doi]
AB  - BACKGROUND: Skipping breakfast is associated with an increased risk of chronic 
      inflammatory diseases. This study aimed to examine the association between 
      breakfast-eating habits and inflammation, using high-sensitivity C-reactive 
      protein (hs-CRP) as a marker. METHODS: A total of 4,000 Korean adult males with 
      no history of myocardial infarction, angina, stroke, diabetes, rheumatoid 
      arthritis, cancer, or current smoking were included. Data from the 2016-2018 
      Korea National Health and Nutrition Examination Survey were used for analysis. 
      The frequency of breakfast consumption was assessed through a questionnaire item 
      in the dietary survey section asking participants about their weekly breakfast 
      consumption routines over the past year. Participants were categorized into two 
      groups, namely "0-2 breakfasts per week" and "3-7 breakfasts per week"; hs-CRP 
      concentrations were measured through blood tests. RESULTS: Comparing between the 
      "infrequent breakfast consumption (0-2 breakfasts per week)" and "frequent 
      breakfast consumption (3-7 breakfasts per week)" groups, the mean hs-CRP was 
      found to be significantly higher in the "infrequent breakfast consumption" group, 
      even after adjusting for age, body mass index, physical activity, alcohol 
      consumption, systolic blood pressure, blood pressure medication, fasting blood 
      glucose, and triglycerides (mean hs-CRP: frequent breakfast consumption, 
      1.36±0.09 mg/L; infrequent breakfast consumption, 1.17±0.05 mg/L; P-value=0.036). 
      CONCLUSION: Less frequent breakfast consumption was associated with elevated 
      hs-CRP levels. Further large-scale studies incorporating adjusted measures of 
      daily eating patterns as well as food quality and quantity are required for a 
      deeper understanding of the role of breakfast in the primary prevention of 
      chronic inflammatory diseases.
FAU - Han, Eun Ji
AU  - Han EJ
AD  - Department of Family Medicine, Pusan National University Yangsan Hospital, 
      Yangsan, Korea.
FAU - Park, Eun Ju
AU  - Park EJ
AD  - Department of Family Medicine, Pusan National University Yangsan Hospital, 
      Yangsan, Korea.
FAU - Lee, Sae Rom
AU  - Lee SR
AD  - Department of Family Medicine, Pusan National University Yangsan Hospital, 
      Yangsan, Korea.
FAU - Lee, Sang Yeoup
AU  - Lee SY
AD  - Department of Family Medicine, Pusan National University Yangsan Hospital, 
      Yangsan, Korea.
AD  - Department of Medical Education, Pusan National University School of Medicine, 
      Yangsan, Korea.
FAU - Cho, Young Hye
AU  - Cho YH
AD  - Department of Family Medicine, Pusan National University Yangsan Hospital, 
      Yangsan, Korea.
AD  - Department of Medical Education, Pusan National University School of Medicine, 
      Yangsan, Korea.
FAU - Lee, Young In
AU  - Lee YI
AD  - Department of Family Medicine, Pusan National University Yangsan Hospital, 
      Yangsan, Korea.
FAU - Choi, Jung In
AU  - Choi JI
AD  - Department of Family Medicine, Pusan National University Yangsan Hospital, 
      Yangsan, Korea.
FAU - Kwon, Ryuk Jun
AU  - Kwon RJ
AD  - Department of Family Medicine, Pusan National University Yangsan Hospital, 
      Yangsan, Korea.
FAU - Son, Soo Min
AU  - Son SM
AD  - Department of Family Medicine, Pusan National University Yangsan Hospital, 
      Yangsan, Korea.
FAU - Kim, Yun Jin
AU  - Kim YJ
AD  - Department of Family Medicine, Pusan National University Hospital, Busan, Korea.
FAU - Lee, Jeong Gyu
AU  - Lee JG
AD  - Department of Family Medicine, Pusan National University Hospital, Busan, Korea.
FAU - Yi, Yu Hyeon
AU  - Yi YH
AD  - Department of Family Medicine, Pusan National University Hospital, Busan, Korea.
FAU - Tak, Young Jin
AU  - Tak YJ
AD  - Department of Family Medicine, Pusan National University Hospital, Busan, Korea.
FAU - Lee, Seung Hun
AU  - Lee SH
AD  - Department of Family Medicine, Pusan National University Hospital, Busan, Korea.
FAU - Kim, Gyu Lee
AU  - Kim GL
AD  - Department of Family Medicine, Pusan National University Hospital, Busan, Korea.
FAU - Ra, Young Jin
AU  - Ra YJ
AD  - Department of Family Medicine, Pusan National University Hospital, Busan, Korea.
LA  - eng
PT  - Journal Article
DEP - 20240705
PL  - Korea (South)
TA  - Korean J Fam Med
JT  - Korean journal of family medicine
JID - 101502902
OTO - NOTNLM
OT  - Breakfast Frequency
OT  - C-Reactive Protein
OT  - Cardiovascular Diseases
OT  - Chronic Inflammation
OT  - Metabolic Diseases
EDAT- 2024/07/05 06:42
MHDA- 2024/07/05 06:42
CRDT- 2024/07/05 02:22
PHST- 2023/08/28 00:00 [received]
PHST- 2024/01/16 00:00 [accepted]
PHST- 2024/07/05 06:42 [medline]
PHST- 2024/07/05 06:42 [pubmed]
PHST- 2024/07/05 02:22 [entrez]
AID - kjfm.23.0151 [pii]
AID - 10.4082/kjfm.23.0151 [doi]
PST - aheadofprint
SO  - Korean J Fam Med. 2024 Jul 5. doi: 10.4082/kjfm.23.0151.

PMID- 38923870
OWN - NLM
STAT- MEDLINE
DCOM- 20241029
LR  - 20241031
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Print)
IS  - 2326-5191 (Linking)
VI  - 76
IP  - 11
DP  - 2024 Nov
TI  - Association of Cardiovascular Outcomes With Low-Dose Glucocorticoid Prescription 
      in Patients With Rheumatoid Arthritis.
PG  - 1585-1593
LID - 10.1002/art.42928 [doi]
AB  - OBJECTIVE: Many guidelines recommend limiting glucocorticoids in patients with 
      rheumatoid arthritis (RA), but 40% of patients remain on glucocorticoids long 
      term. We evaluated the cardiovascular risk of long-term glucocorticoid 
      prescription by studying patients on stable disease-modifying antirheumatic drugs 
      (DMARDs). METHODS: Using two claims databases, we identified patients with RA on 
      stable DMARD therapy for >180 days. Proportional hazards models with 
      inverse-probability weights and clustering to account for multiple observations 
      were used to estimate the effect of glucocorticoid dose on composite 
      cardiovascular outcomes (stroke or myocardial infarction [MI]). RESULTS: There 
      were 135,583 patients in Medicare and 39,272 in Optum's de-identified 
      Clinformatics Data Mart (CDM) database. Medicare and CDM patients had an 
      incidence of 1.3 and 0.8 composite cardiovascular outcomes per 100 person-years, 
      respectively. In the older, comorbid Medicare cohort, glucocorticoids were 
      associated with a dose-dependent increase in composite cardiovascular outcomes in 
      adjusted models with predicted one-year incidence of 1.4% (95% confidence 
      interval [CI] 1.2%-1.6%) for ≤5 mg, 1.6% (95% CI 1.4%-1.9%) for >5 to 10 mg, and 
      1.8% (95% CI 1.2%-2.5%) for >10 mg versus 1.1% (95% CI 1.1%-1.2%) among patients 
      not receiving glucocorticoids. There was no significant association among the CDM 
      cohort. However, in the subgroup of younger patients with RA and higher 
      cardiovascular risk, glucocorticoids were associated with a dose-dependent 
      increase in composite cardiovascular outcomes. CONCLUSION: Among older patients 
      with more comorbidities and younger patients with higher cardiovascular risk with 
      RA on stable DMARD therapy, glucocorticoids were associated with a dose-dependent 
      increased risk of MI and stroke, even at doses ≤5 mg/day. By contrast, no 
      association was noted among younger, healthier patients with RA.
CI  - © 2024 The Author(s). Arthritis & Rheumatology published by Wiley Periodicals LLC 
      on behalf of American College of Rheumatology.
FAU - Coburn, Brian W
AU  - Coburn BW
AUID- ORCID: 0000-0002-0587-9478
AD  - University of Pennsylvania, Philadelphia.
FAU - Baker, Joshua F
AU  - Baker JF
AUID- ORCID: 0000-0003-0799-7563
AD  - University of Pennsylvania and Philadelphia Veterans Affairs Medical Center, 
      Philadelphia, Pennsylvania.
FAU - Hsu, Jesse Y
AU  - Hsu JY
AD  - University of Pennsylvania, Philadelphia.
FAU - Wu, Qufei
AU  - Wu Q
AD  - University of Pennsylvania, Philadelphia.
FAU - Xie, Fenglong
AU  - Xie F
AD  - University of Alabama at Birmingham, Birmingham.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AUID- ORCID: 0000-0002-8907-8976
AD  - University of Alabama at Birmingham, Birmingham.
FAU - George, Michael D
AU  - George MD
AUID- ORCID: 0000-0002-0398-2308
AD  - University of Pennsylvania, Philadelphia.
LA  - eng
GR  - P30 AR072583/AR/NIAMS NIH HHS/United States
GR  - P30-AR-072583/GF/NIH HHS/United States
GR  - K23 AR073931/AR/NIAMS NIH HHS/United States
GR  - K23-AR-073931-01/GF/NIH HHS/United States
GR  - National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)/
PT  - Journal Article
DEP - 20240723
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Glucocorticoids)
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Humans
MH  - *Arthritis, Rheumatoid/drug therapy/complications
MH  - *Glucocorticoids/adverse effects/therapeutic use/administration & dosage
MH  - Male
MH  - Female
MH  - Aged
MH  - Middle Aged
MH  - *Antirheumatic Agents/therapeutic use/adverse effects/administration & dosage
MH  - United States/epidemiology
MH  - *Myocardial Infarction/epidemiology/chemically induced
MH  - Medicare/statistics & numerical data
MH  - Cardiovascular Diseases/epidemiology/chemically induced
MH  - Incidence
MH  - Stroke/epidemiology
MH  - Dose-Response Relationship, Drug
MH  - Proportional Hazards Models
MH  - Adult
PMC - PMC11521768
MID - NIHMS2002990
EDAT- 2024/06/26 18:42
MHDA- 2024/10/29 06:23
PMCR- 2025/11/01
CRDT- 2024/06/26 13:25
PHST- 2024/04/13 00:00 [revised]
PHST- 2023/11/14 00:00 [received]
PHST- 2024/05/31 00:00 [accepted]
PHST- 2025/11/01 00:00 [pmc-release]
PHST- 2024/10/29 06:23 [medline]
PHST- 2024/06/26 18:42 [pubmed]
PHST- 2024/06/26 13:25 [entrez]
AID - 10.1002/art.42928 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2024 Nov;76(11):1585-1593. doi: 10.1002/art.42928. Epub 2024 
      Jul 23.

PMID- 38918258
OWN - NLM
STAT- Publisher
LR  - 20240625
IS  - 1435-1250 (Electronic)
IS  - 0340-1855 (Linking)
DP  - 2024 Jun 25
TI  - All-cause and cause-specific mortality in rheumatoid arthritis: a meta-analysis.
LID - 10.1007/s00393-024-01538-3 [doi]
AB  - OBJECTIVE: This study aimed to evaluate standardized mortality ratios (SMRs) for 
      both all-cause and cause-specific mortality in patients with rheumatoid arthritis 
      (RA). METHODS: We conducted an extensive search across the Medline, Embase, and 
      Cochrane databases to identify studies investigating SMRs for all-cause and/or 
      cause-specific mortality in individuals with RA compared to the general 
      population. Subsequently, we performed a comprehensive meta-analysis, examining 
      SMRs across various categories, including all-cause, sex-specific, 
      ethnicity-specific, and cause-specific SMRs in RA patients. RESULTS: Seventeen 
      studies involving 486,098 patients with RA and 63,988 deaths met the inclusion 
      criteria. Patients with RA had a 1.522-fold increase in all-cause SMR (SMR 1.522, 
      95% CI 1.340-1.704, p < 0.001) compared to the general population. Stratification 
      by ethnicity revealed that the all-cause SMR was 1.575 (95% CI 1.207-1.943) in 
      Caucasians and 1.355 (95% CI 1.140-1.569) in Asians. The gender-specific 
      meta-analysis revealed elevated SMR in both women and men. RA patients exhibited 
      an increased risk of mortality attributed to cardiovascular disease (CVD), 
      respiratory disease, infection, and cerebrovascular accidents (CVA). However, no 
      significant increase in SMR was observed for mortality due to malignancy. 
      CONCLUSION: This meta-analysis study highlights a 1.522-fold increase in SMR in 
      patients with RA compared to that in the general population, irrespective of sex 
      or region. Additionally, a notable increase in mortality associated with specific 
      causes, including CVD, respiratory disease, infection, and CVA, underscores the 
      critical need for targeted interventions to manage these heightened risks in 
      patients with RA.
CI  - © 2024. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, 
      ein Teil von Springer Nature.
FAU - Lee, Young Ho
AU  - Lee YH
AD  - Department of Rheumatology, Korea University Anam Hospital, Korea University 
      College of Medicine, 73, Goryeodae-ro, Seongbuk-gu, 02841, Seoul, Korea (Republic 
      of). lyhcgh@korea.ac.kr.
FAU - Song, Gwan Gyu
AU  - Song GG
AD  - Department of Rheumatology, Korea University Anam Hospital, Korea University 
      College of Medicine, 73, Goryeodae-ro, Seongbuk-gu, 02841, Seoul, Korea (Republic 
      of).
LA  - eng
PT  - Journal Article
TT  - Gesamtmortalität und ursachenspezifische Mortalität bei rheumatoider Arthritis: 
      eine Metaanalyse.
DEP - 20240625
PL  - Germany
TA  - Z Rheumatol
JT  - Zeitschrift fur Rheumatologie
JID - 0414162
SB  - IM
OTO - NOTNLM
OT  - Metaanalyse
OT  - Mortalität
OT  - Rheumatoide Arthritis
OT  - Standardisierte Sterblichkeitsquote
OT  - Systematische Überprüfung
EDAT- 2024/06/26 00:42
MHDA- 2024/06/26 00:42
CRDT- 2024/06/25 23:15
PHST- 2024/06/01 00:00 [accepted]
PHST- 2024/06/26 00:42 [medline]
PHST- 2024/06/26 00:42 [pubmed]
PHST- 2024/06/25 23:15 [entrez]
AID - 10.1007/s00393-024-01538-3 [pii]
AID - 10.1007/s00393-024-01538-3 [doi]
PST - aheadofprint
SO  - Z Rheumatol. 2024 Jun 25. doi: 10.1007/s00393-024-01538-3.

PMID- 38886005
OWN - NLM
STAT- MEDLINE
DCOM- 20240617
LR  - 20240901
IS  - 2056-5933 (Electronic)
IS  - 2056-5933 (Linking)
VI  - 10
IP  - 2
DP  - 2024 Jun 17
TI  - Increased risk of cardiovascular events under the treatments with Janus kinase 
      inhibitors versus biological disease-modifying antirheumatic drugs in patients 
      with rheumatoid arthritis: a retrospective longitudinal population-based study 
      using the Japanese health insurance database.
LID - 10.1136/rmdopen-2023-003885 [doi]
LID - e003885
AB  - OBJECTIVES: To compare the risk of cardiovascular events among Janus kinase 
      inhibitors (JAKIs), biological disease-modifying antirheumatic drugs (bDMARDs) 
      (tumour necrosis factor inhibitors (TNFIs) and non-TNFIs) and methotrexate (MTX) 
      in Japanese patients with rheumatoid arthritis (RA). METHODS: Using Japanese 
      claims data, patients with RA were enrolled in this study if they had at least 
      one ICD-10 code (M05 or M06), were new users of JAKIs, bDMARDs or MTX between 
      July 2013 and July 2020 and being 18 years old or older. The incidence rate (IR), 
      IR ratio and adjusted hazard ratio (aHR (95% CI)) of cardiovascular events 
      including venous thromboembolism, arterial thrombosis, acute myocardial 
      infarction and stroke were calculated. A time-dependent Cox regression model 
      adjusted for patient characteristics at baseline was used to calculate aHR. 
      RESULTS: In 53 448 cases, IRs/1000 patient-years of the overall cardiovascular 
      events were 10.1, 6.8, 5.4, 9.1 and 11.3 under the treatments with JAKIs, 
      bDMARDs, TNFIs, non-TNFIs and MTX, respectively. The adjusted HRs of JAKIs for 
      overall cardiovascular events were 1.7 (1.1 to 2.5) versus TNFIs without MTX and 
      1.7 (1.1 to 2.7) versus TNFIs with MTX. CONCLUSIONS: Among patients with RA, 
      individuals using JAKIs had a significantly higher risk of overall cardiovascular 
      events than TNFIs users, which was attributed to the difference in the risk 
      between JAKIs and TNFIs versus MTX. These data should be interpreted with caution 
      because of the limitations associated with the claims database.
CI  - © Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No 
      commercial re-use. See rights and permissions. Published by BMJ.
FAU - Sakai, Ryoko
AU  - Sakai R
AUID- ORCID: 0000-0002-1640-1373
AD  - Department of Publich Health and Epidemiology, Meiji Pharmaceutical University, 
      Kiyose, Tokyo, Japan.
AD  - Division of Rheumatology, Department of Internal Medicine, Tokyo Women's Medical 
      University School of Medicine, Shinjuku-ku, Tokyo, Japan.
FAU - Tanaka, Eiichi
AU  - Tanaka E
AD  - Division of Rheumatology, Department of Internal Medicine, Tokyo Women's Medical 
      University School of Medicine, Shinjuku-ku, Tokyo, Japan.
AD  - Institute of Rheumatology, Tokyo Women's Medical University Hospital, 
      Shinjuku-ku, Tokyo, Japan.
FAU - Inoue, Eisuke
AU  - Inoue E
AD  - Showa University Research Administration Center, Showa University, Shinagawa-ku, 
      Tokyo, Japan.
FAU - Harigai, Masayoshi
AU  - Harigai M
AUID- ORCID: 0000-0002-6418-2603
AD  - Division of Rheumatology, Department of Internal Medicine, Tokyo Women's Medical 
      University School of Medicine, Shinjuku-ku, Tokyo, Japan 
      harigai.masayoshi@twmu.ac.jp.
AD  - Institute of Rheumatology, Tokyo Women's Medical University Hospital, 
      Shinjuku-ku, Tokyo, Japan.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20240617
PL  - England
TA  - RMD Open
JT  - RMD open
JID - 101662038
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Janus Kinase Inhibitors)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Antirheumatic Agents/therapeutic use/adverse effects
MH  - *Arthritis, Rheumatoid/drug therapy/complications
MH  - *Cardiovascular Diseases/epidemiology/etiology
MH  - Databases, Factual
MH  - East Asian People
MH  - Incidence
MH  - Insurance, Health
MH  - *Janus Kinase Inhibitors/therapeutic use/adverse effects
MH  - Japan/epidemiology
MH  - Longitudinal Studies
MH  - *Methotrexate/therapeutic use/adverse effects
MH  - Retrospective Studies
MH  - Risk Factors
PMC - PMC11184193
OTO - NOTNLM
OT  - arthritis, rheumatoid
OT  - biological therapy
OT  - cardiovascular diseases
OT  - epidemiology
COIS- Competing interests: Ryoko Sakai has nothing to declare. Eiichi Tanaka has 
      received research funding from Pfizer Inc., UCB Japan Co. Ltd, and has received 
      lecture fees or consulting fees from AbbVie, Asahi Kasei Pharma Co., Astellas 
      Pharmaceutical, Ayumi Pharmaceutical, Boehringer Ingelheim Japan, Inc., Bristol 
      Myers Squibb Co., Ltd., Chugai Pharmaceutical, Daiichi-Sankyo, Inc., Eisai 
      Pharmaceutical, Eli Lilly Japan K.K., Gilead Sciences, Inc., GlaxoSmithKline 
      K.K., Kyowa Pharma Chemical Co., Ltd., Janssen Pharmaceutical K.K., Mitsubishi 
      Tanabe Pharma Co., Mochida Pharmaceutical Co., Ltd., Nippon Kayaku Co., Ltd., 
      Pfizer Japan Inc., Takeda Pharmaceutical, and Teijin Pharma Ltd., and Viatris 
      Japan. Eisuke Inoue has received lecture fees or consulting fees from Nippn tect 
      systems Co., Ltd., Cyberdine Inc., Bristol-Myers Squibb, Eisai Co., Ltd., and 
      Chugai Pharmaceutical Co., Ltd. Masayoshi Harigai has received grants or contacts 
      from AbbVie Japan GK, Asahi Kasei Corp., Boehringer Ingelheim Japan, Inc., Eli 
      Lilly Japan K.K., Kaken Pharmaceutical Co., Mitsubishi 16 Tanabe Pharma Co., 
      Mochida Pharmaceutical Co., Nippon Shinyaku Co., Ltd., Taisho Pharmaceutical Co., 
      Ltd., Teijin Pharma Ltd., UCB Japan Co., Ltd., and Viatris Japan, and has 
      received lecture fees or consulting fees from Bristol Myers Squibb Co., Ltd., Ono 
      Pharmaceutical Co., Ltd., Eli Lilly Japan K.K., AbbVie Japan GK, AbbVie Japan GK, 
      Asahi Kasei Corp., Ayumi Pharmaceutical Co., Bristol Myers Squibb Co., Ltd., 
      Chugai Pharmaceutical Co., Ltd., Eisai Co., Ltd., Gilead Sciences Inc., Janssen 
      Pharmaceutical K.K., Mitsubishi Tanabe Pharma Co., Taisho Pharmaceutical Co., 
      Ltd., Teijin Pharma Ltd and UCB Japan.
EDAT- 2024/06/18 00:43
MHDA- 2024/06/18 00:44
PMCR- 2024/06/17
CRDT- 2024/06/17 20:33
PHST- 2023/12/18 00:00 [received]
PHST- 2024/05/31 00:00 [accepted]
PHST- 2024/06/18 00:44 [medline]
PHST- 2024/06/18 00:43 [pubmed]
PHST- 2024/06/17 20:33 [entrez]
PHST- 2024/06/17 00:00 [pmc-release]
AID - rmdopen-2023-003885 [pii]
AID - 10.1136/rmdopen-2023-003885 [doi]
PST - epublish
SO  - RMD Open. 2024 Jun 17;10(2):e003885. doi: 10.1136/rmdopen-2023-003885.

PMID- 38832312
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240607
IS  - 2297-055X (Print)
IS  - 2297-055X (Electronic)
IS  - 2297-055X (Linking)
VI  - 11
DP  - 2024
TI  - Anti-apolipoprotein A-1 IgG, incident cardiovascular events, and lipid paradox in 
      rheumatoid arthritis.
PG  - 1386192
LID - 10.3389/fcvm.2024.1386192 [doi]
LID - 1386192
AB  - OBJECTIVE: To validate the prognostic accuracy of anti-apolipoprotein A-1 (AAA1) 
      IgG for incident major adverse cardiovascular (CV) events (MACE) in rheumatoid 
      arthritis (RA) and study their associations with the lipid paradox at a 
      multicentric scale. METHOD: Baseline AAA1 IgG, lipid profile, atherogenic 
      indexes, and cardiac biomarkers were measured on the serum of 1,472 patients with 
      RA included in the prospective Swiss Clinical Quality Management registry with a 
      median follow-up duration of 4.4 years. MACE was the primary endpoint defined as 
      CV death, incident fatal or non-fatal stroke, or myocardial infarction (MI), 
      while elective coronary revascularization (ECR) was the secondary endpoint. 
      Discriminant accuracy and incidence rate ratios (IRR) were respectively assessed 
      using C-statistics and Poisson regression models. RESULTS: During follow-up, 2.4% 
      (35/1,472) of patients had a MACE, consisting of 6 CV deaths, 11 MIs, and 18 
      strokes; ECR occurred in 2.1% (31/1,472) of patients. C-statistics indicated that 
      AAA1 had a significant discriminant accuracy for incident MACE [C-statistics: 
      0.60, 95% confidence interval (95% CI): 0.57-0.98, p = 0.03], mostly driven by CV 
      deaths (C-statistics: 0.77; 95% CI: 0.57-0.98, p = 0.01). IRR indicated that each 
      unit of AAA1 IgG increase was associated with a fivefold incident CV death rate, 
      independent of models' adjustments. At the predefined and validated cut-off, AAA1 
      displayed negative predictive values above 97% for MACE. AAA1 inversely 
      correlated with total and HDL cholesterol. CONCLUSIONS: AAA1 independently 
      predicts CV deaths, and marginally MACE in RA. Further investigations are 
      requested to ascertain whether AAA1 could enhance CV risk stratification by 
      identifying patients with RA at low CV risk.
CI  - © 2024 Mongin, Pagano, Lamacchia, Juillard, Antinori-Malaspina, Dan, Ciurea, 
      Möller, Gabay, Finckh and Vuilleumier.
FAU - Mongin, Denis
AU  - Mongin D
AD  - Division of Rheumatology, Geneva University Hospital and Faculty of Medicine, 
      University of Geneva, Geneva, Switzerland.
FAU - Pagano, Sabrina
AU  - Pagano S
AD  - Division of Laboratory Medicine, Department of Diagnostics and of Medical 
      Specialties, Geneva University Hospitals and Geneva University, Geneva, 
      Switzerland.
FAU - Lamacchia, Celine
AU  - Lamacchia C
AD  - Division of Rheumatology, Geneva University Hospital and Faculty of Medicine, 
      University of Geneva, Geneva, Switzerland.
FAU - Juillard, Catherine
AU  - Juillard C
AD  - Division of Laboratory Medicine, Department of Diagnostics and of Medical 
      Specialties, Geneva University Hospitals and Geneva University, Geneva, 
      Switzerland.
FAU - Antinori-Malaspina, Paola
AU  - Antinori-Malaspina P
AD  - Division of Laboratory Medicine, Department of Diagnostics and of Medical 
      Specialties, Geneva University Hospitals and Geneva University, Geneva, 
      Switzerland.
FAU - Dan, Diana
AU  - Dan D
AD  - Division of Rheumatology, Lausanne University Hospital and Faculty of Medicine, 
      University of Lausanne, Lausanne, Switzerland.
FAU - Ciurea, Adrian
AU  - Ciurea A
AD  - Division of Rheumatology, Zurich University Hospital and Faculty of Medicine, 
      University of Zurich, Zurich, Switzerland.
FAU - Möller, Burkhard
AU  - Möller B
AD  - Division of Rheumatology and Immunology, Bern University Hospital and Faculty of 
      Medicine, University of Bern, Bern, Switzerland.
FAU - Gabay, Cem
AU  - Gabay C
AD  - Division of Rheumatology, Geneva University Hospital and Faculty of Medicine, 
      University of Geneva, Geneva, Switzerland.
FAU - Finckh, Axel
AU  - Finckh A
AD  - Division of Rheumatology, Geneva University Hospital and Faculty of Medicine, 
      University of Geneva, Geneva, Switzerland.
FAU - Vuilleumier, Nicolas
AU  - Vuilleumier N
AD  - Division of Laboratory Medicine, Department of Diagnostics and of Medical 
      Specialties, Geneva University Hospitals and Geneva University, Geneva, 
      Switzerland.
LA  - eng
PT  - Journal Article
DEP - 20240520
PL  - Switzerland
TA  - Front Cardiovasc Med
JT  - Frontiers in cardiovascular medicine
JID - 101653388
PMC - PMC11144907
OTO - NOTNLM
OT  - anti-apolipoprotein A-1 IgG
OT  - autoantibodies
OT  - cardiovascular disease
OT  - major adverse cardiovascular events
OT  - rheumatoid arthritis
COIS- AF and DD have received consultancies from AbbVie, AstraZeneca, BMS, Lilly, 
      Pfizer, and UCB; and research support to their institution from AbbVie, BMS, 
      Galapagos, Lilly, and Pfizer. NV declared to be president of the FAMH 
      (Association of Medical Laboratories of Switzerland) and past president of the 
      Swiss Society of Clinical Chemistry. No other relationships or activities appear 
      to have influenced the submitted work. NV and SP are named as co-inventors of the 
      patent related to cterA1, peptide (“Mimetic peptides for prognosis, diagnosis or 
      treatment of a cardiovascular disease”, No. P1347EP00). The remaining authors 
      declare that the research was conducted in the absence of any commercial or 
      financial relationships that could be construed as a potential conflict of 
      interest. The authors declared that they were an editorial board member of 
      Frontiers at the time of submission. This had no impact on the peer review 
      process and the final decision.
EDAT- 2024/06/04 06:42
MHDA- 2024/06/04 06:43
PMCR- 2024/01/01
CRDT- 2024/06/04 03:46
PHST- 2024/02/14 00:00 [received]
PHST- 2024/04/24 00:00 [accepted]
PHST- 2024/06/04 06:43 [medline]
PHST- 2024/06/04 06:42 [pubmed]
PHST- 2024/06/04 03:46 [entrez]
PHST- 2024/01/01 00:00 [pmc-release]
AID - 10.3389/fcvm.2024.1386192 [doi]
PST - epublish
SO  - Front Cardiovasc Med. 2024 May 20;11:1386192. doi: 10.3389/fcvm.2024.1386192. 
      eCollection 2024.

PMID- 38829806
OWN - NLM
STAT- MEDLINE
DCOM- 20240603
LR  - 20240614
IS  - 0040-3660 (Print)
IS  - 0040-3660 (Linking)
VI  - 96
IP  - 5
DP  - 2024 Jun 3
TI  - [The effect of hypothyroidism on cardiovascular events and type 2 diabetes 
      mellitus developing in rheumatoid arthritis].
PG  - 459-464
LID - 10.26442/00403660.2024.05.202700 [doi]
AB  - AIM: To compare the frequency of cardiovascular events (CVE), to assess the risk 
      of cardiovascular death using the mSCORE and the development of type 2 diabetes 
      mellitus (DM) using the FINDRISC in patients with rheumatoid arthritis (RA) with 
      and without hypothyroidism. MATERIALS AND METHODS: The study included 149 
      patients (125 women, 24 men) with RA (median age - 57 [52; 61] years). In all 
      patients, traditional factors of cardiovascular risk and glucose metabolism 
      disorders (age, smoking status, total blood cholesterol, blood pressure, 
      overweight, abdominal obesity - AO, heredity burdened by diabetes, insufficient 
      physical activity, the lack of the necessary amount of berries, fruits and 
      vegetables in the daily diet, history of hyperglycemia episodes), the 10-year 
      risk of death from cardiovascular causes according to the mSCORE and the risk of 
      developing type 2 DM according to the FINDRISС were assessed, a history of CVE 
      (myocardial infarctions, and its revascularization, stroke) was recorded. 
      RESULTS: Hypothyroidism was diagnosed in 17.4% of RA patients. Patients with 
      hypothyroidism (group 1) were more likely to have AO and less likely to consume 
      unsufficient dietary fiber than patients with euthyroidism (group 2). Moderate, 
      high and very high risk of development according to the mSCORE and FINDRISC was 
      detected in 61.5% of hypothyroid patients and 48.8% euthyroid patients, according 
      to mSCORE alone - in 30.8 and 44.7%, according to FINDRISC - in 0 and 2.4%, 
      respectively (p>0.05 in all cases); 11.5% of patients in group 1 and 6.5% in 
      group 2 suffered from CVE (OR 1.875, 95% CI 0.462-7.607; p=0.63). CONCLUSION: It 
      is necessary to evaluate the thyroid gland function, especially in patients with 
      AO due to the high frequency of hypothyroidism in RA. Hypothyroidism did not have 
      an independent effect on the severe CVЕ rates, as well as risk assessment 
      according to the score and FINDRISC in RA patients. Theses, with and without 
      hypothyroidism, were predominantly in the moderate, high, very high risk groups 
      according to both scales.
FAU - Kondratyeva, L V
AU  - Kondratyeva LV
AUID- ORCID: 0000-0003-1147-5936
AD  - Nasonova Research Institute of Rheumatology.
FAU - Popkova, T V
AU  - Popkova TV
AUID- ORCID: 0000-0001-5793-4689
AD  - Nasonova Research Institute of Rheumatology.
FAU - Nasonov, E L
AU  - Nasonov EL
AUID- ORCID: 0000-0002-1598-8360
AD  - Nasonova Research Institute of Rheumatology.
AD  - Sechenov First Moscow State Medical University (Sechenov University).
LA  - rus
PT  - English Abstract
PT  - Journal Article
DEP - 20240603
PL  - Russia (Federation)
TA  - Ter Arkh
JT  - Terapevticheskii arkhiv
JID - 2984818R
SB  - IM
MH  - Humans
MH  - *Arthritis, Rheumatoid/complications/epidemiology
MH  - *Diabetes Mellitus, Type 2/complications/epidemiology
MH  - Female
MH  - *Hypothyroidism/epidemiology/complications
MH  - Middle Aged
MH  - Male
MH  - *Cardiovascular Diseases/etiology/epidemiology
MH  - Risk Factors
MH  - Risk Assessment/methods
MH  - Ukraine/epidemiology
OTO - NOTNLM
OT  - FINDRISC
OT  - cardiovascular events
OT  - diabetes mellitus
OT  - hypothyroidism
OT  - mSCORE
OT  - rheumatoid arthritis
OT  - risk
OT  - scale
EDAT- 2024/06/03 18:42
MHDA- 2024/06/03 18:43
CRDT- 2024/06/03 13:13
PHST- 2024/05/15 00:00 [received]
PHST- 2024/05/16 00:00 [accepted]
PHST- 2024/06/03 18:43 [medline]
PHST- 2024/06/03 18:42 [pubmed]
PHST- 2024/06/03 13:13 [entrez]
AID - 10.26442/00403660.2024.05.202700 [doi]
PST - epublish
SO  - Ter Arkh. 2024 Jun 3;96(5):459-464. doi: 10.26442/00403660.2024.05.202700.

PMID- 38772185
OWN - NLM
STAT- MEDLINE
DCOM- 20240627
LR  - 20240627
IS  - 1532-866X (Electronic)
IS  - 0049-0172 (Linking)
VI  - 67
DP  - 2024 Aug
TI  - Adverse cardiovascular events in rheumatoid arthritis patients treated with JAK 
      inhibitors: An analysis of postmarketing spontaneous safety reports.
PG  - 152461
LID - S0049-0172(24)00101-X [pii]
LID - 10.1016/j.semarthrit.2024.152461 [doi]
AB  - OBJECTIVES: The ORAL Surveillance trial, a postmarketing safety clinical trial, 
      found an increased risk of adverse cardiovascular events and venous 
      thromboembolism (VTE) in patients treated with Janus Kinase (JAK) inhibitors 
      compared to tumor necrosis factor (TNF) inhibitors. However, additional studies 
      yielded mixed results and data on other JAK inhibitors are limited. METHODS: A 
      retrospective, pharmacovigilance study using the FDA adverse event reporting 
      system (FAERS) to assess reporting of adverse cardiovascular events following 
      treatment with JAK inhibitors in rheumatoid arthritis (RA) patients between 
      January 2015 and June 2023. To identify disproportionately increased reporting, 
      an adjusted reporting odds ratio (adj.ROR) was calculated with a multivariable 
      logistic regression model. RESULTS: We identified safety reports of 75,407 RA 
      patients treated with JAK inhibitors (tofacitinib, n = 52,181; upadacitinib, n = 
      21,006; baricitinib, n = 2,220) and 303,278 patients treated with biologic 
      disease-modifying antirheumatic drugs (bDMARDs; TNF inhibitors, rituximab, and 
      tocilizumab). The mean age was 61.2(±12) and 59.0(±13), respectively; 82 % and 81 
      % were women. Compared to bDMARDs, JAK inhibitors were associated with an 
      increased reporting of VTE [n = 1,393, adj.ROR=2.11 (1.97-2.25)], stroke [n = 
      973, adj.ROR=1.25 (1.16-1.34)], ischemic heart disease [IHD, n = 999, 
      adj.ROR=1.23 (1.13-1.33)], peripheral edema [n = 2699, adj.ROR=1.22 (1.17-1.28)], 
      and tachyarrhythmias [n = 370, adj.ROR=1.15 (1.00-1.33)]. Most of the events 
      occurred in the first year after treatment initiation. When different JAK 
      inhibitors were compared, VTE, stroke, and IHD were more frequently reported with 
      upadacitinib and baricitinib than tofacitinib. When stratified by age category, 
      all safety signals were statistically significant in patients aged≤65 years. 
      CONCLUSION: In this global postmarketing study, JAK inhibitors are associated 
      with increased reporting of VTE, stroke, IHD, and tachyarrhythmias. These adverse 
      events were reported following all JAK inhibitors that were studied, suggesting a 
      class effect.
CI  - Copyright © 2024 Elsevier Inc. All rights reserved.
FAU - Goldman, Adam
AU  - Goldman A
AD  - Department of Internal Medicine F, Sheba Medical Center, Ramat-Gan, Israel; 
      Department of Epidemiology and Preventive Medicine, School of Public Health, 
      Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel; The Sheba 
      Talpiot Medical Leadership Program, Sheba Medical Center, Ramat-Gan, Israel.
FAU - Galper, Bat-El Lugassy
AU  - Galper BL
AD  - Department of Internal Medicine F, Sheba Medical Center, Ramat-Gan, Israel.
FAU - Druyan, Amit
AU  - Druyan A
AD  - Department of Internal Medicine F, Sheba Medical Center, Ramat-Gan, Israel; 
      School of Medicine, Sackler Faculty of Medicine, Tel-Aviv University, Tel‑Aviv, 
      Israel.
FAU - Grossman, Chagai
AU  - Grossman C
AD  - Department of Internal Medicine F, Sheba Medical Center, Ramat-Gan, Israel; 
      School of Medicine, Sackler Faculty of Medicine, Tel-Aviv University, Tel‑Aviv, 
      Israel.
FAU - Sharif, Kassem
AU  - Sharif K
AD  - School of Medicine, Sackler Faculty of Medicine, Tel-Aviv University, Tel‑Aviv, 
      Israel; Department of Gastroenterology, Sheba Medical Center, Ramat-Gan, Israel.
FAU - Shechtman, Liran
AU  - Shechtman L
AD  - Department of Critical Care Medicine, Sunnybrook Hospital, Toronto, Canada; 
      Department of Medicine, University of Toronto, Toronto, Canada.
FAU - Moshkovits, Yonatan
AU  - Moshkovits Y
AD  - Department of Internal Medicine F, Sheba Medical Center, Ramat-Gan, Israel; 
      School of Medicine, Sackler Faculty of Medicine, Tel-Aviv University, Tel‑Aviv, 
      Israel.
FAU - Lahat, Adi
AU  - Lahat A
AD  - School of Medicine, Sackler Faculty of Medicine, Tel-Aviv University, Tel‑Aviv, 
      Israel; Department of Gastroenterology, Sheba Medical Center, Ramat-Gan, Israel.
FAU - Ben-Zvi, Ilan
AU  - Ben-Zvi I
AD  - Department of Internal Medicine F, Sheba Medical Center, Ramat-Gan, Israel; The 
      Sheba Talpiot Medical Leadership Program, Sheba Medical Center, Ramat-Gan, 
      Israel; School of Medicine, Sackler Faculty of Medicine, Tel-Aviv University, 
      Tel‑Aviv, Israel. Electronic address: Ilan.BenZvi@sheba.health.gov.il.
LA  - eng
PT  - Journal Article
DEP - 20240517
PL  - United States
TA  - Semin Arthritis Rheum
JT  - Seminars in arthritis and rheumatism
JID - 1306053
RN  - 0 (Janus Kinase Inhibitors)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Azetidines)
RN  - 0 (Pyrimidines)
RN  - 0 (Piperidines)
RN  - ISP4442I3Y (baricitinib)
RN  - 0 (Pyrazoles)
RN  - 0 (Purines)
RN  - 87LA6FU830 (tofacitinib)
RN  - 4RA0KN46E0 (upadacitinib)
RN  - 0 (Sulfonamides)
RN  - 0 (Heterocyclic Compounds, 3-Ring)
SB  - IM
MH  - Humans
MH  - *Arthritis, Rheumatoid/drug therapy
MH  - *Janus Kinase Inhibitors/adverse effects
MH  - Female
MH  - Male
MH  - Middle Aged
MH  - Aged
MH  - *Antirheumatic Agents/adverse effects
MH  - Retrospective Studies
MH  - *Cardiovascular Diseases/chemically induced/epidemiology
MH  - *Azetidines/adverse effects
MH  - *Pyrimidines/adverse effects/therapeutic use
MH  - *Piperidines/adverse effects/therapeutic use
MH  - *Pharmacovigilance
MH  - Pyrazoles/adverse effects
MH  - Purines/adverse effects
MH  - Adult
MH  - Sulfonamides/adverse effects/therapeutic use
MH  - Adverse Drug Reaction Reporting Systems
MH  - Product Surveillance, Postmarketing
MH  - Heterocyclic Compounds, 3-Ring/adverse effects/therapeutic use
MH  - Venous Thromboembolism/chemically induced/epidemiology
OTO - NOTNLM
OT  - Disease-modifying antirheumatic drug
OT  - Jak inhibitors
OT  - Major adverse cardiovascular events
OT  - Pharmacovigilance
OT  - Rheumatoid arthritis
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2024/05/22 01:40
MHDA- 2024/06/28 00:42
CRDT- 2024/05/21 18:05
PHST- 2024/03/06 00:00 [received]
PHST- 2024/04/14 00:00 [revised]
PHST- 2024/04/29 00:00 [accepted]
PHST- 2024/06/28 00:42 [medline]
PHST- 2024/05/22 01:40 [pubmed]
PHST- 2024/05/21 18:05 [entrez]
AID - S0049-0172(24)00101-X [pii]
AID - 10.1016/j.semarthrit.2024.152461 [doi]
PST - ppublish
SO  - Semin Arthritis Rheum. 2024 Aug;67:152461. doi: 10.1016/j.semarthrit.2024.152461. 
      Epub 2024 May 17.

PMID- 38756933
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240518
IS  - 2529-198X (Electronic)
IS  - 2529-198X (Linking)
VI  - 35
IP  - Suppl 1
DP  - 2024 Mar
TI  - Risk of Major Adverse Cardiovascular Events and Venous Thromboembolism with JAK 
      Inhibitors versus TNF Inhibitors in Rheumatoid Arthritis Patients: A Systematic 
      Review and Meta-Analysis.
PG  - 10-19
LID - 10.31138/mjr.171023.rof [doi]
AB  - OBJECTIVE: The aim of this study was to compare the risk of major cardiovascular 
      events (MACE) and venous thromboembolic events (VTE) between tumour necrosis 
      factor (TNF) and Janus kinase (JAK) inhibitors in patients with rheumatoid 
      arthritis (RA). METHODS: We researched PubMed, Scopus, Cochrane Library, and 
      clinicaltrials.gov until December of 2023 for randomised controlled trials (RCTs) 
      and observational studies. The outcomes studied were MACE (stroke, heart attack, 
      myocardial infarction, sudden cardiac death) and VTE (deep vein thrombosis, 
      pulmonary embolism). We pooled data using random effects model. Risk for the 
      reported outcomes was expressed as odds ratio (OR) with a 95% confidential 
      interval (CI). We performed a subgroup analysis based on study design. RESULTS: 
      We identified 23 studies, 20 of which compared the odds for MACE and 14 the odds 
      for VTE between JAK and TNF inhibitors in RA patients. Ten studies were RCTs and 
      the rest were observational. Regarding MACE risk we pooled data from a total of 
      215,278 patients (52,243 were treated with JAK inhibitors, while the rest 163,035 
      were under TNF inhibitors). Compared with TNF inhibitors, the OR for JAK 
      inhibitors in regards with MACE risk was 0.87 (0.64-1.17, p<0.01). Regarding VTE, 
      a total of 176,951 patients were analysed (41,375 JAK inhibitors users and 
      135,576 TNF inhibitors users). The OR for VTE for JAK inhibitors compared with 
      TNF inhibitors was 1.28 (0.89-1.84, p<0.01). CONCLUSION: According to our 
      results, there is no statistically significant difference for MACE or VTE in RA 
      patients who receive either JAK or TNF inhibitors.
CI  - © 2024 The Mediterranean Journal of Rheumatology (MJR).
FAU - Partalidou, Styliani
AU  - Partalidou S
AD  - 1 Department of Internal Medicine, 424 Military Hospital of Thessaloniki, 56429, 
      Thessaloniki, Greece.
FAU - Patoulias, Dimitrios
AU  - Patoulias D
AD  - Outpatient Department of Cardiometabolic Medicine, Second Department of 
      Cardiology, Aristotle University of Thessaloniki, General Hospital 
      "Hippokration", 54642 Thessaloniki, Greece.
FAU - Deuteraiou, Kleopatra
AU  - Deuteraiou K
AD  - 4 Department of Internal Medicine, Hippokration General Hospital, School of 
      Medicine, Aristotle University of Thessaloniki, 54642, Thessaloniki, Greece.
FAU - Avgerou, Paraskevi
AU  - Avgerou P
AD  - 4 Department of Internal Medicine, Hippokration General Hospital, School of 
      Medicine, Aristotle University of Thessaloniki, 54642, Thessaloniki, Greece.
FAU - Kitas, George
AU  - Kitas G
AD  - Research & Development, Dudley Group NHS Foundation Trust and University of 
      Birmingham, United Kingdom.
FAU - Tzitiridou-Chatzopoulou, Maria
AU  - Tzitiridou-Chatzopoulou M
AD  - 4 Department of Internal Medicine, Hippokration General Hospital, School of 
      Medicine, Aristotle University of Thessaloniki, 54642, Thessaloniki, Greece.
FAU - Dimitroulas, Theodoros
AU  - Dimitroulas T
AD  - 4 Department of Internal Medicine, Hippokration General Hospital, School of 
      Medicine, Aristotle University of Thessaloniki, 54642, Thessaloniki, Greece.
LA  - eng
PT  - Journal Article
DEP - 20240330
PL  - Greece
TA  - Mediterr J Rheumatol
JT  - Mediterranean journal of rheumatology
JID - 101730166
PMC - PMC11094442
OTO - NOTNLM
OT  - JAK inhibitors
OT  - TNF inhibitors
OT  - cardiovascular events
OT  - rheumatoid arthritis
OT  - thromboembolic events
COIS- The authors declare no conflict of interest.
EDAT- 2024/05/17 06:43
MHDA- 2024/05/17 06:44
PMCR- 2024/03/30
CRDT- 2024/05/17 03:57
PHST- 2023/10/17 00:00 [received]
PHST- 2023/12/07 00:00 [revised]
PHST- 2023/12/11 00:00 [accepted]
PHST- 2024/05/17 06:44 [medline]
PHST- 2024/05/17 06:43 [pubmed]
PHST- 2024/05/17 03:57 [entrez]
PHST- 2024/03/30 00:00 [pmc-release]
AID - MJR-35-Suppl-1-10 [pii]
AID - 10.31138/mjr.171023.rof [doi]
PST - epublish
SO  - Mediterr J Rheumatol. 2024 Mar 30;35(Suppl 1):10-19. doi: 
      10.31138/mjr.171023.rof. eCollection 2024 Mar.

PMID- 38754248
OWN - NLM
STAT- MEDLINE
DCOM- 20240616
LR  - 20240616
IS  - 2211-0356 (Electronic)
IS  - 2211-0348 (Linking)
VI  - 87
DP  - 2024 Jul
TI  - Carotid intima media thickness in multiple sclerosis: A CLSA study.
PG  - 105660
LID - S2211-0348(24)00237-2 [pii]
LID - 10.1016/j.msard.2024.105660 [doi]
AB  - BACKGROUND: People with multiple sclerosis (MS) have an increased incidence of 
      atherosclerotic disease, including ischemic heart disease and stroke, compared to 
      people without MS even after accounting for risk factors such as hypertension, 
      dyslipidemia, diabetes and smoking. We compared carotid intima media thickness 
      (CIMT), a surrogate of atherosclerosis, in people with MS and in two groups of 
      people without MS (rheumatoid arthritis [RA]; all other participants). METHODS: 
      We used data from participants in the Canadian Longitudinal Study on Aging (CLSA) 
      who did not have known vascular disease (ischemic heart disease, stroke, 
      transient ischemic attack, peripheral vascular disease) and who underwent carotid 
      ultrasound for assessment of CIMT. We selected participants with MS, RA and 
      controls who did not have MS or RA. Using age and gender-stratified norms for 
      average CIMT in the CLSA, we identified participants in each cohort with a CIMT 
      ≥75th percentile (subclinical atherosclerosis). We also calculated ten-year level 
      of cardiovascular risk using the Framingham Risk Score (FRS). We tested the 
      association between cohort membership (MS, RA, controls) and atherosclerosis 
      using logistic regression, adjusted for FRS, abdominal obesity, excess alcohol 
      intake, education and elevated symptoms of depression. We adjusted all analyses 
      for the stratified sampling design. RESULTS: We included 78 participants with MS, 
      364 participants with RA and 13,891 controls. Overall, the average (SE) CIMT was 
      0.699 (0.002), and this did not differ between cohorts. Logistic regression 
      analyses revealed that cohort membership was not associated with atherosclerosis 
      based on the average CIMT in unadjusted or adjusted models. However, a 1-point 
      higher FRS was associated with 1.032 (95 %CI: 1.021, 1.043) increased odds of 
      atherosclerosis. CONCLUSION: Average CIMT does not differ between people with MS, 
      people with RA and people without these diseases. Subclinical atherosclerosis as 
      defined by a CIMT ≥75 % is not observed in people with MS at an increased rate 
      beyond what FRS would predict. Further evaluation is needed to determine what 
      mechanisms underlie the increased rates of cardiovascular disease and stroke in 
      MS.
CI  - Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.
FAU - Marrie, Ruth Ann
AU  - Marrie RA
AD  - Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of 
      Health Sciences, University of Manitoba, Winnipeg, Can; Department of Community 
      Health Sciences, Max Rady College of Medicine, Rady Faculty of Health Sciences, 
      University of Manitoba, Winnipeg, Can. Electronic address: rmarrie@hsc.mb.ca.
FAU - Patel, Ronak
AU  - Patel R
AD  - Department of Clinical Health Psychology, Max Rady College of Medicine, Rady 
      Faculty of Health Sciences, University of Manitoba, Winnipeg, Can.
FAU - Schaffer, Stephen Allan
AU  - Schaffer SA
AD  - Department of Internal Medicine, Max Rady College of Medicine, Rady Faculty of 
      Health Sciences, University of Manitoba, Winnipeg, Can.
LA  - eng
PT  - Journal Article
DEP - 20240510
PL  - Netherlands
TA  - Mult Scler Relat Disord
JT  - Multiple sclerosis and related disorders
JID - 101580247
SB  - IM
MH  - Humans
MH  - *Carotid Intima-Media Thickness
MH  - Female
MH  - Male
MH  - Middle Aged
MH  - *Multiple Sclerosis/epidemiology/diagnostic imaging
MH  - Longitudinal Studies
MH  - Canada/epidemiology
MH  - Aged
MH  - Atherosclerosis/epidemiology/diagnostic imaging
MH  - Arthritis, Rheumatoid/complications/epidemiology/diagnostic imaging
MH  - Adult
MH  - Risk Factors
OTO - NOTNLM
OT  - Atherosclerosis
OT  - CLSA
OT  - Carotid intima media thickness
OT  - Multiple sclerosis
OT  - Rheumatoid arthritis
COIS- Declaration of competing interest This research has been conducted using the CLSA 
      dataset Baseline Comprehensive Dataset Version 7.0, under Application Number 
      2,203,003. The CLSA is led by Drs. Parminder Raina, Christina Wolfson and Susan 
      Kirkland. The opinions expressed in this manuscript are the authors’ own and do 
      not reflect the views of the Canadian Longitudinal Study on Aging. Ruth Ann 
      Marrie receives research funding from: CIHR, Research Manitoba, MS Canada, 
      Crohn's and Colitis Canada, National Multiple Sclerosis Society, CMSC, the 
      Arthritis Society and the US Department of Defense, and is a co-investigator on 
      studies receiving funding from Biogen Idec and Roche Canada. She holds the Waugh 
      Family Chair in Multiple Sclerosis. R Patel receives research funding from MS 
      Canada. SA Schaffer receives research funding from MS Canada, Merck, Pfizer and 
      Novo Nordisk.
EDAT- 2024/05/17 00:43
MHDA- 2024/06/17 00:42
CRDT- 2024/05/16 18:06
PHST- 2024/01/10 00:00 [received]
PHST- 2024/04/07 00:00 [revised]
PHST- 2024/04/28 00:00 [accepted]
PHST- 2024/06/17 00:42 [medline]
PHST- 2024/05/17 00:43 [pubmed]
PHST- 2024/05/16 18:06 [entrez]
AID - S2211-0348(24)00237-2 [pii]
AID - 10.1016/j.msard.2024.105660 [doi]
PST - ppublish
SO  - Mult Scler Relat Disord. 2024 Jul;87:105660. doi: 10.1016/j.msard.2024.105660. 
      Epub 2024 May 10.

PMID- 38709770
OWN - NLM
STAT- MEDLINE
DCOM- 20240506
LR  - 20240508
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 19
IP  - 5
DP  - 2024
TI  - External validation of a multi-biomarker-based score for predicting risk of 
      cardiovascular disease in patients with rheumatoid arthritis.
PG  - e0296459
LID - 10.1371/journal.pone.0296459 [doi]
LID - e0296459
AB  - BACKGROUND: A multi-biomarker disease activity (MBDA)-based cardiovascular 
      disease (CVD) risk score was developed and internally validated in a Medicare 
      cohort to predict 3-year risk for myocardial infarction (MI), stroke or CVD death 
      in patients with rheumatoid arthritis (RA). It combines the MBDA score, leptin, 
      MMP-3, TNF-R1, age and four clinical variables. We are now externally validating 
      it in a younger RA cohort. METHODS: Claims data from a private aggregator were 
      linked to MBDA test data to create a cohort of RA patients ≥18 years old. A 
      univariable Cox proportional hazards regression model was fit using the 
      MBDA-based CVD risk score as sole predictor of time-to-a-CVD event (hospitalized 
      MI or stroke). Hazard ratio (HR) estimate was determined for all patients and for 
      clinically relevant subgroups. A multivariable Cox model evaluated whether the 
      MBDA-based CVD risk score adds predictive information to clinical data. RESULTS: 
      49,028 RA patients (340 CVD events) were studied. Mean age was 52.3 years; 18.3% 
      were male. HR for predicting 3-year risk of a CVD event by the MBDA-based CVD 
      risk score in the full cohort was 3.99 (95% CI: 3.51-4.49, p = 5.0×10-95). HR 
      were also significant for subgroups based on age, comorbidities, disease 
      activity, and drug use. In a multivariable model, the MBDA-based CVD risk score 
      added significant information to hypertension, diabetes, tobacco use, history of 
      CVD, age, sex and CRP (HR = 2.27, p = 1.7×10-7). CONCLUSION: The MBDA-based CVD 
      risk score has been externally validated in an RA cohort that is younger than and 
      independent of the Medicare cohort that was used for development and internal 
      validation.
CI  - Copyright: © 2024 Sasso et al. This is an open access article distributed under 
      the terms of the Creative Commons Attribution License, which permits unrestricted 
      use, distribution, and reproduction in any medium, provided the original author 
      and source are credited.
FAU - Sasso, Eric H
AU  - Sasso EH
AD  - Medical and Scientific Affairs, Crescendo Bioscience, South San Francisco, CA, 
      United States of America.
AD  - Myriad Genetics Laboratories, Myriad, Salt Lake City, UT, United States of 
      America.
FAU - Mabey, Brent
AU  - Mabey B
AD  - Myriad Genetics Laboratories, Myriad, Salt Lake City, UT, United States of 
      America.
FAU - Flake, Darl D 2nd
AU  - Flake DD 2nd
AD  - Myriad Genetics Laboratories, Myriad, Salt Lake City, UT, United States of 
      America.
FAU - Hitraya, Elena
AU  - Hitraya E
AD  - Medical and Scientific Affairs, Crescendo Bioscience, South San Francisco, CA, 
      United States of America.
AD  - Myriad Genetics Laboratories, Myriad, Salt Lake City, UT, United States of 
      America.
FAU - Chin, Cheryl L
AU  - Chin CL
AD  - Medical and Scientific Affairs, Crescendo Bioscience, South San Francisco, CA, 
      United States of America.
AD  - Myriad Genetics Laboratories, Myriad, Salt Lake City, UT, United States of 
      America.
FAU - Ben-Shachar, Rotem
AU  - Ben-Shachar R
AD  - Myriad Genetics Laboratories, Myriad, Salt Lake City, UT, United States of 
      America.
FAU - Gutin, Alexander
AU  - Gutin A
AD  - Myriad Genetics Laboratories, Myriad, Salt Lake City, UT, United States of 
      America.
FAU - Lanchbury, Jerry S
AU  - Lanchbury JS
AD  - Myriad Genetics Laboratories, Myriad, Salt Lake City, UT, United States of 
      America.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AUID- ORCID: 0000-0002-8907-8976
AD  - Division of Clinical Immunology and Rheumatology, University of Alabama at 
      Birmingham, Birmingham, AL, United States of America.
LA  - eng
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Validation Study
DEP - 20240506
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Biomarkers)
SB  - IM
MH  - Humans
MH  - *Arthritis, Rheumatoid/complications/blood
MH  - Male
MH  - Female
MH  - Middle Aged
MH  - *Biomarkers/blood
MH  - *Cardiovascular Diseases/epidemiology
MH  - Adult
MH  - Proportional Hazards Models
MH  - Aged
MH  - Risk Factors
MH  - Risk Assessment/methods
MH  - Myocardial Infarction/epidemiology
MH  - Cohort Studies
PMC - PMC11073667
COIS- I have read the journal’s policy and the authors of this manuscript have the 
      following competing interests: ES, BM, DDFII, EH, CLC, RB-S, AG, and JSL are or 
      were employed by Myriad Genetics during the conduct of the study and received 
      salaries and may have received stock grants/options as compensation. EH has been 
      employed by Labcorp. JC received grants or contracts from Abbvie, Amgen, BMS, 
      Corevitas, Janssen, Lilly, Novartis, Myriad, Pfizer, Sanofi, Setpoint, Scipher, 
      and UCB and received consulting fees from Abbvie, Amgen, BMS, Corevitas, Janssen, 
      Lilly, Novartis, Myriad, Pfizer, Sanofi, Setpoint, Scipher, and UCB. This does 
      not alter our adherence to PLOS ONE policies on sharing data and materials.
EDAT- 2024/05/06 19:14
MHDA- 2024/05/06 19:15
PMCR- 2024/05/06
CRDT- 2024/05/06 13:44
PHST- 2023/06/20 00:00 [received]
PHST- 2023/12/13 00:00 [accepted]
PHST- 2024/05/06 19:15 [medline]
PHST- 2024/05/06 19:14 [pubmed]
PHST- 2024/05/06 13:44 [entrez]
PHST- 2024/05/06 00:00 [pmc-release]
AID - PONE-D-23-19235 [pii]
AID - 10.1371/journal.pone.0296459 [doi]
PST - epublish
SO  - PLoS One. 2024 May 6;19(5):e0296459. doi: 10.1371/journal.pone.0296459. 
      eCollection 2024.

PMID- 38699413
OWN - NLM
STAT- MEDLINE
DCOM- 20240503
LR  - 20240701
IS  - 2296-2565 (Electronic)
IS  - 2296-2565 (Linking)
VI  - 12
DP  - 2024
TI  - Temporal change in multimorbidity prevalence, clustering patterns, and the 
      association with mortality: findings from the China Kadoorie Biobank study in 
      Jiangsu Province.
PG  - 1389635
LID - 10.3389/fpubh.2024.1389635 [doi]
LID - 1389635
AB  - OBJECTIVES: The characteristics of multimorbidity in the Chinese population are 
      currently unclear. We aimed to determine the temporal change in multimorbidity 
      prevalence, clustering patterns, and the association of multimorbidity with 
      mortality from all causes and four major chronic diseases. METHODS: This study 
      analyzed data from the China Kadoorie Biobank study performed in Wuzhong 
      District, Jiangsu Province. A total of 53,269 participants aged 30-79 years were 
      recruited between 2004 and 2008. New diagnoses of 15 chronic diseases and death 
      events were collected during the mean follow-up of 10.9 years. Yule's Q cluster 
      analysis method was used to determine the clustering patterns of multimorbidity. 
      A Cox proportional hazards model was used to estimate the associations of 
      multimorbidity with mortalities. RESULTS: The overall multimorbidity prevalence 
      rate was 21.1% at baseline and 27.7% at the end of follow-up. Multimorbidity 
      increased more rapidly during the follow-up in individuals who had a higher risk 
      at baseline. Three main multimorbidity patterns were identified: (i) 
      cardiometabolic multimorbidity (diabetes, coronary heart disease, stroke, and 
      hypertension), (ii) respiratory multimorbidity (tuberculosis, asthma, and chronic 
      obstructive pulmonary disease), and (iii) mental, kidney and arthritis 
      multimorbidity (neurasthenia, psychiatric disorders, chronic kidney disease, and 
      rheumatoid arthritis). There were 3,433 deaths during the follow-up. The 
      mortality risk increased by 24% with each additional disease [hazard ratio (HR) = 
      1.24, 95% confidence interval (CI) = 1.20-1.29]. Compared with those without 
      multimorbidity at baseline, both cardiometabolic multimorbidity and respiratory 
      multimorbidity were associated with increased mortality from all causes and four 
      major chronic diseases. Cardiometabolic multimorbidity was additionally 
      associated with mortality from cardiovascular diseases and diabetes, with HRs of 
      2.64 (95% CI = 2.19-3.19) and 28.19 (95% CI = 14.85-53.51), respectively. 
      Respiratory multimorbidity was associated with respiratory disease mortality, 
      with an HR of 9.76 (95% CI = 6.22-15.31). CONCLUSION: The prevalence of 
      multimorbidity has increased substantially over the past decade. This study has 
      revealed that cardiometabolic multimorbidity and respiratory multimorbidity have 
      significantly increased mortality rates. These findings indicate the need to 
      consider high-risk populations and to provide local evidence for intervention 
      strategies and health management in economically developed regions.
CI  - Copyright © 2024 Yu, Tao, Zhou, Su, Lu, Hua, Jin, Pei, Yu, Sun, Chen, Li and Lv.
FAU - Yu, Hao
AU  - Yu H
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing, China.
AD  - Department of Noncommunicable Chronic Disease and Prevention, Jiangsu Provincial 
      Center for Disease Control and Prevention, Nanjing, China.
FAU - Tao, Ran
AU  - Tao R
AD  - Department of Noncommunicable Chronic Disease and Prevention, Jiangsu Provincial 
      Center for Disease Control and Prevention, Nanjing, China.
FAU - Zhou, Jinyi
AU  - Zhou J
AD  - Department of Noncommunicable Chronic Disease and Prevention, Jiangsu Provincial 
      Center for Disease Control and Prevention, Nanjing, China.
FAU - Su, Jian
AU  - Su J
AD  - Department of Noncommunicable Chronic Disease and Prevention, Jiangsu Provincial 
      Center for Disease Control and Prevention, Nanjing, China.
FAU - Lu, Yan
AU  - Lu Y
AD  - Department of Noncommunicable Chronic Disease Control and Prevention, Suzhou City 
      Center for Disease Control and Prevention, Suzhou, China.
FAU - Hua, Yujie
AU  - Hua Y
AD  - Department of Noncommunicable Chronic Disease Control and Prevention, Suzhou City 
      Center for Disease Control and Prevention, Suzhou, China.
FAU - Jin, Jianrong
AU  - Jin J
AD  - Department of Noncommunicable Chronic Disease Control and Prevention, Wuzhong 
      District Center for Disease Control and Prevention, Suzhou, China.
FAU - Pei, Pei
AU  - Pei P
AD  - Peking University Center for Public Health, Epidemic Preparedness and Response, 
      Beijing, China.
FAU - Yu, Canqing
AU  - Yu C
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing, China.
AD  - Peking University Center for Public Health, Epidemic Preparedness and Response, 
      Beijing, China.
AD  - Key Laboratory of Epidemiology of Major Diseases, Peking University, Ministry of 
      Education, Beijing, China.
FAU - Sun, Dianjianyi
AU  - Sun D
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing, China.
AD  - Peking University Center for Public Health, Epidemic Preparedness and Response, 
      Beijing, China.
AD  - Key Laboratory of Epidemiology of Major Diseases, Peking University, Ministry of 
      Education, Beijing, China.
FAU - Chen, Zhengming
AU  - Chen Z
AD  - Clinical Trial Service Unit and Epidemiological Studies Unit, Nuffield Department 
      of Population Health, University of Oxford, Oxford, United Kingdom.
FAU - Li, Liming
AU  - Li L
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing, China.
AD  - Peking University Center for Public Health, Epidemic Preparedness and Response, 
      Beijing, China.
AD  - Key Laboratory of Epidemiology of Major Diseases, Peking University, Ministry of 
      Education, Beijing, China.
FAU - Lv, Jun
AU  - Lv J
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing, China.
AD  - Peking University Center for Public Health, Epidemic Preparedness and Response, 
      Beijing, China.
AD  - Key Laboratory of Epidemiology of Major Diseases, Peking University, Ministry of 
      Education, Beijing, China.
LA  - eng
GR  - 202922/Z/16/Z/WT_/Wellcome Trust/United Kingdom
GR  - CH/1996001/9454/BHF_/British Heart Foundation/United Kingdom
GR  - MC_U137686851/Medical Research Council UK/
GR  - 088158/Z/09/Z/WT_/Wellcome Trust/United Kingdom
GR  - 212946/Z/18/Z/WT_/Wellcome Trust/United Kingdom
GR  - WT_/Wellcome Trust/United Kingdom
GR  - MC_UU_00017/1/Medical Research Council UK/
GR  - 104085/Z/14/Z/WT_/Wellcome Trust/United Kingdom
GR  - MC_UU_12026/2/Medical Research Council UK/
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20240418
PL  - Switzerland
TA  - Front Public Health
JT  - Frontiers in public health
JID - 101616579
SB  - IM
MH  - Humans
MH  - Middle Aged
MH  - *Multimorbidity
MH  - Male
MH  - Female
MH  - China/epidemiology
MH  - Aged
MH  - Prevalence
MH  - Adult
MH  - Cluster Analysis
MH  - Chronic Disease/epidemiology/mortality
MH  - Proportional Hazards Models
MH  - Biological Specimen Banks
MH  - Mortality/trends
MH  - Risk Factors
PMC - PMC11064014
OTO - NOTNLM
OT  - cluster analysis
OT  - cohort study
OT  - mortality
OT  - multimorbidity
OT  - prevalence
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2024/05/03 06:43
MHDA- 2024/05/03 06:44
PMCR- 2024/04/18
CRDT- 2024/05/03 03:54
PHST- 2024/02/21 00:00 [received]
PHST- 2024/03/18 00:00 [accepted]
PHST- 2024/05/03 06:44 [medline]
PHST- 2024/05/03 06:43 [pubmed]
PHST- 2024/05/03 03:54 [entrez]
PHST- 2024/04/18 00:00 [pmc-release]
AID - 10.3389/fpubh.2024.1389635 [doi]
PST - epublish
SO  - Front Public Health. 2024 Apr 18;12:1389635. doi: 10.3389/fpubh.2024.1389635. 
      eCollection 2024.

PMID- 38609322
OWN - NLM
STAT- MEDLINE
DCOM- 20240415
LR  - 20240421
IS  - 2056-5933 (Electronic)
IS  - 2056-5933 (Linking)
VI  - 10
IP  - 2
DP  - 2024 Apr 12
TI  - Risk of extended major adverse cardiovascular event endpoints with tofacitinib 
      versus TNF inhibitors in patients with rheumatoid arthritis: a post hoc analysis 
      of a phase 3b/4 randomised safety study.
LID - 10.1136/rmdopen-2023-003912 [doi]
LID - e003912
AB  - OBJECTIVES: Compare the risk of extended major adverse cardiovascular (CV) event 
      (MACE) composite outcomes and component events in patients with rheumatoid 
      arthritis (RA) treated with tofacitinib versus tumour necrosis factor inhibitors 
      (TNFi) in Oral Rheumatoid Arthritis Trial (ORAL) Surveillance. METHODS: Patients 
      with RA aged ≥50 years and with ≥1 additional CV risk factor received tofacitinib 
      5 mg or 10 mg two times per day or TNFi. MACE (non-fatal myocardial infarction 
      (MI), non-fatal stroke or CV death (MACE-3)) was extended by sequential addition 
      of CV events (hospitalisation for unstable angina (MACE-4), coronary 
      revascularisation (MACE-5), transient ischaemic attack (MACE-6), peripheral 
      vascular disease (MACE-7)), heart failure (HF) hospitalisation (MACE-8) and 
      venous thromboembolism (VTE; (MACE-8 plus VTE)). HRs (tofacitinib vs TNFi) were 
      evaluated for MACE and individual components. RESULTS: HRs for MACE-4 to MACE-8 
      with combined and individual tofacitinib doses versus TNFi were similar. Risk of 
      MACE-8 plus VTE appeared similar with tofacitinib 5 mg two times per day versus 
      TNFi (HR 1.12 (0.82 to 1.52)), but higher with tofacitinib 10 mg two times per 
      day versus TNFi (HR 1.38 (1.02 to 1.85)). Risk of MI was higher with tofacitinib 
      versus TNFi, but difference in risk of other individual CV events was not 
      suggested. Across extended MACE definitions, risk appeared higher with 
      tofacitinib versus TNFi in those with atherosclerotic CV disease or age ≥65 
      years. CONCLUSION: In ORAL Surveillance, risk of composite CV endpoints combining 
      all ischaemic CV events and HF did not appear different with tofacitinib versus 
      TNFi. The totality of CV risk was higher with tofacitinib 10 mg two times per day 
      versus TNFi, driven by an increase in VTE. TRIAL REGISTRATION NUMBER: 
      NCT02092467.
CI  - © Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY. Published 
      by BMJ.
FAU - Buch, Maya H
AU  - Buch MH
AUID- ORCID: 0000-0002-8962-5642
AD  - Centre for Musculoskeletal Research, Division of Musculoskeletal and 
      Dermatological Sciences, The University of Manchester, Manchester, UK 
      maya.buch@manchester.ac.uk.
AD  - NIHR Manchester Biomedical Research Centre, Manchester, UK.
FAU - Bhatt, Deepak L
AU  - Bhatt DL
AD  - Mount Sinai Heart, Icahn School of Medicine at Mount Sinai Health System, New 
      York, New York, USA.
FAU - Charles-Schoeman, Christina
AU  - Charles-Schoeman C
AUID- ORCID: 0000-0002-1768-7019
AD  - Division of Rheumatology, Department of Medicine, University of California, Los 
      Angeles, California, USA.
FAU - Giles, Jon T
AU  - Giles JT
AD  - Division of Rheumatology, Columbia University, College of Physicians and 
      Surgeons, New York, New York, USA.
FAU - Mikuls, Ted
AU  - Mikuls T
AD  - Department of Medicine, University of Nebraska Medical Center, Omaha, Nebraska, 
      USA.
FAU - Koch, Gary G
AU  - Koch GG
AD  - University of North Carolina at Chapel Hill Department of Biostatistics, Chapel 
      Hill, North Carolina, USA.
FAU - Ytterberg, Steven
AU  - Ytterberg S
AD  - Division of Rheumatology, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Nagy, Edward
AU  - Nagy E
AD  - Pfizer Ltd, Tadworth, UK.
FAU - Jo, Hyejin
AU  - Jo H
AD  - Pfizer Inc, New York, New York, USA.
FAU - Kwok, Kenneth
AU  - Kwok K
AD  - Pfizer Inc, New York, New York, USA.
FAU - Connell, Carol A
AU  - Connell CA
AD  - Pfizer Inc, Groton, Connecticut, USA.
FAU - Masri, Karim Richard
AU  - Masri KR
AUID- ORCID: 0000-0002-2178-9747
AD  - Pfizer Inc, Collegeville, Pennsylvania, USA.
FAU - Yndestad, Arne
AU  - Yndestad A
AD  - Pfizer Inc, Oslo, Norway.
LA  - eng
SI  - ClinicalTrials.gov/NCT02092467
PT  - Clinical Trial, Phase II
PT  - Clinical Trial, Phase III
PT  - Journal Article
PT  - Randomized Controlled Trial
DEP - 20240412
PL  - England
TA  - RMD Open
JT  - RMD open
JID - 101662038
RN  - 0 (Piperidines)
RN  - 0 (Pyrimidines)
RN  - 87LA6FU830 (tofacitinib)
RN  - 0 (Tumor Necrosis Factor Inhibitors)
SB  - IM
MH  - Humans
MH  - *Arthritis, Rheumatoid/complications/drug therapy
MH  - *Heart Failure
MH  - *Myocardial Infarction/epidemiology/etiology
MH  - Piperidines/adverse effects
MH  - *Pyrimidines
MH  - Tumor Necrosis Factor Inhibitors
MH  - *Venous Thromboembolism
PMC - PMC11029242
OTO - NOTNLM
OT  - Antirheumatic Agents
OT  - Arthritis, Rheumatoid
OT  - Cardiovascular Diseases
OT  - Therapeutics
OT  - Tumor Necrosis Factor Inhibitors
COIS- Competing interests: MHB has acted as a consultant for AbbVie, Arxx therapeutics, 
      Eli Lilly, Galapagos, Gilead Sciences, and Pfizer Inc with all funding paid to 
      the University of Manchester; has received grant/research support paid to the 
      University of Manchester from Gilead, Pfizer Inc and UCB; was a member of the 
      Speakers’ Bureau for AbbVie and received honoraria from Boehringer Ingelheim, 
      CESAS Medical, Galapagos, Medistream and Pfizer, all paid to the University of 
      Manchester; and is supported by the National Institute for Health Research (NIHR) 
      Manchester Biomedical Research Centre and is in receipt of an NIHR Senior 
      Investigator award. DLB served as a member of the Steering Committee for ORAL 
      Surveillance, with funding from Pfizer Inc paid to Brigham and Women’s Hospital; 
      has served on Advisory Boards for Angiowave, Bayer, Boehringer Ingelheim, Cardax, 
      CellProthera, Cereno Scientific, Elsevier Practice Update Cardiology, High 
      Enroll, Janssen, Level Ex, McKinsey, Medscape Cardiology, Merck, MyoKardia, 
      NirvaMed, Novo Nordisk, PhaseBio, PLx Pharma, Regado Biosciences, Stasys; Board 
      of Directors: Angiowave (stock options), Boston VA Research Institute, Bristol 
      Myers Squibb (stock), DRS.LINQ (stock options), High Enroll (stock), Society of 
      Cardiovascular Patient Care, TobeSoft; Chair: Inaugural Chair, American Heart 
      Association Quality Oversight Committee; Consultant: Broadview Ventures, Hims; 
      Data Monitoring Committees: Acesion Pharma, Assistance Publique-Hôpitaux de 
      Paris, Baim Institute for Clinical Research (formerly Harvard Clinical Research 
      Institute, for the PORTICO trial, funded by St. Jude Medical, now Abbott), Boston 
      Scientific (Chair, PEITHO trial), Cleveland Clinic (including for the ExCEED 
      trial, funded by Edwards), Contego Medical (Chair, PERFORMANCE 2), Duke Clinical 
      Research Institute, Mayo Clinic, Mount Sinai School of Medicine (for the ENVISAGE 
      trial, funded by Daiichi Sankyo; for the ABILITY-DM trial, funded by Concept 
      Medical), Novartis, Population Health Research Institute; Rutgers University (for 
      the NIH-funded MINT Trial); Honoraria: American College of Cardiology (Senior 
      Associate Editor, Clinical Trials and News, ACC.org; Chair, ACC Accreditation 
      Oversight Committee), Arnold and Porter law firm (work related to 
      Sanofi/Bristol-Myers Squibb clopidogrel litigation), Baim Institute for Clinical 
      Research (formerly Harvard Clinical Research Institute; RE-DUAL PCI clinical 
      trial steering committee funded by Boehringer Ingelheim; AEGIS-II executive 
      committee funded by CSL Behring), Belvoir Publications (Editor in Chief, Harvard 
      Heart Letter), Canadian Medical and Surgical Knowledge Translation Research Group 
      (clinical trial steering committees), Cowen and Company, Duke Clinical Research 
      Institute (clinical trial steering committees, including for the PRONOUNCE trial, 
      funded by Ferring Pharmaceuticals), HMP Global (Editor in Chief, Journal of 
      Invasive Cardiology), Journal of the American College of Cardiology (Guest 
      Editor; Associate Editor), K2P (Co-Chair, interdisciplinary curriculum), Level 
      Ex, Medtelligence/ReachMD (CME steering committees), MJH Life Sciences, Oakstone 
      CME (Course Director, Comprehensive Review of Interventional Cardiology), Piper 
      Sandler, Population Health Research Institute (for the COMPASS operations 
      committee, publications committee, steering committee, and USA national 
      co-leader, funded by Bayer), Slack Publications (Chief Medical Editor, Cardiology 
      Today’s Intervention), Society of Cardiovascular Patient Care 
      (Secretary/Treasurer), WebMD (CME steering committees), Wiley (steering 
      committee); Other: Clinical Cardiology (Deputy Editor), NCDR-ACTION Registry 
      Steering Committee (Chair), VA CART Research and Publications Committee (Chair); 
      Patent: Sotagliflozin (named on a patent for sotagliflozin assigned to Brigham 
      and Women's Hospital who assigned to Lexicon; neither I nor Brigham and Women's 
      Hospital receive any income from this patent); Research Funding: Abbott, Acesion 
      Pharma, Afimmune, Aker Biomarine, Amarin, Amgen, AstraZeneca, Bayer, Beren, 
      Boehringer Ingelheim, Boston Scientific, Bristol-Myers Squibb, Cardax, 
      CellProthera, Cereno Scientific, Chiesi, CinCor, Cleerly, CSL Behring, Eisai, 
      Ethicon, Faraday Pharmaceuticals, Ferring Pharmaceuticals, Forest Laboratories, 
      Fractyl, Garmin, HLS Therapeutics, Idorsia, Ironwood, Ischemix, Janssen, Javelin, 
      Lexicon, Lilly, Medtronic, Merck, Moderna, MyoKardia, NirvaMed, Novartis, Novo 
      Nordisk, Owkin, Pfizer, PhaseBio, PLx Pharma, Recardio, Regeneron, Reid Hoffman 
      Foundation, Roche, Sanofi, Stasys, Synaptic, The Medicines Company, Youngene, 
      89Bio; Royalties: Elsevier (Editor, Braunwald’s Heart Disease); Site 
      Co-Investigator: Abbott, Biotronik, Boston Scientific, CSI, Endotronix, St. Jude 
      Medical (now Abbott), Philips, SpectraWAVE, Svelte, Vascular Solutions; Trustee: 
      American College of Cardiology; Unfunded Research: FlowCo, Takeda. CC-S has acted 
      as a consultant for AbbVie, Gilead Sciences, Pfizer Inc and Regeneron-Sanofi; and 
      has received grant/research support from AbbVie, Bristol-Myers Squibb and Pfizer 
      Inc. JTG has acted as a consultant for AbbVie, Bristol-Myers Squibb, Eli Lilly, 
      Genentech, Gilead Sciences and UCB; and has received grant/research support from 
      Pfizer Inc. TRM has been a consultant for Pfizer and served on the ORAL 
      Surveillance Steering Committee; he has been a consultant for Horizon 
      Therapeutics, Sanofi, Gilead, and UCB and has research support from Horizon. GGK 
      is a shareholder of IQVIA, has received grant/research support from AbbVie, 
      Acceleron, Amgen, Arena, AstraZeneca, Cytokinetics, Eli Lilly, Gilead Sciences, 
      GlaxoSmithKline, Huya Bioscience International, Johnson & Johnson, Landos 
      Biopharma, Merck, Momentum, Novartis, Otsuka, Pfizer Inc, Sanofi, UCB, and vTv 
      Therapeutics, is an employee of the University of North Carolina at Chapel Hill. 
      He served as a member of the Steering Committee for ORAL Surveillance, with 
      funding from Pfizer Inc paid to the University of North Carolina at Chapel Hill. 
      SY has acted as a consultant for Corbus, Janssen, Kezar Life Sciences and Pfizer 
      Inc; and has received remuneration from Pfizer Inc for his services as a member 
      of the Steering Committee for ORAL Surveillance. EN, KK, CAC, KM, and AY are 
      employees and stockholders of Pfizer Inc. HJ is an employee of Syneos Health 
      which was a paid contractor to Pfizer in connection with the development of this 
      manuscript and data and statistical analysis.
EDAT- 2024/04/13 10:42
MHDA- 2024/04/15 06:43
PMCR- 2024/04/12
CRDT- 2024/04/12 21:33
PHST- 2023/11/15 00:00 [received]
PHST- 2024/03/24 00:00 [accepted]
PHST- 2024/04/15 06:43 [medline]
PHST- 2024/04/13 10:42 [pubmed]
PHST- 2024/04/12 21:33 [entrez]
PHST- 2024/04/12 00:00 [pmc-release]
AID - rmdopen-2023-003912 [pii]
AID - 10.1136/rmdopen-2023-003912 [doi]
PST - epublish
SO  - RMD Open. 2024 Apr 12;10(2):e003912. doi: 10.1136/rmdopen-2023-003912.

PMID- 38589871
OWN - NLM
STAT- MEDLINE
DCOM- 20240410
LR  - 20240411
IS  - 1741-7015 (Electronic)
IS  - 1741-7015 (Linking)
VI  - 22
IP  - 1
DP  - 2024 Apr 8
TI  - Characterizing the polygenic overlap and shared loci between rheumatoid arthritis 
      and cardiovascular diseases.
PG  - 152
LID - 10.1186/s12916-024-03376-1 [doi]
LID - 152
AB  - BACKGROUND: Despite substantial research revealing that patients with rheumatoid 
      arthritis (RA) have excessive morbidity and mortality of cardiovascular disease 
      (CVD), the mechanism underlying this association has not been fully known. This 
      study aims to systematically investigate the phenotypic and genetic correlation 
      between RA and CVD. METHODS: Based on UK Biobank, we conducted two cohort studies 
      to evaluate the phenotypic relationships between RA and CVD, including atrial 
      fibrillation (AF), coronary artery disease (CAD), heart failure (HF), and stroke. 
      Next, we used linkage disequilibrium score regression, Local Analysis of 
      [co]Variant Association, and bivariate causal mixture model (MiXeR) methods to 
      examine the genetic correlation and polygenic overlap between RA and CVD, using 
      genome-wide association summary statistics. Furthermore, we explored specific 
      shared genetic loci by conjunctional false discovery rate analysis and 
      association analysis based on subsets. RESULTS: Compared with the general 
      population, RA patients showed a higher incidence of CVD (hazard ratio 
      [HR] = 1.21, 95% confidence interval [CI]: 1.15-1.28). We observed positive 
      genetic correlations of RA with AF and stroke, and a mixture of negative and 
      positive local genetic correlations underlying the global genetic correlation for 
      CAD and HF, with 13 ~ 33% of shared genetic variants for these trait pairs. We 
      further identified 23 pleiotropic loci associated with RA and at least one CVD, 
      including one novel locus (rs7098414, TSPAN14, 10q23.1). Genes mapped to these 
      shared loci were enriched in immune and inflammatory-related pathways, and 
      modifiable risk factors, such as high diastolic blood pressure. CONCLUSIONS: This 
      study revealed the shared genetic architecture of RA and CVD, which may 
      facilitate drug target identification and improved clinical management.
CI  - © 2024. The Author(s).
FAU - Sun, Xiaohui
AU  - Sun X
AD  - Department of Epidemiology, School of Public Health, Zhejiang Chinese Medical 
      University, Hangzhou, 310053, China.
FAU - Qian, Yu
AU  - Qian Y
AD  - Department of Epidemiology, School of Public Health, Zhejiang Chinese Medical 
      University, Hangzhou, 310053, China.
AD  - School of Life Sciences, Westlake University, Hangzhou, 310024, China.
FAU - Cheng, Weiqiu
AU  - Cheng W
AD  - NORMENT, Institute of Clinical Medicine, University of Oslo, Oslo, 0407, Norway.
FAU - Ye, Ding
AU  - Ye D
AD  - Department of Epidemiology, School of Public Health, Zhejiang Chinese Medical 
      University, Hangzhou, 310053, China.
FAU - Liu, Bin
AU  - Liu B
AD  - Department of Epidemiology, School of Public Health, Zhejiang Chinese Medical 
      University, Hangzhou, 310053, China.
FAU - Zhou, Dan
AU  - Zhou D
AD  - School of Public Health and the Second Affiliated Hospital, Zhejiang University 
      School of Medicine, Hangzhou, China.
FAU - Wen, Chengping
AU  - Wen C
AD  - College of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 
      310053, China.
FAU - Andreassen, Ole A
AU  - Andreassen OA
AD  - NORMENT, Institute of Clinical Medicine, University of Oslo, Oslo, 0407, Norway. 
      ole.andreassen@medisin.uio.no.
FAU - Mao, Yingying
AU  - Mao Y
AUID- ORCID: 0000-0003-3644-9160
AD  - Department of Epidemiology, School of Public Health, Zhejiang Chinese Medical 
      University, Hangzhou, 310053, China. myy@zcmu.edu.cn.
LA  - eng
GR  - 82174208/National Natural Science Foundation of China/
GR  - 81973663/National Natural Science Foundation of China/
GR  - LQ21H260001/Natural Science Foundation of Zhejiang Province/
GR  - LQ20H260008/Natural Science Foundation of Zhejiang Province/
GR  - KC201905/he Foundation of Zhejiang Chinese Medical University/
GR  - 2020ZG01/he Foundation of Zhejiang Chinese Medical University/
GR  - 2020ZG016/the Foundation of Zhejiang Chinese Medical University/
GR  - 2021JKZKTS004A/the Foundation of Zhejiang Chinese Medical University/
GR  - #801133/part of convergence environment [4MENT] funded by UiO:Life Science and 
      Scientia Fellows, European Union's Horizon2020 Research and Innovation programme/
GR  - No. 847776/part of convergence environment [4MENT] funded by UiO:Life Science and 
      Scientia Fellows, European Union's Horizon2020 Research and Innovation programme/
GR  - #223273/Research Council of Norway/
GR  - #324252/Research Council of Norway/
PT  - Journal Article
DEP - 20240408
PL  - England
TA  - BMC Med
JT  - BMC medicine
JID - 101190723
SB  - IM
MH  - Humans
MH  - *Cardiovascular Diseases/epidemiology/genetics
MH  - Genome-Wide Association Study/methods
MH  - Genetic Predisposition to Disease/genetics
MH  - *Arthritis, Rheumatoid/genetics/epidemiology
MH  - *Coronary Artery Disease/genetics
MH  - *Heart Failure
MH  - *Stroke/epidemiology/genetics
MH  - Polymorphism, Single Nucleotide/genetics
PMC - PMC11003061
OTO - NOTNLM
OT  - Cardiovascular diseases
OT  - Epidemiological association
OT  - Genetic correlation
OT  - Pleiotropic loci
OT  - Rheumatoid arthritis
COIS- OAA is a consultant to HealtLytics. The other authors declare that they have no 
      competing interests.
EDAT- 2024/04/09 00:42
MHDA- 2024/04/10 06:42
PMCR- 2024/04/08
CRDT- 2024/04/08 23:45
PHST- 2023/07/05 00:00 [received]
PHST- 2024/03/26 00:00 [accepted]
PHST- 2024/04/10 06:42 [medline]
PHST- 2024/04/09 00:42 [pubmed]
PHST- 2024/04/08 23:45 [entrez]
PHST- 2024/04/08 00:00 [pmc-release]
AID - 10.1186/s12916-024-03376-1 [pii]
AID - 3376 [pii]
AID - 10.1186/s12916-024-03376-1 [doi]
PST - epublish
SO  - BMC Med. 2024 Apr 8;22(1):152. doi: 10.1186/s12916-024-03376-1.

PMID- 38586849
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240409
IS  - 1880-4276 (Print)
IS  - 1883-2148 (Electronic)
IS  - 1880-4276 (Linking)
VI  - 40
IP  - 2
DP  - 2024 Apr
TI  - Association between rheumatoid arthritis and atrial fibrillation: A systematic 
      review and meta-analysis.
PG  - 203-213
LID - 10.1002/joa3.12995 [doi]
AB  - Rheumatoid arthritis (RA) is an autoimmune disorder with a varying range of 
      organs involved leading to adverse outcomes. However, very little is known, with 
      conflicting results about the association between RA and atrial fibrillation 
      (AF). We aim to evaluate the association between RA and AF, and other clinical 
      outcomes. We performed a systematic literature search using PubMed, Embase, and 
      Scopus for relevant articles from inception until September 10, 2023. Primary 
      clinical outcomes were AF. Secondary outcomes were acute coronary syndrome (ACS), 
      stroke, and all-cause mortality (ACM). A total of 4 679 930 patients were 
      included in the analysis, with 81 677 patients in the RA group and 4 493 993 
      patients in the nonrheumatoid arthritis (NRA) group. The mean age of the patients 
      was 57.2 years. Pooled analysis of primary outcomes shows that RA groups of 
      patients had a significantly higher risk of AF (odds ratios [OR], 1.53; 95% 
      confidence interval [CI]: [1.16-2.03], p < .001) compared with NRA groups. 
      Secondary Outcomes show that the RA group of patients had significantly higher 
      odds of ACS (OR, 1.39; 95% CI: [1.26-1.52], p < .001), and ACM (OR, 1.19; 95% CI: 
      [1.03-1.37], p = .02) compared with the NRA groups. However, the likelihood of 
      stroke (OR, 1.02; 95% CI: [0.94-1.11], p = .61) was comparable between both 
      groups of patients. Our study shows that RA groups of patients are at increased 
      risk of having AF, ACS, and ACM.
CI  - © 2024 The Authors. Journal of Arrhythmia published by John Wiley & Sons 
      Australia, Ltd on behalf of Japanese Heart Rhythm Society.
FAU - Jaiswal, Vikash
AU  - Jaiswal V
AUID- ORCID: 0000-0002-2021-1660
AD  - Department of Cardiovascular Research Larkin Community Hospital South Miami 
      Florida USA.
FAU - Roy, Poulami
AU  - Roy P
AD  - Department of Internal Medicine North Bengal Medical College and Hospital 
      Siliguri India.
FAU - Ang, Song Peng
AU  - Ang SP
AD  - Department of Internal Medicine Rutgers Health/Community Medical Center Toms 
      River New Jersey USA.
FAU - Shama, Nishat
AU  - Shama N
AD  - Department of Internal Medicine Bangladesh Institute of Research and 
      Rehabilitation in Diabetes, Endocrine and Metabolic Disorders Dhaka Bangladesh.
FAU - Deb, Novonil
AU  - Deb N
AD  - Department of Internal Medicine North Bengal Medical College and Hospital 
      Siliguri India.
FAU - Taha, Amira Mohamed
AU  - Taha AM
AD  - Department of Medicine Fayoum University Fayoum Egypt.
FAU - Rajak, Kripa
AU  - Rajak K
AD  - Department of Internal Medicine UPMC Harrisburg Harrisburg Pennsylvania USA.
FAU - Sharma, Akanksha
AU  - Sharma A
AD  - Department of Internal Medicine UPMC Mercy Pittsburgh Pennsylvania USA.
FAU - Halder, Anupam
AU  - Halder A
AD  - Department of Internal Medicine UPMC Harrisburg Harrisburg Pennsylvania USA.
FAU - Wajid, Zarghoona
AU  - Wajid Z
AD  - Department of Internal Medicine, School of Medicine Wayne State University 
      Detroit Michigan USA.
FAU - Agrawal, Vibhor
AU  - Agrawal V
AUID- ORCID: 0000-0003-3174-2886
AD  - Department of Medicine King George's Medical University Lucknow India.
FAU - Khela, Harpriya
AU  - Khela H
AD  - Department of Medicine Royal College of Surgeons in Ireland Dublin Ireland.
FAU - Biswas, Monodeep
AU  - Biswas M
AD  - Department of Electrophysiology University of Maryland Baltimore Maryland USA.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20240123
PL  - Japan
TA  - J Arrhythm
JT  - Journal of arrhythmia
JID - 101263026
PMC - PMC10995606
OTO - NOTNLM
OT  - acute coronary syndrome
OT  - atrial fibrillation
OT  - mortality
OT  - rheumatoid arthritis
COIS- Vikash Jaiswal serves as an Associate editor section of Cardiology in the 
      European Journal of Medical Research, Frontiers in Cardiology, European Heart 
      Journal Imaging Methods and Practice, and Plos One.
EDAT- 2024/04/08 06:42
MHDA- 2024/04/08 06:43
PMCR- 2024/01/23
CRDT- 2024/04/08 04:51
PHST- 2023/07/05 00:00 [received]
PHST- 2023/12/26 00:00 [revised]
PHST- 2024/01/09 00:00 [accepted]
PHST- 2024/04/08 06:43 [medline]
PHST- 2024/04/08 06:42 [pubmed]
PHST- 2024/04/08 04:51 [entrez]
PHST- 2024/01/23 00:00 [pmc-release]
AID - JOA312995 [pii]
AID - 10.1002/joa3.12995 [doi]
PST - epublish
SO  - J Arrhythm. 2024 Jan 23;40(2):203-213. doi: 10.1002/joa3.12995. eCollection 2024 
      Apr.

PMID- 38531708
OWN - NLM
STAT- MEDLINE
DCOM- 20240717
LR  - 20240717
IS  - 1878-0938 (Electronic)
IS  - 1878-0938 (Linking)
VI  - 65
DP  - 2024 Aug
TI  - In-hospital outcomes and trends of patients with autoimmune diseases undergoing 
      percutaneous coronary intervention: A nationwide analysis.
PG  - 37-43
LID - S1553-8389(24)00073-3 [pii]
LID - 10.1016/j.carrev.2024.02.020 [doi]
AB  - BACKGROUND: The risk of coronary artery disease is exaggerated in patients with 
      autoimmune diseases (AID). A higher risk of complications has been reported 
      during and after percutaneous coronary intervention (PCI) in these patients. We 
      aimed to analyze the in-hospital outcomes and trends of patients with AID, 
      including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and 
      inflammatory bowel disease (IBD) undergoing PCI. METHOD: We identified all PCI 
      procedures using the National In-patient Sample database from 2016 to 2020. 
      Stratified them into cohorts with RA, SLE and IBD and compared them to cohorts 
      without AID. The Chi-square test and multivariate logistic regression were used 
      for analysis. A p-value <0.005 was considered statistically significant. RESULT: 
      We identified 2,367,475 patients who underwent PCI. Of these, 1.6 %, 0.5 %, and 
      0.4 % had RA, IBD and SLE respectively. The odds of mortality were lower among 
      patients with IBD (aOR: 0.56; CI 0.38-0.81, p = 0.002) but patients with RA had 
      higher odds of having composite major complications [(MC) including 
      cerebrovascular accident (CVA), cardiac arrest, acute heart failure (AHF), 
      ventricular arrhythmia (VA), major bleeding, and acute kidney injury (AKI)] (aOR: 
      0.90; CI 0.83-0.98, p = 0.013). Our SLE cohort had higher rates of CVA 
      (p = 0.017) and AKI (p = 0.002). Our cohort with IBD had lower rates of cardiac 
      arrest but had longer hospital length of stay (4.9 days vs 3.9 days) and they 
      incurred higher hospital charges compared to cohort without IBD. CONCLUSION: This 
      study depicts the immediate adverse outcomes observed in patients with AID 
      undergoing PCI. In contrast to those without AID, our cohorts with RA exhibited 
      worse outcomes, as indicated by the higher odds of major complications. IBD is 
      associated with lower risks of in-hospital adverse outcomes but with higher 
      resource utilization.
CI  - Copyright © 2024 Elsevier Inc. All rights reserved.
FAU - Antia, Akanimo
AU  - Antia A
AD  - Department of Medicine, Lincoln Medical Center, Bronx, NY, United States of 
      America. Electronic address: akanimousenantia@gmail.com.
FAU - Aomreore, Kessiena
AU  - Aomreore K
AD  - Department of Medicine, Lincoln Medical Center, Bronx, NY, United States of 
      America.
FAU - Udongwo, Ndausung
AU  - Udongwo N
AD  - Department of Medicine, Division of Cardiovascular Medicine, Morehouse School of 
      Medicine, Atlanta, GA, United States of America.
FAU - Menon, Sharika
AU  - Menon S
AD  - Department of Medicine, Division of Rheumatology, Lincoln Medical Center, Bronx, 
      NY, United States of America.
FAU - Ibebuogu, Uzoma
AU  - Ibebuogu U
AD  - Department of Medicine, Division of Cardiovascular Medicine, University of 
      Tennessee Health Science Center, Memphis, TN, United States of America.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20240325
PL  - United States
TA  - Cardiovasc Revasc Med
JT  - Cardiovascular revascularization medicine : including molecular interventions
JID - 101238551
SB  - IM
MH  - Humans
MH  - *Percutaneous Coronary Intervention/adverse effects/mortality/trends
MH  - Male
MH  - Female
MH  - Middle Aged
MH  - Aged
MH  - Treatment Outcome
MH  - *Databases, Factual
MH  - Risk Factors
MH  - *Coronary Artery Disease/mortality/therapy/diagnostic imaging
MH  - Time Factors
MH  - United States/epidemiology
MH  - Risk Assessment
MH  - *Hospital Mortality
MH  - Retrospective Studies
MH  - Lupus Erythematosus, 
      Systemic/mortality/diagnosis/therapy/complications/epidemiology
MH  - Length of Stay
MH  - Arthritis, Rheumatoid/mortality/diagnosis
MH  - Inflammatory Bowel Diseases/mortality/therapy
MH  - Autoimmune Diseases/mortality/epidemiology/therapy
OTO - NOTNLM
OT  - Autoimmune disease
OT  - Inflammatory bowel disease
OT  - Outcomes
OT  - Percutaneous coronary intervention
OT  - Rheumatoid arthritis
OT  - Systemic lupus erythematosus
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2024/03/27 00:44
MHDA- 2024/07/18 00:41
CRDT- 2024/03/26 22:55
PHST- 2024/01/04 00:00 [received]
PHST- 2024/02/21 00:00 [revised]
PHST- 2024/02/26 00:00 [accepted]
PHST- 2024/07/18 00:41 [medline]
PHST- 2024/03/27 00:44 [pubmed]
PHST- 2024/03/26 22:55 [entrez]
AID - S1553-8389(24)00073-3 [pii]
AID - 10.1016/j.carrev.2024.02.020 [doi]
PST - ppublish
SO  - Cardiovasc Revasc Med. 2024 Aug;65:37-43. doi: 10.1016/j.carrev.2024.02.020. Epub 
      2024 Mar 25.

PMID- 38443230
OWN - NLM
STAT- MEDLINE
DCOM- 20240319
LR  - 20240319
IS  - 2173-5743 (Electronic)
IS  - 2173-5743 (Linking)
VI  - 20
IP  - 3
DP  - 2024 Mar
TI  - Cardiovascular event in a cohort of rheumatoid arthritis patients in Castilla-La 
      Mancha: Utility of carotid ultrasound.
PG  - 150-154
LID - S2173-5743(24)00028-5 [pii]
LID - 10.1016/j.reumae.2024.02.005 [doi]
AB  - Rheumatoid Arthritis (RA) has a mortality rate 1,3 to 3 times higher than the 
      general population, with cardiovascular mortality accounting for 40-50% of cases. 
      Currently, cardiovascular disease is considered an extraarticular manifestation 
      of RA (OR: 1,5-4,0). Ultrasound measurement of the intima-media thickness (IMT) 
      of the common carotid artery and the presence of atherosclerotic plaques (AP) is 
      a non-invasive method and a surrogate marker of subclinical arteriosclerosis. 
      OBJECTIVE: To determine if subclinical arteriosclerosis findings through carotid 
      ultrasound can serve as a good predictor of cardiovascular events (CVE) 
      development in a cohort of RA patients over a 10-year period. METHODOLOGY: A 
      cohort of RA patients seen in the Rheumatology outpatient clinic of a hospital in 
      Castilla La Mancha in 2013 was evaluated. A prospective evaluation for the 
      development of CVE over the following 10 years was conducted, and its correlation 
      with previous ultrasound findings of IMT and AP was analyzed. RESULTS: Eight 
      (24%) patients experienced a CVE. Three (9%) had heart failure, three (9%) had a 
      stroke, and two (6%) experienced acute myocardial infarction. RA patients who 
      developed a CVE had a higher IMT (0,97 +/- 0.08 mm) compared to the RA patients 
      without CV complications (0,74 +/- 0.15 mm) (p = 0,003). The presence of 
      IMT ≥ 0.9 mm and AP had a relative risk of 12,25 (p = 0,012) and 18,66 
      (p = 0,003), respectively, for the development of a CVE. CONCLUSIONS: Carotid 
      ultrasound in RA patients may allow for early detection of subclinical 
      atherosclerosis before the development of CVE, with IMT ≥ 0.9 mm being the most 
      closely associated finding with CVE, unaffected by age.
CI  - Copyright © 2023 Elsevier España, S.L.U. and Sociedad Española de Reumatología y 
      Colegio Mexicano de Reumatología. All rights reserved.
FAU - Ramírez Huaranga, Marco Aurelio
AU  - Ramírez Huaranga MA
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain. Electronic address: maramirezh@sescam.jccm.es.
FAU - Velasco Sánchez, David
AU  - Velasco Sánchez D
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
FAU - Calvo Pascual, Luis Ángel
AU  - Calvo Pascual LÁ
AD  - Departamento de Métodos Cuantitativos, ICADE, Universidad Pontificia de Comillas, 
      Madrid, Spain.
FAU - Castro Corredor, David
AU  - Castro Corredor D
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
FAU - Mínguez Sánchez, María Dolores
AU  - Mínguez Sánchez MD
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
FAU - Salas Manzanedo, Verónica
AU  - Salas Manzanedo V
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
FAU - Revuelta Evrard, Eva
AU  - Revuelta Evrard E
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
FAU - Arenal López, Rocío
AU  - Arenal López R
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
FAU - Anino Fernández, Joaquín
AU  - Anino Fernández J
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
FAU - González Peñas, Marina
AU  - González Peñas M
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
FAU - Martin de la Sierra López, Lourdes
AU  - Martin de la Sierra López L
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
FAU - Jiménez Rodríguez, Laura María
AU  - Jiménez Rodríguez LM
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
FAU - López Menchero Mora, Alberto
AU  - López Menchero Mora A
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
FAU - Huertas, Marcos Paulino
AU  - Huertas MP
AD  - Servicio de Reumatología, Hospital General Universitario de Ciudad Real, Ciudad 
      Real, Spain.
LA  - eng
PT  - Case Reports
DEP - 20240304
PL  - Spain
TA  - Reumatol Clin (Engl Ed)
JT  - Reumatologia clinica
JID - 101717526
SB  - IM
MH  - Humans
MH  - Carotid Intima-Media Thickness
MH  - Risk Factors
MH  - *Arthritis, Rheumatoid/complications/diagnostic imaging
MH  - *Atherosclerosis/complications
MH  - *Cardiovascular Diseases/diagnostic imaging/etiology
OTO - NOTNLM
OT  - Artritis reumatoide
OT  - Atheromatous plaque
OT  - Cardiovascular event
OT  - Carotid ultrasound
OT  - Ecografía carotídea
OT  - Evento cardiovascular
OT  - Grosor íntimo medial
OT  - Medial intima thickness
OT  - Placa ateromatosa
OT  - Rheumatoid arthritis
EDAT- 2024/03/06 00:42
MHDA- 2024/03/19 06:44
CRDT- 2024/03/05 21:56
PHST- 2023/08/04 00:00 [received]
PHST- 2023/11/11 00:00 [accepted]
PHST- 2024/03/19 06:44 [medline]
PHST- 2024/03/06 00:42 [pubmed]
PHST- 2024/03/05 21:56 [entrez]
AID - S2173-5743(24)00028-5 [pii]
AID - 10.1016/j.reumae.2024.02.005 [doi]
PST - ppublish
SO  - Reumatol Clin (Engl Ed). 2024 Mar;20(3):150-154. doi: 
      10.1016/j.reumae.2024.02.005. Epub 2024 Mar 4.

PMID- 38404587
OWN - NLM
STAT- MEDLINE
DCOM- 20240227
LR  - 20240325
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 15
DP  - 2024
TI  - Evaluating the risk of ischemic stroke at a young age in patients with autoimmune 
      inflammatory rheumatic diseases: a population-based cohort study in Taiwan.
PG  - 1272557
LID - 10.3389/fimmu.2024.1272557 [doi]
LID - 1272557
AB  - BACKGROUND: Recent studies have demonstrated an increased incidence of ischemic 
      stroke among patients with certain autoimmune inflammatory rheumatic diseases 
      (AIIRDs). However, the associations between young stroke and AIIRDs have not been 
      fully investigated. This study aimed to evaluate the risk of ischemic stroke 
      among young patients with AIIRDs. METHODS: The National Health Insurance Research 
      Database in Taiwan was utilized to establish cohorts of patients with AIIRDs 
      diagnosed between 2004 and 2015, who were compared with 1,000,000 control 
      participants. Cox proportional hazards regression models were used to calculate 
      the hazard ratio of ischemic stroke and young ischemic stroke for individual 
      AIIRDs after adjustment for relative risk factors. RESULTS: During the study 
      period, a total of 64,120 patients with AIIRDss and 1,000,000 control patients 
      were identified. The overall mean follow-up time was 5.33 years. There were 223 
      (0.8%) and 1,923 (0.3%) young ischemic stroke-related hospitalizations among 
      patients with AIIRDs and controls, respectively. The incidence rate of young 
      ischemic stroke was 0.08 in patients with rheumatoid arthritis, 0.08 in patients 
      with Sjögren's syndrome, 0.26 in patients with systemic lupus erythematosus, 0.17 
      in patients with idiopathic inflammatory myositis, 0.24 in patients with systemic 
      sclerosis, 0.05 in patients with Behçet's disease, and 0.44 in patients with 
      systemic vasculitis, versus 0.05 per 100 person-years in the general population. 
      The adjusted hazard ratios for young ischemic stroke were 1.07 (95% CI 0.70-1.43) 
      for rheumatoid arthritis, 1.39 (95% CI 0.94-2.06) for Sjögren's syndrome, 5.79 
      (95% CI 4.68-7.17) for systemic lupus erythematosus, 2.07 for idiopathic 
      inflammatory myositis (95% CI 0.98-4.38), 2.79 for systemic sclerosis (95% CI 
      1.38-5.63), 0.82 for Behçet's disease (95% CI 0.26-2.55), and 4.15 (95% CI 
      1.96-8.82) for systemic vasculitis. CONCLUSIONS: Patients younger than 50 years 
      with systemic lupus erythematosus, systemic sclerosis, or systemic vasculitis 
      have a significantly elevated risk of developing ischemic stroke. Further 
      research is needed to elucidate the pathogenesis of accelerated atherosclerosis 
      in these AIIRDs.
CI  - Copyright © 2024 Huang, Lai, Liao and Weng.
FAU - Huang, Ya-Chun
AU  - Huang YC
AD  - Division of Allergy, Immunology, and Rheumatology, Department of Internal 
      Medicine, National Cheng Kung University Hospital, College of Medicine, National 
      Cheng Kung University, Tainan, Taiwan.
FAU - Lai, Edward Chia-Cheng
AU  - Lai EC
AD  - School of Pharmacy, Institute of Clinical Pharmacy and Pharmaceutical Sciences, 
      College of Medicine, National Cheng Kung University, Tainan, Taiwan.
FAU - Liao, Tzu-Chi
AU  - Liao TC
AD  - School of Pharmacy, Institute of Clinical Pharmacy and Pharmaceutical Sciences, 
      College of Medicine, National Cheng Kung University, Tainan, Taiwan.
FAU - Weng, Meng-Yu
AU  - Weng MY
AD  - Division of Allergy, Immunology, and Rheumatology, Department of Internal 
      Medicine, National Cheng Kung University Hospital, College of Medicine, National 
      Cheng Kung University, Tainan, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20240209
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
SB  - IM
MH  - Humans
MH  - *Sjogren's Syndrome/complications
MH  - *Ischemic Stroke/epidemiology/etiology
MH  - Cohort Studies
MH  - *Behcet Syndrome/complications
MH  - Taiwan/epidemiology
MH  - *Arthritis, Rheumatoid/complications
MH  - *Lupus Erythematosus, Systemic/diagnosis
MH  - *Scleroderma, Systemic/complications
MH  - *Rheumatic Fever
MH  - *Myositis/complications
MH  - *Systemic Vasculitis
PMC - PMC10884215
OTO - NOTNLM
OT  - autoimmune inflammatory rheumatic disease
OT  - epidemiology
OT  - incidence
OT  - ischemic stroke
OT  - young stroke
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2024/02/26 06:43
MHDA- 2024/02/27 06:44
PMCR- 2024/01/01
CRDT- 2024/02/26 04:28
PHST- 2023/08/04 00:00 [received]
PHST- 2024/01/22 00:00 [accepted]
PHST- 2024/02/27 06:44 [medline]
PHST- 2024/02/26 06:43 [pubmed]
PHST- 2024/02/26 04:28 [entrez]
PHST- 2024/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2024.1272557 [doi]
PST - epublish
SO  - Front Immunol. 2024 Feb 9;15:1272557. doi: 10.3389/fimmu.2024.1272557. 
      eCollection 2024.

PMID- 38351113
OWN - NLM
STAT- MEDLINE
DCOM- 20240215
LR  - 20240217
IS  - 2044-6055 (Electronic)
IS  - 2044-6055 (Linking)
VI  - 14
IP  - 2
DP  - 2024 Feb 13
TI  - Effect of acupuncture on ischaemic stroke in patients with rheumatoid arthritis: 
      a nationwide propensity score-matched study.
PG  - e075218
LID - 10.1136/bmjopen-2023-075218 [doi]
LID - e075218
AB  - OBJECTIVE: To demonstrate that acupuncture is beneficial for decreasing the risk 
      of ischaemic stroke in patients with rheumatoid arthritis (RA). DESIGN: A 
      propensity score-matched cohort study. SETTING: A nationwide population-based 
      study. PARTICIPANTS: Patients with RA diagnosed between 1 January 1997 and 31 
      December 2010, through the National Health Insurance Research Database in Taiwan. 
      INTERVENTIONS: Patients who were administered acupuncture therapy from the 
      initial date of RA diagnosis to 31 December 2010 were included in the acupuncture 
      cohort. Patients who did not receive acupuncture treatment during the same time 
      interval constituted the no-acupuncture cohort. PRIMARY OUTCOME MEASURES: A Cox 
      regression model was used to adjust for age, sex, comorbidities, and types of 
      drugs used. We compared the subhazard ratios (SHRs) of ischaemic stroke between 
      these two cohorts through competing-risks regression models. RESULTS: After 1:1 
      propensity score matching, a total of 23 226 patients with newly diagnosed RA 
      were equally subgrouped into acupuncture cohort or no-acupuncture cohort 
      according to their use of acupuncture. The basic characteristics of these 
      patients were similar. A lower cumulative incidence of ischaemic stroke was found 
      in the acupuncture cohort (log-rank test, p<0.001; immortal time (period from 
      initial diagnosis of RA to index date) 1065 days; mean number of acupuncture 
      visits 9.83. In the end, 341 patients in the acupuncture cohort (5.95 per 1000 
      person-years) and 605 patients in the no-acupuncture cohort (12.4 per 1000 
      person-years) experienced ischaemic stroke (adjusted SHR 0.57, 95% CI 0.50 to 
      0.65). The advantage of lowering ischaemic stroke incidence through acupuncture 
      therapy in RA patients was independent of sex, age, types of drugs used, and 
      comorbidities. CONCLUSIONS: This study showed the beneficial effect of 
      acupuncture in reducing the incidence of ischaemic stroke in patients with RA.
CI  - © Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No 
      commercial re-use. See rights and permissions. Published by BMJ.
FAU - Huang, Chia-Yu
AU  - Huang CY
AUID- ORCID: 0000-0003-2696-808X
AD  - Department of Family Medicine, Taichung Tzu Chi Hospital, Buddhist Tzu Chi 
      Medical Foundation, Taichung, Taiwan.
AD  - Graduate Institute of Chinese Medicine, School of Chinese Medicine, College of 
      Chinese Medicine, China Medical University, Taichung, Taiwan.
FAU - Huang, Ming-Cheng
AU  - Huang MC
AD  - Graduate Institute of Chinese Medicine, School of Chinese Medicine, College of 
      Chinese Medicine, China Medical University, Taichung, Taiwan.
AD  - Department of Chinese Medicine, China Medical University Hospital, Taichung, 
      Taiwan.
AD  - Graduate Institute of Acupuncture Science, College of Chinese Medicine, China 
      Medical University, Taichung, Taiwan.
FAU - Liao, Hou-Hsun
AU  - Liao HH
AD  - Graduate Institute of Chinese Medicine, School of Chinese Medicine, College of 
      Chinese Medicine, China Medical University, Taichung, Taiwan.
AD  - Department of Chinese Medicine, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical 
      Foundation, Chiayi, Taiwan.
AD  - Department of Nursing, Tzu Chi University of Science and Technology, Hualien, 
      Taiwan.
FAU - Lin, Cheng-Li
AU  - Lin CL
AD  - Management Office for Health Data, China Medical University Hospital, Taichung, 
      Taiwan.
AD  - College of Medicine, China Medical University, Taichung, Taiwan.
FAU - Lee, Yu-Chen
AU  - Lee YC
AUID- ORCID: 0000-0002-9510-3146
AD  - Department of Chinese Medicine, China Medical University Hospital, Taichung, 
      Taiwan.
AD  - Graduate Institute of Acupuncture Science, College of Chinese Medicine, China 
      Medical University, Taichung, Taiwan.
FAU - Zimmerman, Gregory
AU  - Zimmerman G
AD  - Graduate Institute of Acupuncture Science, College of Chinese Medicine, China 
      Medical University, Taichung, Taiwan.
AD  - International Master Program in Acupuncture, College of Chinese Medicine, China 
      Medical University, Taichung, Taiwan.
FAU - Wu, Mei-Yao
AU  - Wu MY
AD  - Department of Chinese Medicine, China Medical University Hospital, Taichung, 
      Taiwan hungrongyen@gmail.com hungrongyen@mail.cmu.edu.tw Meiyaowu0919@gmail.com.
AD  - School of Post-Baccalaureate Chinese Medicine, College of Chinese Medicine, China 
      Medical University, Taichung, Taiwan.
AD  - Research Center for Traditional Chinese Medicine, Department of Medical Research, 
      China Medical University Hospital, Taichung, Taiwan.
FAU - Yen, Hung-Rong
AU  - Yen HR
AUID- ORCID: 0000-0002-0131-1658
AD  - Graduate Institute of Chinese Medicine, School of Chinese Medicine, College of 
      Chinese Medicine, China Medical University, Taichung, Taiwan 
      hungrongyen@gmail.com hungrongyen@mail.cmu.edu.tw Meiyaowu0919@gmail.com.
AD  - Department of Chinese Medicine, China Medical University Hospital, Taichung, 
      Taiwan.
AD  - International Master Program in Acupuncture, College of Chinese Medicine, China 
      Medical University, Taichung, Taiwan.
AD  - Research Center for Traditional Chinese Medicine, Department of Medical Research, 
      China Medical University Hospital, Taichung, Taiwan.
AD  - Chinese Medicine Research Center, China Medical University, Taichung, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20240213
PL  - England
TA  - BMJ Open
JT  - BMJ open
JID - 101552874
SB  - IM
MH  - Humans
MH  - Cohort Studies
MH  - *Stroke/epidemiology/therapy/etiology
MH  - Propensity Score
MH  - *Brain Ischemia/epidemiology/etiology/therapy
MH  - *Acupuncture Therapy/adverse effects
MH  - *Arthritis, Rheumatoid/complications/therapy
MH  - *Ischemic Stroke/complications
MH  - Incidence
MH  - Taiwan/epidemiology
MH  - Risk Factors
MH  - Retrospective Studies
PMC - PMC10868250
OTO - NOTNLM
OT  - Acupuncture
OT  - Cardiovascular diseases
OT  - National Health Insurance Research Database
OT  - Rheumatoid arthritis
OT  - Stroke
COIS- Competing interests: The authors declare that the research was conducted in the 
      absence of any commercial or financial relationships that could be construed as 
      potential conflicts of interest.
EDAT- 2024/02/14 00:44
MHDA- 2024/02/15 06:43
PMCR- 2024/02/13
CRDT- 2024/02/13 23:46
PHST- 2024/02/15 06:43 [medline]
PHST- 2024/02/14 00:44 [pubmed]
PHST- 2024/02/13 23:46 [entrez]
PHST- 2024/02/13 00:00 [pmc-release]
AID - bmjopen-2023-075218 [pii]
AID - 10.1136/bmjopen-2023-075218 [doi]
PST - epublish
SO  - BMJ Open. 2024 Feb 13;14(2):e075218. doi: 10.1136/bmjopen-2023-075218.

PMID- 38294723
OWN - NLM
STAT- MEDLINE
DCOM- 20240201
LR  - 20241023
IS  - 1591-9528 (Electronic)
IS  - 1591-8890 (Print)
IS  - 1591-8890 (Linking)
VI  - 24
IP  - 1
DP  - 2024 Jan 31
TI  - Stroke risk in rheumatoid arthritis patients: exploring connections and 
      implications for patient care.
PG  - 30
LID - 10.1007/s10238-023-01288-7 [doi]
LID - 30
AB  - Rheumatoid arthritis (RA) can independently increase the risk of stroke, 
      affecting both young and adult RA patients. Recent attention has been drawn to 
      the association between stroke and RA, supported by mounting evidence. Given that 
      stroke is a significant and an urgent public health concern, this review aims to 
      highlight the relationship between stroke and RA, covering mechanisms, underlying 
      risk factors, early detection tools, and treatment implications. By uncovering 
      the connection that links RA to stroke, we can pave the way for targeted 
      healthcare practices and the development of preventive strategies for individuals 
      with RA. Therefore, further research is imperative to deepen our understanding of 
      this association and, ideally, guide treatment decisions for individuals at risk 
      of both RA and stroke.
CI  - © 2024. The Author(s).
FAU - Al-Ewaidat, Ola A
AU  - Al-Ewaidat OA
AD  - Department of Internal Medicine, Ascension Saint Francis Hospital, Evanston, IL, 
      60202, USA.
FAU - Naffaa, Moawiah M
AU  - Naffaa MM
AD  - Department of Psychology and Neuroscience, Duke University, Durham, NC, 27708, 
      USA. Moawiah.naffaa@duke.edu.
AD  - Department of Cell Biology, Duke University School of Medicine, Durham, NC, 
      27710, USA. Moawiah.naffaa@duke.edu.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20240131
PL  - Italy
TA  - Clin Exp Med
JT  - Clinical and experimental medicine
JID - 100973405
SB  - IM
MH  - Adult
MH  - Humans
MH  - Patient Care
MH  - *Arthritis, Rheumatoid/complications/epidemiology
MH  - Risk Factors
MH  - *Stroke/epidemiology/etiology
PMC - PMC10830780
OTO - NOTNLM
OT  - Anti-cyclic citrullinated peptide (Anti-CCP2) test
OT  - Cardiovascular disease (CVD)
OT  - Chronic inflammation
OT  - Multi-biomarker disease activity (MBDA)
OT  - Rheumatoid arthritis (RA)
OT  - Rheumatoid factor (RF)
OT  - Stroke
COIS- The authors declare no conflicts of interest.
EDAT- 2024/01/31 12:43
MHDA- 2024/02/01 06:42
PMCR- 2024/01/31
CRDT- 2024/01/31 11:20
PHST- 2023/09/17 00:00 [received]
PHST- 2023/11/04 00:00 [accepted]
PHST- 2024/02/01 06:42 [medline]
PHST- 2024/01/31 12:43 [pubmed]
PHST- 2024/01/31 11:20 [entrez]
PHST- 2024/01/31 00:00 [pmc-release]
AID - 10.1007/s10238-023-01288-7 [pii]
AID - 1288 [pii]
AID - 10.1007/s10238-023-01288-7 [doi]
PST - epublish
SO  - Clin Exp Med. 2024 Jan 31;24(1):30. doi: 10.1007/s10238-023-01288-7.

PMID- 38288824
OWN - NLM
STAT- MEDLINE
DCOM- 20240403
LR  - 20240528
IS  - 1875-5828 (Electronic)
IS  - 1567-2050 (Linking)
VI  - 20
IP  - 10
DP  - 2023
TI  - Association of Autoimmune Disorders and Disease-modifying Antirheumatic Drugs: 
      (DMARDs) with the Risk of Alzheimer's and/or Dementia: A Population Study Using 
      Medicare Beneficiary Data.
PG  - 725-737
LID - 10.2174/0115672050289966240110041616 [doi]
AB  - OBJECTIVES: Alzheimer's disease (AD) and/or dementia is a prevalent 
      neurocognitive disorder primarily affecting individuals over the age of 65. 
      Identifying specific causes of AD and/or dementia can be challenging, with 
      emerging evidence suggesting a potential association with autoimmune inflammatory 
      conditions such as rheumatoid arthritis (RA). This study aimed to assess the 
      prevalence rate of AD and/or dementia among Medicare beneficiaries reporting an 
      autoimmune disorder. Additionally, this study sought to identify the comparative 
      prevalence of AD and/or dementia in patients with an autoimmune disorder who were 
      using disease-modifying antirheumatic drugs (DMARDs) compared to those not using 
      DMARDs. METHODS: Cross-sectional secondary data analyses were conducted on 
      Medicare Current Beneficiary Survey (MCBS) data from 2017 and 2018. The MCBS data 
      consists of a nationally representative sample of the Medicare population, a 
      population that is largely 65 and older, and provides de-identified patient 
      information. Patients from this dataset with a self-reported autoimmune disorder 
      were included in the analyses. Descriptive analyses were conducted on demographic 
      variables, chronic conditions, and medication use. The prevalence of AD and/or 
      dementia was compared between patients with and without an autoimmune disorder. A 
      backward stepwise selection regression was used to identify the risk factors 
      associated with the prevalence of AD and/or dementia. RESULTS: The study included 
      18,929 Medicare beneficiaries, with 4,405 identified as having one autoimmune 
      disorder. The prevalence of AD and/or dementia was significantly higher in 
      patients with an autoimmune disorder. The multivariate regression showed that RA 
      was significantly associated with a higher risk of AD and/or dementia. Other 
      demographic factors, including advanced age, African-American or Hispanic 
      ethnicity, low body mass index, and chronic conditions of ischemic heart disease, 
      history of myocardial infarction, history of stroke, depression, mental health 
      disorder(s), and traumatic brain injury also showed statistically significant 
      associations with AD and/or dementia. Patients using DMARDs demonstrated a 
      reduced likelihood of having AD and/or dementia, compared to patients not using 
      DMARDs. CONCLUSION: This study provides evidence of an association between RA and 
      increased risk of AD and/or dementia. The findings suggest that DMARD use may 
      have a protective effect against the development of AD and/or dementia in 
      patients with an autoimmune disorder.
CI  - Copyright© Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Ding, Qian
AU  - Ding Q
AUID- ORCID: 0000-0002-7948-9827
AD  - Ferris State University College of Pharmacy, 220 Ferris Drive, Big Rapids, MI 
      49307, USA.
FAU - Lamberts, Jennifer
AU  - Lamberts J
AUID- ORCID: 0000-0002-2135-0814
AD  - Ferris State University College of Pharmacy, 220 Ferris Drive, Big Rapids, MI 
      49307, USA.
FAU - Konieczny, Alison M
AU  - Konieczny AM
AUID- ORCID: 0000-0002-8892-1044
AD  - Ferris Library for Information, Technology, and Education, Big Rapids, MI 49307, 
      USA.
FAU - Bringedahl, Tyler B
AU  - Bringedahl TB
AD  - Trinity Health Muskegon, 1500 East Sherman Blvd., Muskegon, MI 49444, USA.
FAU - Torres Garcia, Kiara Y
AU  - Torres Garcia KY
AD  - St. Joseph Health System Family Medicine Center, 611 E Douglas Rd., Mishawaka, IN 
      46545, USA.
LA  - eng
PT  - Journal Article
PL  - United Arab Emirates
TA  - Curr Alzheimer Res
JT  - Current Alzheimer research
JID - 101208441
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Humans
MH  - Aged
MH  - United States/epidemiology
MH  - *Antirheumatic Agents/therapeutic use
MH  - *Alzheimer Disease/drug therapy/epidemiology
MH  - Medicare
MH  - Cross-Sectional Studies
MH  - *Arthritis, Rheumatoid/complications/drug therapy/epidemiology
MH  - Chronic Disease
OTO - NOTNLM
OT  - Alzheimer’s disease
OT  - Dementia
OT  - Medicare Current Beneficiary Survey.
OT  - autoimmune disorders
OT  - disease-modifying antirheumatic drugs
OT  - rheumatoid arthritis
EDAT- 2024/01/30 12:42
MHDA- 2024/04/03 06:45
CRDT- 2024/01/30 07:58
PHST- 2023/10/28 00:00 [received]
PHST- 2023/12/26 00:00 [revised]
PHST- 2024/01/02 00:00 [accepted]
PHST- 2024/04/03 06:45 [medline]
PHST- 2024/01/30 12:42 [pubmed]
PHST- 2024/01/30 07:58 [entrez]
AID - CAR-EPUB-138074 [pii]
AID - 10.2174/0115672050289966240110041616 [doi]
PST - ppublish
SO  - Curr Alzheimer Res. 2023;20(10):725-737. doi: 
      10.2174/0115672050289966240110041616.

PMID- 38157014
OWN - NLM
STAT- MEDLINE
DCOM- 20240119
LR  - 20240202
IS  - 1437-160X (Electronic)
IS  - 0172-8172 (Linking)
VI  - 44
IP  - 2
DP  - 2024 Feb
TI  - Prevalence of cardiovascular diseases and traditional cardiovascular risk factors 
      in patients with rheumatoid arthritis: a real-life evidence from BioSTAR 
      nationwide registry.
PG  - 291-301
LID - 10.1007/s00296-023-05515-y [doi]
AB  - Patients with rheumatoid arthritis (RA) have increased morbidity and mortality 
      due to cardiovascular (CV) comorbidities. The association of CV diseases (CVD) 
      and traditional CV risk factors has been debated, depending on patient and RA 
      characteristics. This study aimed to find the prevalence of CVD and CV risk 
      factors in patients with RA. A multi-center cross-sectional study was performed 
      on RA patients using the BioSTAR (Biological and Targeted Synthetic 
      Disease-Modifying Antirheumatic Drugs Registry) in September 2022. 
      Socio-demographic, clinical, and follow-up data were collected. Myocardial 
      infarction, ischemic heart disease, peripheral vascular disorders, congestive 
      heart failure, ischemic stroke, and transient ischemic attack were regarded as 
      major adverse cardiovascular events (MACEs). CVD was defined as the presence of 
      at least one clinical situation of MACE. Group 1 and Group 2 included patients 
      with and without CVD. Prevalence rates of CVD and traditional CV risk factors 
      were the primary outcomes. Secondary outcomes were the differences in the 
      clinical characteristics between patients with and without CVD. An analysis of 
      724 patients with a mean age of 55.1 ± 12.8 years diagnosed with RA was 
      conducted. There was a female preponderance (79.6%). The prevalence rate of CVD 
      was 4.6% (n = 33). The frequencies of the diseases in the MACE category were 
      ischemic heart disease in 27, congestive heart failure in five, peripheral 
      vascular disorders in three, and cerebrovascular events in three patients. The 
      patients with CVD (Group 1) were significantly male, older, and had higher BMI 
      (p = 0.027, p < 0.001, and p = 0.041). Obesity (33.4%) and hypertension (27.2%) 
      were the two CV risk factors most frequently. Male sex (HR = 7.818, 95% CI 
      3.030-20.173, p < 0.001) and hypertension (HR = 4.570, 95% CI 1.567-13.328, 
      p = 0.005) were the independent risk factors for CVD. The prevalence of CVD in RA 
      patients was 4.6%. Some common risk factors for CVD in the general population, 
      including male sex, older age, and hypertension, were evident in RA patients. 
      Male sex and hypertension were the independent risk factors for developing CVD in 
      patients with RA.
CI  - © 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, 
      part of Springer Nature.
FAU - Duruöz, Mehmet Tuncay
AU  - Duruöz MT
AUID- ORCID: 0000-0003-3584-2788
AD  - Division of Rheumatology, Department of Physical Medicine and Rehabilitaton, 
      Faculty of Medicine, Marmara University, İstanbul, Türkiye. 
      tuncayduruoz@gmail.com.
FAU - Ataman, Şebnem
AU  - Ataman Ş
AUID- ORCID: 0000-0003-3570-3825
AD  - Division of Rheumatology, Department of Physical Medicine and Rehabilitaton, 
      Faculty of Medicine, Ankara University, Ankara, Türkiye.
FAU - Bodur, Hatice
AU  - Bodur H
AUID- ORCID: 0000-0003-3008-7007
AD  - Department of Physical Medicine and Rehabilitaton, Ankara City Hospital, Faculty 
      of Medicine, Yıldırım Beyazıt University, Ankara, Türkiye.
FAU - Çay, Hasan Fatih
AU  - Çay HF
AUID- ORCID: 0000-0003-4838-1650
AD  - Department of Physical Medicine Rehabilitation and Rheumatology, Antalya Training 
      and Research Hospital, University of Health Sciences, Antalya, Türkiye.
FAU - Melikoğlu, Meltem Alkan
AU  - Melikoğlu MA
AUID- ORCID: 0000-0001-7519-9470
AD  - Department of Physical Medicine Rehabilitation and Rheumatology, School of 
      Medicine, Atatürk University, Erzurum, Türkiye.
FAU - Akgül, Özgür
AU  - Akgül Ö
AUID- ORCID: 0000-0003-3012-2968
AD  - Division of Rheumatology, Department of Physical Medicine and Rehabilitation, 
      School of Medicine, Manisa Celal Bayar University, Manisa, Türkiye.
FAU - Çapkın, Erhan
AU  - Çapkın E
AUID- ORCID: 0000-0003-2728-5934
AD  - Department of Physical Medicine and Rehabilitaton, School of Medicine, Karadeniz 
      Technical University, Trabzon, Türkiye.
FAU - Gürer, Gülcan
AU  - Gürer G
AUID- ORCID: 0000-0001-8287-2264
AD  - Department of Physical Medicine Rehabilitation and Rheumatology, University 
      School of Medicine, Adnan Menderes University, Aydın, Türkiye.
FAU - Çevik, Remzi
AU  - Çevik R
AUID- ORCID: 0000-0002-4124-1586
AD  - Department of Physical Medicine and Rehabilitaton, School of Medicine, Dicle 
      University, Diyarbakır, Türkiye.
FAU - Göğüş, Feride Nur
AU  - Göğüş FN
AUID- ORCID: 0000-0003-0921-5991
AD  - Department of Physical Medicine Rehabilitation and Rheumatology, School of 
      Medicine, Gazi University, Ankara, Türkiye.
FAU - Kamanlı, Ayhan
AU  - Kamanlı A
AUID- ORCID: 0000-0001-5299-7250
AD  - Department of Physical Medicine Rehabilitation and Rheumatology, School of 
      Medicine, Sakarya University, Sakarya, Türkiye.
FAU - Yurdakul, Fatma Gül
AU  - Yurdakul FG
AUID- ORCID: 0000-0001-8630-9233
AD  - Department of Physical Medicine and Rehabilitaton, Ankara City Hospital, 
      University of Health Sciences, Ankara, Türkiye.
FAU - Yağcı, İlker
AU  - Yağcı İ
AUID- ORCID: 0000-0002-5988-7369
AD  - Department of Physical Medicine and Rehabilitaton, Faculty of Medicine, Marmara 
      University, İstanbul, Türkiye.
FAU - Rezvani, Aylin
AU  - Rezvani A
AUID- ORCID: 0000-0002-5852-3854
AD  - Department of Physical Medicine and Rehabilitaton, Internatonal School of 
      Medicine, İstanbul Medipol University, İstanbul, Türkiye.
FAU - Altan, Lale
AU  - Altan L
AUID- ORCID: 0000-0002-6453-8382
AD  - Department of Physical Medicine Rehabilitation and Rheumatology, Faculty of 
      Medicine, Uludağ University, Bursa, Türkiye.
LA  - eng
PT  - Journal Article
DEP - 20231229
PL  - Germany
TA  - Rheumatol Int
JT  - Rheumatology international
JID - 8206885
SB  - IM
MH  - Humans
MH  - Male
MH  - Female
MH  - Adult
MH  - Middle Aged
MH  - Aged
MH  - *Cardiovascular Diseases/etiology
MH  - Risk Factors
MH  - Prevalence
MH  - Cross-Sectional Studies
MH  - *Arthritis, Rheumatoid/drug therapy/epidemiology/complications
MH  - *Hypertension/epidemiology
MH  - *Heart Failure/epidemiology/complications
MH  - Heart Disease Risk Factors
MH  - Registries
OTO - NOTNLM
OT  - Cardiovascular risk
OT  - Comorbidity
OT  - Major adverse cardiac events
OT  - Prevalence
OT  - Rheumatoid arthritis
OT  - Secondary disease prevention
EDAT- 2024/01/02 11:45
MHDA- 2024/01/19 06:42
CRDT- 2023/12/29 11:05
PHST- 2023/10/23 00:00 [received]
PHST- 2023/11/27 00:00 [accepted]
PHST- 2024/01/19 06:42 [medline]
PHST- 2024/01/02 11:45 [pubmed]
PHST- 2023/12/29 11:05 [entrez]
AID - 10.1007/s00296-023-05515-y [pii]
AID - 10.1007/s00296-023-05515-y [doi]
PST - ppublish
SO  - Rheumatol Int. 2024 Feb;44(2):291-301. doi: 10.1007/s00296-023-05515-y. Epub 2023 
      Dec 29.

PMID- 38147328
OWN - NLM
STAT- MEDLINE
DCOM- 20240214
LR  - 20241023
IS  - 2168-6157 (Electronic)
IS  - 2168-6149 (Print)
IS  - 2168-6149 (Linking)
VI  - 81
IP  - 2
DP  - 2024 Feb 1
TI  - Risk Factors for Young-Onset Dementia in the UK Biobank.
PG  - 134-142
LID - 10.1001/jamaneurol.2023.4929 [doi]
AB  - IMPORTANCE: There is limited information on modifiable risk factors for 
      young-onset dementia (YOD). OBJECTIVE: To examine factors that are associated 
      with the incidence of YOD. DESIGN, SETTING, AND PARTICIPANTS: This prospective 
      cohort study used data from the UK Biobank, with baseline assessment between 2006 
      and 2010 and follow-up until March 31, 2021, for England and Scotland, and 
      February 28, 2018, for Wales. Participants younger than 65 years and without a 
      dementia diagnosis at baseline assessment were included in this study. 
      Participants who were 65 years and older and those with dementia at baseline were 
      excluded. Data were analyzed from May 2022 to April 2023. EXPOSURES: A total of 
      39 potential risk factors were identified from systematic reviews of late-onset 
      dementia and YOD risk factors and grouped into domains of sociodemographic 
      factors (education, socioeconomic status, and sex), genetic factors 
      (apolipoprotein E), lifestyle factors (physical activity, alcohol use, alcohol 
      use disorder, smoking, diet, cognitive activity, social isolation, and marriage), 
      environmental factors (nitrogen oxide, particulate matter, pesticide, and 
      diesel), blood marker factors (vitamin D, C-reactive protein, estimated 
      glomerular filtration rate function, and albumin), cardiometabolic factors 
      (stroke, hypertension, diabetes, hypoglycemia, heart disease, atrial 
      fibrillation, and aspirin use), psychiatric factors (depression, anxiety, 
      benzodiazepine use, delirium, and sleep problems), and other factors (traumatic 
      brain injury, rheumatoid arthritis, thyroid dysfunction, hearing impairment, and 
      handgrip strength). MAIN OUTCOME AND MEASURES: Multivariable Cox proportional 
      hazards regression was used to study the association between the risk factors and 
      incidence of YOD. Factors were tested stepwise first within domains and then 
      across domains. RESULTS: Of 356 052 included participants, 197 036 (55.3%) were 
      women, and the mean (SD) age at baseline was 54.6 (7.0) years. During 2 891 409 
      person-years of follow-up, 485 incident YOD cases (251 of 485 men [51.8%]) were 
      observed, yielding an incidence rate of 16.8 per 100 000 person-years (95% CI, 
      15.4-18.3). In the final model, 15 factors were significantly associated with a 
      higher YOD risk, namely lower formal education, lower socioeconomic status, 
      carrying 2 apolipoprotein ε4 allele, no alcohol use, alcohol use disorder, social 
      isolation, vitamin D deficiency, high C-reactive protein levels, lower handgrip 
      strength, hearing impairment, orthostatic hypotension, stroke, diabetes, heart 
      disease, and depression. CONCLUSIONS AND RELEVANCE: In this study, several 
      factors, mostly modifiable, were associated with a higher risk of YOD. These 
      modifiable risk factors should be incorporated in future dementia prevention 
      initiatives and raise new therapeutic possibilities for YOD.
FAU - Hendriks, Stevie
AU  - Hendriks S
AD  - Department of Psychiatry and Neuropsychology, School for Mental Health and 
      Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, the 
      Netherlands.
FAU - Ranson, Janice M
AU  - Ranson JM
AD  - University of Exeter Medical School, Exeter, United Kingdom.
FAU - Peetoom, Kirsten
AU  - Peetoom K
AD  - Department of Psychiatry and Neuropsychology, School for Mental Health and 
      Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, the 
      Netherlands.
FAU - Lourida, Ilianna
AU  - Lourida I
AD  - University of Exeter Medical School, Exeter, United Kingdom.
FAU - Tai, Xin You
AU  - Tai XY
AD  - Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, 
      United Kingdom.
AD  - Division of Clinical Neurology, John Radcliffe Hospital, Oxford University 
      Hospitals Trust, Oxford, United Kingdom.
FAU - de Vugt, Marjolein
AU  - de Vugt M
AD  - Department of Psychiatry and Neuropsychology, School for Mental Health and 
      Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, the 
      Netherlands.
FAU - Llewellyn, David J
AU  - Llewellyn DJ
AD  - University of Exeter Medical School, Exeter, United Kingdom.
AD  - Alan Turing Institute, London, United Kingdom.
FAU - Köhler, Sebastian
AU  - Köhler S
AD  - Department of Psychiatry and Neuropsychology, School for Mental Health and 
      Neuroscience, Alzheimer Center Limburg, Maastricht University, Maastricht, the 
      Netherlands.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - JAMA Neurol
JT  - JAMA neurology
JID - 101589536
RN  - 9007-41-4 (C-Reactive Protein)
RN  - 0 (Apolipoproteins)
SB  - IM
MH  - Male
MH  - Humans
MH  - Female
MH  - Middle Aged
MH  - Prospective Studies
MH  - *Alcoholism/complications
MH  - UK Biobank
MH  - Biological Specimen Banks
MH  - C-Reactive Protein
MH  - Hand Strength
MH  - *Dementia/diagnosis
MH  - Risk Factors
MH  - *Diabetes Mellitus
MH  - *Stroke/epidemiology
MH  - *Heart Diseases/complications
MH  - Apolipoproteins
MH  - *Hearing Loss/complications
PMC - PMC10751655
COIS- Conflict of Interest Disclosures: Drs Ranson and Llewellyn reported grants from 
      Alzheimer’s Research UK and the Alan Turing Institute/Engineering and Physical 
      Sciences Research Council. Dr de Vugt reported grants from Alzheimer Nederland 
      and Gieskes Strijbis Fonds during the conduct of the study. Dr Llewellyn reported 
      funding from the Medical Research Council, National Institute for Health Research 
      Applied Research Collaboration South West Peninsula, National Health and Medical 
      Research Council, and National Institute on Aging. No other disclosures were 
      reported.
EDAT- 2023/12/26 12:42
MHDA- 2024/02/12 15:43
PMCR- 2024/12/26
CRDT- 2023/12/26 11:33
PHST- 2024/12/26 00:00 [pmc-release]
PHST- 2024/02/12 15:43 [medline]
PHST- 2023/12/26 12:42 [pubmed]
PHST- 2023/12/26 11:33 [entrez]
AID - 2813439 [pii]
AID - noi230092 [pii]
AID - 10.1001/jamaneurol.2023.4929 [doi]
PST - ppublish
SO  - JAMA Neurol. 2024 Feb 1;81(2):134-142. doi: 10.1001/jamaneurol.2023.4929.

PMID- 38107217
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231219
IS  - 2168-8184 (Print)
IS  - 2168-8184 (Electronic)
IS  - 2168-8184 (Linking)
VI  - 15
IP  - 12
DP  - 2023 Dec
TI  - The Mystery of Clopidogrel-Associated Inflammatory Arthritis.
PG  - e50564
LID - 10.7759/cureus.50564 [doi]
LID - e50564
AB  - Clopidogrel is an antiplatelet medication that plays an important role in the 
      management and prevention of thrombotic vascular events in patients with acute 
      coronary syndrome (ACS) and ischemic stroke. We report a case of a male patient 
      who received a maintenance dose of clopidogrel as part of stroke treatment and 
      developed inflammatory arthritis after five days of starting the medication. He 
      underwent extensive evaluation and testing to explore other common causes of 
      inflammatory arthritis, including autoimmune etiologies. None of the test results 
      were helpful, and we hypothesized that his arthritis was induced by clopidogrel. 
      Discontinuing this agent resulted in the complete resolution of the patient's 
      symptoms. Since medication-induced arthritis is a diagnosis of exclusion, these 
      patients should undergo a complete workup for inflammatory arthritis. If 
      possible, a risk-benefit analysis of dual antiplatelet therapy (DAPT) in ischemic 
      stroke patients with a prior history of rheumatoid arthritis (RA) should be done 
      in collaboration with neurology.
CI  - Copyright © 2023, Javed et al.
FAU - Javed, Faiza
AU  - Javed F
AD  - Hospital Medicine, University of Kentucky College of Medicine, Lexington, USA.
FAU - Champaneria, Shivam U
AU  - Champaneria SU
AD  - Oncology, University of Kentucky College of Medicine, Bowling Green, USA.
LA  - eng
PT  - Case Reports
DEP - 20231215
PL  - United States
TA  - Cureus
JT  - Cureus
JID - 101596737
PMC - PMC10724009
OTO - NOTNLM
OT  - arthritis and orthopaedic rheumatology
OT  - clopidogrel
OT  - clopidogrel hypersensitivity
OT  - migratory arthritis
OT  - oligo-arthritis
COIS- The authors have declared that no competing interests exist.
EDAT- 2023/12/18 06:42
MHDA- 2023/12/18 06:43
PMCR- 2023/12/15
CRDT- 2023/12/18 04:54
PHST- 2023/12/14 00:00 [accepted]
PHST- 2023/12/18 06:43 [medline]
PHST- 2023/12/18 06:42 [pubmed]
PHST- 2023/12/18 04:54 [entrez]
PHST- 2023/12/15 00:00 [pmc-release]
AID - 10.7759/cureus.50564 [doi]
PST - epublish
SO  - Cureus. 2023 Dec 15;15(12):e50564. doi: 10.7759/cureus.50564. eCollection 2023 
      Dec.

PMID- 38084174
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231212
IS  - 2168-8184 (Print)
IS  - 2168-8184 (Electronic)
IS  - 2168-8184 (Linking)
VI  - 15
IP  - 11
DP  - 2023 Nov
TI  - Utilizing Clinical and Non-clinical Patient Factors in Predicting Cardiovascular 
      Events in Patients on JAK Inhibitor Therapy: A Retrospective Cohort Study.
PG  - e48595
LID - 10.7759/cureus.48595 [doi]
LID - e48595
AB  - BACKGROUND: Patients with autoimmune rheumatic diseases (ARDs) taking JAK 
      inhibitors may have an increased risk of cardiovascular events, especially if 
      they have other health conditions. Identifying high-risk patients can inform 
      targeted preventive care. This study assessed the value of age and deprivation 
      decile in predicting cardiovascular events in patients on JAK inhibitors for 
      ARDs. OBJECTIVE: To assess the predictive value of age and deprivation decile in 
      identifying patients at risk of cardiovascular events while on JAK inhibitor 
      therapy for ARDs. METHODS: This cross-sectional cohort study enrolled 309 
      patients with ARDs (mean age 59.3 years, 77% female) treated with JAK inhibitors 
      at a UK teaching hospital. Baseline characteristics, including age, gender, 
      ethnicity, and comorbidities, were collected. Cardiovascular events (myocardial 
      infarctions, strokes, and cardiovascular-related deaths) that occurred while on 
      JAK inhibitor therapy were identified retrospectively. Deprivation indices were 
      calculated using socioeconomic factors. RESULTS: Multivariate logistic regression 
      analysis, adjusting for potential confounders, showed that a model combining age 
      and deprivation decile was statistically significant (p = 0.031) in predicting 
      cardiovascular events. Neither age nor deprivation decile alone was statistically 
      significant. Older patients had an odds ratio of 1.06 (95% CI: 1.00-1.13) for 
      increased risk of cardiovascular events. The logistic regression model as a whole 
      was statistically significant (Chi2(14) = 24.04, p = 0.031, n = 309). The AUC of 
      the ROC curve was 0.837. CONCLUSION: Age and deprivation decile can effectively 
      predict cardiovascular events in patients on JAK inhibitor therapy for ARDs. 
      Incorporating these predictive tools into routine clinical practice can help 
      identify patients who warrant intensified cardiovascular risk management.
CI  - Copyright © 2023, Sunmboye et al.
FAU - Sunmboye, Kehinde O
AU  - Sunmboye KO
AD  - Rheumatology, College of Health Sciences, University of Leicester, Leicester, 
      GBR.
AD  - Rheumatology, University Hospitals of Leicester NHS Trust, Leicester, GBR.
FAU - Petrie, Tom
AU  - Petrie T
AD  - Rheumatology, University Hospitals of Leicester NHS Trust, Leicester, GBR.
FAU - Bui, Billy
AU  - Bui B
AD  - Rheumatology, University of Leicester, Leicester, GBR.
FAU - Salim, Hassan
AU  - Salim H
AD  - Rheumatology, University of Leicester, Leicester, GBR.
FAU - Khan, Mutal
AU  - Khan M
AD  - Rheumatology, University of Leicester, Leicester, GBR.
LA  - eng
PT  - Journal Article
DEP - 20231110
PL  - United States
TA  - Cureus
JT  - Cureus
JID - 101596737
PMC - PMC10710663
OTO - NOTNLM
OT  - cardiovascular prevention strategy for cardiovascular events
OT  - jak inhibitors
OT  - psoriatic arthritis
OT  - social deprivation
OT  - • rheumatoid arthritis
COIS- The authors have declared that no competing interests exist.
EDAT- 2023/12/12 06:42
MHDA- 2023/12/12 06:43
PMCR- 2023/11/10
CRDT- 2023/12/12 03:36
PHST- 2023/11/09 00:00 [accepted]
PHST- 2023/12/12 06:43 [medline]
PHST- 2023/12/12 06:42 [pubmed]
PHST- 2023/12/12 03:36 [entrez]
PHST- 2023/11/10 00:00 [pmc-release]
AID - 10.7759/cureus.48595 [doi]
PST - epublish
SO  - Cureus. 2023 Nov 10;15(11):e48595. doi: 10.7759/cureus.48595. eCollection 2023 
      Nov.

PMID- 38040097
OWN - NLM
STAT- MEDLINE
DCOM- 20240205
LR  - 20240206
IS  - 1873-6963 (Electronic)
IS  - 0965-2299 (Linking)
VI  - 80
DP  - 2024 Mar
TI  - Incidence of nerve injury following acupuncture treatments in Taiwan.
PG  - 103007
LID - S0965-2299(23)00094-8 [pii]
LID - 10.1016/j.ctim.2023.103007 [doi]
AB  - OBJECTIVE: Acupuncture, a widely employed traditional therapeutic modality known 
      for its efficacy in pain alleviation and diverse condition management, may 
      inadvertently result in mechanical nerve injury due to its invasive nature. This 
      research aimed to ascertain the incidence of nerve injuries post-acupuncture, 
      identify associated risk factors, and map the distribution of nerve injury sites. 
      METHODS: A case-control study nested in the National Health Insurance Research 
      Database (NHIRD) 2000-2018 two million cohort was conducted. Patients previously 
      diagnosed with nerve injury, surgery, or degeneration before acupuncture were 
      excluded. Cases were defined as patients receiving acupuncture and seeking 
      medical attention for nerve injury (ICD9-CM code 950-957) within 14 days 
      post-procedure, while control groups comprised patients undergoing acupuncture 
      without subsequent adverse events. Invasive treatments prior to adverse events 
      and adverse events occurring more than 14 days post-acupuncture were excluded. To 
      ensure case-control comparability, factors such as age, gender, socioeconomic 
      status, and medical facility environment were controlled using propensity score 
      matching. RESULTS: The study encompassed 14,507,847 acupuncture treatments 
      administered to 886,753 patients, with 8361 instances of post-acupuncture nerve 
      injury identified, representing an incidence rate of approximately 5.76 per 
      10,000 procedures. Age emerged as a significant risk factor, with the adjusted 
      odds ratios escalating with age. Several comorbidities including diabetes, 
      hypothyroidism, liver cirrhosis, chronic kidney disease, herpes zoster, hepatitis 
      virus, rheumatoid arthritis, systemic lupus erythematosus, dementia, and 
      cerebrovascular accidents were associated with an elevated risk of nerve injury 
      post-acupuncture. CONCLUSION: This study underscores the importance of meticulous 
      patient profiling and cautious therapeutic approach in acupuncture, considering 
      the evident influence of various demographic, systemic, and treatment-related 
      factors on the incidence of nerve injuries.
CI  - Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.
FAU - Lin, Chia-Lin
AU  - Lin CL
AD  - Department of Chinese medicine, Taipei City Hospital, Renai Branch, Taipei, 
      Taiwan, ROC; Institute of Traditional Medicine, School of Medicine, National Yang 
      Ming Chiao Tung University, Taipei, Taiwan, ROC. Electronic address: 
      103318121@gms.tcu.edu.tw.
FAU - Chern, Andy
AU  - Chern A
AD  - Department of Chinese medicine, Taipei City Hospital, Renai Branch, Taipei, 
      Taiwan, ROC; Institute of Traditional Medicine, School of Medicine, National Yang 
      Ming Chiao Tung University, Taipei, Taiwan, ROC.
FAU - Wang, Ming-Jen
AU  - Wang MJ
AD  - Department of Chinese medicine, Taipei City Hospital, Renai Branch, Taipei, 
      Taiwan, ROC; Institute of Public Health, School of Medicine, National Yang Ming 
      Chiao Tung University, Taipei, Taiwan, ROC; Institute of Traditional Medicine, 
      School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan, 
      ROC.
FAU - Lin, Shun-Ku
AU  - Lin SK
AD  - Department of Chinese medicine, Taipei City Hospital, Renai Branch, Taipei, 
      Taiwan, ROC; Institute of Public Health, School of Medicine, National Yang Ming 
      Chiao Tung University, Taipei, Taiwan, ROC; Institute of Traditional Medicine, 
      School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan, 
      ROC; University of Taipei, Taipei, Taiwan, ROC.
LA  - eng
PT  - Journal Article
DEP - 20231130
PL  - Scotland
TA  - Complement Ther Med
JT  - Complementary therapies in medicine
JID - 9308777
SB  - IM
MH  - Humans
MH  - Incidence
MH  - Cohort Studies
MH  - Case-Control Studies
MH  - Taiwan/epidemiology
MH  - *Acupuncture Therapy/adverse effects/methods
OTO - NOTNLM
OT  - Acupuncture
OT  - Distribution of nerve injury, sites
OT  - Incidence rate
OT  - Nerve injury
OT  - Risk factors
COIS- Declaration of Competing Interest The authors declare no conflict of interest.
EDAT- 2023/12/02 00:42
MHDA- 2024/02/05 06:43
CRDT- 2023/12/01 19:26
PHST- 2023/05/26 00:00 [received]
PHST- 2023/10/20 00:00 [revised]
PHST- 2023/11/21 00:00 [accepted]
PHST- 2024/02/05 06:43 [medline]
PHST- 2023/12/02 00:42 [pubmed]
PHST- 2023/12/01 19:26 [entrez]
AID - S0965-2299(23)00094-8 [pii]
AID - 10.1016/j.ctim.2023.103007 [doi]
PST - ppublish
SO  - Complement Ther Med. 2024 Mar;80:103007. doi: 10.1016/j.ctim.2023.103007. Epub 
      2023 Nov 30.

PMID- 37996125
OWN - NLM
STAT- MEDLINE
DCOM- 20240216
LR  - 20241023
IS  - 2056-5933 (Electronic)
IS  - 2056-5933 (Linking)
VI  - 9
IP  - 4
DP  - 2023 Nov 23
TI  - Comparative cardiovascular safety with janus kinase inhibitors and biological 
      disease-modifying antirheumatic drugs as used in clinical practice: an 
      observational cohort study from Sweden in patients with rheumatoid arthritis.
LID - 10.1136/rmdopen-2023-003630 [doi]
LID - e003630
AB  - OBJECTIVES: To compare the incidence of cardiovascular (CV) events in rheumatoid 
      arthritis (RA) treated with janus kinase inhibitors (JAKi), tumour necrosis 
      factor inhibitors (TNFi), or other biological disease-modifying antirheumatic 
      drugs (bDMARDs), in clinical practice, and to contextualise these findings by 
      comparing to the Swedish RA population and general population at large. METHODS: 
      Patients with RA initiating JAKi, TNFi and non-TNFi bDMARDs were identified in 
      the Swedish Rheumatology Quality Register between 2016 and 2021. Through linkages 
      to national registers, a cohort of patients with RA, general population 
      comparators, as well as covariates and incident major acute CV event (MACE, 
      including myocardial infarction, stroke and fatal CV events) were identified 
      until 2022. Crude and age-sex standardised rates were calculated and HRs 
      estimated from multivariable Cox regression models using TNFi as reference. 
      RESULTS: We identified 13 492 patients with RA initiating a JAKi, non-TNFi bDMARD 
      or TNFi treatment. Among 3037 JAKi-initiators, 59 MACE events were observed. The 
      age-sex standardised rates for MACE were similar in the JAKi (0.88 per 100 person 
      years) and TNFi (0.91) cohorts. Fully adjusted models showed no increased rate of 
      MACE with JAKi (HR=0.71, 95% CI 0.51 to 0.99), or non-TNFi bDMARD (HR=0.98; 95% 
      CI 0.78 to 1.23) in comparison to TNFi. We found no evidence that this HR changed 
      over time since treatment initiation. In a CV-enriched subset, we observed higher 
      rates but similar HRs. CONCLUSIONS: As used in present clinical practice in 
      Sweden, we found no evidence that CV risk is higher with JAKis than TNFis in RA.
CI  - © Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No 
      commercial re-use. See rights and permissions. Published by BMJ.
FAU - Bower, Hannah
AU  - Bower H
AUID- ORCID: 0000-0002-2046-3833
AD  - Clinical Epidemiology Division, Department of Medicine Solna, Karolinska 
      Institutet, Stockholm, Sweden hannah.bower@ki.se.
FAU - Frisell, Thomas
AU  - Frisell T
AUID- ORCID: 0000-0002-5735-9626
AD  - Clinical Epidemiology Division, Department of Medicine Solna, Karolinska 
      Institutet, Stockholm, Sweden.
FAU - di Giuseppe, Daniela
AU  - di Giuseppe D
AUID- ORCID: 0000-0003-3817-8288
AD  - Clinical Epidemiology Division, Department of Medicine Solna, Karolinska 
      Institutet, Stockholm, Sweden.
FAU - Delcoigne, Benedicte
AU  - Delcoigne B
AUID- ORCID: 0000-0002-2716-5679
AD  - Clinical Epidemiology Division, Department of Medicine Solna, Karolinska 
      Institutet, Stockholm, Sweden.
FAU - Askling, Johan
AU  - Askling J
AUID- ORCID: 0000-0003-0433-0616
AD  - Clinical Epidemiology Division, Department of Medicine Solna, Karolinska 
      Institutet, Stockholm, Sweden.
AD  - Rheumatology, Theme Inflammation and Ageing, Karolinska University Hospital, 
      Stockholm, Sweden.
LA  - eng
PT  - Journal Article
PT  - Observational Study
DEP - 20231123
PL  - England
TA  - RMD Open
JT  - RMD open
JID - 101662038
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Janus Kinase Inhibitors)
SB  - IM
MH  - Humans
MH  - *Antirheumatic Agents/adverse effects
MH  - *Arthritis, Rheumatoid/drug therapy/epidemiology
MH  - Cohort Studies
MH  - *Janus Kinase Inhibitors/adverse effects
MH  - Sweden/epidemiology
PMC - PMC10668277
OTO - NOTNLM
OT  - Biological Therapy
OT  - Cardiovascular Diseases
OT  - Epidemiology
OT  - Rheumatoid Arthritis
COIS- Competing interests: Karolinska Institutet, with JA as principal investigator, 
      has or has had research agreements with AbbVie, Astra-Zeneca, BMS, Eli Lilly, 
      Galapagos, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB, mainly in the 
      context of safety monitoring of biologics via ARTIS/Swedish Biologics Register.
EDAT- 2023/11/24 00:42
MHDA- 2023/11/27 12:42
PMCR- 2023/11/23
CRDT- 2023/11/23 20:53
PHST- 2023/08/21 00:00 [received]
PHST- 2023/11/05 00:00 [accepted]
PHST- 2023/11/27 12:42 [medline]
PHST- 2023/11/24 00:42 [pubmed]
PHST- 2023/11/23 20:53 [entrez]
PHST- 2023/11/23 00:00 [pmc-release]
AID - rmdopen-2023-003630 [pii]
AID - 10.1136/rmdopen-2023-003630 [doi]
PST - epublish
SO  - RMD Open. 2023 Nov 23;9(4):e003630. doi: 10.1136/rmdopen-2023-003630.

PMID- 37964868
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240212
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 14
DP  - 2023
TI  - Cardiovascular risk of Janus kinase inhibitors compared with biologic 
      disease-modifying antirheumatic drugs in patients with rheumatoid arthritis 
      without underlying cardiovascular diseases: a nationwide cohort study.
PG  - 1165711
LID - 10.3389/fphar.2023.1165711 [doi]
LID - 1165711
AB  - Objectives: Despite the ethnic differences in cardiovascular (CV) risks and 
      recent increase in the prescription of Janus kinase (JAK) inhibitors, limited 
      evidence is available for their CV outcomes in Asian patients with rheumatoid 
      arthritis (RA). We aimed to compare the major adverse CV events (MACEs) of JAK 
      inhibitors to those of biologic disease-modifying antirheumatic drugs (bDMARDs) 
      in Korean patients with RA without baseline CV disease (CVD). Methods: In a 
      nationwide retrospective cohort study, patients newly diagnosed with RA without a 
      history of CVD between 2013 and 2018 were identified using the National Health 
      Insurance Service database. The cohort was followed up until the end of 2019 for 
      the development of MACEs. Hazard ratios (HRs) for MACEs such as myocardial 
      infarction, stroke, coronary revascularization, or all-cause death, were 
      estimated using Cox proportional hazard regression in a propensity score-matched 
      cohort. Results: In total, 4,230 matched patients with RA were included (846 JAK 
      inhibitor users and 3,384 bDMARD users). The crude incidence rate (95% confidence 
      intervals, CI) per 100 patient-years for MACEs was 0.83 (0.31-1.81) and 0.74 
      (0.53-1.02) in the JAK inhibitor and bDMARD groups, respectively. The risk of 
      MACEs was not significantly different between JAK inhibitor and bDMARD users with 
      an adjusted HR (95% CI) of 1.28 (0.53-3.11). There were no significant 
      differences in the risk of MACEs between JAK inhibitors and bDMARDs in each 
      subgroup according to the types of bDMARDs, age, sex, Charlson comorbidity index 
      score, and comorbidities. Conclusion: Compared to bDMARDs, JAK inhibitors were 
      not associated with the occurrence of MACEs in Korean patients with RA without a 
      history of CVD.
CI  - Copyright © 2023 Song, Lee, Hwang, Kim and Kwon.
FAU - Song, Yun-Kyoung
AU  - Song YK
AD  - College of Pharmacy, Daegu Catholic University, Gyeongsangbuk-do, Republic of 
      Korea.
FAU - Lee, Gaeun
AU  - Lee G
AD  - Department of Statistics, Daegu University, Gyeongsangbuk-do, Republic of Korea.
FAU - Hwang, Jinseub
AU  - Hwang J
AD  - Department of Statistics, Daegu University, Gyeongsangbuk-do, Republic of Korea.
FAU - Kim, Ji-Won
AU  - Kim JW
AD  - Division of Rheumatology, Department of Internal Medicine, Daegu Catholic 
      University School of Medicine, Daegu, Republic of Korea.
FAU - Kwon, Jin-Won
AU  - Kwon JW
AD  - BK21 FOUR Community-Based Intelligent Novel Drug Discovery Education Unit, 
      College of Pharmacy and Research Institute of Pharmaceutical Sciences, Kyungpook 
      National University, Daegu, Republic of Korea.
LA  - eng
PT  - Journal Article
DEP - 20231030
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC10642260
OTO - NOTNLM
OT  - asian
OT  - biologic DMARDs
OT  - cardiovascular risk
OT  - janus kinase inhibitors
OT  - rheumatoid arthritis
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2023/11/15 06:42
MHDA- 2023/11/15 06:43
PMCR- 2023/10/30
CRDT- 2023/11/15 04:11
PHST- 2023/02/14 00:00 [received]
PHST- 2023/10/16 00:00 [accepted]
PHST- 2023/11/15 06:43 [medline]
PHST- 2023/11/15 06:42 [pubmed]
PHST- 2023/11/15 04:11 [entrez]
PHST- 2023/10/30 00:00 [pmc-release]
AID - 1165711 [pii]
AID - 10.3389/fphar.2023.1165711 [doi]
PST - epublish
SO  - Front Pharmacol. 2023 Oct 30;14:1165711. doi: 10.3389/fphar.2023.1165711. 
      eCollection 2023.

PMID- 37945426
OWN - NLM
STAT- MEDLINE
DCOM- 20231219
LR  - 20231219
IS  - 1444-2892 (Electronic)
IS  - 1443-9506 (Linking)
VI  - 32
IP  - 12
DP  - 2023 Dec
TI  - Sex Differences in Pharmacotherapy and Long-Term Outcomes in Patients With 
      Ischaemic Heart Disease and Comorbid Left Ventricular Dysfunction.
PG  - 1457-1464
LID - S1443-9506(23)04321-4 [pii]
LID - 10.1016/j.hlc.2023.09.008 [doi]
AB  - BACKGROUND: Left ventricular (LV) dysfunction and ischaemic heart disease (IHD) 
      are common among women. However, women tend to present later and are less likely 
      to receive guideline-directed medical therapy (GDMT) compared with men. METHODS: 
      We analysed prospectively collected data (2005-2018) from a multicentre registry 
      on GDMT 30 days after percutaneous coronary intervention in 13,015 patients with 
      LV ejection fraction <50%. Guideline-directed medical therapy was defined as beta 
      blocker, angiotensin-converting enzyme inhibitor/angiotensin receptor 
      blocker±mineralocorticoid receptor antagonist. Long-term mortality was determined 
      by linkage with the Australian National Death Index. RESULTS: Women represented 
      20% (2,634) of the total cohort. Mean age was 65±12 years. Women were on average 
      >5 years, with higher body mass index and higher rates of hypertension, diabetes, 
      renal dysfunction, prior stroke, and rheumatoid arthritis. Guideline-directed 
      medical therapy was similar between sexes (73% vs 72%; p=0.58), although women 
      were less likely to be on an angiotensin-converting enzyme inhibitor/angiotensin 
      receptor blocker (80% vs 82%; p=0.02). Women were less likely to be on statin 
      therapy (p<0.001) or a second antiplatelet agent (p=0.007). Women had higher 
      unadjusted long-term mortality (25% vs 19%; p<0.001); however, there were no 
      differences in long-term mortality between sexes on adjusted analysis (hazard 
      ratio 0.99; 95% confidence interval 0.87-1.14; p=0.94). CONCLUSIONS: Rates of 
      GDMT for LV dysfunction were high and similar between sexes; however, women were 
      less likely to be on appropriate IHD secondary prevention. The increased 
      unadjusted long-term mortality in women was attenuated in adjusted analysis, 
      which highlights the need for optimisation of baseline risk to improve long-term 
      outcomes of women with IHD and comorbid LV dysfunction.
CI  - Copyright © 2023 Australian and New Zealand Society of Cardiac and Thoracic 
      Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). 
      Published by Elsevier B.V. All rights reserved.
FAU - Dagan, Misha
AU  - Dagan M
AD  - Department of Cardiology, Alfred Hospital, Melbourne, Vic, Australia. Electronic 
      address: http://www.twitter.com/misha_dagan.
FAU - Dinh, Diem T
AU  - Dinh DT
AD  - Centre of Cardiovascular Research and Education in Therapeutics, Department of 
      Epidemiology and Preventive Medicine, Monash University, Melbourne, Vic, 
      Australia.
FAU - Stehli, Julia
AU  - Stehli J
AD  - Department of Cardiology, Alfred Hospital, Melbourne, Vic, Australia.
FAU - Nan Tie, Emilia
AU  - Nan Tie E
AD  - Department of Cardiology, Alfred Hospital, Melbourne, Vic, Australia.
FAU - Brennan, Angela
AU  - Brennan A
AD  - Department of Cardiology, Alfred Hospital, Melbourne, Vic, Australia; Centre of 
      Cardiovascular Research and Education in Therapeutics, Department of Epidemiology 
      and Preventive Medicine, Monash University, Melbourne, Vic, Australia.
FAU - Ajani, Andrew E
AU  - Ajani AE
AD  - Centre of Cardiovascular Research and Education in Therapeutics, Department of 
      Epidemiology and Preventive Medicine, Monash University, Melbourne, Vic, 
      Australia; Department of Cardiology, Royal Melbourne Hospital, Melbourne, Vic, 
      Australia.
FAU - Clark, David J
AU  - Clark DJ
AD  - Department of Cardiology, Austin Hospital, Melbourne, Vic, Australia.
FAU - Freeman, Melanie
AU  - Freeman M
AD  - Department of Cardiology, Box Hill Hospital, Melbourne, Vic, Australia.
FAU - Reid, Christopher M
AU  - Reid CM
AD  - Centre of Cardiovascular Research and Education in Therapeutics, Department of 
      Epidemiology and Preventive Medicine, Monash University, Melbourne, Vic, 
      Australia; School of Population Health, Curtin University, Perth, WA, Australia.
FAU - Hiew, Chin
AU  - Hiew C
AD  - Department of Cardiology, University Hospital Geelong, Geelong, Vic, Australia; 
      School of Medicine, Deakin University, Melbourne, Vic, Australia.
FAU - Oqueli, Ernesto
AU  - Oqueli E
AD  - Department of Cardiology, Ballarat Base Hospital, Melbourne, Vic, Australia.
FAU - Kaye, David M
AU  - Kaye DM
AD  - Department of Cardiology, Alfred Hospital, Melbourne, Vic, Australia; 
      Monash-Alfred-Baker Centre for Cardiovascular Research, Monash University, 
      Melbourne, Vic, Australia.
FAU - Duffy, Stephen J
AU  - Duffy SJ
AD  - Centre of Cardiovascular Research and Education in Therapeutics, Department of 
      Epidemiology and Preventive Medicine, Monash University, Melbourne, Vic, 
      Australia; Monash-Alfred-Baker Centre for Cardiovascular Research, Monash 
      University, Melbourne, Vic, Australia. Electronic address: 
      stephenjamesduffy@gmail.com.
CN  - Melbourne Interventional Group
LA  - eng
PT  - Journal Article
DEP - 20231107
PL  - Australia
TA  - Heart Lung Circ
JT  - Heart, lung & circulation
JID - 100963739
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Adrenergic beta-Antagonists)
RN  - 0 (Angiotensin Receptor Antagonists)
SB  - IM
MH  - Humans
MH  - Female
MH  - Male
MH  - Middle Aged
MH  - Aged
MH  - Sex Characteristics
MH  - Australia/epidemiology
MH  - *Myocardial Ischemia/complications/drug therapy/epidemiology
MH  - *Coronary Artery Disease/drug therapy
MH  - Angiotensin-Converting Enzyme Inhibitors/therapeutic use
MH  - Adrenergic beta-Antagonists/therapeutic use
MH  - *Ventricular Dysfunction, Left/drug therapy/epidemiology
MH  - Stroke Volume/physiology
MH  - Angiotensin Receptor Antagonists/therapeutic use
MH  - *Heart Failure
OTO - NOTNLM
OT  - Optimal medical therapy
OT  - Pharmacotherapy
OT  - Secondary prevention
OT  - Sex differences
OT  - Women's heart disease
COIS- Competing Interest Statement SJD’s work is supported by a National Health and 
      Medical Research Council of Australia (NHMRC) Grant (number 1111170). CMR’s work 
      is supported by a NHMRC Principal Research Fellowship (reference no. 1136372).
EDAT- 2023/11/10 00:44
MHDA- 2023/12/19 06:42
CRDT- 2023/11/09 21:54
PHST- 2022/09/24 00:00 [received]
PHST- 2023/06/07 00:00 [revised]
PHST- 2023/09/02 00:00 [accepted]
PHST- 2023/12/19 06:42 [medline]
PHST- 2023/11/10 00:44 [pubmed]
PHST- 2023/11/09 21:54 [entrez]
AID - S1443-9506(23)04321-4 [pii]
AID - 10.1016/j.hlc.2023.09.008 [doi]
PST - ppublish
SO  - Heart Lung Circ. 2023 Dec;32(12):1457-1464. doi: 10.1016/j.hlc.2023.09.008. Epub 
      2023 Nov 7.

PMID- 37942277
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231110
IS  - 1759-720X (Print)
IS  - 1759-7218 (Electronic)
IS  - 1759-720X (Linking)
VI  - 15
DP  - 2023
TI  - Rheumatoid arthritis disease activity and adverse events in patients receiving 
      tofacitinib or tumor necrosis factor inhibitors: a post hoc analysis of ORAL 
      Surveillance.
PG  - 1759720X231201047
LID - 10.1177/1759720X231201047 [doi]
LID - 1759720X231201047
AB  - BACKGROUND: In patients with rheumatoid arthritis (RA), persistent inflammation 
      and increasing disease activity are associated with increased risk of adverse 
      events (AEs). OBJECTIVES: To assess relationships between RA disease activity and 
      AEs of interest in patients treated with tofacitinib or tumor necrosis factor 
      inhibitors (TNFi). DESIGN: This was a post hoc analysis of a long-term, 
      postauthorization safety endpoint trial of tofacitinib versus TNFi. METHODS: In 
      ORAL Surveillance, 4362 patients aged ⩾50 years with active RA despite 
      methotrexate, and ⩾1 additional cardiovascular (CV) risk factor, were randomized 
      1:1:1 to tofacitinib 5 or 10 mg twice daily or TNFi for up to 72 months. Post hoc 
      time-dependent multivariable Cox analysis evaluated the relationships between 
      disease activity [Clinical Disease Activity Index (CDAI)], inflammation 
      [C-reactive protein (CRP)], and AEs of interest. The AEs included major adverse 
      CV events (MACE), malignancies excluding nonmelanoma skin cancer (NMSC), venous 
      thromboembolism (VTE), serious infections, herpes zoster (HZ), nonserious 
      infections excluding HZ (NSI), and death. RESULTS: Across treatments, risk for 
      NSI was higher when patients had CDAI-defined active disease versus remission; 
      MACE and VTE risks trended higher, but did not reach significance. Hazard ratios 
      for MACE, malignancies excluding NMSC, VTE, infections, and death rose by 2-9% 
      for each 5-mg/L increment in serum CRP. The interaction terms evaluating the 
      impact of treatment assignment on the relationship between disease activity and 
      AEs were all p > 0.05. CONCLUSION: In ORAL Surveillance, higher NSI risk was 
      observed in the presence of active RA versus remission. The risk of MACE and VTE 
      directionally increased in active disease versus remission, although statistical 
      power was limited due to small event numbers in these categories. The 
      relationship between active disease and AEs was not impacted by treatment with 
      tofacitinib versus TNFi. REGISTRATION: NCT02092467.
CI  - © The Author(s), 2023.
FAU - Karpouzas, George A
AU  - Karpouzas GA
AD  - Division of Rheumatology, Harbor-UCLA Medical Center, and the Lundquist 
      Institute, Torrance, CA, USA.
FAU - Szekanecz, Zoltán
AU  - Szekanecz Z
AD  - Department of Rheumatology, Faculty of Medicine, University of Debrecen, 
      Debrecen, Hungary.
FAU - Baecklund, Eva
AU  - Baecklund E
AD  - Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
FAU - Mikuls, Ted R
AU  - Mikuls TR
AD  - Division of Rheumatology, University of Nebraska Medical Center and VA 
      Nebraska-Western Iowa Health Care System, Omaha, NE, USA.
FAU - Bhatt, Deepak L
AU  - Bhatt DL
AD  - Mount Sinai Heart, Icahn School of Medicine at Mount Sinai Health System, New 
      York, NY, USA.
FAU - Wang, Cunshan
AU  - Wang C
AD  - Inflammation and Immunology, Pfizer Inc, Groton, CT, USA.
FAU - Sawyerr, Gosford A
AU  - Sawyerr GA
AD  - Inflammation and Immunology, Pfizer Inc, New York, NY, USA.
FAU - Chen, Yan
AU  - Chen Y
AD  - Inflammation and Immunology, Pfizer Inc, Collegeville, PA, USA.
FAU - Menon, Sujatha
AU  - Menon S
AD  - Inflammation and Immunology, Pfizer Inc, Groton, CT, USA.
FAU - Connell, Carol A
AU  - Connell CA
AD  - Inflammation and Immunology, Pfizer Inc, Groton, CT, USA.
FAU - Ytterberg, Steven R
AU  - Ytterberg SR
AD  - Division of Rheumatology, Mayo Clinic, Rochester, MN, USA.
FAU - Mortezavi, Mahta
AU  - Mortezavi M
AUID- ORCID: 0000-0003-4666-071X
AD  - Inflammation and Immunology, Pfizer Inc, 66 Hudson Boulevard, New York, NY 10001, 
      USA.
LA  - eng
SI  - ClinicalTrials.gov/NCT02092467
PT  - Journal Article
DEP - 20231106
PL  - England
TA  - Ther Adv Musculoskelet Dis
JT  - Therapeutic advances in musculoskeletal disease
JID - 101517322
PMC - PMC10629315
OAB - The link between disease activity and adverse medical events in people with 
      rheumatoid arthritis taking tofacitinib or tumor necrosis factor inhibitors. Why 
      was the study done? • People with rheumatoid arthritis (RA) who have uncontrolled 
      symptoms (high disease activity) have a higher chance of having adverse medical 
      events (medical problems that occur during treatment with a medication) than 
      people who have mild symptoms (low disease activity). • We looked at the link 
      between levels of disease activity and the risk of having adverse medical events 
      in people with RA who took tofacitinib or a tumor necrosis factor inhibitor 
      (TNFi) medication. What did the researchers do? • We used the results of ORAL 
      Surveillance, a long-term safety trial in people with RA.  ○ In this study, 
      people with RA were 50 years or older and at high risk of a major cardiovascular 
      event such as heart attack or stroke. • For up to 6 years, people took 
      tofacitinib 5 or 10mg tablets two times a day or TNFi injections. • We used 
      statistical tests to examine the link between different levels of RA disease 
      activity or inflammation and different adverse medical events, such as:  ○ major 
      cardiovascular events (such as heart attack, stroke, or death due to heart 
      failure)  ○ cancers  ○ blood clots  ○ infections  ○ deaths. What did the 
      researchers find? • In people who took tofacitinib or TNFi:  ○ People with active 
      disease (those with RA symptoms) had a higher risk of infections that did not 
      lead to hospitalization (nonserious infections) than people in remission (those 
      with very mild symptoms or no symptoms at all).  ○ People with active disease 
      also had a slightly higher risk of major cardiovascular events and blood clots 
      than those in remission.  ○ Higher levels of inflammation led to increased risk 
      of major cardiovascular events, cancers, blood clots, infections, and deaths. 
      What do the findings mean? • Active RA disease leads to higher risk of adverse 
      medical events. • The medication used (tofacitinib or TNFi) did not affect the 
      link between levels of RA disease activity and adverse medical events. • This 
      study was limited by the low number of adverse medical events recorded.
OABL- eng
OTO - NOTNLM
OT  - DMARDs
OT  - autoinflammatory conditions
OT  - inflammation
OT  - outcome measures
OT  - rheumatoid arthritis
COIS- GAK has received research grants from Pfizer Inc, has acted as a consultant for 
      Janssen and Sanofi-Genzyme-Regeneron, and has participated in speakers’ bureau 
      activities for Sanofi-Genzyme-Regeneron. ZS has acted as a consultant for AbbVie, 
      Eli Lilly, Novartis, Pfizer Inc, Roche, and Sanofi, has acted as a paid 
      instructor for AbbVie, Eli Lilly, Gedeon Richter, Novartis, Pfizer Inc, and 
      Roche, and has participated in speakers’ bureau activities for AbbVie, Eli Lilly, 
      Novartis, Pfizer Inc, Roche, and Sanofi. EB declares no competing interests. TRM 
      has received research grants from Bristol Myers Squibb and Horizon, has acted as 
      a consultant for Gilead Sciences, Horizon, Sanofi and UCB, and served on the 
      Steering Committee for ORAL Surveillance for Pfizer Inc. DLB served as a member 
      of the Steering Committee for ORAL Surveillance, with funding from Pfizer Inc 
      paid to Brigham and Women’s Hospital. DLB has also served as an advisory board 
      member for ANGIOWave, Bayer, Boehringer Ingelheim, Cardax, CellProthera, Cereno 
      Scientific, Elsevier Practice Update Cardiology, High Enroll, Janssen, Level Ex, 
      McKinsey, Medscape Cardiology, Merck, MyoKardia, NirvaMed, Novo Nordisk, 
      PhaseBio, PLx Pharma, Regado Biosciences, and Stasys; has served on the Board of 
      Directors for AngioWave (stock options), Boston VA Research Institute, Bristol 
      Myers Squibb (stock), DRS.LINQ (stock options), High Enroll (stock), Society of 
      Cardiovascular Patient Care, and TOBESOFT; has acted as the Inaugural Chair of 
      the American Heart Association Quality Oversight Committee; has acted as a 
      consultant for Broadview Ventures; has been a member of the Data Monitoring 
      Committees for Acesion Pharma, Assistance Publique-Hôpitaux de Paris, Baim 
      Institute for Clinical Research (formerly Harvard Clinical Research Institute, 
      for the PORTICO trial, funded by St. Jude Medical, now Abbott), Boston Scientific 
      (Chair, PEITHO trial), Cleveland Clinic (including for the ExCEED trial, funded 
      by Edwards), Contego Medical (Chair, PERFORMANCE 2), Duke Clinical Research 
      Institute, Mayo Clinic, Mount Sinai School of Medicine (for the ENVISAGE trial, 
      funded by Daiichi Sankyo; for the ABILITY-DM trial, funded by Concept Medical), 
      Novartis, Population Health Research Institute, and Rutgers University (for the 
      NIH-funded MINT Trial); has received honoraria from the American College of 
      Cardiology (Senior Associate Editor, Clinical Trials and News, ACC.org; Chair, 
      ACC Accreditation Oversight Committee), Arnold and Porter law firm (work related 
      to Sanofi/Bristol Myers Squibb clopidogrel litigation), Baim Institute for 
      Clinical Research (formerly Harvard Clinical Research Institute; RE-DUAL PCI 
      Clinical Trial Steering Committee funded by Boehringer Ingelheim; AEGIS-II 
      Executive Committee funded by CSL Behring), Belvoir Publications (Editor in 
      Chief, Harvard Heart Letter), Canadian Medical and Surgical Knowledge Translation 
      Research Group (Clinical Trial Steering Committees), Cowen and Company, Duke 
      Clinical Research Institute (Clinical Trial Steering Committees, including for 
      the PRONOUNCE trial, funded by Ferring Pharmaceuticals), HMP Global (Editor in 
      Chief, Journal of Invasive Cardiology), Journal of the American College of 
      Cardiology (Guest Editor; Associate Editor), K2P (Co-Chair, interdisciplinary 
      curriculum), Level Ex, Medtelligence/ReachMD (CME Steering Committees), MJH Life 
      Sciences, Oakstone CME (Course Director, Comprehensive Review of Interventional 
      Cardiology), Piper Sandler, Population Health Research Institute (for the COMPASS 
      Operations Committee, Publications Committee, Steering Committee, and USA 
      national co-leader, funded by Bayer), Slack Publications (Chief Medical Editor, 
      Cardiology Today’s Intervention), Society of Cardiovascular Patient Care 
      (Secretary/Treasurer), WebMD (CME Steering Committees), and Wiley (Steering 
      Committee); has acted as Deputy Editor for Clinical Cardiology, Chaired the 
      NCDR-ACTION Registry Steering Committee, and Chaired the VA CART Research and 
      Publications Committee; has been named on a patent for sotagliflozin assigned to 
      Brigham and Women’s Hospital, who assigned to Lexicon (neither DLB nor Brigham 
      and Women’s Hospital receive any income from this patent); has received research 
      funding from Abbott, Acesion Pharma, Afimmune, Aker BioMarine, Amarin, Amgen, 
      AstraZeneca, Bayer, Beren, Boehringer Ingelheim, Boston Scientific, Bristol Myers 
      Squibb, Cardax, CellProthera, Cereno Scientific, Chiesi, CinCor, CSL Behring, 
      Eisai, Eli Lilly, Ethicon, Faraday Pharmaceuticals, Ferring Pharmaceuticals, 
      Forest Laboratories, Fractyl, Garmin, HLS Therapeutics, Idorsia, Ironwood, 
      Ischemix, Janssen, Javelin, Lexicon, Medtronic, Merck, Moderna, MyoKardia, 
      NirvaMed, Novartis, Novo Nordisk, Owkin, Pfizer, PhaseBio, PLx Pharma, Recardio, 
      Regeneron, Reid Hoffman Foundation, Roche, Sanofi, Stasys, Synaptic, The 
      Medicines Company, Youngene, and 89Bio; has received royalties from Elsevier 
      (Editor, Braunwald’s Heart Disease), has been a site co-investigator for Abbott, 
      BIOTRONIK, Boston Scientific, CSI, Endotronix, St. Jude Medical (now Abbott), 
      Philips, SpectraWAVE, Svelte, and Vascular Solutions; has been a trustee for the 
      American College of Cardiology; and has worked on unfunded research for FlowCo 
      and Takeda. GAS has acted as a consultant for Pfizer Inc, and was an employee of 
      Syneos Health Inc at the time of the analysis, who were paid contractors to 
      Pfizer Inc in the development of this manuscript and in providing statistical 
      support. SRY has acted as a consultant for Corbus Pharmaceuticals, Kezar Life 
      Sciences, and Pfizer Inc. SRY also acted as a member of the Steering Committee 
      for ORAL Surveillance. CW, YC, SM, and MM are employees and shareholders of 
      Pfizer Inc. CAC was an employee and shareholder of Pfizer Inc at the time of the 
      analysis.
EDAT- 2023/11/09 06:42
MHDA- 2023/11/09 06:43
PMCR- 2023/11/06
CRDT- 2023/11/09 04:25
PHST- 2023/05/12 00:00 [received]
PHST- 2023/08/25 00:00 [accepted]
PHST- 2023/11/09 06:43 [medline]
PHST- 2023/11/09 06:42 [pubmed]
PHST- 2023/11/09 04:25 [entrez]
PHST- 2023/11/06 00:00 [pmc-release]
AID - 10.1177_1759720X231201047 [pii]
AID - 10.1177/1759720X231201047 [doi]
PST - epublish
SO  - Ther Adv Musculoskelet Dis. 2023 Nov 6;15:1759720X231201047. doi: 
      10.1177/1759720X231201047. eCollection 2023.

PMID- 37933364
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231108
IS  - 2168-8184 (Print)
IS  - 2168-8184 (Electronic)
IS  - 2168-8184 (Linking)
VI  - 15
IP  - 10
DP  - 2023 Oct
TI  - Mouth-Heart Connection: A Systematic Review on the Impact of Periodontal Disease 
      on Cardiovascular Health.
PG  - e46585
LID - 10.7759/cureus.46585 [doi]
LID - e46585
AB  - Periodontal diseases (PDs) and cardiovascular diseases (CVDs) are highly 
      prevalent global diseases with increasing percentages of morbidity and mortality. 
      Both PD and CVDs independently have multifactorial causation, and emerging 
      evidence shows an association between PD and CVDs. Periodontal diseases like 
      gingivitis and periodontitis are chronic inflammatory conditions that eventually 
      cause systemic inflammation, leading to many systemic diseases like rheumatoid 
      arthritis, cardiovascular diseases, and others. In this study, we followed a 
      systematic review approach to give an overview of the current evidence on the 
      association between PD and CVDs. We used a relevant search strategy to retrieve 
      articles from databases such as PubMed and Google Scholar from 2013 to July 2023. 
      Upon applying filters and screening through titles and abstracts, we could narrow 
      down articles to 21. On full-text screening, we selected 10 articles for in-depth 
      analysis. This study showed a significant correlation between PD and CVDs. Poor 
      oral hygiene, infection, and inflammation in the oral cavity lead to systemic 
      inflammation, causing endothelial dysfunction. There are controversial views 
      about PD acting as an independent risk factor for CVD development, as there are 
      other risk factors such as age, gender, smoking, etc. acting as confounding 
      factors while establishing the link between PD and CVDs. Knowledge about oral 
      health, maintaining good oral hygiene, and proper treatment for PD could reduce 
      the incidence of CVDs. Further research is needed to prove that PD is an 
      independent risk factor for CVDs.
CI  - Copyright © 2023, Etta et al.
FAU - Etta, Indu
AU  - Etta I
AD  - Internal Medicine, Kakatiya Medical College, Warangal, IND.
FAU - Kambham, Saisravika
AU  - Kambham S
AD  - Internal Medicine, Dr. Bhim Rao Ambedkar Medical College and Hospital, Bangalore, 
      IND.
FAU - Girigosavi, Khushal B
AU  - Girigosavi KB
AD  - Neurology, Dr. Vasantrao Pawar Medical College, Hospital and Research Center, 
      Nashik, IND.
FAU - Panjiyar, Binay K
AU  - Panjiyar BK
AD  - Internal Medicine, Harvard Medical School, Boston, USA.
AD  - Internal Medicine, California Institute of Behavioral Neurosciences & Psychology, 
      Fairfield, USA.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20231006
PL  - United States
TA  - Cureus
JT  - Cureus
JID - 101596737
PMC - PMC10625740
OTO - NOTNLM
OT  - cardiovascular diseases (cvd)
OT  - hypertension
OT  - myocardial infarction  
OT  - periodontal disease (pd)
OT  - periodontitis
OT  - stroke
COIS- The authors have declared that no competing interests exist.
EDAT- 2023/11/07 06:46
MHDA- 2023/11/07 06:47
PMCR- 2023/10/06
CRDT- 2023/11/07 03:49
PHST- 2023/10/06 00:00 [accepted]
PHST- 2023/11/07 06:47 [medline]
PHST- 2023/11/07 06:46 [pubmed]
PHST- 2023/11/07 03:49 [entrez]
PHST- 2023/10/06 00:00 [pmc-release]
AID - 10.7759/cureus.46585 [doi]
PST - epublish
SO  - Cureus. 2023 Oct 6;15(10):e46585. doi: 10.7759/cureus.46585. eCollection 2023 
      Oct.

PMID- 37871918
OWN - NLM
STAT- MEDLINE
DCOM- 20231030
LR  - 20241024
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Print)
IS  - 1462-0324 (Linking)
VI  - 62
IP  - SI3
DP  - 2023 Oct 23
TI  - Neuropathologic evaluation of cerebrovascular disease in patients with rheumatoid 
      arthritis.
PG  - SI296-SI303
LID - 10.1093/rheumatology/kead396 [doi]
AB  - OBJECTIVES: Active RA has been associated with an increased risk of both 
      cardiovascular and peripheral vascular disease. We aimed to compare 
      cerebrovascular changes in patients with and without RA, both with and without a 
      neuropathologic diagnosis of neurodegenerative disease. METHODS: Patients with RA 
      (n = 32) who died and underwent autopsy between 1994 and 2021 were matched to 
      non-RA controls (n = 32) on age, sex and level of neurodegenerative 
      proteinopathy. Routine neuropathologic examination was performed at the time of 
      autopsy. Cerebrovascular disease severity was evaluated using modified Kalaria 
      and Strozyk scales. Clinical dementia diagnoses were manually collected from 
      patients' medical records. RESULTS: Prior to death, 15 (47%) RA patients and 14 
      (44%) controls were diagnosed with dementia; 9 patients in each group (60% and 
      64%, respectively) had Alzheimer's disease. The prevalence of cerebral amyloid 
      angiopathy, microinfarcts, infarcts or strokes was found to be similar between 
      groups. Patients with RA were more likely to have more severe vascular changes in 
      the basal ganglia by Kalaria scale (P = 0.04), but not in other brain areas. 
      There were no significant differences in the presence of large infarcts, lacunar 
      infarcts or leukoencephalopathy by Strozyk scale. Among patients with RA and no 
      clinical diagnosis of dementia, the majority had mild-moderate cerebrovascular 
      abnormalities, and a subset of patients had Alzheimer's disease neuropathologic 
      changes. CONCLUSION: In this small series of autopsies, patients with and without 
      RA had largely similar cerebrovascular pathology when controlling for 
      neurodegenerative proteinopathies, although patients with RA exhibited more 
      pronounced cerebrovascular disease in the basal ganglia.
CI  - © The Author(s) 2023. Published by Oxford University Press on behalf of the 
      British Society for Rheumatology. All rights reserved. For permissions, please 
      email: journals.permissions@oup.com.
FAU - Larsen, Rachel A
AU  - Larsen RA
AD  - Department of Laboratory Medicine and Pathology, Neuropathology Mayo Clinic, 
      Rochester, MN, USA.
FAU - Constantopoulos, Eleni
AU  - Constantopoulos E
AD  - Department of Laboratory Medicine and Pathology, Neuropathology Mayo Clinic, 
      Rochester, MN, USA.
FAU - Kodishala, Chanakya
AU  - Kodishala C
AD  - Division of Rheumatology, Department of Internal Medicine, Mayo Clinic, 
      Rochester, MN, USA.
FAU - Lovering, Edward
AU  - Lovering E
AD  - Division of Rheumatology, Department of Internal Medicine, Mayo Clinic, 
      Rochester, MN, USA.
FAU - Kumar, Rakesh
AU  - Kumar R
AD  - Division of Rheumatology, Department of Internal Medicine, Mayo Clinic, 
      Rochester, MN, USA.
FAU - Hulshizer, Cassondra A
AU  - Hulshizer CA
AD  - Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA.
FAU - Lennon, Ryan J
AU  - Lennon RJ
AD  - Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA.
FAU - Crowson, Cynthia S
AU  - Crowson CS
AUID- ORCID: 0000-0001-5847-7475
AD  - Division of Rheumatology, Department of Internal Medicine, Mayo Clinic, 
      Rochester, MN, USA.
AD  - Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA.
FAU - Nguyen, Aivi T
AU  - Nguyen AT
AD  - Department of Laboratory Medicine and Pathology, Neuropathology Mayo Clinic, 
      Rochester, MN, USA.
FAU - Myasoedova, Elena
AU  - Myasoedova E
AUID- ORCID: 0000-0003-2006-1436
AD  - Division of Rheumatology, Department of Internal Medicine, Mayo Clinic, 
      Rochester, MN, USA.
AD  - Department of Quantitative Health Sciences, Mayo Clinic, Rochester, MN, USA.
LA  - eng
GR  - R01 AR046849/AR/NIAMS NIH HHS/United States
GR  - R01 AG034676/AG/NIA NIH HHS/United States
GR  - K24 AG078179/AG/NIA NIH HHS/United States
GR  - R01 AG068192/AG/NIA NIH HHS/United States
GR  - UL1 TR002377/TR/NCATS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
SB  - IM
MH  - Humans
MH  - *Alzheimer Disease/complications/pathology
MH  - *Neurodegenerative Diseases/complications/pathology
MH  - *Cerebrovascular Disorders/etiology
MH  - Brain/pathology
MH  - *Arthritis, Rheumatoid/complications/pathology
MH  - Infarction
PMC - PMC10593511
OTO - NOTNLM
OT  - RA
OT  - cerebrovascular disease
OT  - neuropathology
EDAT- 2023/10/24 00:41
MHDA- 2023/10/30 06:46
PMCR- 2024/10/23
CRDT- 2023/10/23 20:13
PHST- 2023/03/15 00:00 [received]
PHST- 2023/07/19 00:00 [accepted]
PHST- 2023/10/30 06:46 [medline]
PHST- 2023/10/24 00:41 [pubmed]
PHST- 2023/10/23 20:13 [entrez]
PHST- 2024/10/23 00:00 [pmc-release]
AID - 7328902 [pii]
AID - kead396 [pii]
AID - 10.1093/rheumatology/kead396 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2023 Oct 23;62(SI3):SI296-SI303. doi: 
      10.1093/rheumatology/kead396.

PMID- 37844386
OWN - NLM
STAT- MEDLINE
DCOM- 20231216
LR  - 20240102
IS  - 1532-866X (Electronic)
IS  - 0049-0172 (Linking)
VI  - 63
DP  - 2023 Dec
TI  - Elevated triglyceride levels are associated with increased risk for major adverse 
      cardiovascular events in statin-naïve rheumatoid arthritis patients: A nationwide 
      cohort study.
PG  - 152274
LID - S0049-0172(23)00116-6 [pii]
LID - 10.1016/j.semarthrit.2023.152274 [doi]
AB  - OBJECTIVES: To investigate the association between the four components of the 
      lipid profile (total cholesterol (TC), triglyceride (TG), low-density lipoprotein 
      cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C)) at 
      baseline and composite major adverse cardiovascular events (MACEs) in 
      statin-naïve rheumatoid arthritis (RA) patients with no previous history of 
      cardiovascular events. METHODS: This nationwide population-based cohort study was 
      performed on a total of 15,216 statin-naïve RA patients. The end point was a 
      composite of clinical events, including myocardial infarction (MI), stroke, 
      coronary revascularization, and cardiovascular death. We compared the incidence 
      of and risk for clinical events according to each lipid variable. RESULTS: During 
      follow-up (median 4.70 years), the incidence of MACE per 1000 person-years was 
      7.27. Among the four lipid components, only higher baseline TG levels were 
      significantly associated with increased risk for composite MACE in RA subjects. 
      The risk for composite MACE was significantly higher in the third (adjusted 
      hazard ratio (HR), 1.35 [95% confidence interval (CI), 1.03-1.78]) and highest 
      quartiles (adjusted HR, 1.74 [95%CI, 1.33-2.28]) of baseline TG level versus the 
      lowest quartile. CONCLUSIONS: In statin-naïve RA patients, increased TG level is 
      associated with increased risk for MACE. Therefore, screening and intervention 
      for increased TG level may be clinically beneficial in this population.
CI  - Copyright © 2023 Elsevier Inc. All rights reserved.
FAU - Choi, Wonsuk
AU  - Choi W
AD  - Department of Internal Medicine, Chonnam National University Hwasun Hospital, 
      Chonnam National University Medical School, Hwasun, Korea. Electronic address: 
      cwonsuk1106@gmail.com.
FAU - Kang, Ji-Hyoun
AU  - Kang JH
AD  - Department of Internal Medicine, Division of Rheumatology, Chonnam National 
      University Hospital, Chonnam National University Medical School, Gwangju, Korea.
FAU - Park, Ji Yong
AU  - Park JY
AD  - Department of Internal Medicine, Chonnam National University Hwasun Hospital, 
      Chonnam National University Medical School, Hwasun, Korea.
FAU - Hong, A Ram
AU  - Hong AR
AD  - Department of Internal Medicine, Chonnam National University Hwasun Hospital, 
      Chonnam National University Medical School, Hwasun, Korea.
FAU - Yoon, Jee Hee
AU  - Yoon JH
AD  - Department of Internal Medicine, Chonnam National University Hwasun Hospital, 
      Chonnam National University Medical School, Hwasun, Korea.
FAU - Kim, Hee Kyung
AU  - Kim HK
AD  - Department of Internal Medicine, Chonnam National University Hwasun Hospital, 
      Chonnam National University Medical School, Hwasun, Korea. Electronic address: 
      albeppy@chonnam.ac.kr.
FAU - Kang, Ho-Cheol
AU  - Kang HC
AD  - Department of Internal Medicine, Chonnam National University Hwasun Hospital, 
      Chonnam National University Medical School, Hwasun, Korea.
LA  - eng
PT  - Journal Article
DEP - 20231005
PL  - United States
TA  - Semin Arthritis Rheum
JT  - Seminars in arthritis and rheumatism
JID - 1306053
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Triglycerides)
RN  - 0 (Cholesterol, LDL)
RN  - 0 (Cholesterol, HDL)
SB  - IM
MH  - Humans
MH  - *Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use
MH  - Cohort Studies
MH  - Risk Factors
MH  - *Myocardial Infarction/etiology/chemically induced
MH  - *Arthritis, Rheumatoid/complications/drug therapy/epidemiology
MH  - Triglycerides
MH  - Cholesterol, LDL
MH  - Cholesterol, HDL
MH  - *Cardiovascular Diseases/etiology/chemically induced
OTO - NOTNLM
OT  - Cardiovascular event
OT  - Nationwide cohort
OT  - Rheumatoid arthritis
OT  - Statin-naïve
OT  - Triglyceride
COIS- Declaration of Competing Interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/10/17 00:42
MHDA- 2023/12/17 09:44
CRDT- 2023/10/16 18:02
PHST- 2023/07/26 00:00 [received]
PHST- 2023/09/18 00:00 [revised]
PHST- 2023/10/03 00:00 [accepted]
PHST- 2023/12/17 09:44 [medline]
PHST- 2023/10/17 00:42 [pubmed]
PHST- 2023/10/16 18:02 [entrez]
AID - S0049-0172(23)00116-6 [pii]
AID - 10.1016/j.semarthrit.2023.152274 [doi]
PST - ppublish
SO  - Semin Arthritis Rheum. 2023 Dec;63:152274. doi: 10.1016/j.semarthrit.2023.152274. 
      Epub 2023 Oct 5.

PMID- 37821035
OWN - NLM
STAT- MEDLINE
DCOM- 20240425
LR  - 20240621
IS  - 1542-7714 (Electronic)
IS  - 1542-3565 (Linking)
VI  - 22
IP  - 5
DP  - 2024 May
TI  - Risk of Major Adverse Cardiovascular Events in Immune-Mediated Inflammatory 
      Disorders on Biologics and Small Molecules: Network Meta-Analysis.
PG  - 961-970.e12
LID - S1542-3565(23)00767-X [pii]
LID - 10.1016/j.cgh.2023.09.033 [doi]
AB  - BACKGROUND AND AIMS: Recent studies raise concern for increased risk of major 
      adverse cardiovascular events (MACE) with Janus kinase (JAK) inhibitors used to 
      treat immune-mediated inflammatory disorders (IMIDs). We aimed to examine MACE 
      risk with licensed biologics and small molecules used commonly between IMIDs: 
      inflammatory bowel disease, rheumatoid arthritis, psoriasis/psoriatic arthritis, 
      and ankylosing spondylitis. METHODS: Data were obtained from systematic searches 
      (from inception to May 31, 2022) in PubMed, Embase, Ovid Medline, Scopus, 
      Cochrane Central, and ClinicalTrials.gov. Studies that assessed a predefined MACE 
      (myocardial infarction, cerebrovascular accident, unstable angina, cardiovascular 
      death, or heart failure) risk in those ≥18 years of age with IMIDs treated with 
      anti-interleukin (IL)-23 antibodies, anti-IL-12/23, anti-tumor necrosis factor α 
      antibodies (anti-TNF-α), or JAK inhibitors were included in a network 
      meta-analysis using a random-effects model with pooled odds ratios (ORs) reported 
      with 95% credible intervals (CrIs) by drug class and disease state. RESULTS: 
      Among 3528 studies identified, 40 (36 randomized controlled trials and 4 cohort 
      studies) were included in the systematic review, comprising 126,961 patients with 
      IMIDs. Based on network meta-analysis of randomized controlled trials, regardless 
      of disease state, anti-TNF-α (OR, 2.49; 95% CrI, 1.14-5.62), JAK inhibitors (OR, 
      2.64; 95% CrI, 1.26-5.99), and anti-IL-12/23 (OR, 3.15; 95% CrI, 1.01-13.35) were 
      associated with increased MACE risk compared with placebo. There was no 
      significant difference in the magnitude of the MACE risk between classes or based 
      on IMID type. CONCLUSIONS: Anti-IL-12/23, JAK inhibitors, and anti-TNF-α were 
      associated with higher risk of MACE compared with placebo. The magnitude of the 
      increased MACE risk was not different by IMID type. These results require 
      confirmation in larger prospective studies.
CI  - Copyright © 2024 AGA Institute. Published by Elsevier Inc. All rights reserved.
FAU - Mattay, Shivani Shah
AU  - Mattay SS
AD  - Division of Gastroenterology, Washington University in St. Louis School of 
      Medicine, St. Louis, Missouri.
FAU - Zamani, Mohammad
AU  - Zamani M
AD  - Division of Gastroenterology, Washington University in St. Louis School of 
      Medicine, St. Louis, Missouri; Digestive Diseases Research Center, Digestive 
      Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran.
FAU - Saturno, Dany
AU  - Saturno D
AD  - Division of Gastroenterology, Washington University in St. Louis School of 
      Medicine, St. Louis, Missouri.
FAU - Loftus, Edward V Jr
AU  - Loftus EV Jr
AD  - Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and 
      Science, Rochester, Minnesota.
FAU - Ciorba, Matthew A
AU  - Ciorba MA
AD  - Division of Gastroenterology, Washington University in St. Louis School of 
      Medicine, St. Louis, Missouri.
FAU - Yarur, Andres
AU  - Yarur A
AD  - Division of Gastroenterology, Cedars-Sinai Medical Center, Los Angeles, 
      California.
FAU - Singh, Siddharth
AU  - Singh S
AD  - Division of Gastroenterology, University of California San Diego, San Diego, 
      California.
FAU - Deepak, Parakkal
AU  - Deepak P
AD  - Division of Gastroenterology, Washington University in St. Louis School of 
      Medicine, St. Louis, Missouri. Electronic address: deepak.parakkal@wustl.edu.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PT  - Systematic Review
DEP - 20231010
PL  - United States
TA  - Clin Gastroenterol Hepatol
JT  - Clinical gastroenterology and hepatology : the official clinical practice journal 
      of the American Gastroenterological Association
JID - 101160775
RN  - 0 (Biological Products)
RN  - 0 (Janus Kinase Inhibitors)
SB  - IM
MH  - Humans
MH  - *Cardiovascular Diseases
MH  - *Biological Products/therapeutic use/adverse effects
MH  - *Network Meta-Analysis
MH  - Janus Kinase Inhibitors/therapeutic use/adverse effects
OTO - NOTNLM
OT  - Anti-TNF
OT  - Cardiovascular Disease
OT  - Inflammation
OT  - Inflammatory Bowel Disease
OT  - JAKi
OT  - Ustekinumab
EDAT- 2023/10/12 00:43
MHDA- 2024/04/26 00:52
CRDT- 2023/10/11 19:41
PHST- 2023/05/21 00:00 [received]
PHST- 2023/09/17 00:00 [revised]
PHST- 2023/09/25 00:00 [accepted]
PHST- 2024/04/26 00:52 [medline]
PHST- 2023/10/12 00:43 [pubmed]
PHST- 2023/10/11 19:41 [entrez]
AID - S1542-3565(23)00767-X [pii]
AID - 10.1016/j.cgh.2023.09.033 [doi]
PST - ppublish
SO  - Clin Gastroenterol Hepatol. 2024 May;22(5):961-970.e12. doi: 
      10.1016/j.cgh.2023.09.033. Epub 2023 Oct 10.

PMID- 37778762
OWN - NLM
STAT- Publisher
LR  - 20231115
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
DP  - 2023 Oct 1
TI  - Safety and Health Care Use Following COVID-19 Vaccination Among Adults With 
      Rheumatoid Arthritis: A Population-Based Self-Controlled Case Series Analysis.
LID - jrheum.2023-0355 [pii]
LID - 10.3899/jrheum.2023-0355 [doi]
AB  - OBJECTIVE: To determine if coronavirus disease 2019 (COVID-19) vaccines were 
      associated with adverse events of special interest (AESIs) and healthcare use 
      among adults with rheumatoid arthritis (RA). METHODS: Among adults with RA who 
      received at least 1 COVID-19 vaccine, a self-controlled case series (SCCS) 
      analysis was conducted to evaluate relative incidence (RI) rates of AESIs (Bell 
      palsy, idiopathic thrombocytopenia, acute disseminated encephalomyelitis, 
      pericarditis/myocarditis, Guillain-Barré syndrome, transverse myelitis, 
      myocardial infarction, anaphylaxis, stroke, deep vein thrombosis, pulmonary 
      embolism, narcolepsy, appendicitis, and disseminated intravascular coagulation) 
      in any 21-day period following vaccination compared to control periods. Secondary 
      outcomes included emergency department (ED) visits, hospitalizations, and 
      rheumatology visits. A matched non-RA comparator group was created and a separate 
      SCCS analysis was conducted. RI ratios (RIRs) were used to compare RA and non-RA 
      groups. RESULTS: Among 123,466 patients with RA and 493,864 comparators, the 
      majority received mRNA vaccines. For patients with RA, relative to control 
      periods, AESIs were not increased. ED visits increased after dose 2 (RI 1.06, 95% 
      CI 1.03-1.10) and decreased after dose 3 (RI 0.93, 95% CI 0.89-0.96). 
      Hospitalizations were lower after the first (RI 0.83, 95% CI 0.78-0.88), second 
      (RI 0.86, 95% CI 0.81-0.92), and third (RI 0.89, 95% CI 0.83-0.95) doses. 
      Rheumatology visits increased after dose 1 (RI 1.08, 95% CI 1.07-1.10), and 
      decreased after doses 2 and 3. Relative to comparators, patients with RA had a 
      higher AESI risk after dose 3 (RIR 1.28, 95% CI 1.05-1.56). Patients with RA 
      experienced fewer ED visits (RIR 0.73, 95% CI 0.58-0.90) and hospitalizations 
      (RIR 0.52, 95% CI 0.36-0.75) after dose 4. CONCLUSION: COVID-19 vaccines in 
      patients with RA were not associated with an increase in AESI risk or healthcare 
      use after every dose.
FAU - Lee, Jennifer J Y
AU  - Lee JJY
AUID- ORCID: 0000-0002-5300-2662
AD  - J.J.Y. Lee, MD, MSc, ICES, Toronto, Ontario.
FAU - Bernatsky, Sasha
AU  - Bernatsky S
AUID- ORCID: 0000-0002-9515-2802
AD  - S. Bernatsky, MD, PhD, Division of Rheumatology and Clinical Epidemiology, 
      Department of Medicine, McGill University Health Centre, Montreal, Quebec.
FAU - Kwong, Jeffrey C
AU  - Kwong JC
AUID- ORCID: 0000-0002-7820-2046
AD  - J.C. Kwong, MD, MSc, ICES, and Dalla Lana School of Public Health, University of 
      Toronto, Toronto, Ontario.
FAU - Li, Qing
AU  - Li Q
AUID- ORCID: 0000-0001-7139-464X
AD  - Q. Li, MMath, ICES, Toronto, Ontario.
FAU - Kwok, Timothy S H
AU  - Kwok TSH
AUID- ORCID: 0000-0003-0354-4794
AD  - T.S.H. Kwok, MD, MSc, Department of Medicine, University of Toronto, and ICES, 
      Toronto, Ontario.
FAU - Widdifield, Jessica
AU  - Widdifield J
AUID- ORCID: 0000-0002-7464-0460
AD  - J. Widdifield, PhD, Sunnybrook Research Institute, and ICES, and Institute of 
      Health Policy, Management and Evaluation, University of Toronto, Toronto, 
      Ontario, Canada.
LA  - eng
PT  - Journal Article
DEP - 20231001
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
SB  - IM
EDAT- 2023/10/02 00:41
MHDA- 2023/10/02 00:41
CRDT- 2023/10/01 20:43
PHST- 2023/10/02 00:41 [pubmed]
PHST- 2023/10/02 00:41 [medline]
PHST- 2023/10/01 20:43 [entrez]
AID - jrheum.2023-0355 [pii]
AID - 10.3899/jrheum.2023-0355 [doi]
PST - aheadofprint
SO  - J Rheumatol. 2023 Oct 1:jrheum.2023-0355. doi: 10.3899/jrheum.2023-0355.

PMID- 37726980
OWN - NLM
STAT- MEDLINE
DCOM- 20231102
LR  - 20231102
IS  - 1756-185X (Electronic)
IS  - 1756-1841 (Linking)
VI  - 26
IP  - 11
DP  - 2023 Nov
TI  - Outcomes of hemorrhagic stroke in patients with autoimmune rheumatic diseases: An 
      analysis of the US Nationwide Inpatient Sample.
PG  - 2206-2213
LID - 10.1111/1756-185X.14916 [doi]
AB  - AIM: To determine whether and how rheumatoid arthritis (RA), systemic lupus 
      erythematosus (SLE), and systemic sclerosis (SSc) affect outcomes in patients 
      admitted for hemorrhagic stroke. METHODS: This study screened the Nationwide 
      Inpatient Sample database for adults aged ≥20 years admitted to US hospitals with 
      a principal diagnosis of intracerebral hemorrhage (ICH) between 2005 and 2018. 
      Diagnoses were determined using the International Classification of Diseases, 9th 
      and 10th revisions (ICD-9 and ICD-10) diagnostic codes for ICH (ICD-9: 431, 432; 
      ICD-10: I61, I62). Study outcomes were: (1) in-hospital mortality; (2) 
      unfavorable discharge, defined as transfer to nursing homes or long-term care 
      facilities; and (3) prolonged length of stay (LOS), defined as LOS >75th centile. 
      RESULTS: Associations between comorbid RA, SLE, and SSc and clinical outcomes 
      show a significantly lower risk of in-hospital mortality and prolonged LOS in RA 
      patients. After admissions for ICH, the risk for in-hospital mortality and 
      prolonged LOS was decreased in RA patients, and the risk for unfavorable 
      discharge (long-term care) was reduced in SLE patients. CONCLUSIONS: Among 
      patients admitted to US hospitals for hemorrhagic stroke, patients with RA had 
      decreased risk for in-hospital mortality and prolonged LOS.
CI  - © 2023 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons 
      Australia, Ltd.
FAU - Chen, Mao-Yu
AU  - Chen MY
AD  - Department of Neurosurgery, Chang Gung Memorial Hospital, Keelung, Taiwan.
FAU - Chen, Pin-Yuan
AU  - Chen PY
AD  - Department of Neurosurgery, Chang Gung Memorial Hospital, Keelung, Taiwan.
AD  - School of Medicine, Chang Gung University, Taoyuan, Taiwan.
AD  - Community Medicine Research Center, Chang Gung Memorial Hospital, Keelung, 
      Taiwan.
FAU - Chang, Chen-Nen
AU  - Chang CN
AD  - Department of Neurosurgery, Chang Gung Memorial Hospital, Keelung, Taiwan.
FAU - Chen, Bo-An
AU  - Chen BA
AD  - Department of Neurosurgery, Chang Gung Memorial Hospital, Linkou, Taiwan.
FAU - Deng, Wen-Chun
AU  - Deng WC
AD  - Department of Neurosurgery, Chang Gung Memorial Hospital, Keelung, Taiwan.
FAU - Yan, Jiun-Lin
AU  - Yan JL
AUID- ORCID: 0000-0002-5270-2878
AD  - Department of Neurosurgery, Chang Gung Memorial Hospital, Keelung, Taiwan.
AD  - School of Traditional Chinese Medicine, College of Medicine, Chang Gung 
      University, Taoyuan, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20230919
PL  - England
TA  - Int J Rheum Dis
JT  - International journal of rheumatic diseases
JID - 101474930
SB  - IM
MH  - Adult
MH  - Humans
MH  - *Hemorrhagic Stroke
MH  - Inpatients
MH  - Risk Factors
MH  - *Arthritis, Rheumatoid/diagnosis/epidemiology
MH  - *Lupus Erythematosus, Systemic/diagnosis/epidemiology
MH  - *Scleroderma, Systemic
MH  - *Stroke/diagnosis/epidemiology/therapy
OTO - NOTNLM
OT  - Nationwide Inpatient Sample
OT  - hemorrhagic stroke
OT  - rheumatoid arthritis
OT  - systemic lupus erythematosus
OT  - systemic sclerosis
EDAT- 2023/09/20 06:42
MHDA- 2023/11/02 12:43
CRDT- 2023/09/20 01:54
PHST- 2023/09/01 00:00 [revised]
PHST- 2023/06/09 00:00 [received]
PHST- 2023/09/03 00:00 [accepted]
PHST- 2023/11/02 12:43 [medline]
PHST- 2023/09/20 06:42 [pubmed]
PHST- 2023/09/20 01:54 [entrez]
AID - 10.1111/1756-185X.14916 [doi]
PST - ppublish
SO  - Int J Rheum Dis. 2023 Nov;26(11):2206-2213. doi: 10.1111/1756-185X.14916. Epub 
      2023 Sep 19.

PMID- 37720218
OWN - NLM
STAT- MEDLINE
DCOM- 20230919
LR  - 20240924
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 14
DP  - 2023
TI  - The impact of EMA recommendations on the real-life use of Janus kinases 
      inhibitors for rheumatoid arthritis: the Expanded Risk Score in RA as a tool to 
      quantify the risk of cardiovascular events.
PG  - 1225160
LID - 10.3389/fimmu.2023.1225160 [doi]
LID - 1225160
AB  - OBJECTIVE: To evaluate in patients with rheumatoid arthritis (RA) the impact of 
      EMA recommendations on the real-life prescription of JAK inhibitors (JAKis) and 
      the use of the Expanded Risk Score in RA (ERS-RA) to quantify the risk of major 
      adverse cardiac events (MACE). METHODS: We conducted a retrospective analysis of 
      real-life RA patients treated with JAKis. Patients were classified as ineligible 
      for JAKis if they fulfilled EMA criteria (>65 years-old, history of malignancy, 
      or increased risk of venous thromboembolic events [VTE] or MACE including 
      smoking). Risk of MACE was defined according to ORAL Surveillance trial inclusion 
      criteria (ORALSURV) or by using the ERS-RA. RESULTS: Of 194 patients enrolled, 
      57.9% were classified as ineligible according to EMA definition (ORALSURV 
      criteria). The most frequent reason for ineligibility was increased MACE risk 
      (70.2%), followed by age>65 (34.2%), smoking (30.7%), and increased risk of VTE 
      (20.2%) or malignancy (7%). The use of the ERS-RA reduced the rate of patients 
      carrying an increased CV risk to 18.6% (p<0.001 versus ORALSURV), leading to 
      46.4% overall ineligible patients. Over a drug-exposure of 337 patient/years, we 
      observed 2 VTE, one MACE (non-fatal stroke), and one solid malignancy (all in the 
      group of patients classified as ineligible according to both the definitions). 
      CONCLUSIONS: Rigorous application of EMA indications in clinical practice could 
      result in the exclusion of a large proportion of RA patients from treatment with 
      JAKis. A proper quantification of the risk for MACE by dedicated tools as ERS-RA 
      is advocated to better tailor the management of RA.
CI  - Copyright © 2023 Favalli, Cincinelli, Germinario, Di Taranto, Orsini, Maioli, 
      Biggioggero, Ferrito and Caporali.
FAU - Favalli, Ennio Giulio
AU  - Favalli EG
AD  - Department of Rheumatology and Medical Sciences, ASST Gaetano Pini-CTO, Milan, 
      Italy.
AD  - Department of Clinical Sciences and Community Health, Università degli Studi di 
      Milano, Milan, Italy.
FAU - Cincinelli, Gilberto
AU  - Cincinelli G
AD  - Department of Rheumatology and Medical Sciences, ASST Gaetano Pini-CTO, Milan, 
      Italy.
AD  - Department of Clinical Sciences and Community Health, Università degli Studi di 
      Milano, Milan, Italy.
FAU - Germinario, Sabino
AU  - Germinario S
AD  - Department of Rheumatology and Medical Sciences, ASST Gaetano Pini-CTO, Milan, 
      Italy.
AD  - Department of Clinical Sciences and Community Health, Università degli Studi di 
      Milano, Milan, Italy.
FAU - Di Taranto, Raffaele
AU  - Di Taranto R
AD  - Department of Rheumatology and Medical Sciences, ASST Gaetano Pini-CTO, Milan, 
      Italy.
AD  - Department of Clinical Sciences and Community Health, Università degli Studi di 
      Milano, Milan, Italy.
FAU - Orsini, Francesco
AU  - Orsini F
AD  - Department of Rheumatology and Medical Sciences, ASST Gaetano Pini-CTO, Milan, 
      Italy.
AD  - Department of Clinical Sciences and Community Health, Università degli Studi di 
      Milano, Milan, Italy.
FAU - Maioli, Gabriella
AU  - Maioli G
AD  - Department of Rheumatology and Medical Sciences, ASST Gaetano Pini-CTO, Milan, 
      Italy.
AD  - Department of Clinical Sciences and Community Health, Università degli Studi di 
      Milano, Milan, Italy.
FAU - Biggioggero, Martina
AU  - Biggioggero M
AD  - Department of Rheumatology and Medical Sciences, ASST Gaetano Pini-CTO, Milan, 
      Italy.
FAU - Ferrito, Matteo
AU  - Ferrito M
AD  - Department of Rheumatology and Medical Sciences, ASST Gaetano Pini-CTO, Milan, 
      Italy.
AD  - Department of Clinical Sciences and Community Health, Università degli Studi di 
      Milano, Milan, Italy.
FAU - Caporali, Roberto
AU  - Caporali R
AD  - Department of Rheumatology and Medical Sciences, ASST Gaetano Pini-CTO, Milan, 
      Italy.
AD  - Department of Clinical Sciences and Community Health, Università degli Studi di 
      Milano, Milan, Italy.
LA  - eng
PT  - Journal Article
DEP - 20230831
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
RN  - 0 (Janus Kinase Inhibitors)
RN  - EC 2.7.10.2 (Janus Kinases)
SB  - IM
MH  - Humans
MH  - Aged
MH  - *Janus Kinase Inhibitors/adverse effects
MH  - Retrospective Studies
MH  - *Venous Thromboembolism/epidemiology/etiology
MH  - Risk Factors
MH  - *Arthritis, Rheumatoid/drug therapy
MH  - Janus Kinases
PMC - PMC10500057
OTO - NOTNLM
OT  - JAK inhibitors
OT  - b/tsDMARDs
OT  - cardiovascular risk
OT  - rheumatoid arthritis
OT  - safety
COIS- Author EF has been a consultant for and/or received honoraria as a speaker for 
      the companies AbbVie, BMS, Eli Lilly, Galapagos, Janssen, MSD, Novartis, Pfizer, 
      and UCB Pharma. Author MB received honoraria as a speaker for the company 
      Galapagos. Author RC has been a consultant for and/or received honoraria as a 
      speaker for the companies AbbVie, Amgen, BMS, Celltrion, Fresenius, Galapagos, 
      Janssen, Eli Lilly, Novartis, Pfizer, and UCB Pharma. The remaining authors 
      declare that the research was conducted in the absence of any commercial or 
      financial relationships that could be construed as a potential conflict of 
      interest.
EDAT- 2023/09/18 06:42
MHDA- 2023/09/19 06:42
PMCR- 2023/01/01
CRDT- 2023/09/18 04:36
PHST- 2023/05/18 00:00 [received]
PHST- 2023/08/10 00:00 [accepted]
PHST- 2023/09/19 06:42 [medline]
PHST- 2023/09/18 06:42 [pubmed]
PHST- 2023/09/18 04:36 [entrez]
PHST- 2023/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2023.1225160 [doi]
PST - epublish
SO  - Front Immunol. 2023 Aug 31;14:1225160. doi: 10.3389/fimmu.2023.1225160. 
      eCollection 2023.

PMID- 37691305
OWN - NLM
STAT- MEDLINE
DCOM- 20240227
LR  - 20241002
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Linking)
VI  - 76
IP  - 3
DP  - 2024 Mar
TI  - Antimalarial Adherence and Risk of Cardiovascular Events in Patients With 
      Rheumatoid Arthritis and Systemic Lupus Erythematosus: A Population-Based Study.
PG  - 426-436
LID - 10.1002/acr.25233 [doi]
AB  - OBJECTIVE: We aimed to assess the association between antimalarial adherence and 
      cardiovascular events between incident rheumatoid arthritis (RA) and systemic 
      lupus erythematosus (SLE) population-based cohorts. METHODS: All patients with 
      incident RA/SLE and incident antimalarial use in British Columbia, Canada, 
      between January 1997 and March 2015 were identified using provincial 
      administrative databases. The outcomes were incident cardiovascular events, 
      including myocardial infarction (MI), stroke, or venous thromboembolism (VTE). 
      The exposure was antimalarial adherence with levels: discontinuation (proportion 
      of days covered [PDC = 0]), nonadherence (0 < PDC < 0.90), and adherence (PDC 
      ≥ 0.90). We used marginal structural models to estimate the effect of 
      antimalarial adherence on the rate of cardiovascular events, accounting for 
      potential confounders. RESULTS: We identified 16,538 individuals with incident 
      RA/SLE and incident antimalarial use without any cardiovascular event before the 
      index date. Over nine years mean follow-up, 2,174 incident cardiovascular events 
      (13.2%) were observed. The adjusted hazard ratio (aHR) for incident 
      cardiovascular events for antimalarial adherence relative to discontinuation was 
      0.72 (95% confidence interval [CI] 0.64-0.81) and 1.01 (95% CI 0.90-1.14) for 
      nonadherence. Additionally, the aHRs for all cardiovascular events, MI, stroke, 
      and VTE for adherence relative to nonadherence was 0.71 (95% CI 0.61-0.82), 0.62 
      (95% CI 0.51-0.75), 0.45 (95% CI 0.36-0.58), and 0.65 (95% CI 0.46-0.93), 
      respectively. We found older age modified the association between antimalarial 
      adherence and cardiovascular events (P = 0.02). CONCLUSION: When people newly 
      diagnosed with RA or SLE take their antimalarial regularly as prescribed (PDC 
      ≥ 0.90), they have a 29% lower risk of sustaining a cardiovascular event than 
      patients with a lower degree of adherence (PDC < 0.90) and a 28% lower risk than 
      if they discontinue antimalarials.
CI  - © 2023 The Authors. Arthritis Care & Research published by Wiley Periodicals LLC 
      on behalf of American College of Rheumatology.
FAU - Hoque, Md Rashedul
AU  - Hoque MR
AUID- ORCID: 0000-0002-0852-1850
AD  - Arthritis Research Canada, Vancouver, and Simon Fraser University, Burnaby, 
      British Columbia, Canada.
FAU - Aviña-Zubieta, J Antonio
AU  - Aviña-Zubieta JA
AUID- ORCID: 0000-0001-5526-663X
AD  - Arthritis Research Canada and University of British Columbia, Vancouver, British 
      Columbia, Canada.
FAU - Lacaille, Diane
AU  - Lacaille D
AUID- ORCID: 0000-0002-4065-4151
AD  - Arthritis Research Canada and University of British Columbia, Vancouver, British 
      Columbia, Canada.
FAU - De Vera, Mary A
AU  - De Vera MA
AD  - Arthritis Research Canada and University of British Columbia, Vancouver, British 
      Columbia, Canada.
FAU - Qian, Yi
AU  - Qian Y
AD  - University of British Columbia, Vancouver, British Columbia, Canada.
FAU - McCandless, Lawrence
AU  - McCandless L
AD  - Simon Fraser University, Burnaby, British Columbia, Canada.
FAU - Esdaile, John M
AU  - Esdaile JM
AD  - Arthritis Research Canada and University of British Columbia, Vancouver, British 
      Columbia, Canada.
FAU - Xie, Hui
AU  - Xie H
AUID- ORCID: 0000-0003-3328-7135
AD  - Arthritis Research Canada, Vancouver, and Simon Fraser University, Burnaby, 
      British Columbia, Canada.
LA  - eng
GR  - THC-135235/CIHR/Canada
GR  - THC-135235/CIHR/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20231218
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 0 (Antimalarials)
SB  - IM
MH  - Humans
MH  - *Antimalarials/adverse effects
MH  - *Venous Thromboembolism
MH  - *Lupus Erythematosus, Systemic/diagnosis/drug therapy/epidemiology
MH  - *Arthritis, Rheumatoid/diagnosis/drug therapy/epidemiology
MH  - *Myocardial Infarction
MH  - *Stroke/diagnosis/epidemiology/prevention & control
MH  - British Columbia/epidemiology
MH  - Risk Factors
EDAT- 2023/09/11 06:43
MHDA- 2024/02/27 06:44
CRDT- 2023/09/11 01:47
PHST- 2023/08/21 00:00 [revised]
PHST- 2023/03/05 00:00 [received]
PHST- 2023/09/06 00:00 [accepted]
PHST- 2024/02/27 06:44 [medline]
PHST- 2023/09/11 06:43 [pubmed]
PHST- 2023/09/11 01:47 [entrez]
AID - 10.1002/acr.25233 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2024 Mar;76(3):426-436. doi: 10.1002/acr.25233. 
      Epub 2023 Dec 18.

PMID- 37662776
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230905
IS  - 2405-8440 (Print)
IS  - 2405-8440 (Electronic)
IS  - 2405-8440 (Linking)
VI  - 9
IP  - 9
DP  - 2023 Sep
TI  - Protocol for rheumatoid arthritis complicated with cardiovascular damage treated 
      with Guanxining tablet with a randomized controlled trial.
PG  - e19241
LID - 10.1016/j.heliyon.2023.e19241 [doi]
LID - e19241
AB  - BACKGROUND: Cardiovascular disease (CVD) is the main cause of death in patients 
      with rheumatoid arthritis (RA). Apart from traditional cardiovascular risk 
      factors, immune dysfunction and chronic inflammation of RA are also risk factors 
      for complex cardiovascular damage. Although methotrexate (MTX) is beneficial to 
      CVD in RA patients by inhibiting inflammation, its adverse effects limit its 
      clinical application. Therefore, it is essential to seek safer and more effective 
      drugs. OBJECTIVE: We aimed to assess the efficacy of Guanxining Tablet (GXNT) for 
      rheumatoid arthritis complicated with cardiovascular damage. METHODS: We will 
      conduct a prospective single-center randomized trial. We will randomly divide 56 
      eligible patients into two groups. The treatment group will take GXNT and MTX 
      treatment, and the control group will receive MTX and the placebo. The primary 
      outcome measure will be aortic distensibility (AD). Secondary outcome measures 
      will be Cardiac function which will contain right ventricular outflow tract 
      diameter (RVOTD), aortic diameter (AOD), left atrium diameter (LAD), right 
      ventricular end diastolic diameter (RVDD), left ventricular end diastolic 
      diameter (LVDD), ejection fraction (EF%), fractional shortening (FS%), stroke 
      volume (SV). Adverse events will be closely monitored during the entire trial 
      period. DISCUSSION: This trial is intended to determine whether the addition of 
      GXNT will improve the prognosis of patients with rheumatoid arthritis and 
      cardiovascular damage without severe adverse reactions. Completing this clinical 
      trial might provide these patients with a novel and effective drug while avoiding 
      adverse reactions similar to methotrexate. TRIAL REGISTRATION: ChiCTR2000030247.
CI  - © 2023 The Authors. Published by Elsevier Ltd.
FAU - Yu, Kai
AU  - Yu K
AD  - Department of Rheumatology, The Second Affiliated Hospital of Zhejiang Chinese 
      Medical University, Hangzhou, 310005, China.
FAU - Yang, Kepeng
AU  - Yang K
AD  - Department of Rheumatology, The Second Affiliated Hospital of Zhejiang Chinese 
      Medical University, Hangzhou, 310005, China.
FAU - Han, Tingfen
AU  - Han T
AD  - Department of Rheumatology, The Second Affiliated Hospital of Zhejiang Chinese 
      Medical University, Hangzhou, 310005, China.
FAU - Sun, Qice
AU  - Sun Q
AD  - Department of Rheumatology, The Second Affiliated Hospital of Zhejiang Chinese 
      Medical University, Hangzhou, 310005, China.
FAU - Zhu, Ming
AU  - Zhu M
AD  - Yuyao Hospital of Traditional Chinese Medicine, Ningbo, 315400, China.
FAU - Wang, Xinchang
AU  - Wang X
AD  - Department of Rheumatology, The Second Affiliated Hospital of Zhejiang Chinese 
      Medical University, Hangzhou, 310005, China.
FAU - Wang, Weijie
AU  - Wang W
AD  - Department of Rheumatology, The Second Affiliated Hospital of Zhejiang Chinese 
      Medical University, Hangzhou, 310005, China.
LA  - eng
PT  - Journal Article
DEP - 20230822
PL  - England
TA  - Heliyon
JT  - Heliyon
JID - 101672560
PMC - PMC10474432
OTO - NOTNLM
OT  - Cardiovascular damage
OT  - Chinese herbal medicine
OT  - Guanxining tablet
OT  - Rheumatoid arthritis
COIS- The authors declare that they have no known competing financial interests or 
      personal relationships that could have appeared to influence the work reported in 
      this paper.
EDAT- 2023/09/04 06:42
MHDA- 2023/09/04 06:43
PMCR- 2023/08/22
CRDT- 2023/09/04 04:49
PHST- 2022/12/12 00:00 [received]
PHST- 2023/07/31 00:00 [revised]
PHST- 2023/08/16 00:00 [accepted]
PHST- 2023/09/04 06:43 [medline]
PHST- 2023/09/04 06:42 [pubmed]
PHST- 2023/09/04 04:49 [entrez]
PHST- 2023/08/22 00:00 [pmc-release]
AID - S2405-8440(23)06449-6 [pii]
AID - e19241 [pii]
AID - 10.1016/j.heliyon.2023.e19241 [doi]
PST - epublish
SO  - Heliyon. 2023 Aug 22;9(9):e19241. doi: 10.1016/j.heliyon.2023.e19241. eCollection 
      2023 Sep.

PMID- 37650912
OWN - NLM
STAT- MEDLINE
DCOM- 20240807
LR  - 20240809
IS  - 1861-0692 (Electronic)
IS  - 1861-0684 (Linking)
VI  - 113
IP  - 2
DP  - 2024 Feb
TI  - Cardiovascular events risk in patients with systemic autoimmune diseases: a 
      prognostic systematic review and meta-analysis.
PG  - 246-259
LID - 10.1007/s00392-023-02291-4 [doi]
AB  - BACKGROUND: Chronic inflammation is considered a risk factor for the development 
      of atherosclerosis and cardiovascular (CV) events. We seek to assess the risk of 
      CV events in patients with Systemic autoimmune diseases (SAD), such as Systemic 
      Lupus Erythematosus (SLE), Rheumatoid Arthritis (RA), Psoriasis (Ps) and 
      Ankylosing Spondylitis (AS), compared with the general population. METHODS AND 
      RESULTS: A systematic search of MEDLINE from inception up to May 2021 was 
      performed. Observational studies including individuals with and without 
      autoimmune diseases (SLE, RA, Ps, AS), which reported a measure of association 
      and variability for the effect of SAD on CV events, were included. The random 
      effects meta-analysis was performed using the Hartung-Knapp-Sidik-Jonkman 
      approach to obtain the pooled estimates. Cardiovascular Events including CV 
      mortality, non-fatal myocardial infarction (MI), non-fatal stroke and coronary 
      revascularization were the main outcomes evaluated. Fifty-four studies were 
      selected, with a total of 24,107,072 participants. The presence of SAD was 
      associated with an increased risk of CV mortality (HR 1.49 [95% CI 1.10-2.03]), 
      non-fatal MI (HR 1.42 [95% CI 1.23-1.62]), and non-fatal stroke (HR 1.47 [95% CI 
      1.28-1.70]). RA, SLE, and Ps (particularly with arthritis) were significantly 
      associated with a higher risk of MI and stroke. SAD was also associated with an 
      increased risk of Major Adverse Cardiovascular Events (MACE) (HR 1.45 [95% CI 
      1.16-1.83]). CONCLUSION: Patients with SAD present an increased risk of CV 
      morbidity and mortality, which should be considered when establishing therapeutic 
      strategies. These findings support the role of systemic inflammation in the 
      development of atherosclerosis-driven disease.
CI  - © 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.
FAU - Asenjo-Lobos, Claudia
AU  - Asenjo-Lobos C
AUID- ORCID: 0000-0002-8264-0524
AD  - Centro de Estudios Clínicos, Instituto de Ciencias e Innovación en Medicina 
      (ICIM), Facultad de Medicina Clínica Alemana Universidad de Desarrollo, Santiago, 
      Chile.
FAU - González, Leticia
AU  - González L
AUID- ORCID: 0000-0002-0589-6884
AD  - Centro de Imágenes Biomédicas, Departamento de Radiología, Escuela de Medicina, 
      Pontificia Universidad Católica de Chile, Santiago, Chile.
AD  - Instituto Milenio de Ingeniería e Inteligencia Artificial para la Salud, iHEALTH, 
      Pontificia Universidad Católica de Chile, Santiago, Chile.
FAU - Bulnes, Juan Francisco
AU  - Bulnes JF
AUID- ORCID: 0000-0002-7849-3883
AD  - División de Enfermedades Cardiovasculares, Pontificia Universidad Católica de 
      Chile, Santiago, Chile.
FAU - Roque, Marta
AU  - Roque M
AUID- ORCID: 0000-0003-0043-1364
AD  - Iberoamerican Cochrane Centre, Sant Pau Biomedical Research Institute (IIB-Sant 
      Pau), Barcelona, Spain.
FAU - Muñoz Venturelli, Paula
AU  - Muñoz Venturelli P
AUID- ORCID: 0000-0003-1869-2255
AD  - Centro de Estudios Clínicos, Instituto de Ciencias e Innovación en Medicina 
      (ICIM), Facultad de Medicina Clínica Alemana Universidad de Desarrollo, Santiago, 
      Chile.
AD  - Faculty of Medicine, The George Institute for Global Health, University of New 
      South Wales, Sydney, NSW, Australia.
FAU - Rodríguez, Gonzalo Martínez
AU  - Rodríguez GM
AUID- ORCID: 0000-0002-7120-855X
AD  - División de Enfermedades Cardiovasculares, Pontificia Universidad Católica de 
      Chile, Santiago, Chile. gmartinezr@med.puc.cl.
LA  - eng
GR  - FONDECYT Regular Nº 1210655/Agencia Nacional de Investigación y Desarrollo/
GR  - Programa Iniciativa Científica Milenio/Agencia Nacional de Investigación y 
      Desarrollo/
GR  - Chile - Nº ICN2021_004/Agencia Nacional de Investigación y Desarrollo/
PT  - Journal Article
PT  - Meta-Analysis
PT  - Systematic Review
DEP - 20230831
PL  - Germany
TA  - Clin Res Cardiol
JT  - Clinical research in cardiology : official journal of the German Cardiac Society
JID - 101264123
MH  - Humans
MH  - *Autoimmune Diseases/complications/epidemiology
MH  - *Cardiovascular Diseases/epidemiology/mortality
MH  - Prognosis
MH  - Risk Factors
MH  - Risk Assessment/methods
MH  - Heart Disease Risk Factors
MH  - Global Health
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - Meta-analysis
OT  - Prognosis
OT  - Systemic inflammatory disease
EDAT- 2023/08/31 12:43
MHDA- 2024/02/09 00:42
CRDT- 2023/08/31 11:08
PHST- 2023/02/27 00:00 [received]
PHST- 2023/08/21 00:00 [accepted]
PHST- 2024/02/09 00:42 [medline]
PHST- 2023/08/31 12:43 [pubmed]
PHST- 2023/08/31 11:08 [entrez]
AID - 10.1007/s00392-023-02291-4 [pii]
AID - 10.1007/s00392-023-02291-4 [doi]
PST - ppublish
SO  - Clin Res Cardiol. 2024 Feb;113(2):246-259. doi: 10.1007/s00392-023-02291-4. Epub 
      2023 Aug 31.

PMID- 37648884
OWN - NLM
STAT- MEDLINE
DCOM- 20230912
LR  - 20230922
IS  - 1437-160X (Electronic)
IS  - 0172-8172 (Linking)
VI  - 43
IP  - 11
DP  - 2023 Nov
TI  - Artificial intelligence-based preventive, personalized and precision medicine for 
      cardiovascular disease/stroke risk assessment in rheumatoid arthritis patients: a 
      narrative review.
PG  - 1965-1982
LID - 10.1007/s00296-023-05415-1 [doi]
AB  - The challenges associated with diagnosing and treating cardiovascular disease 
      (CVD)/Stroke in Rheumatoid arthritis (RA) arise from the delayed onset of 
      symptoms. Existing clinical risk scores are inadequate in predicting cardiac 
      events, and conventional risk factors alone do not accurately classify many 
      individuals at risk. Several CVD biomarkers consider the multiple pathways 
      involved in the development of atherosclerosis, which is the primary cause of 
      CVD/Stroke in RA. To enhance the accuracy of CVD/Stroke risk assessment in the RA 
      framework, a proposed approach involves combining genomic-based biomarkers (GBBM) 
      derived from plasma and/or serum samples with innovative non-invasive 
      radiomic-based biomarkers (RBBM), such as measurements of synovial fluid, plaque 
      area, and plaque burden. This review presents two hypotheses: (i) RBBM and GBBM 
      biomarkers exhibit a significant correlation and can precisely detect the 
      severity of CVD/Stroke in RA patients. (ii) Artificial Intelligence (AI)-based 
      preventive, precision, and personalized (aiP(3)) CVD/Stroke risk AtheroEdge™ 
      model (AtheroPoint™, CA, USA) that utilizes deep learning (DL) to accurately 
      classify the risk of CVD/stroke in RA framework. The authors conducted a 
      comprehensive search using the PRISMA technique, identifying 153 studies that 
      assessed the features/biomarkers of RBBM and GBBM for CVD/Stroke. The study 
      demonstrates how DL models can be integrated into the AtheroEdge™-aiP(3) 
      framework to determine the risk of CVD/Stroke in RA patients. The findings of 
      this review suggest that the combination of RBBM with GBBM introduces a new 
      dimension to the assessment of CVD/Stroke risk in the RA framework. Synovial 
      fluid levels that are higher than normal lead to an increase in the plaque 
      burden. Additionally, the review provides recommendations for novel, unbiased, 
      and pruned DL algorithms that can predict CVD/Stroke risk within a RA framework 
      that is preventive, precise, and personalized.
CI  - © 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, 
      part of Springer Nature.
FAU - Al-Maini, Mustafa
AU  - Al-Maini M
AUID- ORCID: 0000-0003-2553-591X
AD  - Allergy, Clinical Immunology and Rheumatology Institute, Toronto, ON, L4Z 4C4, 
      Canada.
FAU - Maindarkar, Mahesh
AU  - Maindarkar M
AUID- ORCID: 0000-0002-0813-4906
AD  - Stroke Monitoring and Diagnostic Division, AtheroPoint™, Roseville, CA, 95661, 
      USA.
AD  - Asia Pacific Vascular Society, New Delhi, 110001, India.
FAU - Kitas, George D
AU  - Kitas GD
AUID- ORCID: 0000-0002-0828-6176
AD  - Academic Affairs, Dudley Group NHS Foundation Trust, Dudley, DY1 2HQ, UK.
AD  - Arthritis Research UK Epidemiology Unit, Manchester University, Manchester, M13 
      9PL, UK.
FAU - Khanna, Narendra N
AU  - Khanna NN
AUID- ORCID: 0000-0002-6935-0039
AD  - Asia Pacific Vascular Society, New Delhi, 110001, India.
AD  - Department of Cardiology, Indraprastha APOLLO Hospitals, New Delhi, 110001, 
      India.
FAU - Misra, Durga Prasanna
AU  - Misra DP
AUID- ORCID: 0000-0002-5035-7396
AD  - Department of Immunology, SGPIMS, Lucknow, 226014, India.
FAU - Johri, Amer M
AU  - Johri AM
AUID- ORCID: 0000-0001-7044-8212
AD  - Division of Cardiology, Department of Medicine, Queen's University, Kingston, 
      Canada.
FAU - Mantella, Laura
AU  - Mantella L
AUID- ORCID: 0000-0002-6527-426X
AD  - Division of Cardiology, Department of Medicine, University of Toronto, Toronto, 
      Canada.
FAU - Agarwal, Vikas
AU  - Agarwal V
AUID- ORCID: 0000-0002-4508-1233
AD  - Department of Immunology, SGPIMS, Lucknow, 226014, India.
FAU - Sharma, Aman
AU  - Sharma A
AD  - Department of Immunology, SGPIMS, Lucknow, 226014, India.
FAU - Singh, Inder M
AU  - Singh IM
AUID- ORCID: 0000-0002-2844-6050
AD  - Stroke Monitoring and Diagnostic Division, AtheroPoint™, Roseville, CA, 95661, 
      USA.
FAU - Tsoulfas, George
AU  - Tsoulfas G
AUID- ORCID: 0000-0001-5043-7962
AD  - Department of Surgery, Aristoteleion University of Thessaloniki, 54124, 
      Thessaloniki, Greece.
FAU - Laird, John R
AU  - Laird JR
AD  - Heart and Vascular Institute, Adventist Health St. Helena, St Helena, CA, 94574, 
      USA.
FAU - Faa, Gavino
AU  - Faa G
AD  - Department of Pathology, Azienda Ospedaliero Universitaria, 09124, Cagliari, 
      Italy.
FAU - Teji, Jagjit
AU  - Teji J
AUID- ORCID: 0000-0001-7773-2144
AD  - Ann and Robert H. Lurie Children's Hospital of Chicago, Chicago, IL, 60611, USA.
FAU - Turk, Monika
AU  - Turk M
AD  - The Hanse-Wissenschaftskolleg Institute for Advanced Study, 27753, Delmenhorst, 
      Germany.
FAU - Viskovic, Klaudija
AU  - Viskovic K
AUID- ORCID: 0000-0002-5927-3201
AD  - Department of Radiology and Ultrasound, UHID, 10 000, Zagreb, Croatia.
FAU - Ruzsa, Zoltan
AU  - Ruzsa Z
AUID- ORCID: 0000-0002-2474-5723
AD  - Invasive Cardiology Division, University of Szeged, Szeged, Hungary.
FAU - Mavrogeni, Sophie
AU  - Mavrogeni S
AUID- ORCID: 0000-0003-1089-7766
AD  - Cardiology Clinic, Onassis Cardiac Surgery Centre, Athens, Greece.
FAU - Rathore, Vijay
AU  - Rathore V
AUID- ORCID: 0000-0003-4315-5072
AD  - Nephrology Department, Kaiser Permanente, Sacramento, CA, 95823, USA.
FAU - Miner, Martin
AU  - Miner M
AUID- ORCID: 0000-0001-6813-9242
AD  - Men's Health Centre, Miriam Hospital Providence, Providence, RI, 02906, USA.
FAU - Kalra, Manudeep K
AU  - Kalra MK
AUID- ORCID: 0000-0001-9938-7476
AD  - Department of Radiology, Harvard Medical School, Boston, MA, USA.
FAU - Isenovic, Esma R
AU  - Isenovic ER
AUID- ORCID: 0000-0002-0012-2636
AD  - Department of Radiobiology and Molecular Genetics, National Institute of the 
      Republic of Serbia, University of Belgrade, 11000, Belgrade, Serbia.
FAU - Saba, Luca
AU  - Saba L
AUID- ORCID: 0000-0003-3610-8526
AD  - Department of Radiology, Azienda Ospedaliero Universitaria, 40138, Cagliari, 
      Italy.
FAU - Fouda, Mostafa M
AU  - Fouda MM
AUID- ORCID: 0000-0003-1790-8640
AD  - Department of Electrical and Computer Engineering, Idaho State University, 
      Pocatello, ID, 83209, USA.
FAU - Suri, Jasjit S
AU  - Suri JS
AUID- ORCID: 0000-0001-6499-396X
AD  - Stroke Monitoring and Diagnostic Division, AtheroPoint™, Roseville, CA, 95661, 
      USA. jasjit.suri@atheropoint.com.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20230830
PL  - Germany
TA  - Rheumatol Int
JT  - Rheumatology international
JID - 8206885
SB  - IM
MH  - Humans
MH  - Artificial Intelligence
MH  - *Cardiovascular Diseases/diagnosis/etiology/prevention & control
MH  - Precision Medicine
MH  - *Arthritis, Rheumatoid/complications
MH  - *Stroke/etiology/prevention & control
MH  - *Myocardial Infarction
MH  - Risk Assessment
OTO - NOTNLM
OT  - Bias
OT  - Biomarkers
OT  - Cardiovascular disease
OT  - Deep learning
OT  - Explainable AI
OT  - Genomics
OT  - Radiomics
OT  - Rheumatoid arthritis
OT  - Stroke
EDAT- 2023/08/31 00:42
MHDA- 2023/09/12 06:42
CRDT- 2023/08/30 23:31
PHST- 2023/07/10 00:00 [received]
PHST- 2023/07/31 00:00 [accepted]
PHST- 2023/09/12 06:42 [medline]
PHST- 2023/08/31 00:42 [pubmed]
PHST- 2023/08/30 23:31 [entrez]
AID - 10.1007/s00296-023-05415-1 [pii]
AID - 10.1007/s00296-023-05415-1 [doi]
PST - ppublish
SO  - Rheumatol Int. 2023 Nov;43(11):1965-1982. doi: 10.1007/s00296-023-05415-1. Epub 
      2023 Aug 30.

PMID- 37616328
OWN - NLM
STAT- MEDLINE
DCOM- 20230828
LR  - 20230828
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 18
IP  - 8
DP  - 2023
TI  - Clinical characteristics and outcomes of patients with chronic systemic 
      inflammatory disease in acute myocardial infarction.
PG  - e0289794
LID - 10.1371/journal.pone.0289794 [doi]
LID - e0289794
AB  - BACKGROUND: Chronic systemic inflammatory diseases (CSIDs) such as rheumatoid 
      arthritis (RA) are reportedly associated with an increased risk of ischemic 
      cardiovascular events including acute myocardial infarction (MI). However, data 
      are limited on clinical characteristics and ischemic and bleeding outcomes after 
      acute MI in patients with CSIDs. METHODS: This bi-center registry included a 
      total of 1001 patients with acute MI undergoing percutaneous coronary 
      intervention. CSIDs included inflammatory rheumatological conditions (RA, 
      systemic lupus erythematosus, vasculitis, etc.) and organ-specific diseases 
      (chronic hepatitis, psoriasis, inflammatory bowel disease, etc.). The primary 
      endpoint was net adverse clinical events (NACE), a composite of ischemic 
      (all-cause death, MI, and ischemic stroke) and major bleeding (Bleeding Academic 
      Research Consortium type 3 or 5) events, during hospitalization and after 
      discharge. RESULTS: Of the 1001 patients, 58 (5.8%) had CSIDs. The proportion of 
      women was higher in patients with CSIDs than those without (37.9% vs. 22.1%, p = 
      0.009). During the hospitalization, no significant differences in the primary 
      endpoint of NACE were observed between patients with and without CSIDs (10.3% vs. 
      12.7%, p = 0.84). During the median follow-up of 42.6 months after discharge, 
      patients with CSIDs had a higher risk of NACE (22.5% vs. 10.1%, p = 0.01) than 
      those without, mainly driven by an increased risk of ischemic events (18.4% vs. 
      8.4%, p = 0.03). CONCLUSIONS: A small but significant proportion of patients with 
      acute MI (5.8%) had CSIDs. While the incidence of in-hospital events was similar, 
      patients with CSIDs had worse outcomes after discharge, suggesting that further 
      clinical investigations and therapeutic approaches are needed in this patient 
      subset.
CI  - Copyright: © 2023 Yaginuma et al. This is an open access article distributed 
      under the terms of the Creative Commons Attribution License, which permits 
      unrestricted use, distribution, and reproduction in any medium, provided the 
      original author and source are credited.
FAU - Yaginuma, Hiroaki
AU  - Yaginuma H
AD  - Department of Cardiovascular Medicine, Chiba University Graduate School of 
      Medicine, Chiba, Japan.
FAU - Saito, Yuichi
AU  - Saito Y
AUID- ORCID: 0000-0003-3574-0685
AD  - Department of Cardiovascular Medicine, Chiba University Graduate School of 
      Medicine, Chiba, Japan.
FAU - Sato, Takanori
AU  - Sato T
AD  - Department of Cardiovascular Medicine, Chiba University Graduate School of 
      Medicine, Chiba, Japan.
FAU - Yamashita, Daichi
AU  - Yamashita D
AD  - Department of Cardiovascular Medicine, Chiba University Graduate School of 
      Medicine, Chiba, Japan.
FAU - Matsumoto, Tadahiro
AU  - Matsumoto T
AD  - Department of Cardiovascular Medicine, Chiba University Graduate School of 
      Medicine, Chiba, Japan.
FAU - Suzuki, Sakuramaru
AU  - Suzuki S
AD  - Department of Cardiovascular Medicine, Eastern Chiba Medical Center, Togane, 
      Japan.
FAU - Wakabayashi, Shinichi
AU  - Wakabayashi S
AD  - Department of Cardiovascular Medicine, Eastern Chiba Medical Center, Togane, 
      Japan.
FAU - Kitahara, Hideki
AU  - Kitahara H
AD  - Department of Cardiovascular Medicine, Chiba University Graduate School of 
      Medicine, Chiba, Japan.
FAU - Sano, Koichi
AU  - Sano K
AD  - Department of Cardiovascular Medicine, Eastern Chiba Medical Center, Togane, 
      Japan.
FAU - Kobayashi, Yoshio
AU  - Kobayashi Y
AD  - Department of Cardiovascular Medicine, Chiba University Graduate School of 
      Medicine, Chiba, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230824
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
SB  - IM
MH  - Humans
MH  - Female
MH  - Chronic Disease
MH  - *Myocardial Infarction/complications/therapy
MH  - Hospitalization
MH  - Patient Discharge
MH  - *Arthritis, Rheumatoid
PMC - PMC10449159
COIS- The authors have declared that no competing interests exist.
EDAT- 2023/08/24 18:41
MHDA- 2023/08/28 06:42
PMCR- 2023/08/24
CRDT- 2023/08/24 13:55
PHST- 2023/03/18 00:00 [received]
PHST- 2023/07/21 00:00 [accepted]
PHST- 2023/08/28 06:42 [medline]
PHST- 2023/08/24 18:41 [pubmed]
PHST- 2023/08/24 13:55 [entrez]
PHST- 2023/08/24 00:00 [pmc-release]
AID - PONE-D-23-07824 [pii]
AID - 10.1371/journal.pone.0289794 [doi]
PST - epublish
SO  - PLoS One. 2023 Aug 24;18(8):e0289794. doi: 10.1371/journal.pone.0289794. 
      eCollection 2023.

PMID- 37567896
OWN - NLM
STAT- MEDLINE
DCOM- 20230814
LR  - 20231121
IS  - 2055-1010 (Electronic)
IS  - 2055-1010 (Linking)
VI  - 33
IP  - 1
DP  - 2023 Aug 11
TI  - Chronic comorbid conditions and asthma exacerbation occurrence in a general 
      population sample.
PG  - 29
LID - 10.1038/s41533-023-00350-x [doi]
LID - 29
AB  - Chronic comorbid conditions are common in adults with asthma, and some may 
      influence a patient's asthma exacerbation risk. We explored associations between 
      eighteen chronic comorbid conditions and asthma exacerbation occurrence in adults 
      with asthma in a cross-sectional study nested within a cohort study using data 
      from the two-yearly US National Health and Nutrition Examination Survey (NHANES) 
      program. Data of 2387 adults with self-reported doctor-diagnosed current asthma 
      from the 2007 to 2018 NHANES surveys were selected. Investigated chronic 
      comorbidities were: angina pectoris; congestive heart failure; coronary heart 
      disease; depression; diabetes mellitus; soft and hard drug use; gastroesophageal 
      reflux; gout; history of heart attack; history of stroke; hypercholesterolemia; 
      hypertension; kidney failure; liver conditions; obesity; rheumatoid arthritis; 
      and thyroid problems. Outcome was defined as asthma exacerbation category: no, 
      moderate, or severe exacerbation(s) in the past year. Ordinal logistic regression 
      analysis with correction for potential confounders was used to estimate odds 
      ratios (OR) for moderate or severe exacerbations. Observed associations with 
      increased severe asthma exacerbation occurrence were: obesity (OR = 1.67; 95% 
      confidence interval 1.24, 2.26), and rheumatoid arthritis (OR = 1.55; 1.04, 
      2.30). History of stroke (OR = 1.95; 1.22, 3.11) and rheumatoid arthritis 
      (OR = 1.33; 1.00, 1.75) showed associations with increased moderate exacerbation 
      occurrence. Age-stratified analysis showed soft drug use, obesity, depression, 
      thyroid problems, and rheumatoid arthritis to be associated with moderate and/or 
      severe exacerbation occurrence in one or more 10-year age strata. In conclusion, 
      several chronic comorbid conditions were associated with asthma exacerbation 
      occurrence, which confirms but also complements previous studies. Our 
      observations contribute to understanding exacerbation risk estimation and, 
      ultimately, personalized asthma management.
CI  - © 2023. Springer Nature Limited.
FAU - Baljet, Emma
AU  - Baljet E
AD  - Department of Primary and Community Care, Radboud Institute for Health Sciences, 
      Radboud University Medical Center, Nijmegen, The Netherlands.
FAU - Luijks, Hilde
AU  - Luijks H
AUID- ORCID: 0000-0002-2709-5770
AD  - Department of Primary and Community Care, Radboud Institute for Health Sciences, 
      Radboud University Medical Center, Nijmegen, The Netherlands.
AD  - General Practice Valkenburg, Valkenburg, The Netherlands.
FAU - van den Bemt, Lisette
AU  - van den Bemt L
AUID- ORCID: 0000-0002-3771-8273
AD  - Department of Primary and Community Care, Radboud Institute for Health Sciences, 
      Radboud University Medical Center, Nijmegen, The Netherlands.
FAU - Schermer, Tjard R
AU  - Schermer TR
AUID- ORCID: 0000-0002-1391-2995
AD  - Department of Primary and Community Care, Radboud Institute for Health Sciences, 
      Radboud University Medical Center, Nijmegen, The Netherlands. 
      tjard.schermer@radboudumc.nl.
AD  - Science Office, Gelre Hospitals, Apeldoorn, The Netherlands. 
      tjard.schermer@radboudumc.nl.
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20230811
PL  - England
TA  - NPJ Prim Care Respir Med
JT  - NPJ primary care respiratory medicine
JID - 101631999
SB  - IM
MH  - Adult
MH  - Humans
MH  - Nutrition Surveys
MH  - Cohort Studies
MH  - Cross-Sectional Studies
MH  - *Asthma/epidemiology
MH  - *Stroke
MH  - *Arthritis, Rheumatoid
MH  - Obesity/epidemiology
PMC - PMC10421910
COIS- The authors declare no competing interests.
EDAT- 2023/08/12 10:42
MHDA- 2023/08/14 06:42
PMCR- 2023/08/11
CRDT- 2023/08/11 23:18
PHST- 2023/02/27 00:00 [received]
PHST- 2023/07/17 00:00 [accepted]
PHST- 2023/08/14 06:42 [medline]
PHST- 2023/08/12 10:42 [pubmed]
PHST- 2023/08/11 23:18 [entrez]
PHST- 2023/08/11 00:00 [pmc-release]
AID - 10.1038/s41533-023-00350-x [pii]
AID - 350 [pii]
AID - 10.1038/s41533-023-00350-x [doi]
PST - epublish
SO  - NPJ Prim Care Respir Med. 2023 Aug 11;33(1):29. doi: 10.1038/s41533-023-00350-x.

PMID- 37527867
OWN - NLM
STAT- Publisher
LR  - 20230922
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
DP  - 2023 Aug 1
TI  - Safety of Janus Kinase Inhibitors: A Real-World Multicenter Retrospective Cohort 
      Study.
LID - jrheum.2023-0145 [pii]
LID - 10.3899/jrheum.2023-0145 [doi]
AB  - OBJECTIVE: Oral Janus kinase inhibitors (JAKis) represent an effective strategy 
      for rheumatoid arthritis (RA) treatment. A previous study supported that 
      tofacitinib (TOF) is associated with higher incidence of cardiovascular (CV) and 
      neoplastic events compared to tumor necrosis factor inhibitors. Given the 
      apparent discrepancy between these data and real-world experience, we aimed to 
      investigate the safety and efficacy of the available JAKis in a multicenter 
      cohort. METHODS: We retrospectively evaluated patients with RA who ever received 
      1 JAKi (TOF, baricitinib [BAR], upadactinib [UPA], filgotinib [FIL]) from 4 
      tertiary care centers in Milan, Italy. Outcomes related to JAKi safety were 
      recorded, particularly major CV events as well as adverse events of special 
      interest (AESIs), which included serious infections, opportunistic infections, 
      venous thromboembolism, herpes zoster infections, liver injury, malignancies, and 
      deaths; retention rates were also calculated. Further analyses included patients 
      fulfilling the risk factors suggested to influence TOF safety. RESULTS: Six 
      hundred eighty-five patients were included and received BAR (48%), TOF (31%), UPA 
      (14%), or FIL (7%) as first-line innovative treatment prior to a biologic. Of a 
      total of 1137 patient-years of observation, we recorded 1 stroke and 123 (18%) 
      AESIs, including 3 deaths, all a result of severe infections. Among patients with 
      a higher CV risk, we observed a higher frequency of AESIs (23%). CONCLUSION: Our 
      real-world data confirm that JAKis are effective and carry a low risk of AESIs, 
      especially in patients who do not display CV risk factors at baseline. Our study 
      could not identify differences between JAKis. Different safety profiles should be 
      defined in larger prospective cohorts.
FAU - Lanzillotta, Marco
AU  - Lanzillotta M
AUID- ORCID: 0000-0002-4522-2921
AD  - M. Lanzillotta, MD, Unit of Immunology, Rheumatology, Allergy, and Rare diseases 
      (UnIRAR), IRCCS San Raffaele Scientific Institute, and Vita-Salute San Raffaele 
      University.
FAU - Boffini, Nicola
AU  - Boffini N
AUID- ORCID: 0000-0002-4416-933X
AD  - N. Boffini, MD, Unit of Immunology, Rheumatology, Allergy, and Rare diseases 
      (UnIRAR), IRCCS San Raffaele Scientific Institute.
FAU - Barone, Elisa
AU  - Barone E
AUID- ORCID: 0000-0002-5444-354X
AD  - E. Barone, MD, Division of Rheumatology and Clinical Immunology, Humanitas 
      Clinical and Research Center-IRCCS, Rozzano, and Department of Biomedical 
      Sciences, Humanitas University, Pieve Emanuele.
FAU - Cincinelli, Gilberto
AU  - Cincinelli G
AUID- ORCID: 0000-0002-4582-5968
AD  - G. Cincinelli, MD, Department of Rheumatology and Medical Sciences, Gaetano Pini 
      Hospital, and Università degli Studi di Milano, School of Medicine.
FAU - Gerardi, Maria C
AU  - Gerardi MC
AUID- ORCID: 0000-0001-7435-2656
AD  - M.C. Gerardi, MD, Division of Rheumatology, Multispecialist Medical Department, 
      ASST Grande Ospedale Metropolitano Niguarda, Milan, Italy.
FAU - Luciano, Nicoletta
AU  - Luciano N
AUID- ORCID: 0000-0002-1822-7882
AD  - N. Luciano, MD, Division of Rheumatology and Clinical Immunology, Humanitas 
      Clinical and Research Center-IRCCS, Rozzano, and Department of Biomedical 
      Sciences, Humanitas University, Pieve Emanuele.
FAU - Manara, Maria
AU  - Manara M
AUID- ORCID: 0000-0002-7357-6217
AD  - M. Manara, MD, Department of Rheumatology and Medical Sciences, Gaetano Pini 
      Hospital, and Università degli Studi di Milano, School of Medicine.
FAU - Ughi, Nicola
AU  - Ughi N
AUID- ORCID: 0000-0003-4637-1133
AD  - N. Ughi, MD, Division of Rheumatology, Multispecialist Medical Department, ASST 
      Grande Ospedale Metropolitano Niguarda, Milan, Italy.
FAU - Epis, Oscar M
AU  - Epis OM
AUID- ORCID: 0000-0002-9986-4030
AD  - O.M. Epis, MD, Division of Rheumatology, Multispecialist Medical Department, ASST 
      Grande Ospedale Metropolitano Niguarda, Milan, Italy.
FAU - Selmi, Carlo
AU  - Selmi C
AUID- ORCID: 0000-0002-0323-0376
AD  - C. Selmi, MD, PhD, Division of Rheumatology and Clinical Immunology, Humanitas 
      Clinical and Research Center-IRCCS, Rozzano, and Department of Biomedical 
      Sciences, Humanitas University, Pieve Emanuele.
FAU - Caporali, Roberto F
AU  - Caporali RF
AUID- ORCID: 0000-0001-9300-6169
AD  - R.F. Caporali, MD, Department of Rheumatology and Medical Sciences, Gaetano Pini 
      Hospital, and Università degli Studi di Milano, School of Medicine.
FAU - Dagna, Lorenzo
AU  - Dagna L
AUID- ORCID: 0000-0002-7428-315X
AD  - L. Dagna, MD, Unit of Immunology, Rheumatology, Allergy, and Rare diseases 
      (UnIRAR), IRCCS San Raffaele Scientific Institute, and Vita-Salute San Raffaele 
      University.
LA  - eng
PT  - Journal Article
DEP - 20230801
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
SB  - IM
EDAT- 2023/08/02 01:07
MHDA- 2023/08/02 01:07
CRDT- 2023/08/01 20:43
PHST- 2023/08/02 01:07 [pubmed]
PHST- 2023/08/02 01:07 [medline]
PHST- 2023/08/01 20:43 [entrez]
AID - jrheum.2023-0145 [pii]
AID - 10.3899/jrheum.2023-0145 [doi]
PST - aheadofprint
SO  - J Rheumatol. 2023 Aug 1:jrheum.2023-0145. doi: 10.3899/jrheum.2023-0145.

PMID- 37520890
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240922
IS  - 2589-9090 (Electronic)
IS  - 2589-9090 (Linking)
VI  - 7
DP  - 2023 Dec
TI  - Inflammation and immunomodulatory therapies influence the relationship between 
      ATP-binding cassette A1 membrane transporter-mediated cholesterol efflux capacity 
      and coronary atherosclerosis in rheumatoid arthritis.
PG  - 100209
LID - 10.1016/j.jtauto.2023.100209 [doi]
LID - 100209
AB  - OBJECTIVES: High-density lipoprotein (HDL) removes cholesterol from cells in 
      atherosclerotic lesions, a function known as cholesterol efflux capacity (CEC). 
      ATP-binding-cassette A1 (ABCA1) membrane transporter starts cholesterol transfer 
      from macrophages to HDL particles. In rheumatoid arthritis (RA), methotrexate and 
      biologic disease modifying drugs (bDMARDs) are atheroprotective whereas 
      corticosteroids and C-reactive protein (CRP) are proatherogenic. We evaluated the 
      influence of these factors on the relationship of ABCA1-CEC with atherosclerosis 
      and cardiovascular events. METHODS: Atherosclerosis was evaluated with computed 
      tomography angiography in 140 patients with RA and repeated in 99 after 6.9 ± 0.3 
      years. Events including acute coronary syndromes, stroke, cardiovascular death, 
      claudication, revascularization, and heart failure were recorded. ABCA1-CEC was 
      quantified in J774A.1 murine macrophages and reported as percentage of effluxed 
      over intracellular cholesterol. RESULTS: Higher ABCA1-CEC associated with (i) 
      more calcified plaques at baseline only in patients with CRP>7 mg/L (median) 
      (p-interaction = 0.001) and methotrexate nonusers (p-interaction = 0.037), and 
      more partially-calcified plaques only in bDMARD nonusers (p-interaction = 0.029); 
      (ii) fewer new calcified plaques in patients with below-median but not higher 
      time-averaged CRP (p-interaction = 0.028); (iii) fewer new total and calcified 
      plaques in prednisone unexposed but not patients exposed to prednisone during 
      follow-up (p-interaction = 0.034 and 0.004) and (iv) more new plaques in baseline 
      bDMARD nonusers and fewer in bDMARD users (p-interaction  ≤  0.001). Also, 
      ABCA1-CEC associated with greater cardiovascular risk only in baseline prednisone 
      users (p-interaction = 0.027). CONCLUSION: ABCA1-CEC associated with decreased 
      atherosclerosis in patients with below-median baseline and time-averaged CRP and 
      bDMARD use. Conversely, ABCA1-CEC associated with increased plaque in those with 
      higher CRP, corticosteroid users, methotrexate nonusers, and bDMARD nonusers. 
      While in well-treated and controlled disease ABCA1-CEC appears atheroprotective, 
      in uncontrolled RA its action may be masked or fail to counteract the 
      inflammation-driven proatherogenic state.
CI  - © 2023 The Authors. Published by Elsevier B.V.
FAU - Karpouzas, George A
AU  - Karpouzas GA
AD  - Division of Rheumatology, Harbor-UCLA and The Lundquist Institute, Torrance, CA, 
      USA.
FAU - Papotti, Bianca
AU  - Papotti B
AD  - Department of Food and Drug, University of Parma, Parco Area delle Scienze 27/A, 
      43124, Parma, Italy.
FAU - Ormseth, Sarah R
AU  - Ormseth SR
AD  - Division of Rheumatology, Harbor-UCLA and The Lundquist Institute, Torrance, CA, 
      USA.
FAU - Palumbo, Marcella
AU  - Palumbo M
AD  - Department of Food and Drug, University of Parma, Parco Area delle Scienze 27/A, 
      43124, Parma, Italy.
FAU - Hernandez, Elizabeth
AU  - Hernandez E
AD  - The Lundquist Institute, 1124 W Carson Street, Torrance, CA, 90502, USA.
FAU - Adorni, Maria Pia
AU  - Adorni MP
AD  - Department of Medicine and Surgery, University of Parma, Parma, Italy.
FAU - Zimetti, Francesca
AU  - Zimetti F
AD  - Department of Food and Drug, University of Parma, Parco Area delle Scienze 27/A, 
      43124, Parma, Italy.
FAU - Budoff, Matthew J
AU  - Budoff MJ
AD  - Division of Cardiology, Harbor-UCLA and The Lundquist Institute, Torrance, CA, 
      USA.
FAU - Ronda, Nicoletta
AU  - Ronda N
AD  - Department of Food and Drug, University of Parma, Parco Area delle Scienze 27/A, 
      43124, Parma, Italy.
LA  - eng
PT  - Journal Article
DEP - 20230718
PL  - Netherlands
TA  - J Transl Autoimmun
JT  - Journal of translational autoimmunity
JID - 101759413
PMC - PMC10371792
OTO - NOTNLM
OT  - ABCA1
OT  - Cardiovascular events
OT  - Cholesterol efflux capacity
OT  - Coronary atherosclerosis
OT  - Corticosteroids
OT  - Rheumatoid arthritis
COIS- The authors declare the following financial interests/personal relationships 
      which may be considered as potential competing interests: George A Karpouzas 
      reports financial support was provided by American Heart Association Inc. George 
      A Karpouzas reports financial support was provided by Pfizer.
EDAT- 2023/07/31 06:42
MHDA- 2023/07/31 06:43
PMCR- 2023/07/18
CRDT- 2023/07/31 04:59
PHST- 2023/07/11 00:00 [received]
PHST- 2023/07/12 00:00 [accepted]
PHST- 2023/07/31 06:43 [medline]
PHST- 2023/07/31 06:42 [pubmed]
PHST- 2023/07/31 04:59 [entrez]
PHST- 2023/07/18 00:00 [pmc-release]
AID - S2589-9090(23)00022-9 [pii]
AID - 100209 [pii]
AID - 10.1016/j.jtauto.2023.100209 [doi]
PST - epublish
SO  - J Transl Autoimmun. 2023 Jul 18;7:100209. doi: 10.1016/j.jtauto.2023.100209. 
      eCollection 2023 Dec.

PMID- 37498463
OWN - NLM
STAT- MEDLINE
DCOM- 20240109
LR  - 20241023
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Print)
IS  - 0770-3198 (Linking)
VI  - 43
IP  - 1
DP  - 2024 Jan
TI  - Hydroxychloroquine use is associated with reduced mortality risk in older adults 
      with rheumatoid arthritis.
PG  - 87-94
LID - 10.1007/s10067-023-06714-5 [doi]
AB  - BACKGROUND: There is little robust data about the cardiovascular safety of 
      hydroxychloroquine in patients with rheumatoid arthritis (RA), who often have 
      cardiovascular comorbidities. We examined the association between use of 
      hydroxychloroquine (HCQ) in patients with RA and major adverse cardiovascular 
      events (MACE). METHODS: In a retrospective cohort of Medicare beneficiaries 
      aged ≥ 65 years with RA, we identified patients who initiated HCQ (users) and who 
      did not initiate HCQ (non-users) between January 2015-June 2017. Each HCQ user 
      was matched to 2 non-users of HCQ using propensity score derived from patient 
      baseline characteristics. The primary outcome was the occurrence of MACE, defined 
      as acute admissions for stroke, myocardial infarction, or heart failure. 
      Secondary outcomes included all-cause mortality and the composite of MACE and 
      all-cause mortality. Cox proportional hazards model was used to compare outcomes 
      between HCQ users to non-users. RESULTS: The study included 2380 RA patients with 
      incident HCQ use and matched 4633 HCQ non-users over the study period. The mean 
      follow-up duration was 1.67 and 1.63 years in HCQ non-users and users, 
      respectively. In multivariable models, use of HCQ was not associated with the 
      risk of MACE (hazard ratio 1.1; 95% CI: 0.832-1.33). However, use of HCQ was 
      associated with a lower risk of all-cause mortality (HR: 0.54; 95% CI: 0.45-0.64) 
      and the composite of all-cause mortality and MACE (HR 0.67; 95% CI: 0.58-0.78). 
      CONCLUSION: HCQ use was independently associated with a lower risk of mortality 
      in older adults with RA but not with incidence of MACE events. Key Points • Using 
      an incident user design (to avoid the biases of a prevalent user design) and a 
      population-based approach, we examined the effect of hydroxychloroquine (HCQ) on 
      the risk of major cardiovascular events (MACE) in older patients with RA. • We 
      did not find an association between HCQ use and incident MACE. We did, however, 
      find a significant association with the composite outcome (MACE and all-cause 
      mortality) driven by a significant reduction in all-cause mortality with HCQ use.
CI  - © 2023. The Author(s), under exclusive licence to International League of 
      Associations for Rheumatology (ILAR).
FAU - Iyer, Priyanka
AU  - Iyer P
AD  - Division of Rheumatology, University of California at Irvine, Irvine, CA, USA.
FAU - Gao, Yubo
AU  - Gao Y
AD  - Division of General Medicine, Department of Internal Medicine, Roy and Lucille 
      Carver College of Medicine, University of Iowa, Iowa City, IA, USA.
FAU - Jalal, Diana
AU  - Jalal D
AD  - Division of Nephrology, Department of Internal Medicine, Roy and Lucille Carver 
      College of Medicine, University of Iowa, and Iowa City VA Health Care System, 
      Iowa City, IA, USA.
FAU - Girotra, Saket
AU  - Girotra S
AD  - Division of Cardiology, Department of Internal Medicine, University of Texas 
      Southwestern Medical Center, Dallas, TX, USA.
FAU - Singh, Namrata
AU  - Singh N
AUID- ORCID: 0000-0001-7149-363X
AD  - Division of Rheumatology, Department of Medicine, University of Washington, 1959 
      NE Pacific Street, Seattle, WA, 98195, USA. nasingh@uw.edu.
FAU - Vaughan-Sarrazin, Mary
AU  - Vaughan-Sarrazin M
AD  - Division of General Medicine, Department of Internal Medicine, Roy and Lucille 
      Carver College of Medicine, University of Iowa, and Iowa City VA Health Care 
      System Center for Access and Delivery Research and Evaluation (CADRE), Iowa City, 
      IA, USA.
LA  - eng
GR  - R01 HL160734/HL/NHLBI NIH HHS/United States
GR  - R01 HL166305/HL/NHLBI NIH HHS/United States
GR  - R56 HL158803/HL/NHLBI NIH HHS/United States
PT  - Journal Article
DEP - 20230727
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
RN  - 4QWG6N8QKH (Hydroxychloroquine)
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Humans
MH  - Aged
MH  - United States/epidemiology
MH  - Hydroxychloroquine/adverse effects
MH  - *Antirheumatic Agents/adverse effects
MH  - Retrospective Studies
MH  - Medicare
MH  - *Arthritis, Rheumatoid/complications
MH  - *Myocardial Infarction/complications
PMC - PMC10818008
MID - NIHMS1953498
OTO - NOTNLM
OT  - Cardiovascular events
OT  - Hydroxychloroquine
OT  - MACE
OT  - Rheumatoid arthritis
COIS- Disclosures None.
EDAT- 2023/07/27 13:10
MHDA- 2024/01/09 06:42
PMCR- 2025/01/01
CRDT- 2023/07/27 11:10
PHST- 2023/02/21 00:00 [received]
PHST- 2023/07/19 00:00 [accepted]
PHST- 2023/06/20 00:00 [revised]
PHST- 2025/01/01 00:00 [pmc-release]
PHST- 2024/01/09 06:42 [medline]
PHST- 2023/07/27 13:10 [pubmed]
PHST- 2023/07/27 11:10 [entrez]
AID - 10.1007/s10067-023-06714-5 [pii]
AID - 10.1007/s10067-023-06714-5 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2024 Jan;43(1):87-94. doi: 10.1007/s10067-023-06714-5. Epub 2023 
      Jul 27.

PMID- 37484708
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230725
IS  - 2589-9090 (Electronic)
IS  - 2589-9090 (Linking)
VI  - 7
DP  - 2023 Dec
TI  - Statins influence the relationship between ATP-binding cassette A1 membrane 
      transporter-mediated cholesterol efflux capacity and coronary atherosclerosis in 
      rheumatoid arthritis.
PG  - 100206
LID - 10.1016/j.jtauto.2023.100206 [doi]
LID - 100206
AB  - OBJECTIVES: Cholesterol efflux capacity (CEC) is the main antiatherogenic 
      function of high-density lipoprotein (HDL). ATP-binding-cassette A1 (ABCA1) 
      membrane transporter initiates cholesterol export from arterial macrophages to 
      pre-β HDL particles fostering their maturation; in turn, those accept cholesterol 
      through ABCG1-mediated export. Impaired pre-β HDL maturation may disrupt the 
      collaborative function of the two transporters and adversely affect 
      atherosclerosis. Statins exert atheroprotective functions systemically and 
      locally on plaque. We here evaluated associations between ABCA1-CEC, coronary 
      atherosclerosis and cardiovascular risk and the influence of statins on those 
      relationships in rheumatoid arthritis (RA). METHODS: Evaluation with computed 
      tomography angiography was undertaken in 140 patients and repeated in 99 after 
      6.9 ± 0.3 years. Events comprising cardiovascular death, acute coronary 
      syndromes, stroke, claudication, revascularization and heart failure were 
      recorded. ABCA1-CEC and ABCG1-CEC were evaluated in J774A.1 macrophages and 
      Chinese hamster ovary (CHO) cells respectively and expressed as percentage of 
      effluxed over total intracellular cholesterol. Covariates in all cardiovascular 
      event risk and plaque outcome models included atherosclerotic cardiovascular 
      disease (ASCVD) risk score and high-density lipoprotein cholesterol. RESULTS: 
      ABCA1-CEC negatively correlated with ABCG1-CEC (r = -0.167, p = 0.049). ABCA1-CEC 
      associated with cardiovascular risk (adjusted hazard ratio 2.05 [95%CI 1.20-3.48] 
      per standard deviation [SD] increment). There was an interaction of ABCA1-CEC 
      with time-varying statin use (p = 0.038) such that current statin use inversely 
      associated with risk only in patients with ABCA1-CEC below the upper tertile. 
      ABCA1-CEC had no main effect on plaque or plaque progression; instead, ABCA1-CEC 
      (per SD) associated with fewer baseline total plaques (adjusted rate ratio [aRR] 
      0.81, [95%CI 0.65-1.00]), noncalcified plaques (aRR 0.78 [95%CI 0.61-0.98]), and 
      vulnerable low-attenuation plaques (aRR 0.41 [95%CI 0.23-0.74]) in statin users, 
      and more low-attenuation plaques (aRR 1.91 [95%CI 1.18-3.08]) in nonusers 
      (p-for-interaction = 0.018, 0.011, 0.025 and < 0.001 respectively). Moreover, 
      ABCA1-CEC (per SD) associated with greater partially/fully-calcified plaque 
      progression (adjusted odds ratio 3.07 [95%CI 1.20-7.86]) only in patients not 
      exposed to statins during follow-up (p-for-interaction = 0.009). CONCLUSION: In 
      patients with RA, higher ABCA1-CEC may reflect a proatherogenic state, associated 
      with enhanced cardiovascular risk. Statin use may unmask the protective impact of 
      ABCA1-mediated cholesterol efflux on plaque formation, progression and 
      cardiovascular risk.
CI  - © 2023 The Authors.
FAU - Karpouzas, George A
AU  - Karpouzas GA
AD  - Division of Rheumatology, Harbor-UCLA Medical Center and the Lundquist Institute 
      for Biomedical Innovation, Torrance, CA, USA.
FAU - Papotti, Bianca
AU  - Papotti B
AD  - Department of Food and Drug, University of Parma, Parma, Italy.
FAU - Ormseth, Sarah R
AU  - Ormseth SR
AD  - Division of Rheumatology, Harbor-UCLA Medical Center and the Lundquist Institute 
      for Biomedical Innovation, Torrance, CA, USA.
FAU - Palumbo, Marcella
AU  - Palumbo M
AD  - Department of Food and Drug, University of Parma, Parma, Italy.
FAU - Hernandez, Elizabeth
AU  - Hernandez E
AD  - Division of Rheumatology, Harbor-UCLA Medical Center and the Lundquist Institute 
      for Biomedical Innovation, Torrance, CA, USA.
FAU - Adorni, Maria Pia
AU  - Adorni MP
AD  - Department of Medicine and Surgery, University of Parma, Parma, Italy.
FAU - Zimetti, Francesca
AU  - Zimetti F
AD  - Department of Food and Drug, University of Parma, Parma, Italy.
FAU - Budoff, Matthew J
AU  - Budoff MJ
AD  - Division of Cardiology, Harbor-UCLA Medical Center and the Lundquist Institute 
      for Biomedical Innovation, Torrance, CA, USA.
FAU - Ronda, Nicoletta
AU  - Ronda N
AD  - Department of Food and Drug, University of Parma, Parma, Italy.
LA  - eng
PT  - Journal Article
DEP - 20230707
PL  - Netherlands
TA  - J Transl Autoimmun
JT  - Journal of translational autoimmunity
JID - 101759413
PMC - PMC10362327
OTO - NOTNLM
OT  - ABCA1
OT  - Cardiovascular events
OT  - Cholesterol efflux capacity
OT  - Coronary atherosclerosis
OT  - Rheumatoid arthritis
OT  - Statins
COIS- The authors declare the following financial interests/personal relationships 
      which may be considered as potential competing interests: George A Karpouzas 
      reports financial support was provided by American Heart Association Inc. George 
      A Karpouzas reports financial support was provided by Pfizer.
EDAT- 2023/07/24 06:43
MHDA- 2023/07/24 06:44
PMCR- 2023/07/07
CRDT- 2023/07/24 04:46
PHST- 2023/05/03 00:00 [received]
PHST- 2023/06/23 00:00 [revised]
PHST- 2023/07/04 00:00 [accepted]
PHST- 2023/07/24 06:44 [medline]
PHST- 2023/07/24 06:43 [pubmed]
PHST- 2023/07/24 04:46 [entrez]
PHST- 2023/07/07 00:00 [pmc-release]
AID - S2589-9090(23)00019-9 [pii]
AID - 100206 [pii]
AID - 10.1016/j.jtauto.2023.100206 [doi]
PST - epublish
SO  - J Transl Autoimmun. 2023 Jul 7;7:100206. doi: 10.1016/j.jtauto.2023.100206. 
      eCollection 2023 Dec.

PMID- 37460169
OWN - NLM
STAT- Publisher
LR  - 20231012
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 82
IP  - 11
DP  - 2023 Nov
TI  - Major adverse cardiovascular events and mortality with opioids versus NSAIDs 
      initiation in patients with rheumatoid arthritis.
PG  - 1487-1494
LID - 10.1136/ard-2023-224339 [doi]
AB  - OBJECTIVE: Assess major adverse cardiovascular event (MACE) risk with opioids 
      compared with non-steroidal anti-inflammatory drugs (NSAIDs) in patients with 
      rheumatoid arthritis (RA) METHODS: We conducted a new-user active comparator 
      cohort study among patients with RA within FORWARD, The National Databank for 
      Rheumatic Diseases, with ≥1 year participation between 1998 and 2021. Each opioid 
      initiator was matched to two NSAID initiators by propensity scores (PSs). 
      Patients were followed until the occurrence of the composite endpoint of MACE 
      (myocardial infarction, stroke, heart failure, cardiovascular disease (CVD) 
      death, venous thromboembolism (VTE)) and all-cause mortality. The risk of 
      outcomes was estimated using Cox proportional hazards with adjustment for PS 
      weights and imbalanced covariables. RESULTS: Among 6866 opioid initiators and 13 
      689 NSAID initiators, 212 vs 253 MACE (20.6/1000 person-years (PY) vs 18.9/1000 
      PY) and 144 vs 150 deaths (13.5/1000 PY vs 10.8/1000 PY) occurred, respectively. 
      The risk of MACE with opioids was similar to NSAIDs (HR=1.02, 95% CI 0.85 to 
      1.22), whereas all-cause mortality with opioids was 33% higher than NSAIDs 
      (HR=1.33, 95% CI 1.06 to 1.67) in PS-weighted models. Among the individual 
      outcomes of MACE, VTE risk tended to be higher in opioid initiators than NSAID 
      initiators (HR=1.41, 95% CI 0.84 to 2.35). Strong opioids had a higher risk for 
      all-cause mortality and VTE than weak opioids compared with NSAIDs suggesting a 
      dose-dependent association. CONCLUSION: Opioids had similar MACE risk compared 
      with NSAIDs in patients with RA with increased all-cause mortality and likely 
      VTE, which suggests that opioids are not safer than NSAIDs, as clinicians have 
      perceived.
CI  - © Author(s) (or their employer(s)) 2023. No commercial re-use. See rights and 
      permissions. Published by BMJ.
FAU - Ozen, Gulsen
AU  - Ozen G
AUID- ORCID: 0000-0002-5423-393X
AD  - Rheumatology, University of Nebraska Medical Center, Omaha, Nebraska, USA 
      ozengs@yahoo.com.
FAU - Pedro, Sofia
AU  - Pedro S
AD  - FORWARD, The National Databank for Rheumatic Diseases, Wichita, Kansas, USA.
FAU - Michaud, Kaleb
AU  - Michaud K
AUID- ORCID: 0000-0002-5350-3934
AD  - Rheumatology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
AD  - FORWARD, The National Databank for Rheumatic Diseases, Wichita, Kansas, USA.
LA  - eng
PT  - Journal Article
DEP - 20230717
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
OTO - NOTNLM
OT  - Analgesics
OT  - Arthritis, Rheumatoid
OT  - Cardiovascular Diseases
OT  - Epidemiology
COIS- Competing interests: None declared.
EDAT- 2023/07/18 01:09
MHDA- 2023/07/18 01:09
CRDT- 2023/07/17 20:53
PHST- 2023/04/21 00:00 [received]
PHST- 2023/07/03 00:00 [accepted]
PHST- 2023/07/18 01:09 [pubmed]
PHST- 2023/07/18 01:09 [medline]
PHST- 2023/07/17 20:53 [entrez]
AID - ard-2023-224339 [pii]
AID - 10.1136/ard-2023-224339 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2023 Nov;82(11):1487-1494. doi: 10.1136/ard-2023-224339. Epub 2023 
      Jul 17.

PMID- 37456442
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230718
IS  - 2168-8184 (Print)
IS  - 2168-8184 (Electronic)
IS  - 2168-8184 (Linking)
VI  - 15
IP  - 6
DP  - 2023 Jun
TI  - Comparison of Cardiovascular Outcomes in Patients With and Without Rheumatoid 
      Arthritis: A Meta-Analysis of Observational Studies.
PG  - e40348
LID - 10.7759/cureus.40348 [doi]
LID - e40348
AB  - The aim of this meta-analysis was to determine the risk of incident 
      cardiovascular disease (CVD) in patients with rheumatoid arthritis compared 
      to patients without rheumatoid arthritis. We conducted a thorough search of 
      online databases, including PubMed, EMBASE, and Web of Science, to identify 
      English-language publications examining cardiovascular outcomes in patients with 
      rheumatoid arthritis from January 1, 2005, to May 15, 2023. We followed the 
      Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 
      guidelines. The search was performed using relevant keywords such as "rheumatoid 
      arthritis," "cardiovascular diseases," and "risk," along with their synonyms. 
      Medical subject heading (MeSH) terms and Boolean operators (AND, OR) were 
      employed to optimize the search. Outcomes assessed in this study included 
      composite cardiovascular events (as defined by individual studies), myocardial 
      infarction, and stroke (including ischemic and hemorrhagic stroke). Overall, 14 
      studies met the inclusion criteria and were included in the present 
      meta-analysis. We found that the risk of composite CVD was higher in patients 
      with rheumatoid arthritis compared to patients without rheumatoid arthritis. We 
      also found a higher risk of myocardial infarction and stroke in rheumatoid 
      arthritis patients compared to their counterparts. This study demonstrates the 
      elevated risk of CVD in patients with rheumatoid arthritis and highlights the 
      importance of incorporating cardiovascular management and assessment into the 
      care of these patients.
CI  - Copyright © 2023, Barkhane et al.
FAU - Barkhane, Zineb
AU  - Barkhane Z
AD  - Medicine and Pharmacy, University of Hassan II Casablanca, Casablanca, MAR.
FAU - Zaree, Amna
AU  - Zaree A
AD  - Medicine, Shalimar Medical and Dental College, Lahore, PAK.
FAU - Zulfiqar, Sualeha
AU  - Zulfiqar S
AD  - Internal Medicine, Rawalpindi Medical University, Rawalpindi, PAK.
FAU - Qudoos, Ahmed
AU  - Qudoos A
AD  - Medicine, Liaquat University of Medical and Health Sciences, Hyderabad, PAK.
FAU - Vaidhyula, Santhoshi
AU  - Vaidhyula S
AD  - Medicine, Dr. Nandamuri Taraka Rama Rao (NTR) University of Health Sciences, 
      Vijayawada, IND.
FAU - Jaiprada, Fnu
AU  - Jaiprada F
AD  - Medicine, Dow University of Health Sciences, Karachi, PAK.
FAU - Dar, Saleha
AU  - Dar S
AD  - Adult Medicine, Louisiana State University Health Sciences Center, Shreveport, 
      USA.
FAU - Ali, Neelum
AU  - Ali N
AD  - Internal Medicine, University of Health Sciences, Lahore, PAK.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20230613
PL  - United States
TA  - Cureus
JT  - Cureus
JID - 101596737
PMC - PMC10339149
OTO - NOTNLM
OT  - cardiovascular outcomes
OT  - meta-analysis
OT  - myocardial infarction
OT  - rheumatoid arthritis
OT  - stroke
COIS- The authors have declared that no competing interests exist.
EDAT- 2023/07/17 06:42
MHDA- 2023/07/17 06:43
PMCR- 2023/06/13
CRDT- 2023/07/17 04:23
PHST- 2023/06/13 00:00 [accepted]
PHST- 2023/07/17 06:43 [medline]
PHST- 2023/07/17 06:42 [pubmed]
PHST- 2023/07/17 04:23 [entrez]
PHST- 2023/06/13 00:00 [pmc-release]
AID - 10.7759/cureus.40348 [doi]
PST - epublish
SO  - Cureus. 2023 Jun 13;15(6):e40348. doi: 10.7759/cureus.40348. eCollection 2023 
      Jun.

PMID- 37444723
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230718
IS  - 2227-9032 (Print)
IS  - 2227-9032 (Electronic)
IS  - 2227-9032 (Linking)
VI  - 11
IP  - 13
DP  - 2023 Jun 29
TI  - The Casual Association Inference for the Chain of Falls Risk Factors-Falls-Falls 
      Outcomes: A Mendelian Randomization Study.
LID - 10.3390/healthcare11131889 [doi]
LID - 1889
AB  - Previous associations have been observed not only between risk factors and falls 
      but also between falls and their clinical outcomes based on some cross-sectional 
      designs, but their causal associations were still largely unclear. We performed 
      Mendelian randomization (MR), multivariate Mendelian randomization (MVMR), and 
      mediation analyses to explore the effects of falls. Our study data are mainly 
      based on White European individuals (40-69 years) downloaded from the UK Biobank. 
      MR analyses showed that osteoporosis (p = 0.006), BMI (p = 0.003), sleeplessness 
      (p < 0.001), rheumatoid arthritis (p = 0.001), waist circumference (p < 0.001), 
      and hip circumference (p < 0.001) have causal effects on falls. In addition, for 
      every one standard deviation increase in fall risk, the risk of fracture 
      increased by 1.148 (p < 0.001), the risk of stroke increased by 2.908 (p = 
      0.003), and a 1.016-fold risk increase in epilepsy (p = 0.009). The MVMR found 
      that sleeplessness is an important risk factor for falls. Finally, our mediation 
      analyses estimated the mediation effects of falls on the hip circumference and 
      fracture (p < 0.001), waist circumference and epilepsy (p < 0.001), and 
      sleeplessness and fracture (p = 0.005). Our study inferred the causal effects 
      between risk factors and falls, falls, and outcomes, and also constructed three 
      causal chains from risk factors → falls → falls outcomes.
FAU - Wu, Jia-Xin
AU  - Wu JX
AUID- ORCID: 0000-0002-7126-1449
AD  - Center for Genetic Epidemiology and Genomics, School of Public Health, Medical 
      College of Soochow University, Suzhou 215123, China.
AD  - Collaborative Innovation Center of Bone and Immunology between Sihong Hospital 
      and Soochow University, Suzhou 215123, China.
AD  - Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric 
      Diseases, Soochow University, Suzhou 215123, China.
FAU - Deng, Fei-Yan
AU  - Deng FY
AD  - Center for Genetic Epidemiology and Genomics, School of Public Health, Medical 
      College of Soochow University, Suzhou 215123, China.
AD  - Collaborative Innovation Center of Bone and Immunology between Sihong Hospital 
      and Soochow University, Suzhou 215123, China.
AD  - Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric 
      Diseases, Soochow University, Suzhou 215123, China.
FAU - Lei, Shu-Feng
AU  - Lei SF
AD  - Center for Genetic Epidemiology and Genomics, School of Public Health, Medical 
      College of Soochow University, Suzhou 215123, China.
AD  - Collaborative Innovation Center of Bone and Immunology between Sihong Hospital 
      and Soochow University, Suzhou 215123, China.
AD  - Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric 
      Diseases, Soochow University, Suzhou 215123, China.
AD  - Changzhou Geriatric Hospital, Soochow University, Changzhou 213000, China.
LA  - eng
PT  - Journal Article
DEP - 20230629
PL  - Switzerland
TA  - Healthcare (Basel)
JT  - Healthcare (Basel, Switzerland)
JID - 101666525
PMC - PMC10340577
OTO - NOTNLM
OT  - Mendelian randomization
OT  - causal relationship
OT  - falls
COIS- The authors declare no conflict of interest.
EDAT- 2023/07/14 13:06
MHDA- 2023/07/14 13:07
PMCR- 2023/06/29
CRDT- 2023/07/14 01:07
PHST- 2023/05/29 00:00 [received]
PHST- 2023/06/20 00:00 [revised]
PHST- 2023/06/28 00:00 [accepted]
PHST- 2023/07/14 13:07 [medline]
PHST- 2023/07/14 13:06 [pubmed]
PHST- 2023/07/14 01:07 [entrez]
PHST- 2023/06/29 00:00 [pmc-release]
AID - healthcare11131889 [pii]
AID - healthcare-11-01889 [pii]
AID - 10.3390/healthcare11131889 [doi]
PST - epublish
SO  - Healthcare (Basel). 2023 Jun 29;11(13):1889. doi: 10.3390/healthcare11131889.

PMID- 37402929
OWN - NLM
STAT- MEDLINE
DCOM- 20240129
LR  - 20240206
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 42
IP  - 11
DP  - 2023 Nov
TI  - Risk factors for cardiovascular disease in primary Sjögren's syndrome (pSS): a 
      20-year follow-up study.
PG  - 3021-3031
LID - 10.1007/s10067-023-06686-6 [doi]
AB  - INTRODUCTION: Primary Sjögren's syndrome (pSS) is a systemic autoimmune disease 
      characterized by a chronic grade of inflammation. Cardiovascular events represent 
      the major causes of morbidity and mortality in patients with inflammatory 
      rheumatic diseases; however, the significance and prevalence of cardiovascular 
      disease in patients with pSS remain unclear. OBJECTIVE: To determine the clinical 
      significance of cardiovascular disease in pSS and analyze the risk of 
      cardiovascular disease according to glandular/extraglandular involvement and 
      positivity to anti-Ro/SSA and/or anti-La/SSB autoantibodies. METHODS: A 
      retrospective study including patients diagnosed with pSS fulfilling the 2016 
      ACR/EULAR classification criteria was followed and evaluated in our outpatient 
      clinic between 2000 and 2022. The prevalence of cardiovascular risk factors with 
      pSS was evaluated, and a possible association with clinical and immunological 
      characteristics, the treatments received, and the impact on cardiovascular 
      disease were determined. Univariate and multivariate regression analyses were 
      performed in an attempt to determine potential risk factors associated with 
      cardiovascular involvement. RESULTS: A total of 102 pSS patients were included. 
      Eighty-two percent were female, with a mean age of 65±24 years and a disease 
      duration of 12.5 ±6 years. Thirty-six patients (36%) had at least one 
      cardiovascular risk factor. Arterial hypertension was diagnosed in 60 (59%) 
      patients, dyslipidemia in 28 (27%), diabetes in 15 (15%), obesity in 22 (22%), 
      and hyperuricemia in 19 (18%). History of arrhythmia was found in 25 (25%), 
      conduction defects in 10 (10%), arterial peripheral vascular disease in 7 (7%), 
      venous thrombosis in 10 (10%), coronary artery disease in 24 (24%), and 
      cerebrovascular disease in 22 (22%) of patients. Patients with extraglandular 
      involvement had a higher prevalence of arterial hypertension (p=0.04), 
      dyslipidemia (p=0.003), LDL mean values (p=0.038), hyperuricemia (p=0.03), and 
      coronary artery disease (p=0.01) after adjusting for age, sex, disease duration, 
      and the significant variables in the univariate analysis. Patients with Ro/SSA 
      and La/SSB autoantibodies had a substantially higher risk of hyperuricemia 
      (p=0.01), arrhythmia (p=0.01), coronary artery disease (p=0.02), cerebrovascular 
      disease (p=0.02), and venous thrombosis (p =0.03). In the multivariate logistic 
      regression analysis, higher odds of cardiovascular risk factors were associated 
      with extraglandular involvement (p=0.02), treatment with corticosteroids 
      (p=0.02), ESSDAI>13 (p=0.02), inflammatory markers including ESR levels (p 
      0.007), and serologic markers such as low C3 levels (p=0.03) and 
      hypergammaglobulinemia (p=0.02). CONCLUSIONS: Extraglandular involvement was 
      associated with a higher prevalence of arterial hypertension, dyslipidemia, 
      hyperuricemia, and coronary artery disease. Anti-Ro/SSA and anti-La/SSB 
      seropositivity was associated with a higher prevalence of cardiac rhythm 
      abnormalities, hyperuricemia, venous thrombosis, coronary artery disease, and 
      cerebrovascular disease. Raised inflammatory markers, disease activity measured 
      by ESSDAI, extraglandular involvement, serologic markers including 
      hypergammaglobulinemia and low C3, and treatment with corticosteroids were 
      associated with a higher risk for cardiovascular comorbidities. Key Points • 
      Patients with pSS are vulnerable to cardiovascular risk factors. There is an 
      interconnection between extraglandular involvement, disease activity, 
      inflammatory markers, and cardiovascular risk comorbidities. • Anti-Ro/SSA and 
      anti-La/SSB seropositivity was associated with a higher frequency of cardiac 
      conduction abnormalities, coronary artery disease, venous thrombosis, and stroke. 
      • Hypergammaglobulinemia, elevated ESR, and low C3 are associated with a higher 
      prevalence of cardiovascular comorbidities. • Valid risk stratification tools to 
      help with prevention and consensus on the management of CVDs in pSS patients are 
      warranted.
CI  - © 2023. The Author(s), under exclusive licence to International League of 
      Associations for Rheumatology (ILAR).
FAU - Santos, Cristiana Sieiro
AU  - Santos CS
AUID- ORCID: 0000-0003-0889-9877
AD  - Rheumatology Department, Complejo Asistencial Universitario de León, Altos de 
      Nava S/N, 24008, León, Spain. cristysieirosantos@gmail.com.
FAU - Salgueiro, Ruben Rego
AU  - Salgueiro RR
AD  - Internal Medicine, Unidade Local de Saúde da Guarda, Guarda, Portugal.
FAU - Morales, Clara Moriano
AU  - Morales CM
AD  - Rheumatology Department, Complejo Asistencial Universitario de León, Altos de 
      Nava S/N, 24008, León, Spain.
FAU - Castro, Carolina Álvarez
AU  - Castro CÁ
AD  - Rheumatology Department, Complejo Asistencial Universitario de León, Altos de 
      Nava S/N, 24008, León, Spain.
FAU - Álvarez, Elvira Díez
AU  - Álvarez ED
AD  - Rheumatology Department, Complejo Asistencial Universitario de León, Altos de 
      Nava S/N, 24008, León, Spain.
LA  - eng
PT  - Journal Article
DEP - 20230704
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
RN  - 0 (Autoantibodies)
RN  - 0 (Adrenal Cortex Hormones)
SB  - IM
MH  - Humans
MH  - Female
MH  - Adult
MH  - Middle Aged
MH  - Aged
MH  - Aged, 80 and over
MH  - Male
MH  - *Sjogren's Syndrome/complications/epidemiology/diagnosis
MH  - Follow-Up Studies
MH  - Retrospective Studies
MH  - *Cardiovascular Diseases/complications/epidemiology
MH  - *Coronary Artery Disease/complications
MH  - *Hyperuricemia/complications
MH  - Hypergammaglobulinemia
MH  - Risk Factors
MH  - Autoantibodies
MH  - *Cerebrovascular Disorders/complications
MH  - Heart Disease Risk Factors
MH  - *Hypertension/complications/epidemiology
MH  - *Dyslipidemias/complications
MH  - *Venous Thrombosis
MH  - Arrhythmias, Cardiac
MH  - Adrenal Cortex Hormones
OTO - NOTNLM
OT  - Autoantibodies
OT  - Cardiovascular disease
OT  - Sjogren
EDAT- 2023/07/05 01:06
MHDA- 2024/01/29 06:44
CRDT- 2023/07/04 23:30
PHST- 2023/05/01 00:00 [received]
PHST- 2023/06/26 00:00 [accepted]
PHST- 2023/06/20 00:00 [revised]
PHST- 2024/01/29 06:44 [medline]
PHST- 2023/07/05 01:06 [pubmed]
PHST- 2023/07/04 23:30 [entrez]
AID - 10.1007/s10067-023-06686-6 [pii]
AID - 10.1007/s10067-023-06686-6 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2023 Nov;42(11):3021-3031. doi: 10.1007/s10067-023-06686-6. Epub 
      2023 Jul 4.

PMID- 37282790
OWN - NLM
STAT- MEDLINE
DCOM- 20230815
LR  - 20230815
IS  - 1365-2796 (Electronic)
IS  - 0954-6820 (Linking)
VI  - 294
IP  - 3
DP  - 2023 Sep
TI  - Cardiovascular risk in rheumatoid arthritis patients treated with targeted 
      synthetic and biological disease-modifying antirheumatic drugs: A multi-centre 
      cohort study.
PG  - 314-325
LID - 10.1111/joim.13681 [doi]
AB  - BACKGROUND: This study aimed to compare the cardiovascular safety of 
      interleukin-6 inhibitors (IL-6i) and Janus Kinase inhibitors (JAKi) to tumour 
      necrosis factor inhibitors (TNFi). METHODS: We conducted a retrospective cohort 
      study using population-based electronic databases from Hong Kong, Taiwan and 
      Korea. We identified newly diagnosed patients with rheumatoid arthritis (RA) who 
      received b/tsDMARDs first time. We followed patients from b/tsDMARD initiation to 
      the earliest outcome (acute coronary heart disease, stroke, heart failure, venous 
      thromboembolism and systemic embolism) or censoring events (death, transformation 
      of b/tsDMARDs on different targets, discontinuation and study end). Using TNFi as 
      reference, we applied generalized linear regression for the incidence rate ratio 
      estimation adjusted by age, sex, disease duration and comorbidities. Random 
      effects meta-analysis was used for pooled analysis. RESULTS: We identified 8689 
      participants for this study. Median (interquartile range) follow-up years were 
      1.45 (2.77) in Hong Kong, 1.72 (2.39) in Taiwan and 1.45 (2.46) in Korea. 
      Compared to TNFi, the adjusted incidence rate ratios (aIRRs) (95% confidence 
      interval [CI]) of IL-6i in Hong Kong, Taiwan and Korea are 0.99 (0.25, 3.95), 
      1.06 (0.57, 1.98) and 1.05 (0.59, 1.86) and corresponding aIRR of JAKi are 1.50 
      (0.42, 5.41), 0.60 (0.26, 1.41), and 0.81 (0.38, 1.74), respectively. Pooled 
      aIRRs showed no significant risk of cardiovascular events (CVEs) associated with 
      IL-6i (1.05 [0.70, 1.57]) nor JAKi (0.80 [0.48, 1.35]) compared to TNFi. 
      CONCLUSION: There was no difference in the risk of CVE among RA patients 
      initiated with IL-6i, or JAKi compared to TNFi. The finding is consistent in Hong 
      Kong, Taiwan and Korea.
CI  - © 2023 The Authors. Journal of Internal Medicine published by John Wiley & Sons 
      Ltd on behalf of Association for Publication of The Journal of Internal Medicine.
FAU - Tong, Xinning
AU  - Tong X
AD  - Department of Medicine, School of Clinical Medicine, Li Ka Shing Faculty of 
      Medicine, The University of Hong Kong, Hong Kong SAR, China.
AD  - Department of Orthopaedics, The Eighth Affiliated Hospital, Sun Yat-sen 
      University, Shenzhen, China.
FAU - Shen, Chin-Yao
AU  - Shen CY
AD  - School of Pharmacy, Institute of Clinical Pharmacy and Pharmaceutical Sciences, 
      College of Medicine, National Cheng Kung University, Tainan, Taiwan.
FAU - Jeon, Ha-Lim
AU  - Jeon HL
AUID- ORCID: 0000-0002-9429-8711
AD  - School of Pharmacy, Jeonbuk National University, Jeonju, South Korea.
FAU - Li, Yihua
AU  - Li Y
AD  - Department of Medicine, School of Clinical Medicine, Li Ka Shing Faculty of 
      Medicine, The University of Hong Kong, Hong Kong SAR, China.
FAU - Shin, Ju-Young
AU  - Shin JY
AUID- ORCID: 0000-0003-1010-7525
AD  - School of Pharmacy, Sungkyunkwan University, Seoul, South Korea.
AD  - Department of Biohealth Regulatory Science, Sungkyunkwan University, Seoul, South 
      Korea.
FAU - Chan, Shirley Cw
AU  - Chan SC
AD  - Department of Medicine, School of Clinical Medicine, Li Ka Shing Faculty of 
      Medicine, The University of Hong Kong, Hong Kong SAR, China.
FAU - Yiu, Kai Hang
AU  - Yiu KH
AUID- ORCID: 0000-0003-2145-3108
AD  - Department of Medicine, School of Clinical Medicine, Li Ka Shing Faculty of 
      Medicine, The University of Hong Kong, Hong Kong SAR, China.
FAU - Pratt, Nicole L
AU  - Pratt NL
AD  - Quality Use of Medicines and Pharmacy Research Centre, Clinical and Health 
      Sciences, University of South Australia, Adelaide, Australia.
FAU - Ward, Michael
AU  - Ward M
AD  - Quality Use of Medicines and Pharmacy Research Centre, Clinical and Health 
      Sciences, University of South Australia, Adelaide, Australia.
FAU - Lau, Chak Sing
AU  - Lau CS
AD  - Department of Medicine, School of Clinical Medicine, Li Ka Shing Faculty of 
      Medicine, The University of Hong Kong, Hong Kong SAR, China.
FAU - Wong, Ian Ck
AU  - Wong IC
AD  - Centre for Safe Medication Practice and Research, Department of Pharmacology and 
      Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong 
      SAR, China.
AD  - Aston School of Pharmacy, Aston University, Birmingham, UK.
FAU - Li, Xue
AU  - Li X
AUID- ORCID: 0000-0003-4836-7808
AD  - Department of Medicine, School of Clinical Medicine, Li Ka Shing Faculty of 
      Medicine, The University of Hong Kong, Hong Kong SAR, China.
AD  - Centre for Safe Medication Practice and Research, Department of Pharmacology and 
      Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong 
      SAR, China.
FAU - Lai, Edward Chia-Cheng
AU  - Lai EC
AUID- ORCID: 0000-0002-5852-7652
AD  - School of Pharmacy, Institute of Clinical Pharmacy and Pharmaceutical Sciences, 
      College of Medicine, National Cheng Kung University, Tainan, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
DEP - 20230613
PL  - England
TA  - J Intern Med
JT  - Journal of internal medicine
JID - 8904841
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Humans
MH  - *Cardiovascular Diseases/epidemiology
MH  - Retrospective Studies
MH  - Risk Factors
MH  - *Arthritis, Rheumatoid/complications/drug therapy
MH  - Heart Disease Risk Factors
MH  - *Antirheumatic Agents/adverse effects
MH  - Multicenter Studies as Topic
OTO - NOTNLM
OT  - JAK inhibitors
OT  - bDMARDs
OT  - cardiovascular safety of biologics
OT  - real-world observational study
OT  - rheumatoid arthritis
EDAT- 2023/06/07 06:42
MHDA- 2023/08/15 06:42
CRDT- 2023/06/07 03:53
PHST- 2023/08/15 06:42 [medline]
PHST- 2023/06/07 06:42 [pubmed]
PHST- 2023/06/07 03:53 [entrez]
AID - 10.1111/joim.13681 [doi]
PST - ppublish
SO  - J Intern Med. 2023 Sep;294(3):314-325. doi: 10.1111/joim.13681. Epub 2023 Jun 13.

PMID- 37256492
OWN - NLM
STAT- MEDLINE
DCOM- 20240705
LR  - 20241018
IS  - 1868-601X (Electronic)
IS  - 1868-4483 (Linking)
VI  - 15
IP  - 4
DP  - 2024 Aug
TI  - Associations of Rheumatoid Factor, Rheumatoid Arthritis, and Interleukin-6 
      Inhibitor with the Prognosis of Ischemic Stroke: a Prospective Multicenter Cohort 
      Study and Mendelian Randomization Analysis.
PG  - 750-760
LID - 10.1007/s12975-023-01161-5 [doi]
AB  - Rheumatoid factor (RF), an established diagnostic biomarker for rheumatoid 
      arthritis (RA), is associated with cardiovascular diseases, but its impact on 
      clinical outcomes of ischemic stroke remains unclear. We aimed to investigate the 
      observational associations between serum RF and prognosis of ischemic stroke, and 
      further examined the genetic associations of RA and its therapeutic strategy, 
      interleukin-6 (IL-6) inhibitor, with prognosis of ischemic stroke. We measured 
      serum RF levels in 3474 Chinese ischemic stroke patients from the China 
      Antihypertensive Trial in Acute Ischemic Stroke. The primary outcome was the 
      composite outcome of death or major disability (modified Rankin Scale score ≥3) 
      at 3 months after stroke onset. Mendelian randomization (MR) analyses were 
      performed to examine the associations of genetically predicted RA and IL-6 
      inhibition with prognosis of ischemic stroke. During 3 months of follow-up, 866 
      patients (25.43%) experienced death or major disability. After multivariate 
      adjustment, RF-positive was significantly associated with a high risk of primary 
      outcome (OR, 1.47; 95% CI, 1.08-2.00; P =0.016) compared with RF-negative. The 
      two-sample MR analyses suggested that genetically predicted RA was associated 
      with an increased risk of primary outcome (OR, 1.09; 95% CI, 1.01-1.18; P=0.021), 
      while genetically predicted IL-6 inhibition was associated with a decreased risk 
      of primary outcome (OR, 0.88; 95% CI, 0.77-0.99; P=0.041). We found that positive 
      RF was associated with increased risks of adverse outcomes after atherosclerotic 
      ischemic stroke, and genetically predicted RA and IL-6 inhibition increased and 
      decreased the risks of adverse outcomes after ischemic stroke, respectively.
CI  - © 2023. The Author(s), under exclusive licence to Springer Science+Business 
      Media, LLC, part of Springer Nature.
FAU - Jia, Yiming
AU  - Jia Y
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Suzhou Medical 
      College of Soochow University, 199 Renai Road, Industrial Park District, Suzhou, 
      215123, Jiangsu Province, China.
FAU - Zhang, Kaixin
AU  - Zhang K
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Suzhou Medical 
      College of Soochow University, 199 Renai Road, Industrial Park District, Suzhou, 
      215123, Jiangsu Province, China.
FAU - Shi, Mengyao
AU  - Shi M
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Suzhou Medical 
      College of Soochow University, 199 Renai Road, Industrial Park District, Suzhou, 
      215123, Jiangsu Province, China.
AD  - Department of Epidemiology, Tulane University School of Public Health and 
      Tropical Medicine, New Orleans, LA, USA.
FAU - Guo, Daoxia
AU  - Guo D
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Suzhou Medical 
      College of Soochow University, 199 Renai Road, Industrial Park District, Suzhou, 
      215123, Jiangsu Province, China.
AD  - School of Nursing, Suzhou Medical College of Soochow University, Suzhou, China.
FAU - Yang, Pinni
AU  - Yang P
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Suzhou Medical 
      College of Soochow University, 199 Renai Road, Industrial Park District, Suzhou, 
      215123, Jiangsu Province, China.
FAU - Bu, Xiaoqing
AU  - Bu X
AD  - Department of Epidemiology, School of Public health, Chongqing Medical 
      University, Chongqing, China.
FAU - Chen, Jing
AU  - Chen J
AD  - Department of Epidemiology, Tulane University School of Public Health and 
      Tropical Medicine, New Orleans, LA, USA.
AD  - Department of Medicine, Tulane University School of Medicine, New Orleans, LA, 
      USA.
FAU - Wang, Aili
AU  - Wang A
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Suzhou Medical 
      College of Soochow University, 199 Renai Road, Industrial Park District, Suzhou, 
      215123, Jiangsu Province, China.
FAU - Xu, Tan
AU  - Xu T
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Suzhou Medical 
      College of Soochow University, 199 Renai Road, Industrial Park District, Suzhou, 
      215123, Jiangsu Province, China.
FAU - He, Jiang
AU  - He J
AD  - Department of Epidemiology, Tulane University School of Public Health and 
      Tropical Medicine, New Orleans, LA, USA.
AD  - Department of Medicine, Tulane University School of Medicine, New Orleans, LA, 
      USA.
FAU - Zhu, Zhengbao
AU  - Zhu Z
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Suzhou Medical 
      College of Soochow University, 199 Renai Road, Industrial Park District, Suzhou, 
      215123, Jiangsu Province, China. zbzhu@suda.edu.cn.
AD  - Department of Epidemiology, Tulane University School of Public Health and 
      Tropical Medicine, New Orleans, LA, USA. zbzhu@suda.edu.cn.
FAU - Zhang, Yonghong
AU  - Zhang Y
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Suzhou Medical 
      College of Soochow University, 199 Renai Road, Industrial Park District, Suzhou, 
      215123, Jiangsu Province, China. yhzhang@suda.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
DEP - 20230531
PL  - United States
TA  - Transl Stroke Res
JT  - Translational stroke research
JID - 101517297
RN  - 0 (Interleukin-6)
RN  - 9009-79-4 (Rheumatoid Factor)
RN  - 0 (IL6 protein, human)
SB  - IM
MH  - Humans
MH  - *Mendelian Randomization Analysis
MH  - *Interleukin-6/blood/genetics
MH  - *Ischemic Stroke/genetics/blood
MH  - Male
MH  - Female
MH  - *Arthritis, Rheumatoid/genetics/blood/complications/drug therapy
MH  - Middle Aged
MH  - Aged
MH  - *Rheumatoid Factor/blood
MH  - Prognosis
MH  - Prospective Studies
MH  - Cohort Studies
MH  - China/epidemiology
OTO - NOTNLM
OT  - Interleukin-6 inhibitor
OT  - Ischemic stroke
OT  - Prognosis
OT  - Rheumatoid arthritis
OT  - Rheumatoid factor
EDAT- 2023/05/31 13:12
MHDA- 2024/07/05 12:41
CRDT- 2023/05/31 11:12
PHST- 2023/02/23 00:00 [received]
PHST- 2023/05/21 00:00 [accepted]
PHST- 2023/04/23 00:00 [revised]
PHST- 2024/07/05 12:41 [medline]
PHST- 2023/05/31 13:12 [pubmed]
PHST- 2023/05/31 11:12 [entrez]
AID - 10.1007/s12975-023-01161-5 [pii]
AID - 10.1007/s12975-023-01161-5 [doi]
PST - ppublish
SO  - Transl Stroke Res. 2024 Aug;15(4):750-760. doi: 10.1007/s12975-023-01161-5. Epub 
      2023 May 31.

PMID- 37252810
OWN - NLM
STAT- MEDLINE
DCOM- 20240304
LR  - 20240304
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 63
IP  - 3
DP  - 2024 Mar 1
TI  - Mortality in patients with incident rheumatoid arthritis and depression: a Danish 
      cohort study of 11 071 patients and 55 355 comparators.
PG  - 680-688
LID - 10.1093/rheumatology/kead259 [doi]
AB  - OBJECTIVES: In patients with RA, the association between mortality and depression 
      has been investigated only in patients with prevalent RA. In this study, we 
      estimated the mortality risk associated with depression, defined as the first 
      filling of a prescription for antidepressants, in patients with incident RA and 
      background population comparators. METHODS: From 2008 to 2018, we identified 
      patients with incident RA in the nationwide Danish rheumatologic database, 
      DANBIO. For each patient, we randomly selected five comparators. Participants 
      were not treated with antidepressants or diagnosed with depression 3 years prior 
      to the index date. From other registers we collected data on socioeconomic 
      status, mortality and cause of death using unique personal identifiers. Using Cox 
      models, we calculated hazard rate ratios (HRR) with 95% CI. RESULTS: In depressed 
      patients with RA vs patients without depression, adjusted HRR for all-cause 
      mortality was 5.34 (95% CI 3.02, 9.45) during 0-2 years and 3.15 (95% CI 2.62, 
      3.79) during the total follow-up period, and highest in patients <55 years with 
      HRR 8.13 (95% CI 3.89, 17.02). In comparators with depression vs comparators 
      without depression, the association with mortality was similar to that in 
      patients with RA. There were no unnatural causes of death among depressed 
      patients with RA. The most frequent natural causes of death were cancer, 
      cardiovascular disease, stroke and pneumonia. CONCLUSION: In patients with RA, 
      depression was a predictor of death but with a strength similar to that in 
      matched comparators.
CI  - © The Author(s) 2023. Published by Oxford University Press on behalf of the 
      British Society for Rheumatology. All rights reserved. For permissions, please 
      email: journals.permissions@oup.com.
FAU - Pedersen, Jens K
AU  - Pedersen JK
AUID- ORCID: 0000-0003-2531-9547
AD  - Department of Rheumatology C, Research Unit, Odense University Hospital, Odense, 
      Denmark.
AD  - Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
FAU - Wang, Lei
AU  - Wang L
AD  - Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.
FAU - Risbo, Nickolaj
AU  - Risbo N
AD  - Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.
FAU - Pedersen, Alma B
AU  - Pedersen AB
AD  - Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.
AD  - Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
FAU - Andersen, Kjeld
AU  - Andersen K
AD  - Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
AD  - Department of Mental Health Odense, Mental Health Services Region of Southern 
      Denmark, Odense, Denmark.
FAU - Ellingsen, Torkell
AU  - Ellingsen T
AUID- ORCID: 0000-0003-0426-4962
AD  - Department of Rheumatology C, Research Unit, Odense University Hospital, Odense, 
      Denmark.
AD  - Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
LA  - eng
GR  - Danish Rheumatism Association/
PT  - Journal Article
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
RN  - 0 (Antidepressive Agents)
SB  - IM
MH  - Humans
MH  - Cohort Studies
MH  - *Depression/epidemiology
MH  - *Arthritis, Rheumatoid/drug therapy/epidemiology
MH  - Antidepressive Agents/therapeutic use
MH  - Denmark/epidemiology
OTO - NOTNLM
OT  - RA
OT  - antidepressive agents
OT  - cohort studies
OT  - depression
OT  - mortality
EDAT- 2023/05/30 19:16
MHDA- 2024/03/04 06:48
CRDT- 2023/05/30 12:22
PHST- 2023/02/19 00:00 [received]
PHST- 2023/05/23 00:00 [accepted]
PHST- 2024/03/04 06:48 [medline]
PHST- 2023/05/30 19:16 [pubmed]
PHST- 2023/05/30 12:22 [entrez]
AID - 7186518 [pii]
AID - 10.1093/rheumatology/kead259 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2024 Mar 1;63(3):680-688. doi: 
      10.1093/rheumatology/kead259.

PMID- 37172316
OWN - NLM
STAT- MEDLINE
DCOM- 20230925
LR  - 20240109
IS  - 2047-4881 (Electronic)
IS  - 2047-4873 (Linking)
VI  - 30
IP  - 13
DP  - 2023 Sep 20
TI  - Comprehensive characterization of non-cardiac comorbidities in acute heart 
      failure: an analysis of ESC-HFA EURObservational Research Programme Heart Failure 
      Long-Term Registry.
PG  - 1346-1358
LID - 10.1093/eurjpc/zwad151 [doi]
AB  - AIMS: To evaluate the prevalence and associations of non-cardiac comorbidities 
      (NCCs) with in-hospital and post-discharge outcomes in acute heart failure (AHF) 
      across the ejection fraction (EF) spectrum. METHODS AND RESULTS: The 9326 AHF 
      patients from European Society of Cardiology (ESC)-Heart Failure Association 
      (HFA)-EURObservational Research Programme Heart Failure Long-Term Registry had 
      complete information for the following 12 NCCs: anaemia, chronic obstructive 
      pulmonary disease (COPD), diabetes, depression, hepatic dysfunction, renal 
      dysfunction, malignancy, Parkinson's disease, peripheral vascular disease (PVD), 
      rheumatoid arthritis, sleep apnoea, and stroke/transient ischaemic attack (TIA). 
      Patients were classified by number of NCCs (0, 1, 2, 3, and ≥4). Of the AHF 
      patients, 20.5% had no NCC, 28.5% had 1 NCC, 23.1% had 2 NCC, 15.4% had 3 NCC, 
      and 12.5% had ≥4 NCC. In-hospital and post-discharge mortality increased with 
      number of NCCs from 3.0% and 18.5% for 1 NCC to 12.5% and 36% for ≥4 
      NCCs.Anaemia, COPD, PVD, sleep apnoea, rheumatoid arthritis, stroke/TIA, 
      Parkinson, and depression were more prevalent in HF with preserved EF (HFpEF). 
      The hazard ratio (95% confidence interval) for post-discharge death for each NCC 
      was for anaemia 1.6 (1.4-1.8), diabetes 1.2 (1.1-1.4), kidney dysfunction 1.7 
      (1.5-1.9), COPD 1.4 (1.2-1.5), PVD 1.2 (1.1-1.4), stroke/TIA 1.3 (1.1-1.5), 
      depression 1.2 (1.0-1.5), hepatic dysfunction 2.1 (1.8-2.5), malignancy 1.5 
      (1.2-1.8), sleep apnoea 1.2 (0.9-1.7), rheumatoid arthritis 1.5 (1.1-2.1), and 
      Parkinson 1.4 (0.9-2.1). Anaemia, kidney dysfunction, COPD, and diabetes were 
      associated with post-discharge mortality in all EF categories, PVD, stroke/TIA, 
      and depression only in HF with reduced EF, and sleep apnoea and malignancy only 
      in HFpEF. CONCLUSION: Multiple NCCs conferred poor in-hospital and post-discharge 
      outcomes. Ejection fraction categories had different prevalence and risk profile 
      associated with individual NCCs.
CI  - © The Author(s) 2023. Published by Oxford University Press on behalf of the 
      European Society of Cardiology. All rights reserved. For permissions, please 
      e-mail: journals.permissions@oup.com.
FAU - Chioncel, Ovidiu
AU  - Chioncel O
AUID- ORCID: 0000-0002-3197-3628
AD  - Emergency Institute for Cardiovascular Diseases 'Prof. C.C. Iliescu', Bucharest, 
      Romania.
AD  - University of Medicine Carol Davila, Bucharest, Romania.
FAU - Benson, Lina
AU  - Benson L
AD  - Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
FAU - Crespo-Leiro, Maria G
AU  - Crespo-Leiro MG
AD  - Cardiology Department Complexo Hospitalario Universitario A Coruna, (CHUAC), 
      CIBERCV, INIBIC, UDC, La Coruna, Spain.
FAU - Anker, Stefan D
AU  - Anker SD
AUID- ORCID: 0000-0002-0805-8683
AD  - Department of Cardiology (CVK), Berlin Institute of Health Center for 
      Regenerative Therapies (BCRT), German Centre for Cardiovascular Research (DZHK) 
      partner site Berlin, Berlin, Germany.
AD  - Charité Universitätsmedizin, Berlin, Germany.
FAU - Coats, Andrew J S
AU  - Coats AJS
AD  - Heart Research Institute, Sydney, Monash University, Sidney, Australia.
FAU - Filippatos, Gerasimos
AU  - Filippatos G
AUID- ORCID: 0000-0002-5640-0332
AD  - Heart Failure Unit, Attikon University Hospital, University of Athens, Athens, 
      Greece.
AD  - School of Medicine, University of Cyprus, Nicosia, Cyprus.
FAU - McDonagh, Theresa
AU  - McDonagh T
AD  - Department of Cardiology, King's College Hospital London, London, UK.
AD  - School of Cardiovascular Medicine and Sciences, King's College London British 
      Heart Foundation Centre of Excellence, London, UK.
FAU - Margineanu, Cornelia
AU  - Margineanu C
AD  - Emergency Institute for Cardiovascular Diseases 'Prof. C.C. Iliescu', Bucharest, 
      Romania.
AD  - University of Medicine Carol Davila, Bucharest, Romania.
FAU - Mebazaa, Alexandre
AU  - Mebazaa A
AD  - University of Paris Diderot, Hôpitaux Universitaires Saint Louis Lariboisière, 
      APHP, Paris, France.
FAU - Metra, Marco
AU  - Metra M
AD  - Cardiology, Department of Medical and Surgical Specialties, Radiological 
      Sciences, and Public Health, University of Brescia, Brescia, Italy.
FAU - Piepoli, Massimo F
AU  - Piepoli MF
AD  - Cardiology, IRCCS PoliclinicoSan Donato, San Donato Milanese, Milan, Italy.
AD  - Dipartimento di Scienze Biomediche per la Salute, University of Milan, Milan, 
      Italy.
FAU - Adamo, Marianna
AU  - Adamo M
AUID- ORCID: 0000-0002-3855-1815
AD  - Cardiology, Department of Medical and Surgical Specialties, Radiological 
      Sciences, and Public Health, University of Brescia, Brescia, Italy.
FAU - Rosano, Giuseppe M C
AU  - Rosano GMC
AD  - Cardiology Clinical Academy Group, St Georges Hospital NHS Trust, University of 
      London, London, UK.
AD  - Department of Medical Sciences, Centre for Clinical and Basic Research, IRCCS San 
      Raffaele Pisana, Rome, Italy.
FAU - Ruschitzka, Frank
AU  - Ruschitzka F
AD  - Department of Cardiology, University Hospital Zurich, Zurich, Switzerland.
FAU - Savarese, Gianluigi
AU  - Savarese G
AD  - Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
FAU - Seferovic, Petar
AU  - Seferovic P
AD  - Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
AD  - Serbian Academy of Sciences and Arts, Belgrade, Serbia.
FAU - Volterrani, Maurizio
AU  - Volterrani M
AD  - IRCCS San Raffaele Pisana, Rome, Italy.
FAU - Ferrari, Roberto
AU  - Ferrari R
AUID- ORCID: 0000-0003-2046-9175
AD  - Scientific Department, MTA Group, Lugano, Switzerland.
FAU - Maggioni, Aldo P
AU  - Maggioni AP
AD  - ANMCO Research Centre, Florence, Italy.
FAU - Lund, Lars H
AU  - Lund LH
AD  - Department of Medicine, Karolinska Institute, Stockholm, Sweden.
AD  - Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Eur J Prev Cardiol
JT  - European journal of preventive cardiology
JID - 101564430
SB  - IM
CIN - Eur J Prev Cardiol. 2023 Sep 20;30(13):1343-1345. doi: 10.1093/eurjpc/zwad170. 
      PMID: 37219916
EIN - Eur J Prev Cardiol. 2024 Jan 25;31(2):274. doi: 10.1093/eurjpc/zwad396. PMID: 
      38195099
MH  - Humans
MH  - *Heart Failure/diagnosis/epidemiology/complications
MH  - Stroke Volume
MH  - Aftercare
MH  - *Ischemic Attack, Transient
MH  - *Parkinson Disease/complications
MH  - Prognosis
MH  - Patient Discharge
MH  - *Anemia/diagnosis/epidemiology/complications
MH  - *Cardiology
MH  - *Arthritis, Rheumatoid/complications
MH  - *Sleep Apnea Syndromes/complications
MH  - Registries
MH  - *Stroke
MH  - *Pulmonary Disease, Chronic Obstructive/diagnosis/epidemiology/complications
OAB - The current analysis from ESC-Heart Failure Long-Term Registry represents the 
      largest and most comprehensive study in an acute heart failure (AHF) population 
      with HF with reduced ejection fraction (HFrEF), HF with mildly reduced EF 
      (HFmrEF), and HF with preserved EF (HFpEF), on prevalence and association with 
      in-hospital and post-discharge outcomes of a large number of non-cardiac 
      comorbidities.A greater number of non-cardiac comorbidities (CNNs) were 
      associated at admission with older age, preserved EF, more severe NYHA class, and 
      longer duration of HF. In-hospital and post-discharge mortality gradually 
      increased with number of CNNs.The association between each individual comorbidity 
      and post-discharge outcomes varied substantially in AHF patients with HFrEF, 
      HFmrEF, and HFpEF, suggesting that an ‘EF-specific’ multidisciplinary approach 
      with distinct comorbidity management programs should be applied in post-discharge 
      phase.
OABL- eng
OTO - NOTNLM
OT  - Acute heart failure
OT  - Comorbidities
OT  - Prognosis
COIS- Conflict of interest: O. Chioncel declare no conflict of interest related to 
      present work; ESC meeting support from Servier. L. Benson declare no conflict of 
      interest. M. Crespo-Leiro reports unrelated to the present work: consultancy or 
      speaker's honoraria from Novartis, AstraZeneca, Boehringer Ingelheim, Abbott, 
      Medtronic, CareDx, Astellas and Vifor Pharma. S.D. Anker reports unrelated to the 
      present work: Grants or contracts: Vifor Int, Abbott Vascular; Consulting fees: 
      CVRx, Amgen, Respicardia, Novo Nordisk, Brahms, Novartis, Sanofi, Cordio; 
      Leadership or fiduciary role in other board: Abbott Vascular, Astra Zeneca, Bayer 
      AG, Bioventrix, Boehringer Ingelheim, Cardiac Dimension, Cardior, Impulse 
      Dynamics, Janssen, Occlutech, Servier, Vifor Int, and V-Wave. A.J.S. Coats 
      reports unrelated to the present work: speaker's honoraria from: Astra Zeneca, 
      Bayer, Boehringer Ingelheim, Edwards, Menarini, Novartis, Servier, Vifor, Abbott, 
      Actimed, Arena, Cardiac Dimensions, Corvia, CVRx, Enopace, ESN Cleer, Faraday, 
      Impulse Dynamics, Respicardia, and Viatris. G. Filippatos reports lecture fees 
      and/or committee membership in trials sponsored by Bayer, Vifor, Medtronic, 
      Novartis, Servier, Boehringer Ingelheim, and research support from the European 
      Union. T. McDonagh reports unrelated to the present work: speaker's honoraria 
      from Abbot, Astra Zeneca, Boeringher Ingelheim and Edwards. C. Margineanu none 
      related to the present work. A. Mebazaa reports unrelated to the present work: 
      Grants or contracts from and consulting fees from Roche, 4TEEN4, Corteria; 
      speaker's honoraria from MSD; Patents: S-Form Pharma. M. Metra reports personal 
      fees from Amgen, AstraZeneca, Abbott Vascular, Bayer, Edwards Therapeutics, 
      Livanova, Vifor Pharma, as member of Trials' Committees or advisory boards or for 
      speeches at sponsored meetings in the last 3 years. M. Piepoli reports unrelated 
      to the present work: consultancy, speaker's, institutional fees from 
      Astra-Zeneca, Boehringer- Ingelheim, CHF solution, Menarini, Novartis, Servier M. 
      Adammo reports speaker fees from Abbott Vascular and Medtronic. G.M.C. Rosano 
      declare no conflict of interest. F. Ruschitzka has not received personal payments 
      by pharmaceutical companies or device manufacturers in the last 3 years 
      (remuneration for the time spent in activities, such as participation as steering 
      committee member of clinical trials and member of the Pfizer Research Award 
      selection committee in Switzerland, were made directly to the University of 
      Zurich). The Department of Cardiology (University Hospital of Zurich/University 
      of Zurich) reports research-, educational- and/or travel grants from Abbott, 
      Amgen, Astra Zeneca, Bayer, Berlin Heart, B. Braun, Biosense Webster, Biosensors 
      Europe AG, Biotronik, BMS, Boehringer Ingelheim, Boston Scientific, Bracco, 
      Cardinal Health Switzerland, Corteria, Daiichi, Diatools AG, Edwards 
      Lifesciences, Guidant Europe NV (BS), Hamilton Health Sciences, Kaneka 
      Corporation, Kantar, Labormedizinisches Zentrum, Medtronic, MSD, Mundipharma 
      Medical Company, Novartis, Novo Nordisk, Orion, Pfizer, Quintiles Switzerland 
      Sarl, Roche Diagnostics, Sahajanand IN, Sanofi, Sarstedt AG, Servier, SIS 
      Medical, SSS International Clinical Research, Terumo Deutschland, Trama 
      Solutions, V- Wave, Vascular Medical, Vifor, Wissens Plus, ZOLL. The research and 
      educational grants do not impact on Prof. Ruschitzka`s personal remuneration. G. 
      Savarese reports unrelated to the present work: Grants or contracts: Vifor 
      Pharma, Boehringer Ingelheim, Astra Zeneca, Merck, Cytokinetics; Consulting fees: 
      Societa' Prodotti Antibiotici, Medical Education Global Solutions, Genesis, 
      Agence Recherche (ANR); speaker's honoraria: Servier, Cytokinetics, Medtronic, 
      Dynamicom Education, Vifor Pharma; Support for attending meetings: Boehringer 
      Ingelheim; Data Safety Monitoring Bord or Advisory Board: Astra Zeneca, Uppsala 
      Clinical Research Center, Servier. P. Seferovic reports unrelated to the present 
      work: speaker's honoraria from Servier, Astra Zeneca, Menarini, Boehringer 
      Ingelheim, Novartis and Roche diagnostic. M. Volterrani: none related to the 
      present work. R. Ferrari reports unrelated to the present work: speaker's 
      honoraria and support for attending meetings: Servier International, Merck 
      Serono, Lupin, Sunpharma, Reddys Ltd; leadership or fiduciary role in other 
      board: Scientific Director of Medical Trial Analysis. A. Maggioni: personal fees 
      from AstraZeneca, Bayer, Fresenius, Novartis, outside the submitted work. L.H. 
      Lund is supported by Supported by Karolinska Institutet, the Swedish Research 
      Council [grant 523-2014-2336], the Swedish Heart Lung Foundation [grants 
      20150557, 20190310], and the Stockholm County Council [grants 20170112, 20190525] 
      and reports unrelated to the present work: Grants: AstraZeneca, Vifor, Boston 
      Scientific, Boehringer Ingelheim, Novartis, MSD; Consulting: Vifor, AstraZeneca, 
      Bayer, Pharmacosmos, MSD, MedScape, Sanofi, Lexicon, Myokardia, Boehringer 
      Ingelheim, Servier, Edwards Life Sciences, Alleviant; Speaker's honoraria: 
      Abbott, OrionPharma, MedScape, Radcliffe, AstraZeneca, Novartis, Boehringer 
      Ingelheim, Bayer; Patent: AnaCardio; Stock ownership: AnaCardio.
EDAT- 2023/05/12 19:07
MHDA- 2023/09/25 06:42
CRDT- 2023/05/12 17:12
PHST- 2023/01/26 00:00 [received]
PHST- 2023/05/05 00:00 [revised]
PHST- 2023/05/06 00:00 [accepted]
PHST- 2023/09/25 06:42 [medline]
PHST- 2023/05/12 19:07 [pubmed]
PHST- 2023/05/12 17:12 [entrez]
AID - 7161110 [pii]
AID - 10.1093/eurjpc/zwad151 [doi]
PST - ppublish
SO  - Eur J Prev Cardiol. 2023 Sep 20;30(13):1346-1358. doi: 10.1093/eurjpc/zwad151.

PMID- 37114972
OWN - NLM
STAT- MEDLINE
DCOM- 20230501
LR  - 20230504
IS  - 1552-8456 (Electronic)
IS  - 0193-9459 (Linking)
VI  - 45
IP  - 6
DP  - 2023 Jun
TI  - Risk of Stroke and Cardiovascular Disease According to Diabetes Mellitus Status.
PG  - 520-527
LID - 10.1177/01939459231158212 [doi]
AB  - The purpose of this study was to investigate the importance of prevention and 
      management of diabetes by analyzing stroke and cardiovascular disease (CVD) 
      incidence among people with diabetes. This secondary analysis of the Korea 
      National Health and Nutrition Examination Survey Ⅶ (2016-2018) data included 
      15,039 adults. Diabetes status was significantly associated with sex, age, 
      marital status, household size, education level, employment status, household 
      income, hypertension, dyslipidemia, stroke, CVD, osteoarthritis, osteoporosis, 
      kidney failure, depression, level of stress, smoking, drinking, body mass index, 
      weight control, and the number of days of walking per week; however, it was not 
      associated with rheumatoid arthritis. Stroke and CVD risk significantly increased 
      in the presence of diabetes (by 4.123 times and 3.223 times, respectively). The 
      incidences of stroke and CVD were significantly higher among participants with 
      diabetes than among those without diabetes. Thus, preventing and systematically 
      managing diabetes is crucial to reducing related complications and mortality.
FAU - Kim, Hyunsu
AU  - Kim H
AD  - College of Nursing, Kyungdong University, Wonju, Republic of Korea.
FAU - Lee, Hyunjung
AU  - Lee H
AUID- ORCID: 0000-0003-3307-8480
AD  - College of Nursing, Kyungdong University, Wonju, Republic of Korea.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230302
PL  - United States
TA  - West J Nurs Res
JT  - Western journal of nursing research
JID - 7905435
SB  - IM
MH  - Adult
MH  - Humans
MH  - *Cardiovascular Diseases/complications/epidemiology
MH  - Risk Factors
MH  - Nutrition Surveys
MH  - *Diabetes Mellitus/epidemiology
MH  - *Stroke/complications/epidemiology
OTO - NOTNLM
OT  - cardiovascular disease
OT  - diabetes mellitus
OT  - national surveys
OT  - risk factors
OT  - stroke
EDAT- 2023/04/28 12:42
MHDA- 2023/05/01 06:42
CRDT- 2023/04/28 09:33
PHST- 2023/05/01 06:42 [medline]
PHST- 2023/04/28 12:42 [pubmed]
PHST- 2023/04/28 09:33 [entrez]
AID - 10.1177/01939459231158212 [doi]
PST - ppublish
SO  - West J Nurs Res. 2023 Jun;45(6):520-527. doi: 10.1177/01939459231158212. Epub 
      2023 Mar 2.

PMID- 37080728
OWN - NLM
STAT- MEDLINE
DCOM- 20230706
LR  - 20230805
IS  - 2092-7193 (Electronic)
IS  - 2092-7193 (Linking)
VI  - 45
DP  - 2023
TI  - Risk of cancer, cardiovascular disease, thromboembolism, and mortality in 
      patients with rheumatoid arthritis receiving Janus kinase inhibitors: a 
      real-world retrospective observational study using Korean health insurance data.
PG  - e2023045
LID - 10.4178/epih.e2023045 [doi]
LID - e2023045
AB  - OBJECTIVES: This study investigated whether Janus kinase inhibitors (JAKis) raise 
      the risk of cardiovascular disease (CVD), venous thromboembolism (VTE), and 
      cancer in patients with rheumatoid arthritis (RA). METHODS: We conducted a 
      real-world retrospective observational study using data obtained from the Korean 
      National Health Insurance Service database. Two data sets were analyzed: tumor 
      necrosis factor inhibitor (TNFi)/JAKi-naive RA patients (set 1) and all RA 
      patients who used TNFis or JAKis (set 2). The incidence rate ratios (IRRs) and 
      hazard ratios (HRs) for acute myocardial infarction (AMI), stroke, cardiovascular 
      (CV)-related mortality, major adverse cardiovascular events (MACE), VTE, arterial 
      thromboembolism (ATE), cancer, and all-cause mortality were compared between the 
      JAKi and TNFi groups. RESULTS: Set 1 included 1,596 RA patients (JAKi group: 645; 
      TNFi group: 951), and set 2 included 11,765 RA patients (JAKi group: 2,498; TNFi 
      group: 9,267). No adverse events (AEs) showed significantly higher IRRs in the 
      JAKi groups than in the TNFi groups of sets 1 and 2. The HRs for MACE in the JAKi 
      groups of sets 1 and 2 were 0.59 (95% confidence [CI], 0.35 to 0.99) and 0.80 
      (95% CI, 0.67 to 0.97), respectively. The JAKi group of set 2 showed a 
      significantly higher risk of all-cause mortality (HR, 1.71; 95% CI, 1.32 to 
      2.20), but the other AEs did not demonstrate increased risks in the JAKi groups. 
      CONCLUSIONS: In this study, JAKis did not increase the risk of AMI, stroke, 
      CV-related mortality, MACE, VTE, ATE, or cancer in Korean RA patients relative to 
      TNFis.
FAU - Min, Hong Ki
AU  - Min HK
AD  - Division of Rheumatology, Department of Internal Medicine, Konkuk University 
      Medical Center, Seoul, Korea.
FAU - Kim, Hyeongsu
AU  - Kim H
AD  - Department of Preventive Medicine, Konkuk University School of Medicine, Seoul, 
      Korea.
FAU - Jeong, Ho Jin
AU  - Jeong HJ
AD  - Department of Preventive Medicine, Konkuk University School of Medicine, Seoul, 
      Korea.
FAU - Kim, Se Hee
AU  - Kim SH
AD  - Division of Rheumatology, Department of Internal Medicine, Konkuk University 
      Medical Center, Seoul, Korea.
FAU - Kim, Hae-Rim
AU  - Kim HR
AD  - Division of Rheumatology, Department of Internal Medicine, Konkuk University 
      Medical Center, Seoul, Korea.
AD  - Research Institute of Medical Science, Konkuk University School of Medicine, 
      Seoul, Korea.
FAU - Lee, Sang-Heon
AU  - Lee SH
AD  - Division of Rheumatology, Department of Internal Medicine, Konkuk University 
      Medical Center, Seoul, Korea.
AD  - Research Institute of Medical Science, Konkuk University School of Medicine, 
      Seoul, Korea.
FAU - Lee, KunSei
AU  - Lee K
AD  - Department of Preventive Medicine, Konkuk University School of Medicine, Seoul, 
      Korea.
FAU - Shin, Soon-Ae
AU  - Shin SA
AD  - Big Data Strategy Department, National Health Insurance Service, Wonju, Korea.
FAU - Park, Jong Heon
AU  - Park JH
AD  - Big Data Strategy Department, National Health Insurance Service, Wonju, Korea.
LA  - eng
PT  - Journal Article
PT  - Observational Study
DEP - 20230415
PL  - Korea (South)
TA  - Epidemiol Health
JT  - Epidemiology and health
JID - 101519472
RN  - 0 (Janus Kinase Inhibitors)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Humans
MH  - *Janus Kinase Inhibitors/therapeutic use
MH  - *Antirheumatic Agents/adverse effects
MH  - *Cardiovascular Diseases/epidemiology
MH  - *Venous Thromboembolism/epidemiology/chemically induced/drug therapy
MH  - Tumor Necrosis Factor-alpha/therapeutic use
MH  - *Arthritis, Rheumatoid/drug therapy/chemically induced
MH  - *Myocardial Infarction/epidemiology
MH  - Insurance, Health
MH  - *Neoplasms/drug therapy
MH  - Republic of Korea/epidemiology
PMC - PMC10396807
OTO - NOTNLM
OT  - Cancer
OT  - Cardiovascular disease
OT  - Janus kinase inhibitor
OT  - Rheumatoid arthritis
OT  - Tumor necrosis factor inhibitor
OT  - Venous thromboembolism
COIS- CONFLICT OF INTEREST The authors have no conflicts of interest to declare for 
      this study.
EDAT- 2023/04/21 00:41
MHDA- 2023/07/06 06:42
PMCR- 2023/04/15
CRDT- 2023/04/20 21:08
PHST- 2022/12/15 00:00 [received]
PHST- 2023/04/05 00:00 [accepted]
PHST- 2023/07/06 06:42 [medline]
PHST- 2023/04/21 00:41 [pubmed]
PHST- 2023/04/20 21:08 [entrez]
PHST- 2023/04/15 00:00 [pmc-release]
AID - epih.e2023045 [pii]
AID - epih-45-e2023045 [pii]
AID - 10.4178/epih.e2023045 [doi]
PST - ppublish
SO  - Epidemiol Health. 2023;45:e2023045. doi: 10.4178/epih.e2023045. Epub 2023 Apr 15.

PMID- 37049403
OWN - NLM
STAT- MEDLINE
DCOM- 20230414
LR  - 20230415
IS  - 2072-6643 (Electronic)
IS  - 2072-6643 (Linking)
VI  - 15
IP  - 7
DP  - 2023 Mar 23
TI  - The Interplay between Cardiovascular Risk, Cardiovascular Events, and Disease 
      Activity in Primary Sjögren's Syndrome: Is Uric Acid the Missing Link?
LID - 10.3390/nu15071563 [doi]
LID - 1563
AB  - (1) Background: Uric acid is a well-known cardiovascular (CV) risk factor in the 
      general population but its role in the setting of rheumatic diseases other than 
      gout is unclear. (2) Methods: This is a retrospective study investigating a 
      cohort of 105 pSS patients recording clinical, serological, and CV-related 
      variables including adherence to the Mediterranean diet. (3) Results: We observed 
      a strong relationship between disease activity, interstitial lung disease (ILD), 
      and CV events. The association between ILD and CV events was dependent on higher 
      SUA levels but independent of other traditional CV risk factors. All three cases 
      of previous non-fatal stroke were reported by females aged <65 years, with higher 
      SUA levels, and two of them also had pSS-ILD. Forty (38%) patients had a 10-year 
      risk of fatal and non-fatal CV disease events beyond the cut-off recommended for 
      their age, and using the correction factor of 1.5 currently applied only to 
      rheumatoid arthritis, we could better identify patient subsets characterized by 
      different CV risk profiles including different SUA levels. (4) Conclusions: This 
      study is the first to investigate in depth the role of SUA in the CV scenario of 
      pSS. Our findings underpin the importance of assessing SUA levels in pSS in 
      addition to the other traditional CV risk factors and to consider applying the 
      correction factor for CV risk assessment tools to achieve a better stratification 
      of CV risk.
FAU - Alunno, Alessia
AU  - Alunno A
AUID- ORCID: 0000-0003-1105-5640
AD  - Internal Medicine and Nephrology Division, Department of Life, Health & 
      Environmental Sciences, San Salvatore Hospital, University of L'Aquila, ASL 1 
      Avezzano-Sulmona-L'Aquila, 67100 L'Aquila, Italy.
FAU - Carubbi, Francesco
AU  - Carubbi F
AUID- ORCID: 0000-0003-1958-5136
AD  - Internal Medicine and Nephrology Division, Department of Life, Health & 
      Environmental Sciences, San Salvatore Hospital, University of L'Aquila, ASL 1 
      Avezzano-Sulmona-L'Aquila, 67100 L'Aquila, Italy.
FAU - Mariani, Francesco Maria
AU  - Mariani FM
AD  - Internal Medicine and Nephrology Division, Department of Life, Health & 
      Environmental Sciences, San Salvatore Hospital, University of L'Aquila, ASL 1 
      Avezzano-Sulmona-L'Aquila, 67100 L'Aquila, Italy.
FAU - Martini, Cecilia
AU  - Martini C
AD  - Internal Medicine and Nephrology Division, Department of Life, Health & 
      Environmental Sciences, San Salvatore Hospital, University of L'Aquila, ASL 1 
      Avezzano-Sulmona-L'Aquila, 67100 L'Aquila, Italy.
FAU - Campanozzi, Elena
AU  - Campanozzi E
AD  - Internal Medicine and Nephrology Division, Department of Life, Health & 
      Environmental Sciences, San Salvatore Hospital, University of L'Aquila, ASL 1 
      Avezzano-Sulmona-L'Aquila, 67100 L'Aquila, Italy.
FAU - Ferri, Claudio
AU  - Ferri C
AD  - Internal Medicine and Nephrology Division, Department of Life, Health & 
      Environmental Sciences, San Salvatore Hospital, University of L'Aquila, ASL 1 
      Avezzano-Sulmona-L'Aquila, 67100 L'Aquila, Italy.
LA  - eng
GR  - BANDO PSD-MESVA 2022/University of L'Aquila/
PT  - Journal Article
DEP - 20230323
PL  - Switzerland
TA  - Nutrients
JT  - Nutrients
JID - 101521595
RN  - 268B43MJ25 (Uric Acid)
SB  - IM
MH  - Female
MH  - Humans
MH  - Uric Acid
MH  - *Sjogren's Syndrome/complications/epidemiology
MH  - *Cardiovascular Diseases/etiology/epidemiology
MH  - Risk Factors
MH  - Retrospective Studies
MH  - *Lung Diseases, Interstitial/complications
MH  - Heart Disease Risk Factors
PMC - PMC10096655
OTO - NOTNLM
OT  - Sjögren’s syndrome
OT  - cardiovascular risk
OT  - cerebrovascular disease
COIS- The authors declare no conflict of interest. The funders had no role in the 
      design of the study; in the collection, analysis, or interpretation of data; in 
      the writing of the manuscript; or in the decision to publish the results.
EDAT- 2023/04/14 06:00
MHDA- 2023/04/14 06:41
PMCR- 2023/03/23
CRDT- 2023/04/13 01:24
PHST- 2023/02/13 00:00 [received]
PHST- 2023/03/18 00:00 [revised]
PHST- 2023/03/22 00:00 [accepted]
PHST- 2023/04/14 06:41 [medline]
PHST- 2023/04/13 01:24 [entrez]
PHST- 2023/04/14 06:00 [pubmed]
PHST- 2023/03/23 00:00 [pmc-release]
AID - nu15071563 [pii]
AID - nutrients-15-01563 [pii]
AID - 10.3390/nu15071563 [doi]
PST - epublish
SO  - Nutrients. 2023 Mar 23;15(7):1563. doi: 10.3390/nu15071563.

PMID- 36996698
OWN - NLM
STAT- MEDLINE
DCOM- 20230412
LR  - 20230526
IS  - 1095-9157 (Electronic)
IS  - 0896-8411 (Linking)
VI  - 136
DP  - 2023 Apr
TI  - ATP-binding cassette G1 membrane transporter-mediated cholesterol efflux capacity 
      influences coronary atherosclerosis and cardiovascular risk in Rheumatoid 
      Arthritis.
PG  - 103029
LID - S0896-8411(23)00038-0 [pii]
LID - 10.1016/j.jaut.2023.103029 [doi]
AB  - OBJECTIVES: Cholesterol efflux capacity (CEC) measures the ability of 
      high-density lipoprotein (HDL) to remove cholesterol from macrophages and reduce 
      the lipid content of atherosclerotic plaques. CEC inversely associated with 
      cardiovascular risk beyond HDL-cholesterol levels. CEC through the 
      ATP-binding-cassette G1 (ABCG1) membrane transporter is impaired in rheumatoid 
      arthritis (RA). We evaluated associations of ABCG1-CEC with coronary 
      atherosclerosis, plaque progression and cardiovascular risk in RA. METHODS: 
      Coronary atherosclerosis (noncalcified, partially, fully-calcified, 
      low-attenuation plaque) was assessed with computed tomography angiography in 140 
      patients and reevaluated in 99 after 6.9 ± 0.3 years. Cardiovascular events 
      including acute coronary syndromes, stroke, cardiovascular death, claudication, 
      revascularization and hospitalized heart failure were recorded. ABCG1-CEC was 
      measured in Chinese hamster ovary cells as percentage of effluxed over total 
      intracellular cholesterol. RESULTS: ABCG1-CEC inversely associated with extensive 
      atherosclerosis (≥5 plaques) (adjusted odds ratio 0.50 [95% CI 0.28-0.88]), 
      numbers of partially-calcified (rate ratio [RR] 0.71 [0.53-0.94]) and 
      low-attenuation plaques (RR 0.63 [0.43-0.91] per standard deviation increment). 
      Higher ABCG1-CEC predicted fewer new partially-calcified plaques in patients with 
      lower baseline and time-averaged CRP and fewer new noncalcified and calcified 
      plaques in those receiving higher mean prednisone dose. ABCG1-CEC inversely 
      associated with events in patients with but not without noncalcified plaques, 
      with <median but not higher CRP and in prednisone users but not nonusers 
      (p-for-interaction = 0.021, 0.033 and 0.008 respectively). CONCLUSION: ABCG1-CEC 
      inversely associated with plaque burden and vulnerability, and plaque progression 
      conditionally on cumulative inflammation and corticosteroid dose. ABCG1-CEC 
      inversely associated with events specifically in patients with noncalcified 
      plaques, lower inflammation and in prednisone users.
CI  - Copyright © 2023 Elsevier Ltd. All rights reserved.
FAU - Karpouzas, George A
AU  - Karpouzas GA
AD  - Division of Rheumatology, Harbor-UCLA Medical Center and the Lundquist Institute 
      for Biomedical Innovation, Torrance, CA, USA. Electronic address: 
      gkarpouzas@lundquist.org.
FAU - Papotti, Bianca
AU  - Papotti B
AD  - Department of Food and Drug, University of Parma, Parco Area delle Scienze 27/A, 
      43124, Parma, Italy.
FAU - Ormseth, Sarah R
AU  - Ormseth SR
AD  - Division of Rheumatology, Harbor-UCLA Medical Center and the Lundquist Institute 
      for Biomedical Innovation, Torrance, CA, USA.
FAU - Palumbo, Marcella
AU  - Palumbo M
AD  - Department of Food and Drug, University of Parma, Parco Area delle Scienze 27/A, 
      43124, Parma, Italy.
FAU - Hernandez, Elizabeth
AU  - Hernandez E
AD  - Division of Rheumatology, Harbor-UCLA Medical Center and the Lundquist Institute 
      for Biomedical Innovation, Torrance, CA, USA.
FAU - Adorni, Maria Pia
AU  - Adorni MP
AD  - Department of Food and Drug, University of Parma, Parco Area delle Scienze 27/A, 
      43124, Parma, Italy.
FAU - Zimetti, Francesca
AU  - Zimetti F
AD  - Department of Food and Drug, University of Parma, Parco Area delle Scienze 27/A, 
      43124, Parma, Italy.
FAU - Budoff, Matthew J
AU  - Budoff MJ
AD  - Division of Cardiology, Harbor-UCLA Medical Center and the Lundquist Institute 
      for Biomedical Innovation, Torrance, CA, USA.
FAU - Ronda, Nicoletta
AU  - Ronda N
AD  - Department of Food and Drug, University of Parma, Parco Area delle Scienze 27/A, 
      43124, Parma, Italy.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230328
PL  - England
TA  - J Autoimmun
JT  - Journal of autoimmunity
JID - 8812164
RN  - VB0R961HZT (Prednisone)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - 0 (Membrane Transport Proteins)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
SB  - IM
MH  - Animals
MH  - Cricetinae
MH  - Humans
MH  - *Coronary Artery Disease
MH  - *Cardiovascular Diseases
MH  - Prednisone
MH  - CHO Cells
MH  - Risk Factors
MH  - Cricetulus
MH  - Cholesterol
MH  - *Arthritis, Rheumatoid
MH  - Inflammation
MH  - Heart Disease Risk Factors
MH  - Membrane Transport Proteins
MH  - Adenosine Triphosphate
OTO - NOTNLM
OT  - ABCG1
OT  - Cardiovascular events
OT  - Cholesterol efflux capacity
OT  - Coronary atherosclerosis
OT  - Rheumatoid arthritis
COIS- Declaration of competing interest G.A.K. has received consulting and speaker fees 
      from Sanofi-Genzyme-Regeneron, Bristol-Meyer-Squibb and Janssen. M.J.B. has 
      received consulting and speaker fees from Pfizer. No other disclosures were 
      reported.
EDAT- 2023/03/31 06:00
MHDA- 2023/04/12 06:42
CRDT- 2023/03/30 18:08
PHST- 2023/02/10 00:00 [received]
PHST- 2023/03/06 00:00 [revised]
PHST- 2023/03/17 00:00 [accepted]
PHST- 2023/04/12 06:42 [medline]
PHST- 2023/03/31 06:00 [pubmed]
PHST- 2023/03/30 18:08 [entrez]
AID - S0896-8411(23)00038-0 [pii]
AID - 10.1016/j.jaut.2023.103029 [doi]
PST - ppublish
SO  - J Autoimmun. 2023 Apr;136:103029. doi: 10.1016/j.jaut.2023.103029. Epub 2023 Mar 
      28.

PMID- 36787310
OWN - NLM
STAT- MEDLINE
DCOM- 20230216
LR  - 20230406
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 18
IP  - 2
DP  - 2023
TI  - Clinical outcomes of patients with rheumatoid arthritis who underwent 
      percutaneous coronary intervention: A Korean nationwide cohort study.
PG  - e0281067
LID - 10.1371/journal.pone.0281067 [doi]
LID - e0281067
AB  - OBJECTIVE: Rheumatoid arthritis (RA) increases the risk of cardiovascular 
      disease. This study aimed to investigate the short-and long-term prognosis of 
      patients with and without RA who underwent percutaneous coronary intervention 
      (PCI). METHODS: The Korean National Health Insurance Service claims database was 
      used to extract data on 236,134 patients (34,493 with RA and 201,641 without RA) 
      who underwent PCI between 2008 and 2019. The primary outcome was major adverse 
      cardiovascular events (MACE), including all-cause mortality, myocardial 
      infarction, stroke, transient ischemic attack, or coronary revascularization with 
      short-term (30-day) and long-term outcomes. The secondary outcomes were the 
      individual components of MACE. RESULTS: During a 10-year follow-up, patients with 
      RA showed a shorter median survival time from MACE than their counterparts (with 
      RA: 4.29 years vs. without RA: 6.10 years). RA was significantly associated with 
      an increased risk of MACEs in long-term outcomes (hazard ratio (HR) 1.07, 95% 
      confidence intervals (CI) 1.06-1.09, p<0.001), but not with short-term outcomes 
      (HR 1.02, 95% CI 0.99-1.06, p = 0.222). RA was an independent predictor of an 
      increased risk of all the MACE components. CONCLUSION: In patients who underwent 
      PCI, RA did not increase the risk of short-term cardiovascular outcomes but 
      increased the risk of long-term adverse outcomes.
CI  - Copyright: © 2023 Ha et al. This is an open access article distributed under the 
      terms of the Creative Commons Attribution License, which permits unrestricted 
      use, distribution, and reproduction in any medium, provided the original author 
      and source are credited.
FAU - Ha, Sang Jin
AU  - Ha SJ
AUID- ORCID: 0000-0003-4275-6538
AD  - Division of Cardiology, Department of Internal Medicine, Gangneung Asan Hospital, 
      University of Ulsan College of Medicine, Gangneung, Korea.
FAU - Park, Se-Jun
AU  - Park SJ
AD  - Total Healthcare Center, Kangbuk Samsung Hospital, Sungkyunkwan University School 
      of Medicine, Suwon, Korea.
FAU - Lee, Bora
AU  - Lee B
AD  - Institute of Health & Environment, Seoul National University, Korea.2 Rexsoft 
      Corp., Seoul, Korea.
FAU - Moon, Hyesung
AU  - Moon H
AUID- ORCID: 0000-0003-0898-086X
AD  - Rexsoft Corp., Seoul, Korea.
FAU - Kim, Bo Young
AU  - Kim BY
AUID- ORCID: 0000-0001-9442-3300
AD  - Division of Rheumatology, Department of Internal Medicine, Gangneung Asan 
      Hospital, University of Ulsan College of Medicine, Gangneung, Korea.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230214
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
SB  - IM
MH  - Humans
MH  - *Percutaneous Coronary Intervention/adverse effects
MH  - Cohort Studies
MH  - *Myocardial Infarction/etiology
MH  - *Arthritis, Rheumatoid/etiology
MH  - Republic of Korea/epidemiology
MH  - Treatment Outcome
MH  - Risk Factors
MH  - *Coronary Artery Disease
PMC - PMC9928100
COIS- The authors declare that there are no conflicts of interest related to this 
      manuscript.
EDAT- 2023/02/15 06:00
MHDA- 2023/02/17 06:00
PMCR- 2023/02/14
CRDT- 2023/02/14 13:33
PHST- 2022/10/04 00:00 [received]
PHST- 2023/01/15 00:00 [accepted]
PHST- 2023/02/14 13:33 [entrez]
PHST- 2023/02/15 06:00 [pubmed]
PHST- 2023/02/17 06:00 [medline]
PHST- 2023/02/14 00:00 [pmc-release]
AID - PONE-D-22-27374 [pii]
AID - 10.1371/journal.pone.0281067 [doi]
PST - epublish
SO  - PLoS One. 2023 Feb 14;18(2):e0281067. doi: 10.1371/journal.pone.0281067. 
      eCollection 2023.

PMID- 36776896
OWN - NLM
STAT- MEDLINE
DCOM- 20230214
LR  - 20230307
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 14
DP  - 2023
TI  - A meta-analysis investigating the relationship between inflammation in autoimmune 
      disease, elevated CRP, and the risk of dementia.
PG  - 1087571
LID - 10.3389/fimmu.2023.1087571 [doi]
LID - 1087571
AB  - Alzheimer's Disease (AD) represents the most common type of dementia and is 
      becoming a steadily increasing challenge for health systems globally. 
      Inflammation is developing as the main focus of research into Alzheimer's disease 
      and has been demonstrated to be a major driver of the pathologies associated with 
      AD. This evidence introduces an interesting research question, whether chronic 
      inflammation due to pathologies such as inflammatory bowel disease (IBD) and 
      rheumatoid arthritis (RA) could lead to a higher risk of developing dementia. In 
      both IBD and RA, increased levels of the inflammatory biomarker C-reactive 
      protein (CRP) can be highlighted, the latter being directly implicated in 
      neuroinflammation and AD. In this meta-analysis both the association between 
      chronic inflammatory diseases and elevated levels of CRP during midlife were 
      investigated to examine if they correlated with an augmented risk of dementia. 
      Moreover, the association between increased CRP and modifications in the 
      permeability of the Blood Brain Barrier (BBB) in the presence of CRP is explored. 
      The results displayed that the odds ratio for IBD and dementia was 1.91 
      [1.15-3.15], for RA it was 1.90 [1.09-3.32] following sensitivity analysis and 
      for CRP it was 1.62 [1.22-2.15]. These results demonstrate a higher risk of 
      dementia in patients presenting chronic inflammation and that exists an 
      independent association with high CRP in midlife. This paper builds on published 
      research that suggest a critical role for CRP both in stroke and AD and provides 
      an analysis on currently published research on multiple diseases (IBD and RA) in 
      which CRP is raised as well as chronically elevated. CRP and the associated risk 
      of dementia and further research indicated that the monomeric form of CRP can 
      infiltrate the BBB/be released from damaged micro-vessels to access the brain. 
      This meta-analysis provides first-time evidence that chronic elevation of CRP in 
      autoimmune diseases is directly associated with an increased risk of later 
      development of Alzheimer's disease. Therefore, greater priority should be 
      provided to the effective control of inflammation in patients with chronic 
      inflammatory or autoimmune conditions and further long-term assessment of 
      circulating CRP might inform of an individual's relative risk of developing 
      dementia.
CI  - Copyright © 2023 Cooper, Pastorello and Slevin.
FAU - Cooper, Joseph
AU  - Cooper J
AD  - Department of Life Sciences, Manchester Metropolitan University, Manchester, 
      United Kingdom.
FAU - Pastorello, Ylenia
AU  - Pastorello Y
AD  - George Emil Palade University of Medicine, Pharmacy, Science and Technology, 
      Targu Mures, Romania.
FAU - Slevin, Mark
AU  - Slevin M
AD  - Department of Life Sciences, Manchester Metropolitan University, Manchester, 
      United Kingdom.
AD  - George Emil Palade University of Medicine, Pharmacy, Science and Technology, 
      Targu Mures, Romania.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Review
DEP - 20230127
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Humans
MH  - *Alzheimer Disease
MH  - Inflammation
MH  - *Autoimmune Diseases
MH  - *Arthritis, Rheumatoid
MH  - C-Reactive Protein/metabolism
MH  - *Inflammatory Bowel Diseases
PMC - PMC9912841
OTO - NOTNLM
OT  - C-reactive protein
OT  - autoimmune
OT  - dementia
OT  - inflammatory disease
OT  - meta - analysis
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2023/02/14 06:00
MHDA- 2023/02/15 06:00
PMCR- 2023/01/01
CRDT- 2023/02/13 03:26
PHST- 2022/11/17 00:00 [received]
PHST- 2023/01/16 00:00 [accepted]
PHST- 2023/02/13 03:26 [entrez]
PHST- 2023/02/14 06:00 [pubmed]
PHST- 2023/02/15 06:00 [medline]
PHST- 2023/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2023.1087571 [doi]
PST - epublish
SO  - Front Immunol. 2023 Jan 27;14:1087571. doi: 10.3389/fimmu.2023.1087571. 
      eCollection 2023.

PMID- 36736866
OWN - NLM
STAT- MEDLINE
DCOM- 20230227
LR  - 20230227
IS  - 1879-0038 (Electronic)
IS  - 0378-1119 (Linking)
VI  - 861
DP  - 2023 Apr 20
TI  - A comprehensive meta-analysis comprising 149 case-control studies to investigate 
      the association between IL-6 gene rs1800795 polymorphism and multiple disease 
      risk.
PG  - 147234
LID - S0378-1119(23)00075-6 [pii]
LID - 10.1016/j.gene.2023.147234 [doi]
AB  - BACKGROUND: Individual genome-wide association studies (GWAS) or single 
      case-specific meta-analyses may not be sufficient evidence to take action against 
      a specific gene function. Thus, we tried to determine a consensus association 
      between the IL-6 gene rs1800795 polymorphism and multiple disease risks through 
      an updated statistical meta-analysis. METHOD: After systematically searching 
      online databases, we found 149 case-control relevant datasets with a sample size 
      of 96,153 (cases: 38,291 and controls: 57862) and conducted the meta-analysis 
      using updated statistical models. RESULTS: The analyses of this comprehensive 
      meta-analysis revealed a significant association between IL-6 -174G/C 
      polymorphism and overall disorder risk under all genetic models (C vs G: 
      OR = 1.11, 95% CI = 1.08-1.13; p-value = 4.8E-17; CC vs GG: OR = 1.19, 95% 
      CI = 1.13-1.26; p-value = 9.4E-12; CG vs GG: OR = 1.10, 95% CI = 1.06-1.14; 
      p-value = 1.1E-07; CC + CG vs GG: OR = 1.13, 95% CI = 1.10-1.17; 
      p-value = 1.1E-13; CC vs CG + GG: OR = 1.18, 95% CI = 1.06-1.31; 
      p-value = 0.0019) and (OR > 1) with Asian ethnicity. The subgroup analyses based 
      on the diseases revealed that the polymorphism was highly significantly 
      increasing the risk of coronary artery disease (CAD) under all genetic models. 
      Likewise, a significant association was observed with increased risk under three 
      genetic models of inflammatory diseases (C vs G; CC vs GG; and CC vs CG + GG), 
      and rheumatoid arthritis (C vs G; CG vs GG; and CC + CG vs GG). Conversely, the 
      -174G/C SNP significantly decreased the risk of ischemic stroke under the two 
      genetic models (C vs G; and CG vs GG). However, the other diseases included in 
      this study showed no significant association with IL-6 (-174G/C) polymorphism. 
      CONCLUSION: This meta-analysis provided strong evidence for the association 
      between IL-6 gene rs1800795 polymorphism and multiple disease risks. The IL-6 
      gene could be a useful prognostic biomarker for CAD, inflammatory disease, 
      ischemic stroke, and rheumatoid arthritis.
CI  - Copyright © 2023 Elsevier B.V. All rights reserved.
FAU - Harun-Or-Roshid, Md
AU  - Harun-Or-Roshid M
AD  - Department of Statistics, University of Rajshahi, Rajshahi 6205, Bangladesh. 
      Electronic address: harun.stat.ru@gmail.com.
FAU - Mollah, Md Nurul Haque
AU  - Mollah MNH
AD  - Department of Statistics, University of Rajshahi, Rajshahi 6205, Bangladesh. 
      Electronic address: mollah.stat.bio@ru.ac.bd.
FAU - Jesmin
AU  - Jesmin
AD  - Department of Genetic Engineering & Biotechnology, University of Dhaka, Dhaka 
      1000, Bangladesh. Electronic address: jesmin@du.ac.bd.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
DEP - 20230201
PL  - Netherlands
TA  - Gene
JT  - Gene
JID - 7706761
RN  - 0 (Interleukin-6)
SB  - IM
MH  - Humans
MH  - Genetic Predisposition to Disease
MH  - Interleukin-6/genetics
MH  - Polymorphism, Single Nucleotide
MH  - Genome-Wide Association Study
MH  - *Arthritis, Rheumatoid
MH  - *Ischemic Stroke
MH  - Case-Control Studies
OTO - NOTNLM
OT  - CAD
OT  - Diseases
OT  - IL-6
OT  - Inflammatory disease
OT  - Ischemic stroke
OT  - Meta-analysis
OT  - Rheumatoid arthritis
OT  - SNPs
OT  - rs1800795
COIS- Declaration of Competing Interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/02/04 06:00
MHDA- 2023/03/03 06:00
CRDT- 2023/02/03 19:32
PHST- 2022/09/14 00:00 [received]
PHST- 2022/12/28 00:00 [revised]
PHST- 2023/01/25 00:00 [accepted]
PHST- 2023/02/04 06:00 [pubmed]
PHST- 2023/03/03 06:00 [medline]
PHST- 2023/02/03 19:32 [entrez]
AID - S0378-1119(23)00075-6 [pii]
AID - 10.1016/j.gene.2023.147234 [doi]
PST - ppublish
SO  - Gene. 2023 Apr 20;861:147234. doi: 10.1016/j.gene.2023.147234. Epub 2023 Feb 1.

PMID- 36700719
OWN - NLM
STAT- MEDLINE
DCOM- 20230130
LR  - 20230202
IS  - 2038-1840 (Electronic)
IS  - 0034-1193 (Linking)
VI  - 114
IP  - 2
DP  - 2023 Feb
TI  - [Occurrence of cardiovascular events within a large population of patients 
      affected by rheumatoid arthritis with or without diabetes.].
PG  - 94-109
LID - 10.1701/3966.39449 [doi]
AB  - INTRODUCTION: Rheumatoid arthritis (Ra) and diabetes are often associated with 
      chronic multimorbidity and share the high risk of development of major 
      cardiovascular events (Mace). This study aimed to identify and analyse patients 
      with only Ra, Ra + diabetes, and only diabetes, in terms of comorbidities and new 
      occurrence of Cv events, from the perspective of the Italian national health 
      service (Inhs). METHODS: Starting from the Fondazione ricerca e salute (ReS)'s 
      database, through the record linkage of administrative healthcare data, cohorts 
      with only Ra, Ra + diabetes and only diabetes have been selected, characterized 
      (age and sex), and analysed by comorbidity (depression, dyslipidemia, 
      hypertension, hemorrhagic stroke and ischemic stroke/transient ischemic attack - 
      Tia, coronary artery disease - Cad, heart failure - Hf, chronic liver disease, 
      periphery artery disease - Pad, chronic kidney disease, asthma/chronic 
      obstructive pulmonary disease - Copd, neoplasia) and by new Cv events (Hf, Cad 
      and ischemic stroke/Tia) within two follow-up years (Kaplan-Meier curves). A 
      logistic regression model defined contribution and type of association of some 
      variables on new Cv events. RESULTS: In 2018, from 5.375.531 Inhs beneficiaries 
      in the ReS database, 13.698 (0.25%) were affected by only Ra, 1728 (0.03%) by Ra 
      + diabetes, 347,659 (6.8%) by only diabetes. The only Ra cohort was composed by 
      more females, younger and with less comorbidities patients. Proportions of 79.3%, 
      70.8% and 38.5% of patients with Ra + diabetes, only diabetes and only Ra were 
      affected by 2 to ≥4 comorbidities: among patients with Ra + diabetes, 
      comorbidities showed the highest frequencies, mainly hypertension, dyslipidemia 
      and asthma/Copd. Within two follow-up years, about 8% of patients with diabetes 
      with/without Ra developed a new Cv event (vs 3% with only Ra). The presence of 
      Ra/diabetes or Ra + diabetes, male sex, older age and comorbidities of interest 
      resulted significantly (p<0.01) associated with a higher Cv risk. CONCLUSIONS: 
      Comorbidities and the co-presence of diabetes in patients with Ra determine a 
      complicated framework with high risk of Cv events. It is worthy include more 
      complex patients in clinical trials, in order to generate evidence useful for 
      even more multidisciplinary medical teams.
FAU - Calabria, Silvia
AU  - Calabria S
AD  - Fondazione ricerca e salute (ReS), Roma.
FAU - Ronconi, Giulia
AU  - Ronconi G
AD  - Fondazione ricerca e salute (ReS), Roma.
FAU - Dondi, Letizia
AU  - Dondi L
AD  - Fondazione ricerca e salute (ReS), Roma.
FAU - Piccinni, Carlo
AU  - Piccinni C
AD  - Fondazione ricerca e salute (ReS), Roma.
FAU - Pedrini, Antonella
AU  - Pedrini A
AD  - Fondazione ricerca e salute (ReS), Roma.
FAU - Dondi, Leonardo
AU  - Dondi L
AD  - Fondazione ricerca e salute (ReS), Roma.
FAU - Dell'Anno, Irene
AU  - Dell'Anno I
AD  - Fondazione ricerca e salute (ReS), Roma.
FAU - Esposito, Immacolata
AU  - Esposito I
AD  - Drugs & health, Roma.
FAU - Addesi, Alice
AU  - Addesi A
AD  - Drugs & health, Roma.
FAU - Martini, Nello
AU  - Martini N
AD  - Fondazione ricerca e salute (ReS), Roma.
FAU - Maggioni, Aldo Pietro
AU  - Maggioni AP
AD  - Fondazione ricerca e salute (ReS), Roma - Anmco Research Center Heart Care 
      Foundation, Firenze.
LA  - ita
PT  - English Abstract
PT  - Journal Article
TT  - Sviluppo di eventi cardiovascolari in un’ampia popolazione di pazienti affetti da 
      artrite reumatoide con o senza diabete.
PL  - Italy
TA  - Recenti Prog Med
JT  - Recenti progressi in medicina
JID - 0401271
SB  - IM
MH  - Female
MH  - Humans
MH  - Male
MH  - Risk Factors
MH  - *Ischemic Attack, Transient/complications/epidemiology
MH  - State Medicine
MH  - *Cardiovascular Diseases/epidemiology/etiology
MH  - *Arthritis, Rheumatoid/complications/epidemiology/drug therapy
MH  - Comorbidity
MH  - *Diabetes Mellitus/epidemiology
MH  - *Dyslipidemias/complications/epidemiology
MH  - *Pulmonary Disease, Chronic Obstructive/epidemiology
MH  - *Hypertension
MH  - *Ischemic Stroke/complications/epidemiology
MH  - *Asthma/epidemiology
EDAT- 2023/01/27 06:00
MHDA- 2023/01/31 06:00
CRDT- 2023/01/26 09:23
PHST- 2023/01/26 09:23 [entrez]
PHST- 2023/01/27 06:00 [pubmed]
PHST- 2023/01/31 06:00 [medline]
AID - 10.1701/3966.39449 [doi]
PST - ppublish
SO  - Recenti Prog Med. 2023 Feb;114(2):94-109. doi: 10.1701/3966.39449.

PMID- 36632250
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240910
IS  - 2168-8184 (Print)
IS  - 2168-8184 (Electronic)
IS  - 2168-8184 (Linking)
VI  - 14
IP  - 12
DP  - 2022 Dec
TI  - Increased Risk of Cardiovascular Diseases in Rheumatoid Arthritis: A Systematic 
      Review.
PG  - e32308
LID - 10.7759/cureus.32308 [doi]
LID - e32308
AB  - Rheumatoid arthritis (RA) is an autoimmune condition in which the body's 
      joints are attacked by the immune system, leaving the patient disabled in severe 
      cases, with irreversible joint damage and a lower quality of life. RA patients 
      are more likely to develop cardiovascular (CV) disease, which increases their 
      risk of morbidity and mortality. This study systematically reviews various CV 
      diseases that might occur with RA including heart failure (HF), coronary artery 
      disease, acute coronary syndrome, ischemic heart disease, stroke, cardiac death, 
      venous thromboembolism, and valvular diseases. The relation between these 
      complications and RA is specifically assessed. Systematic search was carried out 
      on literature reporting the risk of each of the CV diseases in RA patients from 
      databases in accordance with Preferred Reporting Items for Systematic Reviews and 
      Meta-Analyses (PRISMA) guidelines. The databases searched were MEDLINE (through 
      PubMed) and Google Scholar using a combination of keywords and medical subject 
      headings (MeSH). Our keywords were mainly "cardiovascular diseases" and 
      "arthritis and rheumatoid". We found a total of 33 articles reporting each CV 
      comorbidity. Interestingly, a wide spectrum of CV diseases is reported in 
      patients with RA. Many tools were implemented in the diagnosis of each disease 
      such as carotid intima-media thickness for atherosclerosis and echocardiography 
      for HF. We confirmed that RA is associated with an increased risk of different CV 
      events, and prophylactic measures should be implemented.
CI  - Copyright © 2022, Farhat et al.
FAU - Farhat, Hadi
AU  - Farhat H
AD  - Cardiology and Rheumatology, University of Balamand, Beirut, LBN.
AD  - Research, California Institute of Behavioral Neurosciences & Psychology, 
      Fairfield, USA.
FAU - Irfan, Huma
AU  - Irfan H
AD  - Research, Larkin Community Hospital, South Miami, USA.
AD  - Research, California Institute of Behavioral Neurosciences & Psychology, 
      Fairfield, USA.
FAU - Muthiah, Kanmani
AU  - Muthiah K
AD  - Neurology, California Institute of Behavioral Neurosciences & Psychology, 
      Fairfield, USA.
FAU - Pallipamu, Namratha
AU  - Pallipamu N
AD  - Internal Medicine, Franciscan Health, Lafayette, USA.
AD  - Internal Medicine, California Institute of Behavioral Neurosciences & Psychology, 
      Fairfield, USA.
FAU - Taheri, Sogand
AU  - Taheri S
AD  - Medical Science, California Institute of Behavioral Neurosciences & Psychology, 
      Fairfield, USA.
FAU - Thiagaraj, Suvedha S
AU  - Thiagaraj SS
AD  - Internal Medicine, California Institute of Behavioral Neurosciences & Psychology, 
      Fairfield, USA.
FAU - Shukla, Twisha S
AU  - Shukla TS
AD  - Pediatrics, California Institute of Behavioral Neurosciences & Psychology, 
      Fairfield, USA.
FAU - Gutlapalli, Sai Dheeraj
AU  - Gutlapalli SD
AD  - Internal Medicine, California Institute of Behavioral Neurosciences & Psychology, 
      Fairfield, USA.
FAU - Giva, Sheiniz
AU  - Giva S
AD  - Neonatology, Children's Health Ireland at Temple Street, Dublin, IRL.
AD  - Research, California Institute of Behavioral Neurosciences & Psychology, 
      Fairfield, USA.
FAU - Penumetcha, Sai Sri
AU  - Penumetcha SS
AD  - General Medicine, California Institute of Behavioral Neurosciences & Psychology, 
      Fairfield, USA.
AD  - General Medicine, Chalmeda Anand Rao Institute of Medical Sciences, Karimnagar, 
      IND.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20221208
PL  - United States
TA  - Cureus
JT  - Cureus
JID - 101596737
PMC - PMC9827945
OTO - NOTNLM
OT  - aortic stenosis
OT  - atherosclerosis
OT  - cardiac death
OT  - cardiovascular disease
OT  - heart failure
OT  - ischemic heart disease
OT  - myocardial infarction
OT  - rheumatoid arthriitis
OT  - stroke
OT  - venous thromboembolism
COIS- The authors have declared that no competing interests exist.
EDAT- 2023/01/13 06:00
MHDA- 2023/01/13 06:01
PMCR- 2022/12/08
CRDT- 2023/01/12 01:57
PHST- 2022/09/29 00:00 [received]
PHST- 2022/12/08 00:00 [accepted]
PHST- 2023/01/12 01:57 [entrez]
PHST- 2023/01/13 06:00 [pubmed]
PHST- 2023/01/13 06:01 [medline]
PHST- 2022/12/08 00:00 [pmc-release]
AID - 10.7759/cureus.32308 [doi]
PST - epublish
SO  - Cureus. 2022 Dec 8;14(12):e32308. doi: 10.7759/cureus.32308. eCollection 2022 
      Dec.

PMID- 36622121
OWN - NLM
STAT- MEDLINE
DCOM- 20230714
LR  - 20230718
IS  - 0392-856X (Print)
IS  - 0392-856X (Linking)
VI  - 41
IP  - 7
DP  - 2023 Jul
TI  - Prevalence and clinical significance of electrocardiographic signs of atrial 
      myopathy in rheumatoid arthritis: results from the EDRA study.
PG  - 1427-1433
LID - 10.55563/clinexprheumatol/d9l4lt [doi]
AB  - OBJECTIVES: We sought to determine whether the increased risk of atrial 
      fibrillation and stroke in rheumatoid arthritis (RA) can be accounted for by an 
      increased prevalence of electrocardiographic markers of atrial myopathy. METHODS: 
      We retrospectively evaluated clinical and electrocardiographic data of 218 RA 
      patients prospectively enrolled in the Endothelial Dysfunction Evaluation for 
      Coronary Heart Disease Risk Estimation in Rheumatoid Arthritis study (EDRA study 
      ClinicalTrials.gov: NCT02341066) and 109 controls matched by age and gender. The 
      prevalence of interatrial blocks (IAB, partial - pIAB or advanced - aIAB), 
      abnormal P-wave terminal force in lead V1 (aPtfV1) and atrial myopathy 
      (electrocardiographically defined as the presence of 1) aIAB, or 2) pIAB plus 
      abnormal aPtfV1) was assessed in each group. RA patients were followed-up for 5 
      years for incident atrial fibrillation and cardiovascular events. RESULTS: 
      Barring the prevalence of hyperlipidaemia and obesity, the demographic 
      characteristics and cardiovascular risk profile of RA patients and controls were 
      comparable. All subjects enrolled in the study were free from previous 
      cardiovascular disease and atrial fibrillation. Compared to controls, RA patients 
      had longer P-wave duration (118±12 vs. 112±10 ms, p<0.001) and higher prevalence 
      of pIAB (43% vs. 21%, p<0.001) and abnormal PtfV1 (27% vs. 10%, p<0.001). 
      Accordingly, atrial myopathy was significantly more prevalent (15% vs 4%, 
      p=0.003) in RA patients. In multiple regression, male gender (OR [95% CI] = 3.09 
      [1.48-6.47], p=0.003) and RA (OR [95% CI] = 4.83 [1.58-14.73], p=0.006) were 
      independently associated with atrial myopathy. Atrial myopathy was not 
      significantly associated with incident atrial fibrillation or cardiovascular 
      events in RA patients after 5 years of follow-up. CONCLUSIONS: 
      Electrocardiographic markers of atrial myopathy are independently associated with 
      RA. Further studies with larger sample size and longer follow-up are needed to 
      determine whether the increased prevalence of atrial myopathy contributes to the 
      increased risk of atrial fibrillation and stroke in this group.
FAU - Sanna, Giuseppe D
AU  - Sanna GD
AD  - Clinical and Interventional Cardiology, Sassari University Hospital, Sassari, 
      Italy.
FAU - Piga, Matteo
AU  - Piga M
AD  - Rheumatology Unit, University Clinic AOU Cagliari, Monserrato, and Department of 
      Medical Sciences and Public Health, University of Cagliari, Italy.
FAU - Piga, Anna
AU  - Piga A
AD  - Dipartimento di Medicina, Chirurgia e Farmacia, University of Sassari, Italy.
FAU - Falco, Olga
AU  - Falco O
AD  - Dipartimento di Medicina, Chirurgia e Farmacia, University of Sassari, Italy.
FAU - Ponti, Enrico
AU  - Ponti E
AD  - Dipartimento di Medicina, Chirurgia e Farmacia, University of Sassari, Italy.
FAU - Cauli, Alberto
AU  - Cauli A
AD  - Rheumatology Unit, University Clinic AOU Cagliari, Monserrato, and Department of 
      Medical Sciences and Public Health, University of Cagliari, Italy.
FAU - Floris, Alberto
AU  - Floris A
AD  - Rheumatology Unit, University Clinic AOU Cagliari, Monserrato, and Department of 
      Medical Sciences and Public Health, University of Cagliari, Italy.
FAU - Mangoni, Arduino A
AU  - Mangoni AA
AD  - Department of Clinical Pharmacology, Flinders University and Flinders Medical 
      Centre, Adelaide, Australia.
FAU - Casu, Gavino
AU  - Casu G
AD  - Clinical and Interventional Cardiology, Sassari University Hospital, Sassari, 
      Italy.
FAU - De Luca, Giuseppe
AU  - De Luca G
AD  - Dipartimento di Medicina, Chirurgia e Farmacia, University of Sassari, and 
      Clinica Cardiologica e Sperimentale, AOU Sassari, Italy.
FAU - Erre, Gian Luca
AU  - Erre GL
AD  - UOC di Reumatologia, Dipartimento di Medicina, Chirurgia e Farmacia, University 
      of Sassari, Italy. glerre@uniss.it.
CN  - EDRA Study Group
LA  - eng
SI  - ClinicalTrials.gov/NCT02341066
PT  - Clinical Study
PT  - Journal Article
DEP - 20230102
PL  - Italy
TA  - Clin Exp Rheumatol
JT  - Clinical and experimental rheumatology
JID - 8308521
SB  - IM
MH  - Humans
MH  - Male
MH  - *Arthritis, Rheumatoid/complications/diagnosis/epidemiology
MH  - *Atrial Fibrillation/diagnosis/epidemiology
MH  - Clinical Relevance
MH  - Electrocardiography
MH  - *Muscular Diseases
MH  - Prevalence
MH  - Retrospective Studies
MH  - Risk Factors
MH  - *Stroke/diagnosis
MH  - Female
FIR - Cadoni, Maria Luisa
IR  - Cadoni ML
FIR - Cangemi, Ignazio
IR  - Cangemi I
FIR - Dessì, Martina
IR  - Dessì M
FIR - Fedele, Anna Laura
IR  - Fedele AL
FIR - Ferraccioli, Gianfranco
IR  - Ferraccioli G
FIR - Gremese, Elisa
IR  - Gremese E
FIR - Mundula, Nicola
IR  - Mundula N
FIR - Piras, Marco
IR  - Piras M
EDAT- 2023/01/10 06:00
MHDA- 2023/07/14 13:06
CRDT- 2023/01/09 08:53
PHST- 2022/07/09 00:00 [received]
PHST- 2022/10/05 00:00 [accepted]
PHST- 2023/07/14 13:06 [medline]
PHST- 2023/01/10 06:00 [pubmed]
PHST- 2023/01/09 08:53 [entrez]
AID - 18970 [pii]
AID - 10.55563/clinexprheumatol/d9l4lt [doi]
PST - ppublish
SO  - Clin Exp Rheumatol. 2023 Jul;41(7):1427-1433. doi: 
      10.55563/clinexprheumatol/d9l4lt. Epub 2023 Jan 2.

PMID- 36514090
OWN - NLM
STAT- MEDLINE
DCOM- 20221215
LR  - 20221222
IS  - 1471-2458 (Electronic)
IS  - 1471-2458 (Linking)
VI  - 22
IP  - 1
DP  - 2022 Dec 13
TI  - Influencing factors of weak grip strength and fall: a study based on the China 
      Health and Retirement Longitudinal Study (CHARLS).
PG  - 2337
LID - 10.1186/s12889-022-14753-x [doi]
LID - 2337
AB  - BACKGROUND: Fall is a major cause of mortality and cause a significant burden on 
      the healthcare system and economic system. Weak grip strength signifies impaired 
      function. Older people with weak grip strength are at a higher risk of death. 
      China has the largest ageing population in the world today. This study aims to 
      analyze the factors contributing to weak grip strength and fall among Chinese. 
      METHODS: This study analyzed data from the 2011 baseline and 2015 follow-up 
      survey of the China Health and Retirement Longitudinal Study (CHARLS). To 
      identify the risk factors of fall and weak grip strength, we used a stepwise 
      multivariable logistic regression model and a least absolute shrinkage and 
      selection operator (LASSO) regression model. RESULTS: In the LASSO regression 
      model, all the risk factors were not shrunken. In the stepwise logistic 
      regression model, adjusted for gender, age, grip strength, depression, and 
      chronic disease, we found that female (aOR = 1.376, 95% CI = 1.243-1.523; 
      P < 0.001), history of ischemic stroke (aOR = 1.786, 95% CI = 1.263-2.524; 
      P = 0.001), depression (aOR = 1.559, 95% CI = 1.396-1.742; P < 0.001), weak grip 
      strength (aOR = 1.285, 95% CI = 1.105-1.494; P = 0.001), older age (aOR = 1.227, 
      95% CI = 1.163-1.294; P < 0.001), rheumatoid arthritis (aOR = 1.410, 95% 
      CI = 1.270-1.560; P < 0.001), history of kidney disease (aOR = 1.383, 95% 
      CI = 1.136-1.682; P = 0.001) were factors associated with fall significantly. 
      After further adjusting, we found the risk factors of weak grip strength included 
      symptomatic knee osteoarthritis (aOR = 1.755, 95% CI 1.158-2.661; P = 0.008), 
      living in rural area (aOR = 2.056, 95% CI 1.290-3.277; P = 0.002), depression 
      (aOR = 1.523, 95% CI 1.116-2.078; P = 0.008), older age (aOR = 2.116, 95% CI 
      1.801-2.486; P < 0.001). CONCLUSION: From the study, we found that older age and 
      depression were risk factors of weak grip strength and fall. Weak grip strength 
      was a risk factor of fall. Female, ischemic stroke, kidney disease, rheumatoid 
      arthritis were risk factors of fall; living in rural area and symptomatic knee 
      osteoarthritis were risk factors of weak grip strength.
CI  - © 2022. The Author(s).
FAU - Liu, Hao
AU  - Liu H
AD  - Arthritis Clinic & Research Center, Peking University People's Hospital, Peking 
      University, 100044, Beijing, China.
FAU - Hou, Yunfei
AU  - Hou Y
AD  - Arthritis Clinic & Research Center, Peking University People's Hospital, Peking 
      University, 100044, Beijing, China.
FAU - Li, Hu
AU  - Li H
AD  - Arthritis Clinic & Research Center, Peking University People's Hospital, Peking 
      University, 100044, Beijing, China. chinalihu@sina.com.
FAU - Lin, Jianhao
AU  - Lin J
AD  - Arthritis Clinic & Research Center, Peking University People's Hospital, Peking 
      University, 100044, Beijing, China. linjianhao@pkuph.edu.cn.
LA  - eng
GR  - RDH2021-09/Peking University People's Hospital Scientific Research Development 
      Funds/
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20221213
PL  - England
TA  - BMC Public Health
JT  - BMC public health
JID - 100968562
SB  - IM
MH  - Humans
MH  - Female
MH  - Aged
MH  - Retirement
MH  - Longitudinal Studies
MH  - *Osteoarthritis, Knee
MH  - Hand Strength
MH  - China/epidemiology
MH  - Muscle Weakness
MH  - *Ischemic Stroke
MH  - *Arthritis, Rheumatoid
PMC - PMC9749312
OTO - NOTNLM
OT  - China Health and Retirement Longitudinal Study (CHARLS)
OT  - Fall
OT  - Risk factors
OT  - Weak grip strength
COIS- The corresponding authors and co-authors declare that there are no conflicts of 
      interest to disclose concerning the publication of this article.
EDAT- 2022/12/14 06:00
MHDA- 2022/12/16 06:00
PMCR- 2022/12/13
CRDT- 2022/12/13 23:53
PHST- 2022/05/09 00:00 [received]
PHST- 2022/11/28 00:00 [accepted]
PHST- 2022/12/13 23:53 [entrez]
PHST- 2022/12/14 06:00 [pubmed]
PHST- 2022/12/16 06:00 [medline]
PHST- 2022/12/13 00:00 [pmc-release]
AID - 10.1186/s12889-022-14753-x [pii]
AID - 14753 [pii]
AID - 10.1186/s12889-022-14753-x [doi]
PST - epublish
SO  - BMC Public Health. 2022 Dec 13;22(1):2337. doi: 10.1186/s12889-022-14753-x.

PMID- 36431290
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20221213
IS  - 2077-0383 (Print)
IS  - 2077-0383 (Electronic)
IS  - 2077-0383 (Linking)
VI  - 11
IP  - 22
DP  - 2022 Nov 17
TI  - Associations between Cardiovascular Outcomes and Rheumatoid Arthritis: A 
      Nationwide Population-Based Cohort Study.
LID - 10.3390/jcm11226812 [doi]
LID - 6812
AB  - Despite a growing burden posed by cardiovascular disease (CVD) in rheumatoid 
      arthritis (RA) patients, large-scale studies on the association between the 
      characteristics of RA patients and CVD risks and studies adjusted for various 
      confounding factors are lacking. In this large-scale nationwide cohort study, we 
      aimed to investigate the association between CVD risk and RA and factors that may 
      increase CVD risk using a dataset provided by the Korean National Health 
      Insurance Service (NHIS). We enrolled 136,469 patients with RA who participated 
      in national health examinations within two years of RA diagnosis between 2010 and 
      2017 and non-RA controls matched by age and sex (n = 682,345). The outcome was 
      the occurrence of myocardial infarction (MI) or stroke. MI was defined as one 
      hospitalization or two outpatient visits with ICD-10-CM codes I21 or I22. Stroke 
      was defined as one hospitalization with ICD-10-CM codes I63 or I64 and a claim 
      for brain imaging (CT or MRI). The Cox proportional hazard model and Kaplan-Meier 
      curve were used for analysis. The mean follow-up duration was 4.7 years, and the 
      incidence rate of CVD was higher in the RA group than the control group (MI: 3.20 
      vs. 2.08; stroke: 2.84 vs. 2.33 per 1000 person-years). The risk of MI and stroke 
      was about 50% and 20% higher, respectively, in RA patients. The association 
      between RA and CVD was prominent in females after adjusting for confounding 
      variables. The association between RA and risk of MI was significant in 
      individuals without DM. Therefore, appropriate screening for CVD is important in 
      all RA patients including females and younger patients.
FAU - Kang, Seonyoung
AU  - Kang S
AD  - Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of 
      Medicine, Seoul 06351, Republic of Korea.
FAU - Han, Kyungdo
AU  - Han K
AD  - Department of Statistics and Actuarial Science, Soongsil University, Seoul 06978, 
      Republic of Korea.
FAU - Jung, Jin-Hyung
AU  - Jung JH
AUID- ORCID: 0000-0002-8920-8777
AD  - Department of Medical Statistics, College of Medicine, Catholic University of 
      Korea, Seoul 06591, Republic of Korea.
FAU - Eun, Yeonghee
AU  - Eun Y
AD  - Division of Rheumatology, Department of Internal Medicine, Kangbuk Samsung 
      Hospital, Sungkyunkwan University School of Medicine, Seoul 03181, Republic of 
      Korea.
FAU - Kim, In Young
AU  - Kim IY
AD  - Department of Medicine, National Police Hospital, Seoul 05715, Republic of Korea.
FAU - Hwang, Jiwon
AU  - Hwang J
AD  - Division of Rheumatology, Department of Internal Medicine, Sungkyunkwan 
      University Samsung Changwon Hospital, Changwon 51353, Republic of Korea.
FAU - Koh, Eun-Mi
AU  - Koh EM
AD  - Korean Health Insurance Review and Assessment Service, Seoul 06653, Republic of 
      Korea.
FAU - Lee, Seulkee
AU  - Lee S
AUID- ORCID: 0000-0002-5551-4178
AD  - Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of 
      Medicine, Seoul 06351, Republic of Korea.
FAU - Cha, Hoon-Suk
AU  - Cha HS
AD  - Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of 
      Medicine, Seoul 06351, Republic of Korea.
FAU - Kim, Hyungjin
AU  - Kim H
AD  - Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of 
      Medicine, Seoul 06351, Republic of Korea.
AD  - Department of Medical Humanities, Samsung Medical Center, Sungkyunkwan University 
      School of Medicine, Seoul 06351, Republic of Korea.
FAU - Lee, Jaejoon
AU  - Lee J
AD  - Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of 
      Medicine, Seoul 06351, Republic of Korea.
LA  - eng
PT  - Journal Article
DEP - 20221117
PL  - Switzerland
TA  - J Clin Med
JT  - Journal of clinical medicine
JID - 101606588
PMC - PMC9695475
OTO - NOTNLM
OT  - cardiovascular disease
OT  - rheumatoid arthritis
COIS- The authors declare no conflict interest.
EDAT- 2022/11/27 06:00
MHDA- 2022/11/27 06:01
PMCR- 2022/11/17
CRDT- 2022/11/26 01:22
PHST- 2022/10/15 00:00 [received]
PHST- 2022/11/10 00:00 [revised]
PHST- 2022/11/12 00:00 [accepted]
PHST- 2022/11/26 01:22 [entrez]
PHST- 2022/11/27 06:00 [pubmed]
PHST- 2022/11/27 06:01 [medline]
PHST- 2022/11/17 00:00 [pmc-release]
AID - jcm11226812 [pii]
AID - jcm-11-06812 [pii]
AID - 10.3390/jcm11226812 [doi]
PST - epublish
SO  - J Clin Med. 2022 Nov 17;11(22):6812. doi: 10.3390/jcm11226812.

PMID- 36411486
OWN - NLM
STAT- MEDLINE
DCOM- 20221123
LR  - 20221213
IS  - 2047-783X (Electronic)
IS  - 0949-2321 (Print)
IS  - 0949-2321 (Linking)
VI  - 27
IP  - 1
DP  - 2022 Nov 21
TI  - Prevalence and influence of hypouricemia on cardiovascular diseases in patients 
      with rheumatoid arthritis.
PG  - 260
LID - 10.1186/s40001-022-00888-5 [doi]
LID - 260
AB  - BACKGROUND: Serum uric acid (SUA) acts as an antioxidant and abnormally low SUA 
      may raise the risk of developing atherosclerotic disorders. There is a U-shaped 
      association between SUA with cardiovascular diseases (CVDs) in general 
      population. However, the prevalence of hypouricemia and its influence on CVDs in 
      rheumatoid arthritis (RA) remains unclear. METHODS: This cross-sectional study 
      collected clinical data from a Chinese RA cohort. Hypouricemia was defined as 
      SUA ≤ 3.0 mg/dL, and hyperuricemia was defined as SUA ≥ 7.0 mg/dL. CVDs were 
      defined as a history of angina pectoris, myocardial infarction, heart failure, 
      stroke and peripheral arterial disease. Restricted cubic spline regression and 
      logistic regression analysis were conducted to evaluate the associations between 
      SUA levels and CVDs. RESULTS: Among 1130 RA patients recruited, the mean age was 
      53.2 years and 79.0% were female. The prevalence of hypouricemia and 
      hyperuricemia were 10.6% and 12.0%, respectively. RA patients with hyperuricemia 
      had a higher rate of CVDs than normouricemic patients (27.9% vs. 7.1%, P < 0.05). 
      Surprisingly, RA patients with hypouricemia also had a higher rate of CVDs (20.7% 
      vs. 7.1%, P < 0.05) even without higher traditional cardiovascular risk factors. 
      A U-shaped association between SUA levels and total CVDs was found 
      (P(non-linear) < 0.001). Multivariate logistic regression analysis revealed that 
      compared with normouricemia, both hypouricemia [adjusted OR (AOR) = 4.707, 95% CI 
      2.570-8.620] and hyperuricemia (AOR = 3.707, 95% CI 2.174-6.321) were associated 
      with higher risk of CVDs. CONCLUSIONS: Hypouricemia may be a potential risk 
      factor of CVDs in RA patients.
CI  - © 2022. The Author(s).
FAU - Zou, Yao-Wei
AU  - Zou YW
AD  - Department of Rheumatology, Sun Yat-sen Memorial Hospital, Sun Yat-sen 
      University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's 
      Republic of China.
FAU - Li, Qian-Hua
AU  - Li QH
AD  - Department of Rheumatology, Sun Yat-sen Memorial Hospital, Sun Yat-sen 
      University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's 
      Republic of China.
FAU - Zhu, Ying-Ying
AU  - Zhu YY
AD  - Division of Clinical Research Design, Sun Yat-sen Memorial Hospital, Sun Yat-sen 
      University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's 
      Republic of China.
FAU - Pan, Jie
AU  - Pan J
AD  - Department of Rheumatology, Sun Yat-sen Memorial Hospital, Sun Yat-sen 
      University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's 
      Republic of China.
FAU - Gao, Jing-Wei
AU  - Gao JW
AD  - Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 
      107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's Republic of 
      China.
FAU - Lin, Jian-Zi
AU  - Lin JZ
AD  - Department of Rheumatology, Sun Yat-sen Memorial Hospital, Sun Yat-sen 
      University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's 
      Republic of China.
FAU - Wu, Tao
AU  - Wu T
AD  - Department of Rheumatology, Sun Yat-sen Memorial Hospital, Sun Yat-sen 
      University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's 
      Republic of China.
FAU - Zhang, Qian
AU  - Zhang Q
AD  - Department of Rheumatology, Sun Yat-sen Memorial Hospital, Sun Yat-sen 
      University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's 
      Republic of China.
FAU - Zheng, Hu-Wei
AU  - Zheng HW
AD  - Department of Rheumatology, Sun Yat-sen Memorial Hospital, Sun Yat-sen 
      University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's 
      Republic of China.
FAU - Mo, Ying-Qian
AU  - Mo YQ
AD  - Department of Rheumatology, Sun Yat-sen Memorial Hospital, Sun Yat-sen 
      University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's 
      Republic of China.
FAU - Ma, Jian-Da
AU  - Ma JD
AD  - Department of Rheumatology, Sun Yat-sen Memorial Hospital, Sun Yat-sen 
      University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's 
      Republic of China. majd@mail.sysu.edu.cn.
FAU - Dai, Lie
AU  - Dai L
AD  - Department of Rheumatology, Sun Yat-sen Memorial Hospital, Sun Yat-sen 
      University, 107 Yan Jiang West Road, Guangzhou, 510120, Guangdong, People's 
      Republic of China. dailie@mail.sysu.edu.cn.
LA  - eng
GR  - 82101892/National Natural Science Foundation of China/
GR  - 82171780/National Natural Science Foundation of China/
GR  - 2020A1515110061/Basic and Applied Basic Research Foundation of Guangdong 
      Province/
GR  - 2022A1515010524/Basic and Applied Basic Research Foundation of Guangdong 
      Province/
GR  - A2021065/Guangdong Medical Research Foundation/
GR  - 202102010188/Guangzhou Municipal Science and Technology Project/
GR  - 22qntd3303/Fundamental Research Funds for the Central Universities, Sun Yat-sen 
      University/
PT  - Journal Article
DEP - 20221121
PL  - England
TA  - Eur J Med Res
JT  - European journal of medical research
JID - 9517857
RN  - 268B43MJ25 (Uric Acid)
SB  - IM
MH  - Humans
MH  - Female
MH  - Middle Aged
MH  - Male
MH  - *Hyperuricemia/complications/epidemiology
MH  - *Cardiovascular Diseases/complications/epidemiology
MH  - Prevalence
MH  - Uric Acid
MH  - Cross-Sectional Studies
MH  - *Arthritis, Rheumatoid/complications/epidemiology
PMC - PMC9677667
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - Hypouricemia
OT  - Rheumatoid arthritis
OT  - Serum uric acid
OT  - U-shaped curve
COIS- The authors declare that they have no competing interests.
EDAT- 2022/11/22 06:00
MHDA- 2022/11/24 06:00
PMCR- 2022/11/21
CRDT- 2022/11/21 23:43
PHST- 2022/10/19 00:00 [received]
PHST- 2022/11/06 00:00 [accepted]
PHST- 2022/11/21 23:43 [entrez]
PHST- 2022/11/22 06:00 [pubmed]
PHST- 2022/11/24 06:00 [medline]
PHST- 2022/11/21 00:00 [pmc-release]
AID - 10.1186/s40001-022-00888-5 [pii]
AID - 888 [pii]
AID - 10.1186/s40001-022-00888-5 [doi]
PST - epublish
SO  - Eur J Med Res. 2022 Nov 21;27(1):260. doi: 10.1186/s40001-022-00888-5.

PMID- 36382679
OWN - NLM
STAT- MEDLINE
DCOM- 20230323
LR  - 20230324
IS  - 1742-481X (Electronic)
IS  - 1742-4801 (Print)
IS  - 1742-4801 (Linking)
VI  - 20
IP  - 4
DP  - 2023 Apr
TI  - Risk factors for venous thromboembolism following surgical treatment of 
      fractures: A systematic review and meta-analysis.
PG  - 995-1007
LID - 10.1111/iwj.13949 [doi]
AB  - This study aimed to determine the risk factors for postoperative venous 
      thromboembolism (VTE) in patients treated surgically for fractures using a 
      meta-analytic approach. Electronic searches were performed in PubMed, Embase, and 
      the Cochrane library from inception until February 2022. The odds ratio (OR) and 
      95% confidence interval (CI) were applied to calculate the pooled effect estimate 
      using the random-effects model. Sensitivity, subgroup, and publication bias tests 
      were also performed. Forty-four studies involving 3 239 291 patients and 
      reporting 11 768 VTE cases were selected for the meta-analysis. We found that 
      elderly (OR: 1.72; 95% CI: 1.38-2.15; P < .001), American Society of 
      Anesthesiologists (ASA) ≥ 3 (OR: 1.82; 95% CI: 1.46-2.29; P < .001), blood 
      transfusion (OR: 1.82; 95% CI: 1.14-2.92; P = .013), cardiovascular disease (CVD) 
      (OR: 1.40; 95% CI: 1.22-1.61; P < .001), elevated D-dimer (OR: 4.55; 95% CI: 
      2.08-9.98; P < .001), diabetes mellitus (DM) (OR: 1.36; 95% CI: 1.19-1.54; 
      P < .001), hypertension (OR: 1.31; 95% CI: 1.09-1.56; P = .003), immobility (OR: 
      3.45; 95% CI: 2.23-5.32; P < .001), lung disease (LD) (OR: 2.40; 95% CI: 
      1.29-4.47; P = .006), obesity (OR: 1.52; 95% CI: 1.27-1.82; P < .001), peripheral 
      artery disease (PAD) (OR: 2.13; 95% CI: 1.21-3.73; P = .008), prior 
      thromboembolic event (PTE) (OR: 5.17; 95% CI: 3.14-8.50; P < .001), and steroid 
      use (OR: 2.37; 95% CI: 1.73-3.24; P < .001) were associated with an increased 
      risk of VTE. Additionally, regional anaesthesia (OR: 0.66; 95% CI: 0.45-0.96; 
      P = .029) was associated with a reduced risk of VTE following surgical treatment 
      of fractures. However, alcohol intake, cancer, current smoking, deep surgical 
      site infection, fusion surgery, heart failure, hypercholesterolemia, liver and 
      kidney disease, sex, open fracture, operative time, preoperative anticoagulant 
      use, rheumatoid arthritis, and stroke were not associated with the risk of VTE. 
      Post-surgical risk factors for VTE include elderly, ASA ≥ 3, blood transfusion, 
      CVD, elevated D-dimer, DM, hypertension, immobility, LD, obesity, PAD, PTE, and 
      steroid use.
CI  - © 2022 The Authors. International Wound Journal published by Medicalhelplines.com 
      Inc (3M) and John Wiley & Sons Ltd.
FAU - Xia, Zhen-Hua
AU  - Xia ZH
AD  - Department of Surgery, Shanghai Shidong Hospital, Shanghai, China.
FAU - Chen, Wei-Hua
AU  - Chen WH
AD  - Department of Surgery, Shanghai Shidong Hospital, Shanghai, China.
FAU - Wang, Qun
AU  - Wang Q
AD  - Department of Surgery, Shanghai Shidong Hospital, Shanghai, China.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Systematic Review
DEP - 20221116
PL  - England
TA  - Int Wound J
JT  - International wound journal
JID - 101230907
RN  - 0 (Steroids)
SB  - IM
MH  - Humans
MH  - Aged
MH  - *Venous Thromboembolism/epidemiology/etiology
MH  - Risk Factors
MH  - *Fractures, Bone
MH  - *Diabetes Mellitus
MH  - Obesity/complications
MH  - *Hypertension
MH  - Steroids
PMC - PMC10030940
OTO - NOTNLM
OT  - fracture
OT  - meta-analysis
OT  - risk factors
OT  - surgical treatments
OT  - venous thromboembolism
COIS- The authors declare that they have no competing interests.
EDAT- 2022/11/17 06:00
MHDA- 2023/03/24 06:00
PMCR- 2022/11/16
CRDT- 2022/11/16 06:03
PHST- 2022/06/21 00:00 [received]
PHST- 2022/08/18 00:00 [accepted]
PHST- 2022/11/17 06:00 [pubmed]
PHST- 2023/03/24 06:00 [medline]
PHST- 2022/11/16 06:03 [entrez]
PHST- 2022/11/16 00:00 [pmc-release]
AID - IWJ13949 [pii]
AID - 10.1111/iwj.13949 [doi]
PST - ppublish
SO  - Int Wound J. 2023 Apr;20(4):995-1007. doi: 10.1111/iwj.13949. Epub 2022 Nov 16.

PMID- 36380120
OWN - NLM
STAT- MEDLINE
DCOM- 20230301
LR  - 20240913
IS  - 1438-7573 (Electronic)
IS  - 1525-3961 (Print)
IS  - 1438-7573 (Linking)
VI  - 24
IP  - 1
DP  - 2023 Feb
TI  - Low Evidence for Tinnitus Risk Factors: A Systematic Review and Meta-analysis.
PG  - 81-94
LID - 10.1007/s10162-022-00874-y [doi]
AB  - AIMS/HYPOTHESIS: Identifying risk factors for tinnitus could facilitate not only 
      the recommendations for prevention measures, but also identifying potential 
      pathways for new interventions. This study reports the first comprehensive 
      systematic review of analytical observational studies able to provide information 
      about causality (i.e., case-control and cohort designs). METHODS: A literature 
      search of four electronic databases identified epidemiological studies published 
      on tinnitus and different exposures. Independent raters screened all studies, 
      extracted data, and evaluated study quality using the Newcastle-Ottawa Scale. 
      Reported relative risks (RR), hazard ratios (HR), odds ratios (OR), and 
      prevalence ratios (PR) with 95% confidence intervals (CI) were used to compute 
      crude estimates of RR for tinnitus risk factors. RESULTS: From 2389 records 
      identified, a total of 374 articles were read as full text (24 reviews, 301 
      cross-sectional studies, 42 cohort studies, and 7 case-control studies). However, 
      from 49 case-control and cohort studies, only 25 adequately reported risk ratios. 
      Using the findings from these studies, positive causal associations were found 
      for various hearing-related factors (i.e., unspecified hearing loss, 
      sensorineural hearing loss, occupational noise exposure, ototoxic platinum 
      therapy, and otitis media). Evidence was also found for a number of 
      non-otological risk factors including temporo-mandibular joint disorder, 
      depression, chronic obstructive pulmonary disease, and hyperlipidemia. Negative 
      associations indicating preventative effects were found for diabetes and high 
      alcohol consumption. No associations were found for low alcohol consumption, body 
      mass index, head injury, heart failure, hypertension, leisure noise exposure, 
      migraine, rheumatoid arthritis, sex, smoking, stroke, and whiplash. However, with 
      the exception of unspecified hearing loss, these findings resulted from pooling 
      no more than 4 studies, illustrating that the vast majority of the associations 
      still remain inconclusive. CONCLUSIONS: These systematic review and meta-analysis 
      confirm a number of otological and non-otological risk factors for tinnitus. By 
      highlighting major gaps in knowledge, our synthesis can help provide direction 
      for future research that will shed light on the pathophysiology, improve 
      management strategies, and inform more effective preventions.
CI  - © 2022. The Author(s).
FAU - Biswas, Roshni
AU  - Biswas R
AD  - Hearing Sciences, School of Medicine, Mental Health and Clinical Neurosciences, 
      University of Nottingham, Nottingham, UK.
AD  - Department of Environmental Health Sciences, Istituto di Ricerche Farmacologiche 
      Mario Negri IRCCS, Milan, Italy.
FAU - Genitsaridi, Eleni
AU  - Genitsaridi E
AD  - Hearing Sciences, School of Medicine, Mental Health and Clinical Neurosciences, 
      University of Nottingham, Nottingham, UK.
AD  - NIHR Nottingham Biomedical Research Centre, Nottingham, UK.
FAU - Trpchevska, Natalia
AU  - Trpchevska N
AD  - Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, 
      Sweden.
FAU - Lugo, Alessandra
AU  - Lugo A
AD  - Department of Environmental Health Sciences, Istituto di Ricerche Farmacologiche 
      Mario Negri IRCCS, Milan, Italy.
FAU - Schlee, Winfried
AU  - Schlee W
AD  - Department of Psychiatry and Psychotherapy, University of Regensburg, Regensburg, 
      Germany.
FAU - Cederroth, Christopher R
AU  - Cederroth CR
AUID- ORCID: 0000-0001-7267-5136
AD  - Hearing Sciences, School of Medicine, Mental Health and Clinical Neurosciences, 
      University of Nottingham, Nottingham, UK. christopher.cederroth@ki.se.
AD  - NIHR Nottingham Biomedical Research Centre, Nottingham, UK. 
      christopher.cederroth@ki.se.
AD  - Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, 
      Sweden. christopher.cederroth@ki.se.
FAU - Gallus, Silvano
AU  - Gallus S
AD  - Department of Environmental Health Sciences, Istituto di Ricerche Farmacologiche 
      Mario Negri IRCCS, Milan, Italy.
FAU - Hall, Deborah A
AU  - Hall DA
AD  - Hearing Sciences, School of Medicine, Mental Health and Clinical Neurosciences, 
      University of Nottingham, Nottingham, UK.
AD  - NIHR Nottingham Biomedical Research Centre, Nottingham, UK.
AD  - School of Social Sciences, Heriot-Watt University Malaysia, Putrajaya, Malaysia.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Systematic Review
DEP - 20221115
PL  - United States
TA  - J Assoc Res Otolaryngol
JT  - Journal of the Association for Research in Otolaryngology : JARO
JID - 100892857
SB  - IM
MH  - Humans
MH  - *Tinnitus/epidemiology/etiology
MH  - Cross-Sectional Studies
MH  - *Hearing Loss/epidemiology/etiology
MH  - Risk Factors
MH  - *Hearing Loss, Sensorineural
MH  - Observational Studies as Topic
PMC - PMC9971395
OTO - NOTNLM
OT  - Case–control
OT  - Cohort
OT  - Epidemiology
OT  - Exposures
OT  - Risk factors
OT  - Tinnitus
COIS- The authors declare no competing interests.
EDAT- 2022/11/16 06:00
MHDA- 2023/03/03 06:00
PMCR- 2022/11/15
CRDT- 2022/11/15 23:46
PHST- 2022/06/16 00:00 [received]
PHST- 2022/09/14 00:00 [accepted]
PHST- 2022/11/16 06:00 [pubmed]
PHST- 2023/03/03 06:00 [medline]
PHST- 2022/11/15 23:46 [entrez]
PHST- 2022/11/15 00:00 [pmc-release]
AID - 10.1007/s10162-022-00874-y [pii]
AID - 874 [pii]
AID - 10.1007/s10162-022-00874-y [doi]
PST - ppublish
SO  - J Assoc Res Otolaryngol. 2023 Feb;24(1):81-94. doi: 10.1007/s10162-022-00874-y. 
      Epub 2022 Nov 15.

PMID- 36369668
OWN - NLM
STAT- MEDLINE
DCOM- 20231207
LR  - 20240702
IS  - 1601-0825 (Electronic)
IS  - 1354-523X (Linking)
VI  - 29
IP  - 8
DP  - 2023 Nov
TI  - A lower prevalence of malignant lymphoma in Sjögren's syndrome patients: A 
      cross-sectional study.
PG  - 3313-3324
LID - 10.1111/odi.14435 [doi]
AB  - OBJECTIVE: This study aims to determine the prevalence and risk factors 
      associated with lymphoma in primary Sjögren's syndrome (pSS). METHODS: We 
      conducted a cross-sectional study on pSS patients who were registered into the 
      Integrated Data Repository (IDR) at the University of Florida (UF) Health Shands 
      Hospital. The parameters, such as age, sex, race, and smoking status, were 
      included. Lymphoma types in pSS were categorized. The clinical and laboratory 
      features were compared between pSS patients with and those without lymphoma by 
      utilizing the items in the EULAR Sjögren's Syndrome Disease Activity Index 
      (ESSDAI). RESULTS: Among 1,211,343 patients, we found 6799 patients (0.56%) with 
      lymphomas and 2562 patients (0.21%) with pSS. Out of the 2562 pSS patients, 67 
      patients (2.6%) were diagnosed with lymphoma. The difference in the clinical and 
      laboratory features listed under the ESSDAI domains between pSS patients with 
      lymphomas and pSS without it was significant (p < 0.05 or 0.01): fever, weight 
      loss, lymphadenopathy, splenomegaly, lacrimal gland diseases, cough, shortness of 
      breath, hematuria, cerebrovascular accident diseases, peripheral nerve 
      involvement due to vasculitis, neutropenia, and thrombocytopenia. CONCLUSION: We 
      report 2.6% of lymphoma prevalence in pSS, lower than previously reported in the 
      literature.
CI  - © 2022 Wiley Periodicals LLC.
FAU - Saleh, Wafaa
AU  - Saleh W
AUID- ORCID: 0000-0003-4143-7084
AD  - Oral Medicine, Periodontology, Diagnosis and Oral Radiology Department, Faculty 
      of Dentistry, Mansoura University, Mansoura City, Egypt.
FAU - Elashry, Mohamed M
AU  - Elashry MM
AD  - Department of Diagnostic Radiology, Faculty of Medicine, Mansoura University, 
      Mansoura City, Egypt.
FAU - Winn, Nicole
AU  - Winn N
AUID- ORCID: 0000-0001-9063-6763
AD  - Oral and Maxillofacial Diagnostic Sciences, University of Florida College of 
      Dentistry, Gainesville, Florida, USA.
AD  - Center for Orphaned Autoimmune Disorders (COAD), University of Florida College of 
      Dentistry, Gainesville, Florida, USA.
FAU - Mona, Mahmoud
AU  - Mona M
AD  - Department of Endodontics, College of Dentistry, University of Florida, 
      Gainesville, Florida, USA.
FAU - Katz, Joseph
AU  - Katz J
AUID- ORCID: 0000-0002-0741-8149
AD  - Oral and Maxillofacial Diagnostic Sciences, University of Florida College of 
      Dentistry, Gainesville, Florida, USA.
AD  - Center for Orphaned Autoimmune Disorders (COAD), University of Florida College of 
      Dentistry, Gainesville, Florida, USA.
FAU - Cha, Seunghee
AU  - Cha S
AD  - Oral and Maxillofacial Diagnostic Sciences, University of Florida College of 
      Dentistry, Gainesville, Florida, USA.
AD  - Center for Orphaned Autoimmune Disorders (COAD), University of Florida College of 
      Dentistry, Gainesville, Florida, USA.
LA  - eng
GR  - center of orphand autoimmune disorders/
GR  - NIH/NIAMS/
PT  - Journal Article
DEP - 20221202
PL  - Denmark
TA  - Oral Dis
JT  - Oral diseases
JID - 9508565
CIN - Oral Dis. 2024 Apr;30(3):828-829. doi: 10.1111/odi.14570. PMID: 36939410
MH  - Humans
MH  - *Sjogren's Syndrome/complications/epidemiology/diagnosis
MH  - Cross-Sectional Studies
MH  - Prevalence
MH  - Risk Factors
MH  - *Lymphoma/epidemiology/complications
OTO - NOTNLM
OT  - Sjögren's syndrome
OT  - lymphoma
OT  - prevalence
OT  - risk factor
EDAT- 2022/11/13 06:00
MHDA- 2023/12/07 12:42
CRDT- 2022/11/12 00:52
PHST- 2022/10/31 00:00 [revised]
PHST- 2022/10/10 00:00 [received]
PHST- 2022/11/09 00:00 [accepted]
PHST- 2023/12/07 12:42 [medline]
PHST- 2022/11/13 06:00 [pubmed]
PHST- 2022/11/12 00:52 [entrez]
AID - 10.1111/odi.14435 [doi]
PST - ppublish
SO  - Oral Dis. 2023 Nov;29(8):3313-3324. doi: 10.1111/odi.14435. Epub 2022 Dec 2.

PMID- 36341096
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20221108
IS  - 1664-2295 (Print)
IS  - 1664-2295 (Electronic)
IS  - 1664-2295 (Linking)
VI  - 13
DP  - 2022
TI  - Celecoxib and Etoricoxib may reduce risk of ischemic stroke in patients with 
      rheumatoid arthritis: A nationwide retrospective cohort study.
PG  - 1018521
LID - 10.3389/fneur.2022.1018521 [doi]
LID - 1018521
AB  - BACKGROUND AND PURPOSE: Previous studies reported conflicting results about the 
      risk of ischemic stroke associated with the use of non-steroidal 
      anti-inflammatory drugs (NSAIDs) in patients with rheumatoid arthritis (RA). We 
      aimed to investigate two specific COX-2 inhibitors, Celecoxib and Etoricoxib, and 
      their corresponding effects on the risk of ischemic stroke in patients with RA. 
      PATIENTS AND METHODS: 10,857 patients newly diagnosed with RA were identified and 
      sampled from the Taiwanese National Health Insurance Research Database during the 
      period from 2001 to 2009. The identification of RA was based on the criteria of 
      ICD-9-CM diagnosis code 714.0. Patients diagnosed with cerebrovascular disease 
      and those receiving RA treatment prior to the first diagnosis of RA were 
      excluded. Study endpoint was ischemic stroke, defined by ICD-9-CM code. Cox 
      proportional hazard models and Kaplan Meier curves were used to reveal covariates 
      and differences by drugs in the risk of ischemic stroke. Dosages for Celecoxib 
      were defined as ≤ 200 and >200 mg/day; those for Etoricoxib were 0 and >0 mg/day. 
      RESULTS: Among 7,904 RA patients, 6,669 did not take Celecoxib and 564 (8.46%) of 
      them experienced an ischemic stroke event. Of the 597 individuals who took ≤ 200 
      mg/day of Celecoxib, 58 (9.72%) had strokes. Of the 638 patients who took >200 
      mg/day of Celecoxib, 38 (5.96%) eventually experienced a stroke. Among the 7,681 
      patients who did not take Etoricoxib, 654 (8.51%) experienced an ischemic stroke, 
      while 6 (2.69%) in 223 patients who consumed Etoricoxib had a stroke event. 
      Consuming more than 200 mg of Celecoxib per day for <3.5 years lowered the 
      incidence rate for strokes [hazard ratio (HR) 0.67, 95% Confidence Interval (CI) 
      0.48-0.93 for dosage and HR 0.22, 95% CI 0.10-0.46 for duration, both p < 0.001], 
      while consuming any dosage of Etoricoxib significantly decreases the possibility 
      (HR 0.35, 95% CI 0.16-0.80, p < 0.001). On the other hand, consuming Etoricoxib 
      for 8 years might have a neutral or even a potentially protective effect compared 
      to at 3.8 years. CONCLUSION: This population-based retrospective cohort study has 
      shown that Celecoxib and Etoricoxib reduce the risk of ischemic stroke in 
      patients with RA in a dose- and time-dependent manner.
CI  - Copyright © 2022 Chen, Lee, Perng, Chiou, Wang, Lin, Wei and Tsou.
FAU - Chen, Acer I-Hung
AU  - Chen AI
AD  - Medical Intensive Care Unit, Ronald Reagan UCLA Medical Center, Los Angeles, CA, 
      United States.
AD  - School of Medicine, Chang Gung University, Taoyuan, Taiwan.
FAU - Lee, Yung-Heng
AU  - Lee YH
AD  - Department of Health Services Administration, China Medical University, Taichung, 
      Taiwan.
AD  - Department of Public Health, China Medical University, Taichung, Taiwan.
AD  - Department of Orthopedics, Cishan Hospital, Ministry of Health and Welfare, 
      Kaohsiung, Taiwan.
AD  - Department of Center for General Education, National United University, Miaoli, 
      Taiwan.
FAU - Perng, Wuu-Tsun
AU  - Perng WT
AD  - Department of Recreational Sport and Health Promotion, National Pingtung 
      University of Science and Technology, Pingtung, Taiwan.
FAU - Chiou, Jeng-Yuan
AU  - Chiou JY
AD  - School of Health Policy and Management, Chung Shan Medical University, Taichung, 
      Taiwan.
FAU - Wang, Yu-Hsun
AU  - Wang YH
AD  - Department of Medical Research, Chung Shan Medical University Hospital, Taichung, 
      Taiwan.
FAU - Lin, Lichi
AU  - Lin L
AD  - Department of Statistics, Oklahoma State University, Stillwater, OK, United 
      States.
FAU - Wei, James Cheng-Chung
AU  - Wei JC
AD  - Division of Allergy, Immunology and Rheumatology, Chung Shan Medical University 
      Hospital, Taichung, Taiwan.
AD  - Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
AD  - Graduate Institute of Integrated Medicine, China Medical University, Taichung, 
      Taiwan.
FAU - Tsou, Hsi-Kai
AU  - Tsou HK
AD  - Functional Neurosurgery Division, Neurological Institute, Taichung Veterans 
      General Hospital, Taichung, Taiwan.
AD  - Department of Rehabilitation, Jen-Teh Junior College of Medicine, Nursing and 
      Management, Miaoli, Taiwan.
AD  - College of Health, National Taichung University of Science and Technology, 
      Taichung, Taiwan.
AD  - Department of Post-baccalaureate Medicine, College of Medicine, National Chung 
      Hsing University, Taichung, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20221020
PL  - Switzerland
TA  - Front Neurol
JT  - Frontiers in neurology
JID - 101546899
PMC - PMC9630581
OTO - NOTNLM
OT  - Celecoxib-compound CID: 2662
OT  - Etoricoxib (CID: 123619)
OT  - ischemic stroke (IS)
OT  - non-steroidal anti-inflammatory drugs (NSAIDs)
OT  - rheumatoid arthritis
OT  - risk
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2022/11/08 06:00
MHDA- 2022/11/08 06:01
PMCR- 2022/10/20
CRDT- 2022/11/07 05:12
PHST- 2022/08/17 00:00 [received]
PHST- 2022/10/06 00:00 [accepted]
PHST- 2022/11/07 05:12 [entrez]
PHST- 2022/11/08 06:00 [pubmed]
PHST- 2022/11/08 06:01 [medline]
PHST- 2022/10/20 00:00 [pmc-release]
AID - 10.3389/fneur.2022.1018521 [doi]
PST - epublish
SO  - Front Neurol. 2022 Oct 20;13:1018521. doi: 10.3389/fneur.2022.1018521. 
      eCollection 2022.

PMID- 36254547
OWN - NLM
STAT- MEDLINE
DCOM- 20221019
LR  - 20221019
IS  - 1847-6538 (Electronic)
IS  - 1330-027X (Linking)
VI  - 30
IP  - 2
DP  - 2022 Sep
TI  - Decreased Arterial Vascular Tone in Small Arteries in Severe Hidradenitis 
      Suppurativa - A Study Using Finger Photopulseplethysmography.
PG  - 119-122
AB  - A previous study has found an association between chronic inflammatory disorders 
      e.g. psoriasis, rheumatoid arthritis, and inflammatory bowel disease and 
      increased vascular stiffness(1). Psoriasis and hidradenitis suppurativa (HS) are 
      believed to have shared comorbidities and pathophysiology despite their 
      morphologically different manifestations in the skin. In order to evaluate a 
      putative association between the chronic inflammatory skin disease HS and 
      arterial stiffness, an observational cross-sectional retrospective study was 
      carried out as part of the Danish General Suburban Population Study (GESUS) (1), 
      in which 430 patients with HS from the general population (representing mild HS; 
      Table 1), 32 patients with HS from a hospital-based out-patient clinic 
      (representing severe HS, Table 1), and 20,780 controls underwent measurements of 
      arterial vascular tone and stiffness using photoplethysmography (Pulse Trace 
      PCA2®; Micro Medical Ltd, Kent, UK). The method of Pulse Trace has been validated 
      by correlation with intra-arterial sensing techniques, and is a simple 
      cost-effective screening method[2]. All analyses were performed using SAS 9.3. 
      This study was accepted by the ethics committee of Region Zealand (project number 
      SJ-191, SJ-113, SJ-114) in Denmark (2,3). RESULTS Reflection index (RI) is an 
      expression of arterial vascular tone and stiffness of small arteries. The raw 
      data showed a significantly lower RI for both HS groups groups, compared to 
      controls. The results remained significant when adjusting for confounders (age, 
      sex, smoking and metabolic syndrome) in the out-patient clinic HS group (-11.26 
      (-17.75- -4.76), P=0.0002*), but not in the population HS group (Table 2). 
      Stiffness index (SI) expresses arterial stiffness in large arteries. Both HS 
      groups showed no significant difference in either SI or vascular age in 
      multivariate analysis, when compared with controls (Table 2). DISCUSSION This 
      study suggests that decreased vascular tone and stiffness of small arteries may 
      be associated with severe HS, and at the same time found no difference in 
      arterial stiffness in large arteries. The significance for the out-patient clinic 
      HS group, but not the population HS group may reflect a dose-response 
      relationship. Vascular tone in vascular smooth muscle cells of small arteries 
      depends on competing vasodilators and vasoconstrictors. We speculate that the 
      inflammation of HS may induce a dysfunctional balance e.g. through increased 
      TNF-alpha with subsequent increase of the vasodilator nitric oxide resulting in 
      the lower arterial vascular tone observed. Additionally, mast cells are increased 
      in HS [4], possibly increasing levels of the vasodilator histamine. HS patients 
      often suffer from stress which could increase sympathetic activity, thereby 
      adrenalin/cortisol and subsequent vasodilation in e.g. muscles. The more 
      peripheral an artery is, the more collagen it contains and the stiffer it is. The 
      finding of lower vascular tone may also be suggestive of a different 
      elastin:collagen ratio in small arteries in HS. The healing process of HS lesions 
      is known to involve scarring formation of sinus tracts [5], which may suggest a 
      hypothesis of altered connective tissue. This study found no difference in SI 
      expressing arterial stiffness of large arteries between HS and controls. Our 
      previous study found an association between HS and myocardial infarction, but no 
      association with stroke, nor peripheral arterial stiffness of lower extremities 
      in medium/large arteries [6], suggesting regional differences in vascular beds in 
      HS. The major limitation of the study is the missing values of pulse trace 
      measurement (Table 1) creating possible selection bias. Although unable to draw 
      any clinical conclusions, we believe these results may contribute to the future 
      research of the complexity of HS and cardiovascular risk profiling. This study 
      suggests that decreased vascular tone and stiffness of small arteries may be 
      associated with severe HS, and at the same time found no difference in arterial 
      stiffness in large arteries. The significance for the out-patient clinic HS 
      group, but not the population HS group may reflect a dose-response relationship. 
      Vascular tone in vascular smooth muscle cells of small arteries depends on 
      competing vasodilators and vasoconstrictors. We speculate that the inflammation 
      of HS may induce a dysfunctional balance e.g. through increased TNF-alpha with 
      subsequent increase of the vasodilator nitric oxide resulting in the lower 
      arterial vascular tone observed. Additionally, mast cells are increased in HS 
      [4], possibly increasing levels of the vasodilator histamine. HS patients often 
      suffer from stress which could increase sympathetic activity, thereby 
      adrenalin/cortisol and subsequent vasodilation in e.g. muscles. The more 
      peripheral an artery is, the more collagen it contains and the stiffer it is. The 
      finding of lower vascular tone may also be suggestive of a different 
      elastin:collagen ratio in small arteries in HS. The healing process of HS lesions 
      is known to involve scarring formation of sinus tracts [5], which may suggest a 
      hypothesis of altered connective tissue. This study found no difference in SI 
      expressing arterial stiffness of large arteries between HS and controls. Our 
      previous study found an association between HS and myocardial infarction, but no 
      association with stroke, nor peripheral arterial stiffness of lower extremities 
      in medium/large arteries [6], suggesting regional differences in vascular beds in 
      HS. The major limitation of the study is the missing values of pulse trace 
      measurement (Table 1) creating possible selection bias. Although unable to draw 
      any clinical conclusions, we believe these results may contribute to the future 
      research of the complexity of HS and cardiovascular risk profiling.
FAU - Miller, Iben Marie
AU  - Miller IM
AD  - Iben Marie Miller, MD, PhD, Department of Dermatology, Zealand University 
      Hospital, Sygehusvej 10, 4000 Roskilde, Faculty of Health and Medical Sciences, 
      University of Copenhagen, Denmark; ibenmariemiller@gmail.com.
FAU - Ahlehoff, Ole
AU  - Ahlehoff O
FAU - Zarchi, Kian
AU  - Zarchi K
FAU - Rytgaard, Helene
AU  - Rytgaard H
FAU - Mogensen, Ulla B
AU  - Mogensen UB
FAU - Ellervik, Christina
AU  - Ellervik C
FAU - E Jemec, Gregor B
AU  - E Jemec GB
LA  - eng
PT  - Journal Article
PL  - Croatia
TA  - Acta Dermatovenerol Croat
JT  - Acta dermatovenerologica Croatica : ADC
JID - 9433781
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vasoconstrictor Agents)
RN  - 0 (Vasodilator Agents)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 820484N8I3 (Histamine)
RN  - 9007-58-3 (Elastin)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - Arteries
MH  - Cicatrix/complications
MH  - Cross-Sectional Studies
MH  - Elastin
MH  - *Hidradenitis Suppurativa/complications
MH  - Histamine
MH  - Humans
MH  - Hydrocortisone
MH  - Inflammation/complications
MH  - *Myocardial Infarction/complications
MH  - Nitric Oxide
MH  - *Psoriasis/complications
MH  - Retrospective Studies
MH  - *Stroke/complications
MH  - Tumor Necrosis Factor-alpha
MH  - Vasoconstrictor Agents
MH  - Vasodilator Agents
EDAT- 2022/10/19 06:00
MHDA- 2022/10/20 06:00
CRDT- 2022/10/18 03:22
PHST- 2022/10/18 03:22 [entrez]
PHST- 2022/10/19 06:00 [pubmed]
PHST- 2022/10/20 06:00 [medline]
PST - ppublish
SO  - Acta Dermatovenerol Croat. 2022 Sep;30(2):119-122.

PMID- 36197529
OWN - NLM
STAT- MEDLINE
DCOM- 20240325
LR  - 20240409
IS  - 1573-7241 (Electronic)
IS  - 0920-3206 (Print)
IS  - 0920-3206 (Linking)
VI  - 38
IP  - 2
DP  - 2024 Apr
TI  - Hydroxychloroquine and Cardiovascular Events in Patients with Rheumatoid 
      Arthritis.
PG  - 297-304
LID - 10.1007/s10557-022-07387-z [doi]
AB  - INTRODUCTION: Cardiovascular disease (CVD) is the leading cause of mortality in 
      patients with rheumatoid arthritis (RA). Some studies have reported a decrease in 
      CVD in patients with RA using hydroxychloroquine (HCQ). Most of these have had 
      fewer participants and have analyzed only composite outcomes. We aimed to 
      identify the association between the use of HCQ in patients with RA and the 
      incidence of major adverse cardiac events (MACEs), cerebral infarction, and AMI. 
      METHODS: This was a retrospective observational study using the TriNetX Diamond 
      Network. Propensity score matching (PSM) was used to equilibrate the cohorts. The 
      dependent variables in our study were MACE, cerebral infarction, and AMI. 
      RESULTS: A total of 2,261,643 patients with RA were identified. Approximately 6% 
      had been prescribed HCQ. Of those prescribed HCQ, 80% (112,743) were females, 
      while of those not prescribed HCQ, 72.5% (1,536,937) were females. HCQ was 
      associated with lower rates of MACE (HR 0.827, 95%CI 0.8,0.86), cerebral 
      infarction (HR 0.824, 95% CI 0.78,0.87), and AMI (HR 0.9, 95% CI 0.85,0.96). 
      These associations were not seen in patients taking biologics. HCQ was associated 
      with lower MACE in all other subgroups. CONCLUSION: In conclusion, HCQ was 
      slightly beneficial in decreasing MACE and cerebral infarction in patients with 
      RA. These associations were significantly lower in patients taking methotrexate 
      or biologics. Although there was a significant decrease in the risk of AMI in all 
      patients with RA, these results were not replicated in subgroup analyses, and 
      there was an apparent increased risk of AMI with the use of HCQ in patients using 
      biologics.
CI  - © 2022. The Author(s), under exclusive licence to Springer Science+Business 
      Media, LLC, part of Springer Nature.
FAU - Cordova Sanchez, Andres
AU  - Cordova Sanchez A
AUID- ORCID: 0000-0003-3763-3971
AD  - Department of Medicine, SUNY Upstate Medical University, Rm. 5138. 750 East Adams 
      Street, Syracuse, NY, 13210, USA. cordovaa@upstate.edu.
FAU - Khokhar, Farzam
AU  - Khokhar F
AD  - Department of Medicine, SUNY Upstate Medical University, Rm. 5138. 750 East Adams 
      Street, Syracuse, NY, 13210, USA.
FAU - Olonoff, Danielle A
AU  - Olonoff DA
AD  - Department of Medicine, SUNY Upstate Medical University, Rm. 5138. 750 East Adams 
      Street, Syracuse, NY, 13210, USA.
FAU - Carhart, Robert L
AU  - Carhart RL
AD  - Division of Cardiology, SUNY Upstate Medical University, Syracuse, NY, 13210, 
      USA.
LA  - eng
PT  - Journal Article
PT  - Observational Study
DEP - 20221005
PL  - United States
TA  - Cardiovasc Drugs Ther
JT  - Cardiovascular drugs and therapy
JID - 8712220
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - 4QWG6N8QKH (Hydroxychloroquine)
SB  - IM
CIN - Cardiovasc Drugs Ther. 2023 Aug;37(4):621-622. doi: 10.1007/s10557-022-07408-x. 
      PMID: 36418627
MH  - Female
MH  - Humans
MH  - Male
MH  - *Antirheumatic Agents/adverse effects
MH  - *Arthritis, Rheumatoid/diagnosis/drug therapy/epidemiology
MH  - *Biological Products/adverse effects
MH  - Cerebral Infarction/complications/drug therapy
MH  - Hydroxychloroquine/adverse effects
PMC - PMC9532807
OTO - NOTNLM
OT  - Cardiovascular Disease
OT  - Hydroxychloroquine
OT  - Myocardial Infarction
OT  - Rheumatoid Arthritis
OT  - Stroke
COIS- The authors declare no competing interests.
EDAT- 2022/10/06 06:00
MHDA- 2024/03/25 06:42
PMCR- 2022/10/05
CRDT- 2022/10/05 11:25
PHST- 2022/09/25 00:00 [accepted]
PHST- 2024/03/25 06:42 [medline]
PHST- 2022/10/06 06:00 [pubmed]
PHST- 2022/10/05 11:25 [entrez]
PHST- 2022/10/05 00:00 [pmc-release]
AID - 10.1007/s10557-022-07387-z [pii]
AID - 7387 [pii]
AID - 10.1007/s10557-022-07387-z [doi]
PST - ppublish
SO  - Cardiovasc Drugs Ther. 2024 Apr;38(2):297-304. doi: 10.1007/s10557-022-07387-z. 
      Epub 2022 Oct 5.

PMID- 36159579
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220928
IS  - 1741-427X (Print)
IS  - 1741-4288 (Electronic)
IS  - 1741-427X (Linking)
VI  - 2022
DP  - 2022
TI  - Analysis of Clinical Characteristics and Influencing Factors for H-Type 
      Hypertension Complicated with Other Chronic Diseases in a Community in Beijing.
PG  - 6974065
LID - 10.1155/2022/6974065 [doi]
LID - 6974065
AB  - OBJECTIVE: The aim of the study is to analyze the clinical characteristics of 
      patients with H-type hypertension complicated with other chronic diseases in a 
      community in Beijing and to explore the influencing factors related to the 
      occurrence of the disease by means of a case-control study. METHODS: A 
      questionnaire was designed. 362 residents with H-type hypertension in a community 
      in Beijing were randomly enrolled from January 2020 to December 2021. The general 
      data and clinical indexes of the patients were collected and their clinical 
      characteristics were analyzed. According to the complications of other chronic 
      diseases, they were divided into the simple hypertension group (n = 65) and the 
      other chronic disease group (n = 297). Univariate and multivariate analyses were 
      used to analyze the influencing factors for H-type hypertension patients with 
      other chronic diseases. RESULTS: Among the 362 H-type hypertension patients, 21 
      cases were aged 35-45 years, 35 cases were aged 45-55 years, and 127 cases were 
      aged 55-65 years. The number of patients aged ≥65 years was 179, and the number 
      of patients aged ≥55 years accounted for the highest proportion with a 
      constituent ratio of 85.00%. Only 65 patients were patients with simple 
      hypertension. The remaining 297 patients were complicated with different kinds of 
      chronic diseases. The types of chronic diseases include malignant tumors, 
      diabetes, rheumatoid arthritis, coronary heart disease, asthma, chronic 
      obstructive pulmonary disease, systemic lupus erythematosus, and stroke. The 
      proportion of H-type hypertension complicated with coronary heart disease, 
      diabetes, and stroke is higher. Among the 297 patients, most of them were local, 
      resident, and nonagricultural patients with a constituent ratio of 89.90%, 
      95.96%, and 98.98%, respectively. The prevalence rate of the male was 59.60% 
      higher than that of the female at 40.40%. The blood types B and AB were more 
      common. 90.57% of patients were married and the proportion of body mass index 
      (BMI) was 45.79%. 60.61% of patients had a history of smoking, 55.56% had a 
      history of drinking, 35.02% had a regular physical examination, 14.81% had 
      regular exercise, and 37.71% had a light diet. There were significant differences 
      in marital status, smoking, alcohol consumption, regular exercise, and light diet 
      between the simple hypertension group and the chronic disease group (P < 0.05). 
      The results of the logistic regression analysis showed that smoking, drinking, 
      little exercise, and not eating lightly were the independent risk factors for 
      other chronic diseases (P < 0.05). CONCLUSION: The incidence of H-type 
      hypertension is higher in people ≥55 years old. Most of them are accompanied by 
      three other chronic diseases: smoking, drinking, little exercise, and no light 
      diet are also risk factors for chronic diseases.
CI  - Copyright © 2022 Tianlong Li et al.
FAU - Li, Tianlong
AU  - Li T
AUID- ORCID: 0000-0001-7027-6828
AD  - School of General Practice and Continuing Education, Capital Medical University, 
      Beijing 100069, China.
AD  - Department of General Medicine, Wanping Community Health Service Center, Fengtai 
      District Beijing, Beijing 100165, China.
FAU - Wang, Chen
AU  - Wang C
AUID- ORCID: 0000-0003-2617-4132
AD  - School of General Practice and Continuing Education, Capital Medical University, 
      Beijing 100069, China.
AD  - Department of General Medicine, Beijing Tiantan Hospital, Capital Medical 
      University, Beijing 100070, China.
FAU - Ma, Li
AU  - Ma L
AD  - Department of General Medicine, Beijing Tiantan Hospital, Capital Medical 
      University, Beijing 100070, China.
LA  - eng
PT  - Journal Article
DEP - 20220915
PL  - United States
TA  - Evid Based Complement Alternat Med
JT  - Evidence-based complementary and alternative medicine : eCAM
JID - 101215021
PMC - PMC9499743
COIS- The authors declare that they have no conflicts of interest.
EDAT- 2022/09/27 06:00
MHDA- 2022/09/27 06:01
PMCR- 2022/09/15
CRDT- 2022/09/26 17:36
PHST- 2022/07/04 00:00 [received]
PHST- 2022/08/18 00:00 [accepted]
PHST- 2022/09/26 17:36 [entrez]
PHST- 2022/09/27 06:00 [pubmed]
PHST- 2022/09/27 06:01 [medline]
PHST- 2022/09/15 00:00 [pmc-release]
AID - 10.1155/2022/6974065 [doi]
PST - epublish
SO  - Evid Based Complement Alternat Med. 2022 Sep 15;2022:6974065. doi: 
      10.1155/2022/6974065. eCollection 2022.

PMID- 36118256
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230504
IS  - 2352-9067 (Print)
IS  - 2352-9067 (Electronic)
IS  - 2352-9067 (Linking)
VI  - 42
DP  - 2022 Oct
TI  - Oral anticoagulant treatment in rheumatoid arthritis patients with atrial 
      fibrillation results of an international audit.
PG  - 101117
LID - 10.1016/j.ijcha.2022.101117 [doi]
LID - 101117
AB  - OBJECTIVE: To describe the prevalence of atrial fibrillation (AF) in patients 
      with rheumatoid arthritis (RA), and to evaluate the proportion of patients with 
      AF receiving guideline-recommended anticoagulation for prevention of stroke, 
      based on data from a large international audit. METHODS: The cohort was derived 
      from the international audit SUrvey of cardiovascular disease Risk Factors in 
      patients with Rheumatoid Arthritis (SURF-RA) which collected data from 17 
      countries during 2014-2019. We evaluated the prevalence of AF across world 
      regions and explored factors associated with the presence of AF with 
      multivariable logistic regression models. The proportion of AF patients at high 
      risk of stroke (CHA(2)DS(2)-VASc ≥ 2 in males and ≥ 3 in females) receiving 
      anticoagulation was examined. RESULTS: Of the total SURF-RA cohort (n = 14,503), 
      we included RA cases with data on whether the diagnosis of AF was present or not 
      (n = 7,665, 75.1% women, mean (SD) age 58.7 (14.1) years). A total of 288 (3.8%) 
      patients had a history of AF (4.4% in North America, 3.4% in Western Europe, 2.8% 
      in Central and Eastern Europe and 1.5% in Asia). Factors associated with the 
      presence of AF were older age, male sex, atherosclerotic cardiovascular disease, 
      heart failure and hypertension. Two-hundred and fifty-five (88.5%) RA patients 
      had a CHA(2)DS(2)-VASc score indicating recommendation for oral anticoagulant 
      treatment, and of them, 164 (64.3%) were anticoagulated. CONCLUSION: 
      Guideline-recommended anticoagulant therapy for prevention of stroke due to AF 
      may not be optimally implemented among RA patients, and requires special 
      attention.
CI  - © 2022 The Authors.
FAU - Semb, Anne Grete
AU  - Semb AG
AD  - Preventive Cardio-Rheuma Clinic, Center for treatment of Rheumatic and 
      Musculoskeletal Diseases (REMEDY), Diakonhjemmet Hospital, Oslo, Norway.
FAU - Rollefstad, Silvia
AU  - Rollefstad S
AD  - Preventive Cardio-Rheuma Clinic, Center for treatment of Rheumatic and 
      Musculoskeletal Diseases (REMEDY), Diakonhjemmet Hospital, Oslo, Norway.
FAU - Sexton, Joseph
AU  - Sexton J
AD  - Division of Rheumatology and Research, REMEDY, Diakonhjemmet Hospital, Oslo, 
      Norway.
FAU - Ikdahl, Eirik
AU  - Ikdahl E
AD  - Preventive Cardio-Rheuma Clinic, Center for treatment of Rheumatic and 
      Musculoskeletal Diseases (REMEDY), Diakonhjemmet Hospital, Oslo, Norway.
FAU - Crowson, Cynthia S
AU  - Crowson CS
AD  - Quantitative Health Sciences, Mayo Clinic Rochester, Rochester, MN, USA.
FAU - van Riel, Piet
AU  - van Riel P
AD  - IQ Healthcare, Radboud University Nijmegen, Nijmegen, the Netherlands.
FAU - Kitas, George
AU  - Kitas G
AD  - Department of Rheumatology, The Dudley Group NHS Foundation Trust, Dudley, UK.
FAU - Graham, Ian
AU  - Graham I
AD  - Cardiology, The University of Dublin Trinity College, Dublin, Ireland.
FAU - Kerola, Anne M
AU  - Kerola AM
AD  - Preventive Cardio-Rheuma Clinic, Center for treatment of Rheumatic and 
      Musculoskeletal Diseases (REMEDY), Diakonhjemmet Hospital, Oslo, Norway.
AD  - Inflammation Center, Helsinki University Hospital, Helsinki, Finland.
CN  - SURF-RA
LA  - eng
PT  - Journal Article
DEP - 20220912
PL  - Ireland
TA  - Int J Cardiol Heart Vasc
JT  - International journal of cardiology. Heart & vasculature
JID - 101649525
PMC - PMC9479366
OTO - NOTNLM
OT  - Anticoagulation
OT  - Atrial fibrillation
OT  - Pharmacotherapy
OT  - Rheumatoid arthritis
COIS- The authors declare that they have no known competing financial interests or 
      personal relationships that could have appeared to influence the work reported in 
      this paper.
FIR - Athanasios Karpouzas, George
IR  - Athanasios Karpouzas G
IRAD- Internal Medicine-Rheumatology, Harbor-UCLA Medical Center, Torrance, CA, USA.
FIR - Gonzalez-Gay, Miguel A
IR  - Gonzalez-Gay MA
IRAD- Rheumatology, Hospital Universitario Marques de Valdecilla, Santander, Spain.
FIR - Sfikakis, Petros P
IR  - Sfikakis PP
IRAD- First Department of Propaedeutic and Internal Medicine, University of Athens, 
      Athens, Greece.
FIR - Tektonidou, Maria G
IR  - Tektonidou MG
IRAD- 2nd Department of Medicine and Laboratory, Clinical Immunology-Rheumatology Unit, 
      National and Kapodistrian University of Athens School of Medicine, Athens, 
      Greece.
FIR - Lazarini, Argyro
IR  - Lazarini A
IRAD- 2nd Department of Medicine and Laboratory, Clinical Immunology-Rheumatology Unit, 
      National and Kapodistrian University of Athens School of Medicine, Athens, 
      Greece.
FIR - Vassilopoulos, Dimitrios
IR  - Vassilopoulos D
IRAD- Medicine, Mount Sinai Hospital, Toronto, Ontario, Canada.
FIR - Kuriya, Bindee
IR  - Kuriya B
IRAD- Medicine, Mount Sinai Hospital, Toronto, Ontario, Canada.
FIR - Hitchon, Carol
IR  - Hitchon C
IRAD- Rheumatology, University of Manitoba, Winnipeg, Manitoba, Canada.
FIR - Simona Stoenoiu, Maria
IR  - Simona Stoenoiu M
IRAD- Rheumatology, Université Catholique de Louvain, Louvain-la-Neuve, Belgium.
FIR - Durez, Patrick
IR  - Durez P
IRAD- Rheumatology, Université Catholique de Louvain, Louvain-la-Neuve, Belgium.
FIR - Pascual-Ramos, Virginia
IR  - Pascual-Ramos V
IRAD- Immunology and Rheumatology, Instituto Nacional de Ciencias Medicas y Nutricion 
      Salvador Zubiran, Mexico City, Mexico.
FIR - Angel Galarza-Delgado, Dionicio
IR  - Angel Galarza-Delgado D
IRAD- Rheumatology, Hospital Universitario Dr Jose Eleuterio Gonzalez, Monterrey, Nuevo 
      León, Mexico.
FIR - Faggiano, Pompilio
IR  - Faggiano P
IRAD- Cardiothoracic, Fondazione Poliambulanza Instituto Ospedaliero, Brescia, Italy.
FIR - Prasanna Misra, Durga
IR  - Prasanna Misra D
IRAD- Department of Clinical Immunology and Rheumatology, Sanjay Gandhi Post Graduate 
      Institute of Medical Sciences, Lucknow, Uttar Pradesh, India.
FIR - Borg, Andrew A
IR  - Borg AA
IRAD- Department of Rheumatology, Mater Dei Hospital, Msida, Malta.
FIR - Mu, Rong
IR  - Mu R
IRAD- Rheumatology, Peking University People's Hospital, Beijing, China.
FIR - Mirrakhimov, Erkin M
IR  - Mirrakhimov EM
IRAD- Kyrgyz State Medical Academy Faculty of General Medicine, Bishkek, Kyrgyzstan.
FIR - Gheta, Diane
IR  - Gheta D
IRAD- Medicine, Tallaght University Hospital, Dublin, Ireland.
FIR - Douglas, Karen
IR  - Douglas K
IRAD- Department of Rheumatology, Dudley Group of Hospitals NHS Trust, Dudley, UK.
FIR - Agarwal, Vikas
IR  - Agarwal V
IRAD- Department of Clinical Immunology and Rheumatology, Sanjay Gandhi Post Graduate 
      Institute of Medical Sciences, Lucknow, Uttar Pradesh, India.
FIR - Myasoedova, Svetlana
IR  - Myasoedova S
IRAD- Rheumatology, Ivanovo State Medical Academy, Ivanovo, Ivanovskaa oblast', Russian 
      Federation.
FIR - Krougly, Lev
IR  - Krougly L
IRAD- Rheumatology, FSBI National Medical and Surgical Center named after N I Pirogov 
      of the Ministry of Healthcare of the Russian Federation, Moskva, Moskva, Russian 
      Federation.
FIR - Valentinovna Popkova, Tatiana
IR  - Valentinovna Popkova T
IRAD- V.A. Nasonova Research Institute of Rheumatology, Moscow, Russian Federation.
FIR - Tuchyňová, Alena
IR  - Tuchyňová A
IRAD- Rheumatology, Narodny Ustav Reumatickych Chorob, Piestany, Slovakia.
FIR - Tomcik, Michal
IR  - Tomcik M
IRAD- 3rd Department of Internal Medicine, General University Hospital and 1st Faculty 
      of Medicine, Charles University, Prague, Czech Republic.
FIR - Vrablik, Michal
IR  - Vrablik M
IRAD- Third Department of Internal Medicine, Department of Endocrinology and 
      Metabolism, Charles University First Faculty of Medicine, Praha, Czech Republic.
FIR - Lastuvka, Jiri
IR  - Lastuvka J
IRAD- Krajska zdravotni a.s, Masaryk Hospital in Usti nad Labem, Usti nad Labem, Czech 
      Republic.
IRAD- First Medical Faculty, Charles University, Praha, Czech Republic.
FIR - Horak, Pavel
IR  - Horak P
IRAD- Department of Internal Medicine III-Nephrology, Rheumatology and Endocrinology, 
      University Hospital Olomouc, Olomouc, Olomoucký, Czech Republic.
FIR - Kaspar Medkova, Helena
IR  - Kaspar Medkova H
IRAD- Division of Rheumatology, 2nd Department of Internal Medicine-Gastroenterology, 
      Charles University First Faculty of Medicine, Hradec Králové, Czech Republic.
EDAT- 2022/09/20 06:00
MHDA- 2022/09/20 06:01
PMCR- 2022/09/12
CRDT- 2022/09/19 04:08
PHST- 2022/08/23 00:00 [received]
PHST- 2022/08/31 00:00 [accepted]
PHST- 2022/09/20 06:00 [pubmed]
PHST- 2022/09/20 06:01 [medline]
PHST- 2022/09/19 04:08 [entrez]
PHST- 2022/09/12 00:00 [pmc-release]
AID - S2352-9067(22)00166-X [pii]
AID - 101117 [pii]
AID - 10.1016/j.ijcha.2022.101117 [doi]
PST - epublish
SO  - Int J Cardiol Heart Vasc. 2022 Sep 12;42:101117. doi: 
      10.1016/j.ijcha.2022.101117. eCollection 2022 Oct.

PMID- 36113961
OWN - NLM
STAT- MEDLINE
DCOM- 20220920
LR  - 20221017
IS  - 2056-5933 (Electronic)
IS  - 2056-5933 (Linking)
VI  - 8
IP  - 2
DP  - 2022 Sep
TI  - Serum cholesterol loading capacity on macrophages is linked to coronary 
      atherosclerosis and cardiovascular event risk in rheumatoid arthritis.
LID - 10.1136/rmdopen-2022-002411 [doi]
LID - e002411
AB  - OBJECTIVES: Cholesterol loading capacity (CLC) describes the ability of serum to 
      deliver cholesterol to cells. It is linked to foam cell formation, a pivotal step 
      in atherosclerotic plaque development. We evaluate the associations of CLC with 
      coronary atherosclerosis presence, burden and cardiovascular risk in patients 
      with rheumatoid arthritis (RA). METHODS: Coronary atherosclerosis (any, high-risk 
      low-attenuation plaque and obstructive plaque) was evaluated with CT angiography 
      in 141 patients. Participants were prospectively followed for 6.0±2.4 years and 
      cardiovascular events including cardiac death, myocardial infarction, unstable 
      angina, stroke, claudication, revascularisation and hospitalised heart failure 
      were recorded. CLC was quantified as intracellular cholesterol in human 
      macrophages after incubation with patient serum. RESULTS: CLC was not linked to 
      overall plaque presence or burden after adjustments for atherosclerotic 
      cardiovascular disease (ASCVD) score, statin use and low-density lipoprotein 
      cholesterol. However, CLC associated with presence and numbers of any, 
      low-attenuation and obstructive plaques exclusively in biologic disease-modifying 
      antirheumatic drugs (bDMARD) non-users (p for interaction ≤0.018). CLC associated 
      with cardiovascular event risk overall after adjustments for ASCVD and number of 
      segments with plaque (HR=1.76 (95% CI 1.16 to 2.67) per 1 SD increase in CLC, 
      p=0.008). Additionally, bDMARD use modified the impact of CLC on event risk; CLC 
      associated with events in bDMARD non-users (HR=2.52 (95% CI 1.36 to 4.65) per 1SD 
      increase in CLC, p=0.003) but not users. CONCLUSION: CLC was linked to long-term 
      cardiovascular event risk in RA and associated with high-risk low attenuation and 
      obstructive coronary plaque presence and burden in bDMARD non-users. Its 
      prospective validation as a predictive biomarker may be, therefore, warranted.
CI  - © Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No 
      commercial re-use. See rights and permissions. Published by BMJ.
FAU - Karpouzas, George Athanasios
AU  - Karpouzas GA
AUID- ORCID: 0000-0003-1065-1563
AD  - Internal Medicine-Rheumatology, Lundquist Institute, Torrance, California, USA 
      gkarpouzas@lundquist.org.
AD  - Department of Rheumatology, Harbor-UCLA Medical Center, Torrance, California, 
      USA.
FAU - Papotti, Bianca
AU  - Papotti B
AD  - Department of Food and Drug, University of Parma, Parma, Italy.
FAU - Ormseth, Sarah
AU  - Ormseth S
AD  - Internal Medicine-Rheumatology, Lundquist Institute, Torrance, California, USA.
FAU - Palumbo, Marcella
AU  - Palumbo M
AD  - Department of Food and Drug, University of Parma, Parma, Italy.
FAU - Hernandez, Elizabeth
AU  - Hernandez E
AD  - Internal Medicine, Lundquist Institute, Torrance, California, USA.
FAU - Adorni, Maria Pia
AU  - Adorni MP
AD  - University of Parma, Parma, Emilia-Romagna, Italy.
FAU - Zimetti, Francesca
AU  - Zimetti F
AD  - Department of Pharmacy, University of Parma, Parma, Emilia-Romagna, Italy.
FAU - Budoff, Matthew
AU  - Budoff M
AD  - Internal Medicine, Lundquist Institute, Torrance, California, USA.
FAU - Ronda, Nicoletta
AU  - Ronda N
AD  - Department of Pharmacy, University of Parma, Parma, Emilia-Romagna, Italy.
LA  - eng
PT  - Journal Article
PL  - England
TA  - RMD Open
JT  - RMD open
JID - 101662038
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - 0 (Biomarkers)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Lipoproteins, LDL)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Antirheumatic Agents/therapeutic use
MH  - *Arthritis, Rheumatoid/complications/drug therapy
MH  - Biological Products/therapeutic use
MH  - Biomarkers
MH  - *Cholesterol/blood/chemistry
MH  - *Coronary Artery Disease/complications/etiology
MH  - Humans
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use
MH  - Lipoproteins, LDL/therapeutic use
MH  - *Macrophages/metabolism
MH  - *Plaque, Atherosclerotic/complications/drug therapy
PMC - PMC9486392
OTO - NOTNLM
OT  - arthritis, rheumatoid
OT  - atherosclerosis
OT  - lipids
COIS- Competing interests: GAK has received consulting and speaker fees from 
      Sanofi-Genzyme-Regeneron, Bristol-Meyer-Squibb and Janssen (less than $10 000 USD 
      each). MJB has received consulting and speaker fees from Pfizer (less than $10 
      000 USD). BP, SRO, MP, EH, MPA, FZ and NR have nothing to disclose.
EDAT- 2022/09/17 06:00
MHDA- 2022/09/21 06:00
PMCR- 2022/09/16
CRDT- 2022/09/16 21:06
PHST- 2022/04/21 00:00 [received]
PHST- 2022/08/03 00:00 [accepted]
PHST- 2022/09/16 21:06 [entrez]
PHST- 2022/09/17 06:00 [pubmed]
PHST- 2022/09/21 06:00 [medline]
PHST- 2022/09/16 00:00 [pmc-release]
AID - rmdopen-2022-002411 [pii]
AID - 10.1136/rmdopen-2022-002411 [doi]
PST - ppublish
SO  - RMD Open. 2022 Sep;8(2):e002411. doi: 10.1136/rmdopen-2022-002411.

PMID- 36050731
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220907
IS  - 1477-9560 (Print)
IS  - 1477-9560 (Electronic)
IS  - 1477-9560 (Linking)
VI  - 20
IP  - 1
DP  - 2022 Sep 1
TI  - The trends in the incidence and thrombosis-related comorbidities of 
      antiphospholipid syndrome: a 14-year nationwide population-based study.
PG  - 50
LID - 10.1186/s12959-022-00409-8 [doi]
LID - 50
AB  - BACKGROUND: This study aims to provide 14-year nationwide epidemiology data to 
      evaluate the incidence ratio of APS in Taiwan and the condition of comorbidities 
      by analyzing the National Health Insurance Research Database. METHODS: Nineteen 
      thousand one hundred sixty-three patients newly diagnosed as having APS during 
      the 2000-2013 period and 76,652 controls (with similar distributions of age and 
      sex) were analyzed. RESULTS: The incidence of APS increased from 4.87 to 6.49 per 
      10,000 person-years in the Taiwan population during 2000-2013. The incidence of 
      APS increased with age after 20 years old, especially in the female population, 
      and it rose rapidly after age over 60 years old. In addition, APS cohorts 
      presented a higher proportion of diabetes mellitus, hypertension, hyperlipidemia, 
      stroke, heart failure, atrial fibrillation, myocardial infarction, PAOD, chronic 
      kidney disease, COPD, deep vein thrombosis, pulmonary embolism, SLE, rheumatoid 
      arthritis, Sjogren's syndrome, and polymyositis. CONCLUSIONS: Our study indicated 
      an increasing trend in APS incidence among the Taiwanese population and a 
      relationship between APS and potential comorbidities. This large national study 
      found that the APS risk is heavily influenced by sex and age. Thus, the 
      distinctive sex and age patterns might be constructive given exploring potential 
      causal mechanisms. Furthermore, our findings indicate that clinicians should have 
      a heightened awareness of the probability of APS, especially in women in certain 
      age groups presenting with symptoms of APS.
CI  - © 2022. The Author(s).
FAU - Yao, Wei-Cheng
AU  - Yao WC
AD  - Department of Anesthesiology and Pain Medicine, Min-Sheng General Hospital, 
      Tao-Yuan City, Taiwan.
FAU - Leong, Kam-Hang
AU  - Leong KH
AD  - Department of Laboratory Medicine, MacKay Memorial Hospital, No. 92, Sec. 2, 
      Zhongshan N. Rd, Taipei City, 10449, Taiwan.
AD  - Department of Medicine, MacKay Medical College, New Taipei City, Taiwan.
FAU - Chiu, Lu-Ting
AU  - Chiu LT
AD  - Management Office for Health Data, China Medical University Hospital, Taichung 
      City, Taiwan.
FAU - Chou, Po-Yi
AU  - Chou PY
AD  - Department of Laboratory Medicine, MacKay Memorial Hospital, No. 92, Sec. 2, 
      Zhongshan N. Rd, Taipei City, 10449, Taiwan.
FAU - Wu, Li-Chih
AU  - Wu LC
AD  - Department of Laboratory Medicine, MacKay Memorial Hospital, No. 92, Sec. 2, 
      Zhongshan N. Rd, Taipei City, 10449, Taiwan.
FAU - Chou, Chih-Yu
AU  - Chou CY
AD  - Department of Medicine, MacKay Medical College, New Taipei City, Taiwan.
FAU - Kuo, Chien-Feng
AU  - Kuo CF
AD  - Department of Medicine, MacKay Medical College, New Taipei City, Taiwan.
AD  - Division of Infectious Diseases, Department of Internal Medicine, MacKay Memorial 
      Hospital, Taipei, Taiwan.
AD  - Department of Nursing, MacKay Junior College of Medicine, Nursing and Management, 
      New Taipei City, Taiwan.
FAU - Tsai, Shin-Yi
AU  - Tsai SY
AD  - Department of Laboratory Medicine, MacKay Memorial Hospital, No. 92, Sec. 2, 
      Zhongshan N. Rd, Taipei City, 10449, Taiwan. stsai22@jhu.edu.
AD  - Department of Medicine, MacKay Medical College, New Taipei City, Taiwan. 
      stsai22@jhu.edu.
AD  - Institute of Biomedical Sciences, MacKay Medical College, New Taipei City, 
      Taiwan. stsai22@jhu.edu.
AD  - Institute of Long-Term Care, MacKay Medical College, New Taipei City, Taiwan. 
      stsai22@jhu.edu.
AD  - Department of Health Policy and Management, Johns Hopkins Bloomberg School of 
      Public Health, Johns Hopkins University, Baltimore, MD, USA. stsai22@jhu.edu.
LA  - eng
PT  - Journal Article
DEP - 20220901
PL  - England
TA  - Thromb J
JT  - Thrombosis journal
JID - 101170542
PMC - PMC9434885
OTO - NOTNLM
OT  - Antiphospholipid syndrome
OT  - Epidemiology
OT  - Incidence
OT  - National health programs
OT  - Nationwide population-based study
COIS- The authors declare that there is no conflict of interest regarding the 
      publication of this paper.
EDAT- 2022/09/02 06:00
MHDA- 2022/09/02 06:01
PMCR- 2022/09/01
CRDT- 2022/09/01 23:46
PHST- 2022/05/23 00:00 [received]
PHST- 2022/08/18 00:00 [accepted]
PHST- 2022/09/01 23:46 [entrez]
PHST- 2022/09/02 06:00 [pubmed]
PHST- 2022/09/02 06:01 [medline]
PHST- 2022/09/01 00:00 [pmc-release]
AID - 10.1186/s12959-022-00409-8 [pii]
AID - 409 [pii]
AID - 10.1186/s12959-022-00409-8 [doi]
PST - epublish
SO  - Thromb J. 2022 Sep 1;20(1):50. doi: 10.1186/s12959-022-00409-8.

PMID- 35974225
OWN - NLM
STAT- MEDLINE
DCOM- 20221115
LR  - 20240406
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Print)
IS  - 0770-3198 (Linking)
VI  - 41
IP  - 12
DP  - 2022 Dec
TI  - Cardiology co-management of rheumatoid arthritis patients with coronary artery 
      disease as an intervention reduces hospitalization rates and adverse event 
      occurrence.
PG  - 3715-3724
LID - 10.1007/s10067-022-06335-4 [doi]
AB  - INTRODUCTION: Rheumatoid arthritis (RA) is a systemic autoimmune disease with 
      important cardiovascular (CV) implications. CV disease represents over half of RA 
      patient deaths and causes significant morbidity. CV manifestations in RA can be 
      complex, raising concerns for adequate patient management and provider-dependent 
      roles. METHODS: This is a retrospective study of patients diagnosed with RA and 
      coronary artery disease (CAD). Patients were identified and filtered via EPIC 
      Database search engine. Parameters were set from January 1, 2014, to December 31, 
      2020. Inclusion criteria consisted of patients who met diagnostic criteria for 
      both RA and CAD. A total of 399 patients met criteria. RESULTS: Of the 399 
      identified patients, 272 were female (68.2%) and 127 were male (31.8%) with a 
      median age of 73 (range 26-98). The population was further divided into two 
      groups: those with established cardiology care versus those without. Patients 
      without cardiology follow-up experienced significantly more hospitalizations (RR 
      1.63 95% CI 1.12, 2.38), higher rates of adverse events including myocardial 
      infarction (MI) (RR 4.82 95% CI 1.94, 11.98), heart failure (HF) (OR 15.81 95% CI 
      3.54, 70.52), and stroke (RR 2.55 95% CI 1.29, 5.03). Patients not followed by 
      cardiology also had numerical increases in CV death (4 deaths compared to none in 
      those with cardiology follow) and all-cause mortality (HR 1.03 95% CI 0.63, 
      1.67). CONCLUSION: Patients with regular cardiology follow-up demonstrated fewer 
      cardiac-related adverse events. This suggests that co-management may have a role 
      in adverse cardiac event risk reduction and should therefore be an early 
      consideration. Key Points • Rheumatoid arthritis patients demonstrate higher 
      rates of coronary disease compared to the general population. Traditional cardiac 
      risk factors may not be entirely responsible for this phenomenon • 
      Hospitalization rates and adverse event occurrence are significantly higher in 
      patients with single-provider care (rheumatology only) compared to dual provider 
      care (rheumatology and cardiology) • Cardiology co-management should be an early 
      consideration in the management of RA patients • Early screening, risk 
      stratification of coronary disease, and utilization of appropriate treatment 
      algorithms are important to decrease morbidity and mortality.
CI  - © 2022. The Author(s), under exclusive licence to International League of 
      Associations for Rheumatology (ILAR).
FAU - Guerra, Jorge D
AU  - Guerra JD
AUID- ORCID: 0000-0003-2554-0567
AD  - Department of Internal Medicine, Baylor Scott & White Medical Center, Texas A&M 
      University College of Medicine, St, MS 01 161B, Temple, TX, 2401 S 3176508, USA. 
      jorgedguerra@gmail.com.
FAU - De Santiago, Andres Belmont
AU  - De Santiago AB
AD  - Department of Internal Medicine, Baylor Scott & White Medical Center, Texas A&M 
      University College of Medicine, St, MS 01 161B, Temple, TX, 2401 S 3176508, USA.
FAU - Reed, Shirley
AU  - Reed S
AD  - Department of Internal Medicine, Baylor Scott & White Medical Center, Texas A&M 
      University College of Medicine, St, MS 01 161B, Temple, TX, 2401 S 3176508, USA.
FAU - Hammonds, Kendall P
AU  - Hammonds KP
AD  - Baylor Scott & White Research Institute, Baylor Scott & White Medical Center, 
      Texas A&M University College of Medicine, Temple, TX, USA.
FAU - Shaver, Courtney
AU  - Shaver C
AD  - Baylor Scott & White Research Institute, Baylor Scott & White Medical Center, 
      Texas A&M University College of Medicine, Temple, TX, USA.
FAU - Widmer, Robert J
AU  - Widmer RJ
AD  - Department of Cardiovascular Disease, Baylor Scott & White Medical Center, Texas 
      A&M University College of Medicine, Temple, TX, USA.
FAU - Scholz, Beth A
AU  - Scholz BA
AD  - Department of Rheumatology, Baylor Scott & White Medical Center, Texas A&M 
      University College of Medicine, Temple, TX, USA.
LA  - eng
PT  - Journal Article
DEP - 20220816
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
SB  - IM
MH  - Humans
MH  - Male
MH  - Female
MH  - *Coronary Artery Disease/complications/epidemiology
MH  - Retrospective Studies
MH  - *Arthritis, Rheumatoid/complications/drug therapy/epidemiology
MH  - Risk Factors
MH  - *Myocardial Infarction/epidemiology
MH  - Hospitalization
MH  - *Cardiology
PMC - PMC9381150
OTO - NOTNLM
OT  - Coronary artery disease
OT  - Hospital mortality
OT  - Rheumatoid arthritis
OT  - Specialization
EDAT- 2022/08/17 06:00
MHDA- 2022/11/16 06:00
PMCR- 2022/08/16
CRDT- 2022/08/16 23:33
PHST- 2022/06/28 00:00 [received]
PHST- 2022/08/09 00:00 [accepted]
PHST- 2022/07/21 00:00 [revised]
PHST- 2022/08/17 06:00 [pubmed]
PHST- 2022/11/16 06:00 [medline]
PHST- 2022/08/16 23:33 [entrez]
PHST- 2022/08/16 00:00 [pmc-release]
AID - 10.1007/s10067-022-06335-4 [pii]
AID - 6335 [pii]
AID - 10.1007/s10067-022-06335-4 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2022 Dec;41(12):3715-3724. doi: 10.1007/s10067-022-06335-4. Epub 
      2022 Aug 16.

PMID- 35919348
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220805
IS  - 2752-4191 (Electronic)
IS  - 2752-4191 (Linking)
VI  - 2
IP  - 3
DP  - 2022 May
TI  - Autoimmune connective tissue diseases and aortic valve replacement outcomes: a 
      population-based study.
PG  - oeac024
LID - 10.1093/ehjopen/oeac024 [doi]
LID - oeac024
AB  - AIMS: Patients with autoimmune connective tissue diseases (CTDs) have a high 
      burden of valvular heart disease and are often thought of as high surgical risk 
      patients. METHODS AND RESULTS: Patients undergoing aortic valve replacement (AVR) 
      were identified in the Nationwide Readmissions Database between January 2012 and 
      December 2018. Patients with a history of systemic lupus erythematosus, 
      rheumatoid arthritis, systemic sclerosis, mixed C, Sjögren syndrome, 
      polymyositis, and dermatomyositis were included in the CTD cohort. Patients 
      undergoing coronary artery bypass grafting concomitantly with AVR were excluded. 
      A total of 569 600 hospitalizations were included, of which16 531 (2.9%) had CTD. 
      CTD patients were more likely to be females, with higher rates of heart failure, 
      pulmonary hypertension, and more likely to be insured by Medicare. CTD patients 
      had lower mortality than non-CTD patients [odds ratio (OR) 0.66; 95% confidence 
      interval (CI): 0.59-0.74] and stroke [OR 0.87; 95% (CI): 0.79-0.97]. CTD patients 
      undergoing SAVR had lower mortality [OR 0.69; 95% (CI): 0.60-0.80] and stroke [OR 
      0.86; 95% (CI): 0.75-0.98). CTD patients undergoing TAVR had lower mortality 
      outcomes [OR 0.67; 95% (CI): 0.56-0.80]; however, they had comparable stroke 
      outcomes [OR 0.97; 95% (CI): 0.83-1.13, P = 0.69]. CONCLUSIONS: Outcomes for 
      patients with CTD requiring AVR are not inferior to their non-CTD counterparts. A 
      comprehensive heart team selection of patients undergoing AVR approaches should 
      place CTD history under consideration; however, pre-existing CTD should not be 
      prohibitive of AVR interventions.
CI  - © The Author(s) 2022. Published by Oxford University Press on behalf of European 
      Society of Cardiology.
FAU - Gad, Mohamed M
AU  - Gad MM
AUID- ORCID: 0000-0003-0218-3317
AD  - Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Heart and 
      Vascular Institute, 9500 Euclid Avenue, J2-3, Cleveland, OH 44195, USA.
FAU - Lichtman, Devora
AU  - Lichtman D
AD  - Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Heart and 
      Vascular Institute, 9500 Euclid Avenue, J2-3, Cleveland, OH 44195, USA.
FAU - Saad, Anas M
AU  - Saad AM
AD  - Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Heart and 
      Vascular Institute, 9500 Euclid Avenue, J2-3, Cleveland, OH 44195, USA.
FAU - Isogai, Toshiaki
AU  - Isogai T
AD  - Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Heart and 
      Vascular Institute, 9500 Euclid Avenue, J2-3, Cleveland, OH 44195, USA.
FAU - Bansal, Agam
AU  - Bansal A
AD  - Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Heart and 
      Vascular Institute, 9500 Euclid Avenue, J2-3, Cleveland, OH 44195, USA.
FAU - Abdallah, Mouin S
AU  - Abdallah MS
AD  - Department of Cardiology, Medstar Heart and Vascular Institute, Fairfax, VA 
      22031, USA.
FAU - Roselli, Eric
AU  - Roselli E
AD  - Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Heart and 
      Vascular Institute, 9500 Euclid Avenue, J2-3, Cleveland, OH 44195, USA.
FAU - Chatterjee, Soumya
AU  - Chatterjee S
AD  - Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Heart and 
      Vascular Institute, 9500 Euclid Avenue, J2-3, Cleveland, OH 44195, USA.
FAU - Reed, Grant W
AU  - Reed GW
AD  - Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Heart and 
      Vascular Institute, 9500 Euclid Avenue, J2-3, Cleveland, OH 44195, USA.
FAU - Kapadia, Samir R
AU  - Kapadia SR
AD  - Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Heart and 
      Vascular Institute, 9500 Euclid Avenue, J2-3, Cleveland, OH 44195, USA.
FAU - Menon, Venu
AU  - Menon V
AD  - Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Heart and 
      Vascular Institute, 9500 Euclid Avenue, J2-3, Cleveland, OH 44195, USA.
FAU - Wassif, Heba
AU  - Wassif H
AD  - Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Heart and 
      Vascular Institute, 9500 Euclid Avenue, J2-3, Cleveland, OH 44195, USA.
LA  - eng
PT  - Journal Article
DEP - 20220406
PL  - England
TA  - Eur Heart J Open
JT  - European heart journal open
JID - 9918282081406676
PMC - PMC9242052
OTO - NOTNLM
OT  - Aortic valve replacement
OT  - Autoimmune connective tissue diseases
OT  - Valvular heart disease
EDAT- 2022/08/04 06:00
MHDA- 2022/08/04 06:01
PMCR- 2022/04/06
CRDT- 2022/08/03 02:07
PHST- 2022/01/06 00:00 [received]
PHST- 2022/03/26 00:00 [revised]
PHST- 2022/08/03 02:07 [entrez]
PHST- 2022/08/04 06:00 [pubmed]
PHST- 2022/08/04 06:01 [medline]
PHST- 2022/04/06 00:00 [pmc-release]
AID - oeac024 [pii]
AID - 10.1093/ehjopen/oeac024 [doi]
PST - epublish
SO  - Eur Heart J Open. 2022 Apr 6;2(3):oeac024. doi: 10.1093/ehjopen/oeac024. 
      eCollection 2022 May.

PMID- 35840149
OWN - NLM
STAT- MEDLINE
DCOM- 20230103
LR  - 20240910
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 50
IP  - 1
DP  - 2023 Jan
TI  - Risk Factors for Dementia in Patients With Incident Rheumatoid Arthritis: A 
      Population-Based Cohort Study.
PG  - 48-55
LID - 10.3899/jrheum.220200 [doi]
AB  - OBJECTIVE: Growing evidence suggests that patients with rheumatoid arthritis (RA) 
      have increased risk for dementia. We assessed risk factors for incident dementia 
      in an inception cohort of patients with RA. METHODS: This retrospective 
      population-based cohort study included residents of 8 counties in Minnesota who 
      were ≥ 50 years of age when they met 1987 American College of Rheumatology 
      criteria for incident RA between 1980 and 2014 and were followed until 
      death/migration or December 31, 2019. Patients with dementia before RA incidence 
      were excluded. Incident dementia was defined as 2 relevant International 
      Classification of Diseases, 9th or 10th revision codes at least 30 days apart. 
      Data on sociodemographics, disease characteristics, 
      cardiovascular/cerebrovascular disease (CVD) risk factors, and comorbidities were 
      abstracted from medical records. RESULTS: The study included 886 patients with RA 
      (mean age 65.1 yrs, 65.2% female). During the follow-up period (median 8.5 yrs), 
      103 patients developed dementia. After adjusting for age, sex, and calendar year 
      of RA incidence, older age at RA incidence (HR 1.14 per 1 year increase, 95% CI 
      1.12-1.17), rheumatoid nodules (HR 1.76, 95% CI 1.05-2.95), hypertension (HR 
      1.84, 95% CI 1.19-2.85), presence of large joint swelling (HR 2.03, 95% CI 
      1.14-3.60), any CVD (HR 2.25, 95% CI 1.38-3.66), particularly ischemic stroke (HR 
      3.16, 95% CI 1.84-5.43) and heart failure (HR 1.82, 95% CI 1.10-3.00), anxiety 
      (HR 1.86, 95% CI 1.16-2.97), and depression (HR 2.63, 95% CI 1.76-3.93) were 
      associated with increased risk of dementia. After adjusting for CVD risk factors 
      and any CVD, all covariates listed above were still significantly associated with 
      risk of dementia. CONCLUSION: Apart from age, hypertension, depression, and 
      anxiety, all of which are universally recognized risk factors for dementia, 
      clinically active RA and presence of CVD were associated with an elevated risk of 
      dementia incidence among patients with RA.
CI  - Copyright © 2023 by the Journal of Rheumatology.
FAU - Kodishala, Chanakya
AU  - Kodishala C
AUID- ORCID: 0000-0003-3553-4304
AD  - C. Kodishala, MBBS, DM, V.L. Kronzer, MD, MSCI, J.M. Davis III, MD, Division of 
      Rheumatology, Mayo Clinic.
FAU - Hulshizer, Cassondra A
AU  - Hulshizer CA
AD  - C.A. Hulshizer, BA, Department of Quantitative Health Sciences, Mayo Clinic.
FAU - Kronzer, Vanessa L
AU  - Kronzer VL
AUID- ORCID: 0000-0002-7489-3134
AD  - C. Kodishala, MBBS, DM, V.L. Kronzer, MD, MSCI, J.M. Davis III, MD, Division of 
      Rheumatology, Mayo Clinic.
FAU - Davis, John M 3rd
AU  - Davis JM 3rd
AUID- ORCID: 0000-0002-9710-8143
AD  - C. Kodishala, MBBS, DM, V.L. Kronzer, MD, MSCI, J.M. Davis III, MD, Division of 
      Rheumatology, Mayo Clinic.
FAU - Ramanan, Vijay K
AU  - Ramanan VK
AUID- ORCID: 0000-0001-6591-8734
AD  - V.K. Ramanan, MD, PhD, Department of Neurology, Mayo Clinic.
FAU - Vassilaki, Maria
AU  - Vassilaki M
AUID- ORCID: 0000-0001-8328-136X
AD  - M. Vassilaki, MD, PhD, Department of Quantitative Health Sciences, Mayo Clinic.
FAU - Mielke, Michelle M
AU  - Mielke MM
AUID- ORCID: 0000-0001-7177-1185
AD  - M.M. Mielke, PhD, Department of Quantitative Health Sciences, Department of 
      Neurology, Mayo Clinic.
FAU - Crowson, Cynthia S
AU  - Crowson CS
AUID- ORCID: 0000-0001-5847-7475
AD  - C.S. Crowson, PhD, Division of Rheumatology, Department of Quantitative Health 
      Sciences, Mayo Clinic.
FAU - Myasoedova, Elena
AU  - Myasoedova E
AUID- ORCID: 0000-0003-2006-1436
AD  - E. Myasoedova, MD, PhD, Division of Rheumatology, Department of Internal 
      Medicine, Division of Epidemiology, Department of Quantitative Health Sciences, 
      Mayo Clinic, Rochester, Minnesota, USA. Myasoedova.elena@mayo.edu.
LA  - eng
GR  - R01 AR046849/AR/NIAMS NIH HHS/United States
GR  - R01 AG034676/AG/NIA NIH HHS/United States
GR  - R33 AG058738/AG/NIA NIH HHS/United States
GR  - K24 AG078179/AG/NIA NIH HHS/United States
GR  - R01 AG068192/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20220715
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
SB  - IM
CIN - J Rheumatol. 2023 Jan;50(1):3-5. doi: 10.3899/jrheum.220991. PMID: 36318997
CIN - J Rheumatol. 2023 Jun;50(6):851-852. doi: 10.3899/jrheum.220934. PMID: 36379582
MH  - Humans
MH  - Female
MH  - Aged
MH  - Male
MH  - Cohort Studies
MH  - Retrospective Studies
MH  - *Arthritis, Rheumatoid/complications/epidemiology
MH  - Risk Factors
MH  - *Hypertension/epidemiology/complications
MH  - Incidence
MH  - *Dementia/epidemiology/complications
MH  - *Cardiovascular Diseases/epidemiology/complications
PMC - PMC9812854
MID - NIHMS1820593
OTO - NOTNLM
OT  - cardiovascular disease
OT  - dementia
OT  - depression
OT  - disease activity
OT  - rheumatoid arthritis
COIS- Conflict of Interest: CK: none, CAH: none, VLK: none, JMD: Research grant from 
      Pfizer, VKR: none, MV: Received research funding from F. Hoffmann-La Roche Ltd 
      and Biogen; consultant for F. Hoffmann-La Roche Ltd; receives research funding 
      from NIA and has equity ownership in Abbott Laboratories, Johnson and Johnson, 
      Medtronic, and Amgen, MMM: Consulted for Biogen, Brain Protection Company, and 
      LabCorp. Receives research funding from NIH and DOD, CSC: none, EM: none
EDAT- 2022/07/16 06:00
MHDA- 2023/01/04 06:00
PMCR- 2024/01/01
CRDT- 2022/07/15 20:43
PHST- 2022/06/30 00:00 [accepted]
PHST- 2022/07/16 06:00 [pubmed]
PHST- 2023/01/04 06:00 [medline]
PHST- 2022/07/15 20:43 [entrez]
PHST- 2024/01/01 00:00 [pmc-release]
AID - jrheum.220200 [pii]
AID - 10.3899/jrheum.220200 [doi]
PST - ppublish
SO  - J Rheumatol. 2023 Jan;50(1):48-55. doi: 10.3899/jrheum.220200. Epub 2022 Jul 15.

PMID- 35821191
OWN - NLM
STAT- MEDLINE
DCOM- 20221003
LR  - 20221116
IS  - 1879-0828 (Electronic)
IS  - 0953-6205 (Linking)
VI  - 104
DP  - 2022 Oct
TI  - C-reactive protein and 10-year cardiovascular risk in rheumatoid arthritis.
PG  - 49-54
LID - S0953-6205(22)00251-5 [pii]
LID - 10.1016/j.ejim.2022.07.001 [doi]
AB  - OBJECTIVES: To evaluate the association between C-reactive protein (CRP) and 
      10-year risk of cardiovascular (CV) events using the Expanded Cardiovascular Risk 
      Prediction Score for Rheumatoid Arthritis (ERS-RA), based on conventional and 
      RA-specific risk factors but not CRP, in RA patients without previous 
      cardiovascular events. METHODS: ERS-RA was calculated in 1,251 "Cardiovascular 
      Obesity and Rheumatic Disease Study (CORDIS)" database patients [(age 60.4(9.3) 
      years; 78% female; disease duration, 11.6(8) years; CDAI, 9(9); CRP, 6.8(12) 
      mg/L]. RESULTS: The mean (SD) 10-year risk of CV events was 12.9% (10). After 
      adjusting for the use of DMARDs and biologics, CRP concentrations were 
      significantly associated with 10-year risk of CV events (coefficient=0.005 for 
      each 10 mg/L CRP increment; 95%CI 0.000-0.111; p = 0.047). In mediation analysis, 
      the association between CRP and ERS-RA was not explained by disease activity. 
      CONCLUSION: In a large cohort of RA patients without previous cardiovascular 
      events, a 20 mg/L increase in CRP concentrations was associated with a 1% 
      increase in 10-year risk of CV events. This suggests that actively targeting 
      residual inflammatory risk beyond conventional and RA-specific risk factors might 
      further reduce CV event rates in RA patients.
CI  - Copyright © 2022 European Federation of Internal Medicine. Published by Elsevier 
      B.V. All rights reserved.
FAU - Erre, Gian Luca
AU  - Erre GL
AD  - University and AOU of Sassari, Dipartimento di Medicina, Chirurgia e Farmacia, 
      Sassari, Italy. Electronic address: glerre@uniss.it.
FAU - Cacciapaglia, Fabio
AU  - Cacciapaglia F
AD  - University and AOU, Policlinico of Bari, Department of Emergency and Organs 
      Transplantation, Bari, Italy.
FAU - Sakellariou, Garifallia
AU  - Sakellariou G
AD  - University of Pavia, Istituti Clinici Scientifici Maugeri IRCCS Pavia, Pavia, 
      Italy.
FAU - Manfredi, Andreina
AU  - Manfredi A
AD  - Azienda Ospedaliera Universitaria Policlinico di Modena, Unit of Rheumatology, 
      Modena, Italy.
FAU - Bartoloni, Elena
AU  - Bartoloni E
AD  - University of Perugia, Department of Medicine and Surgery, Perugia, Italy.
FAU - Viapiana, Ombretta
AU  - Viapiana O
AD  - University of Verona, Dipartimento di Medicina, Verona, Italy.
FAU - Fornaro, Marco
AU  - Fornaro M
AD  - University and AOU, Policlinico of Bari, Department of Emergency and Organs 
      Transplantation, Bari, Italy.
FAU - Cauli, Alberto
AU  - Cauli A
AD  - Rheumatology Unit, Department of Medical Sciences and Public Health, AOU and 
      University of Cagliari, Italy.
FAU - Mangoni, Arduino Aleksander
AU  - Mangoni AA
AD  - Flinders University and Flinders Medical Centre, Discipline of Clinical 
      Pharmacology, College of Medicine and Public Health, Adelaide, Australia.
FAU - Woodman, Richard John
AU  - Woodman RJ
AD  - Flinders University, Centre of Epidemiology and Biostatistics, College of 
      Medicine and Public Health, Adelaide, Australia.
FAU - Palermo, Bianca Lucia
AU  - Palermo BL
AD  - University of Pavia, IRCSS San Matteo, Pavia, Italy.
FAU - Gremese, Elisa
AU  - Gremese E
AD  - Policlinico Gemelli, Università Cattolica del Sacro Cuore, Dipartimento di 
      Scienze Mediche e Chirurgiche, Roma, Italy.
FAU - Cafaro, Giacomo
AU  - Cafaro G
AD  - University of Verona, Dipartimento di Medicina, Verona, Italy.
FAU - Nucera, Valeria
AU  - Nucera V
AD  - University of Messina, Dipartimento di Medicina Clinica e Sperimentale, Messina, 
      Italy.
FAU - Vacchi, Caterina
AU  - Vacchi C
AD  - University of Modena and Reggio Emilia, Clinical and Experimental Medicine PhD 
      Program, Modena, Italy.
FAU - Spinelli, Francesca Romana
AU  - Spinelli FR
AD  - Università La Sapienza, Dipartimento di Scienze Cliniche Internistiche, 
      Anestesiologiche e Cardiovascolari, Roma, Italy.
FAU - Atzeni, Fabiola
AU  - Atzeni F
AD  - University of Messina, Dipartimento di Medicina Clinica e Sperimentale, Messina, 
      Italy.
FAU - Piga, Matteo
AU  - Piga M
AD  - Rheumatology Unit, Department of Medical Sciences and Public Health, AOU and 
      University of Cagliari, Italy.
CN  - “Cardiovascular, Obesity and Rheumatic Disease Study (CORDIS) Group” of the 
      Italian Society of Rheumatology (SIR)
LA  - eng
PT  - Journal Article
DEP - 20220709
PL  - Netherlands
TA  - Eur J Intern Med
JT  - European journal of internal medicine
JID - 9003220
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - 0 (CRP protein, human)
RN  - 0 (Receptors, Immunologic)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - *Antirheumatic Agents/therapeutic use
MH  - *Arthritis, Rheumatoid/complications/drug therapy
MH  - *Biological Products/therapeutic use
MH  - C-Reactive Protein/analysis
MH  - *Cardiovascular Diseases/complications/etiology
MH  - Female
MH  - Heart Disease Risk Factors
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Receptors, Immunologic
MH  - Risk Factors
OTO - NOTNLM
OT  - C-reactive protein
OT  - Cardiovascular risk score
OT  - Inflammation
OT  - Myocardial infarction
OT  - Stroke
COIS- Declaration of Competing Interests All Authors report no conflict of interest.
EDAT- 2022/07/13 06:00
MHDA- 2022/10/04 06:00
CRDT- 2022/07/12 23:57
PHST- 2022/04/14 00:00 [received]
PHST- 2022/06/17 00:00 [revised]
PHST- 2022/07/05 00:00 [accepted]
PHST- 2022/07/13 06:00 [pubmed]
PHST- 2022/10/04 06:00 [medline]
PHST- 2022/07/12 23:57 [entrez]
AID - S0953-6205(22)00251-5 [pii]
AID - 10.1016/j.ejim.2022.07.001 [doi]
PST - ppublish
SO  - Eur J Intern Med. 2022 Oct;104:49-54. doi: 10.1016/j.ejim.2022.07.001. Epub 2022 
      Jul 9.

PMID- 35810846
OWN - NLM
STAT- MEDLINE
DCOM- 20220830
LR  - 20220830
IS  - 1535-6280 (Electronic)
IS  - 0146-2806 (Linking)
VI  - 47
IP  - 10
DP  - 2022 Oct
TI  - Outcomes of the First Episode of STEMI in Rheumatoid Arthritis Patients from the 
      National Inpatient Sample Database, 2016-2019.
PG  - 101310
LID - S0146-2806(22)00207-9 [pii]
LID - 10.1016/j.cpcardiol.2022.101310 [doi]
AB  - Patients with Rheumatoid arthritis (RA) have a higher burden of cardiovascular 
      diseases (CVDs), but conflicting results were seen regarding in-hospital outcomes 
      of STEMI in patients with RA compared to patients without RA. Our study aimed to 
      compare in-hospital outcomes of the first episode of STEMI between patients with 
      and without RA. The NIS database was used to conduct a retrospective study of 
      U.S. hospitalizations with a primary diagnosis of first-time STEMI from 2016 to 
      2019. We divided our study population into two cohorts, with diagnosis codes for 
      RA and those without RA and compared baseline demographics, comorbidities, and 
      in-hospital outcomes and finally performed a multivariate logistic regression 
      analysis after adjusting for baseline factors. Our analysis revealed that 
      patients with RA were statistically more likely to be older, white, and female 
      and had more hypertension, cardiomyopathy, CKD stage 3 or greater and heart 
      failure. After adjusting for potential confounders, we found lower inpatient 
      mortality in the first STEMI with RA cohort (adjusted OR: 0.70, 95% CI of 
      0.56-0.87, p <0.002) compared to the patients without RA. However, there was no 
      statistically significant difference between the two groups in rates of 
      in-hospital complications, including repeat MI, acute heart failure, arrhythmias, 
      cardiac arrest, cardiogenic shock, and stroke. Further patient-level studies are 
      needed to understand better the impact of newer biologics and the effect of risk 
      factor modification on this patient subset.
CI  - Copyright © 2022 Elsevier Inc. All rights reserved.
FAU - Suwal, Amar
AU  - Suwal A
AD  - Department of Medicine, Reading Hospital, Tower Health, Reading, PA. Electronic 
      address: suwalamar15@gmail.com.
FAU - Shrestha, Biraj
AU  - Shrestha B
AD  - Department of Medicine, Reading Hospital, Tower Health, Reading, PA.
FAU - Setyono, Devy
AU  - Setyono D
AD  - Emkey Arthritis and Osteoporosis Clinic.
FAU - Poudel, Bidhya
AU  - Poudel B
AD  - Department of Medicine, AMITA Health Saint Francis Hospital, Evanston, IL, United 
      States of America.
FAU - Donato, Anthony
AU  - Donato A
AD  - Department of Medicine, Reading Hospital, Tower Health, Reading, PA.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220708
PL  - Netherlands
TA  - Curr Probl Cardiol
JT  - Current problems in cardiology
JID - 7701802
SB  - IM
MH  - *Arthritis, Rheumatoid
MH  - Female
MH  - *Heart Failure
MH  - Humans
MH  - Inpatients
MH  - Retrospective Studies
MH  - *ST Elevation Myocardial Infarction
MH  - Shock, Cardiogenic
EDAT- 2022/07/11 06:00
MHDA- 2022/08/31 06:00
CRDT- 2022/07/10 19:24
PHST- 2022/06/28 00:00 [received]
PHST- 2022/07/01 00:00 [accepted]
PHST- 2022/07/11 06:00 [pubmed]
PHST- 2022/08/31 06:00 [medline]
PHST- 2022/07/10 19:24 [entrez]
AID - S0146-2806(22)00207-9 [pii]
AID - 10.1016/j.cpcardiol.2022.101310 [doi]
PST - ppublish
SO  - Curr Probl Cardiol. 2022 Oct;47(10):101310. doi: 10.1016/j.cpcardiol.2022.101310. 
      Epub 2022 Jul 8.

PMID- 35798796
OWN - NLM
STAT- MEDLINE
DCOM- 20220711
LR  - 20220915
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 12
IP  - 1
DP  - 2022 Jul 7
TI  - Effects of immune-mediated inflammatory diseases on cardiovascular diseases in 
      patients with type 2 diabetes: a nationwide population-based study.
PG  - 11548
LID - 10.1038/s41598-022-15436-8 [doi]
LID - 11548
AB  - Both type 2 diabetes and immune-mediated inflammatory diseases (IMIDs), such as 
      Crohn's disease (CD), ulcerative colitis, rheumatoid arthritis (RA), ankylosing 
      spondylitis (AS), and psoriasis (PsO) are risk factors of cardiovascular disease. 
      Whether presence of IMIDs in patients with type 2 diabetes increases their 
      cardiovascular risk remains unclear. We aimed to investigate the risk of 
      cardiovascular morbidity and mortality in patients with type 2 diabetes and 
      IMIDs. Patients with type 2 diabetes without cardiovascular disease were 
      retrospectively enrolled from nationwide data provided by the Korean National 
      Health Insurance Service. The primary outcome was cardiovascular mortality, and 
      the secondary outcomes were myocardial infarction (MI), stroke, and all-cause 
      mortality. Inverse probability of treatment weighting (IPTW)-adjusted Cox 
      proportional hazard regression analysis was performed to estimate the hazard 
      ratios (HRs) and 95% confidence intervals (95% CIs) for each IMID. Overall 
      2,263,853 patients with type 2 diabetes were analyzed. CD was associated with a 
      significantly higher risk of stroke (IPTW-adjusted HR: 1.877 [95%CI 1.046, 
      3.367]). UC was associated with a significantly higher risk of MI (1.462 [1.051, 
      2.032]). RA was associated with a significantly higher risk of cardiovascular 
      mortality (2.156 [1.769, 2.627]), MI (1.958 [1.683, 2.278]), stroke (1.605 
      [1.396, 1.845]), and all-cause mortality (2.013 [1.849, 2.192]). AS was 
      associated with a significantly higher risk of MI (1.624 [1.164, 2.266]), stroke 
      (2.266 [1.782, 2.882]), and all-cause mortality (1.344 [1.089, 1.658]). PsO was 
      associated with a significantly higher risk of MI (1.146 [1.055, 1.246]), stroke 
      (1.123 [1.046, 1.205]) and all-cause mortality (1.115 [1.062, 1.171]). In 
      patients with type 2 diabetes, concomitant IMIDs increase the risk of 
      cardiovascular morbidity and mortality. Vigilant surveillance for cardiovascular 
      disease is needed in patients with type 2 diabetes and IMIDs.
CI  - © 2022. The Author(s).
FAU - Kwon, Oh Chan
AU  - Kwon OC
AD  - Division of Rheumatology, Department of Internal Medicine, Yonsei University 
      College of Medicine, Seoul, Korea.
FAU - Han, Kyungdo
AU  - Han K
AD  - Department of Statistics and Actuarial Science, Soongsil University, 369 
      Sangdo-ro, Dongjak-gu, Seoul, 06978, Korea. hkd917@naver.com.
FAU - Chun, Jaeyoung
AU  - Chun J
AD  - Division of Gastroenterology, Department of Internal Medicine, Yonsei University 
      College of Medicine, 20, Eonju-ro 63-gil, Gangnam-gu, Seoul, 06229, Korea. 
      j40479@gmail.com.
FAU - Kim, Ryul
AU  - Kim R
AD  - Department of Neurology, Inha University Hospital, Incheon, Korea.
FAU - Hong, Seung Wook
AU  - Hong SW
AD  - Department of Gastroenterology, University of Ulsan College of Medicine, Asan 
      Medical Center, Seoul, Korea.
FAU - Kim, Jie-Hyun
AU  - Kim JH
AD  - Division of Gastroenterology, Department of Internal Medicine, Yonsei University 
      College of Medicine, 20, Eonju-ro 63-gil, Gangnam-gu, Seoul, 06229, Korea.
FAU - Youn, Young Hoon
AU  - Youn YH
AD  - Division of Gastroenterology, Department of Internal Medicine, Yonsei University 
      College of Medicine, 20, Eonju-ro 63-gil, Gangnam-gu, Seoul, 06229, Korea.
FAU - Park, Hyojin
AU  - Park H
AD  - Division of Gastroenterology, Department of Internal Medicine, Yonsei University 
      College of Medicine, 20, Eonju-ro 63-gil, Gangnam-gu, Seoul, 06229, Korea.
FAU - Park, Min-Chan
AU  - Park MC
AD  - Division of Rheumatology, Department of Internal Medicine, Yonsei University 
      College of Medicine, Seoul, Korea.
CN  - Gastroenterology, Neurology and Rheumatology National Data Science Research 
      (GUARANTEE) Group
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220707
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
SB  - IM
MH  - *Arthritis, Rheumatoid/complications
MH  - *Cardiovascular Diseases
MH  - *Colitis, Ulcerative/epidemiology
MH  - *Crohn Disease/complications
MH  - *Diabetes Mellitus, Type 2/complications/epidemiology
MH  - Humans
MH  - *Myocardial Infarction/complications/epidemiology
MH  - *Psoriasis/complications
MH  - Retrospective Studies
MH  - Risk Factors
MH  - *Spondylitis, Ankylosing/complications
MH  - *Stroke/complications/epidemiology
PMC - PMC9262934
COIS- Dr. Chun received a grant given by Eisai Co. All other authors disclose that they 
      have no financial, professional, or personal conflicts related to this 
      publication.
FIR - Kwon, Oh Chan
IR  - Kwon OC
FIR - Han, Kyungdo
IR  - Han K
FIR - Chun, Jaeyoung
IR  - Chun J
FIR - Kim, Ryul
IR  - Kim R
FIR - Hong, Seung Wook
IR  - Hong SW
FIR - Kim, Jie-Hyun
IR  - Kim JH
FIR - Youn, Young Hoon
IR  - Youn YH
FIR - Park, Hyojin
IR  - Park H
FIR - Park, Min-Chan
IR  - Park MC
EDAT- 2022/07/08 06:00
MHDA- 2022/07/12 06:00
PMCR- 2022/07/07
CRDT- 2022/07/07 23:24
PHST- 2022/03/10 00:00 [received]
PHST- 2022/06/23 00:00 [accepted]
PHST- 2022/07/07 23:24 [entrez]
PHST- 2022/07/08 06:00 [pubmed]
PHST- 2022/07/12 06:00 [medline]
PHST- 2022/07/07 00:00 [pmc-release]
AID - 10.1038/s41598-022-15436-8 [pii]
AID - 15436 [pii]
AID - 10.1038/s41598-022-15436-8 [doi]
PST - epublish
SO  - Sci Rep. 2022 Jul 7;12(1):11548. doi: 10.1038/s41598-022-15436-8.

PMID- 35772915
OWN - NLM
STAT- MEDLINE
DCOM- 20220704
LR  - 20230706
IS  - 1558-3597 (Electronic)
IS  - 0735-1097 (Print)
IS  - 0735-1097 (Linking)
VI  - 80
IP  - 1
DP  - 2022 Jul 5
TI  - Cardiovascular Risks of Hydroxychloroquine vs Methotrexate in Patients With 
      Rheumatoid Arthritis.
PG  - 36-46
LID - S0735-1097(22)04935-X [pii]
LID - 10.1016/j.jacc.2022.04.039 [doi]
AB  - BACKGROUND: Hydroxychloroquine is often used as a first-line treatment of 
      rheumatoid arthritis despite limited evidence on its cardiovascular risk. 
      OBJECTIVES: We conducted a cardiovascular safety evaluation comparing 
      hydroxychloroquine to methotrexate among patients with rheumatoid arthritis. 
      METHODS: Using Medicare data (2008-2016), we identified 54,462 propensity 
      score-matched patients with rheumatoid arthritis, aged ≥65 years, who initiated 
      hydroxychloroquine or methotrexate. Primary outcomes were sudden cardiac arrest 
      or ventricular arrythmia (SCA/VA) and major adverse cardiovascular event (MACE). 
      Secondary outcomes were cardiovascular mortality, all-cause mortality, myocardial 
      infarction, stroke, and hospitalized heart failure (HF). We also examined 
      treatment effect modification by history of HF. RESULTS: Hydroxychloroquine was 
      not associated with risk of SCA/VA (HR: 1.03; 95% CI: 0.79-1.35) or MACE (HR: 
      1.07; 95% CI: 0.97-1.18) compared with methotrexate. In patients with history of 
      HF, hydroxychloroquine initiators had a higher risk of MACE (HR: 1.30; 95% CI: 
      1.08-1.56), cardiovascular mortality (HR: 1.34; 95% CI: 1.06-1.70), all-cause 
      mortality (HR: 1.22; 95% CI: 1.04-1.43), myocardial infarction (HR: 1.74; 95% CI: 
      1.25-2.42), and hospitalized HF (HR: 1.29; 95% CI: 1.07-1.54) compared to 
      methotrexate initiators. Cardiovascular risks were not different in patients 
      without history of HF except for an increased hospitalized HF risk (HR: 1.57; 
      95% CI: 1.30-1.90) among hydroxychloroquine initiators. CONCLUSIONS: In older 
      patients with rheumatoid arthritis, hydroxychloroquine and methotrexate showed 
      similar SCA/VA and MACE risks; however, hydroxychloroquine initiators with 
      history of HF had higher risks of MACE, cardiovascular mortality, all-cause 
      mortality, and myocardial infarction. An increased hospitalized HF risk was 
      observed among hydroxychloroquine initiators regardless of an HF history.
CI  - Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier 
      Inc. All rights reserved.
FAU - D'Andrea, Elvira
AU  - D'Andrea E
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital and Harvard Medical School, Boston, Massachusetts, USA.
FAU - Desai, Rishi J
AU  - Desai RJ
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital and Harvard Medical School, Boston, Massachusetts, USA.
FAU - He, Mengdong
AU  - He M
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital and Harvard Medical School, Boston, Massachusetts, USA.
FAU - Glynn, Robert J
AU  - Glynn RJ
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital and Harvard Medical School, Boston, Massachusetts, USA.
FAU - Lee, Hemin
AU  - Lee H
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital and Harvard Medical School, Boston, Massachusetts, USA.
FAU - Weinblatt, Michael E
AU  - Weinblatt ME
AD  - Division of Rheumatology, Inflammation, and Immunity, Brigham and Women's 
      Hospital and Harvard Medical School, Boston, Massachusetts, USA.
FAU - Kim, Seoyoung C
AU  - Kim SC
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital and Harvard Medical School, Boston, Massachusetts, USA; Division of 
      Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital and 
      Harvard Medical School, Boston, Massachusetts, USA. Electronic address: 
      sykim@bwh.harvard.edu.
LA  - eng
GR  - K24 AR078959/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Am Coll Cardiol
JT  - Journal of the American College of Cardiology
JID - 8301365
RN  - 0 (Antirheumatic Agents)
RN  - 4QWG6N8QKH (Hydroxychloroquine)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
CIN - J Am Coll Cardiol. 2022 Jul 5;80(1):47-49. doi: 10.1016/j.jacc.2022.04.038. PMID: 
      35772916
MH  - Aged
MH  - *Antirheumatic Agents/adverse effects
MH  - *Arthritis, Rheumatoid/drug therapy
MH  - *Cardiovascular Diseases/chemically induced/drug therapy/epidemiology
MH  - Heart Disease Risk Factors
MH  - Humans
MH  - Hydroxychloroquine/adverse effects
MH  - Medicare
MH  - Methotrexate/adverse effects
MH  - *Myocardial Infarction/chemically induced/drug therapy/epidemiology
MH  - Risk Factors
MH  - United States/epidemiology
PMC - PMC9722228
MID - NIHMS1851197
OTO - NOTNLM
OT  - administrative data
OT  - cardiovascular
OT  - disease-modifying antirheumatic drugs (DMARDs)
OT  - pharmacoepidemiology
OT  - rheumatoid arthritis
COIS- Funding Support and Author Disclosures This work was supported by the National 
      Institutes of Health K24-AR078959 as well as internal resources in the Division 
      of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women’s Hospital, 
      Harvard Medical School. Dr Desai has received research grants from Vertex, Bayer, 
      and Novartis for unrelated studies. Dr Gynn has received research grants from 
      AstraZeneca, Kowa, Novartis, and Pfizer for unrelated studies. Dr Weinblatt has 
      received research grants from Amgen, Bristol Myers Squibb, Eli Lilly, and Sanofi 
      for unrelated studies; has stock options from Canfite, Scipher, Vorso, and 
      Inmedix; and has provided consulting for AbbVie, Amgen, Aclaris, Arena, Bristol 
      Myers Squibb, CorEvitas, EqRx, Genosco, GlaxoSmithKline, Gilead, Eli Lilly, 
      Merck, Novartis, Pfizer, Roche, Scipher, SetPoint, and Tremeau. Dr Kim has 
      received research grants from Roche, Pfizer, AbbVie, and Bristol Myers Squibb for 
      unrelated studies. All other authors have reported that they have no 
      relationships relevant to the contents of this paper to disclose.
EDAT- 2022/07/01 06:00
MHDA- 2022/07/06 06:00
PMCR- 2023/07/05
CRDT- 2022/06/30 21:04
PHST- 2022/04/01 00:00 [received]
PHST- 2022/04/05 00:00 [accepted]
PHST- 2022/06/30 21:04 [entrez]
PHST- 2022/07/01 06:00 [pubmed]
PHST- 2022/07/06 06:00 [medline]
PHST- 2023/07/05 00:00 [pmc-release]
AID - S0735-1097(22)04935-X [pii]
AID - 10.1016/j.jacc.2022.04.039 [doi]
PST - ppublish
SO  - J Am Coll Cardiol. 2022 Jul 5;80(1):36-46. doi: 10.1016/j.jacc.2022.04.039.

PMID- 35743556
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220716
IS  - 2077-0383 (Print)
IS  - 2077-0383 (Electronic)
IS  - 2077-0383 (Linking)
VI  - 11
IP  - 12
DP  - 2022 Jun 17
TI  - Management of Cardiovascular Disease Risk in Rheumatoid Arthritis.
LID - 10.3390/jcm11123487 [doi]
LID - 3487
AB  - Cardiovascular diseases, including ischemic heart disease and stroke, reportedly 
      comprise the top two causes of global mortality [...].
FAU - Dessein, Patrick H
AU  - Dessein PH
AUID- ORCID: 0000-0002-9357-4630
AD  - Departments of Medicine and Physiology, Faculty of Health Sciences, Universtiy of 
      Witwatersrand, Johannesburg 2000, South Africa.
FAU - Gonzalez-Gay, Miguel A
AU  - Gonzalez-Gay MA
AUID- ORCID: 0000-0002-7924-7406
AD  - Division of Rheumatology and Epidemiology, Genetics and Atherosclerosis Research 
      Group on Systemic Inflammatory Diseases, Hospital Universitario Marques de 
      Valdecilla, Instituto de Investigacion Marques de Valdecilla (IDIVAL), 39011 
      Santander, Spain.
AD  - Department of Medicine and Psychiatry, Universidad de Cantabria, 39011 Santander, 
      Spain.
LA  - eng
PT  - Editorial
DEP - 20220617
PL  - Switzerland
TA  - J Clin Med
JT  - Journal of clinical medicine
JID - 101606588
PMC - PMC9225346
COIS- The authors declare that they have no conflict of interest in relation to this 
      manuscript.
EDAT- 2022/06/25 06:00
MHDA- 2022/06/25 06:01
PMCR- 2022/06/17
CRDT- 2022/06/24 01:25
PHST- 2022/06/12 00:00 [received]
PHST- 2022/06/15 00:00 [accepted]
PHST- 2022/06/24 01:25 [entrez]
PHST- 2022/06/25 06:00 [pubmed]
PHST- 2022/06/25 06:01 [medline]
PHST- 2022/06/17 00:00 [pmc-release]
AID - jcm11123487 [pii]
AID - jcm-11-03487 [pii]
AID - 10.3390/jcm11123487 [doi]
PST - epublish
SO  - J Clin Med. 2022 Jun 17;11(12):3487. doi: 10.3390/jcm11123487.

PMID- 35734296
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220716
IS  - 2666-5018 (Electronic)
IS  - 2666-5018 (Linking)
VI  - 3
IP  - 3
DP  - 2022 Jun
TI  - Safety and efficacy outcomes of atrial fibrillation ablation in patients with 
      rheumatoid arthritis.
PG  - 261-268
LID - 10.1016/j.hroo.2022.03.001 [doi]
AB  - BACKGROUND: Rheumatoid arthritis (RA) is an immune-mediated inflammatory disease 
      associated with atrial fibrillation (AF) and stroke. OBJECTIVE: The purpose of 
      this study was to evaluate the safety and efficacy of AF ablation in patients 
      with RA. METHODS: All patients with RA undergoing AF ablation at our institution 
      from 2010 to 2021 were propensity matched to patients without RA using 9 baseline 
      characteristics. The primary outcome was procedural efficacy defined by clinical 
      AF recurrence, the need for antiarrhythmic drugs (AADs), and repeat catheter 
      ablation. Secondary outcome was safety. RESULTS: A total of 45 patients with RA 
      (age 66.3 ± 7.7 years) were matched to 45 patients without a history of RA (age 
      68.0 ± 7.3 years). Both groups had similar procedural and periprocedural 
      characteristics. Before ablation, RA patients had statistically higher C-reactive 
      protein (CRP) levels (P ≤.01) and erythrocyte sedimentation rates (ESRs) (P <.05) 
      compared to non-RA patients. After ablation, RA patients had statistically 
      significant higher rates of AF recurrence (P = .006), were more likely to be 
      taking AADs (P <.05), and more likely to undergo repeat ablations (P <.05). The 
      use of immunosuppression or corticosteroids at the time of ablation did not 
      influence the primary endpoint of AF recurrence, AADs, or repeat ablation. 
      Multivariate regression analysis showed CRP and ESR were independent predictors 
      of AF recurrence. CRP was an independent predictor of repeat ablation. 
      CONCLUSION: Patients with RA are at higher risk of clinical AF recurrence, and 
      are more likely to be taking AADs and require repeat ablation. Preablation CRP 
      and ESR are independent predictors of AF recurrence, and CRP is an independent 
      predictor of repeat catheter ablation.
CI  - © 2022 Heart Rhythm Society. Published by Elsevier Inc.
FAU - Haq, Ikram U
AU  - Haq IU
AD  - Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota.
FAU - Lodhi, Fahad K
AU  - Lodhi FK
AD  - Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.
FAU - Anan, Abu Rmilah
AU  - Anan AR
AD  - Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.
FAU - Alzu'bi, Hossam
AU  - Alzu'bi H
AD  - Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.
FAU - Agboola, Kolade M
AU  - Agboola KM
AD  - Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.
FAU - Lee, Hon-Chi
AU  - Lee HC
AD  - Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.
FAU - Asirvatham, Samuel J
AU  - Asirvatham SJ
AD  - Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.
FAU - Deshmukh, Abhishek J
AU  - Deshmukh AJ
AD  - Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.
FAU - DeSimone, Christopher V
AU  - DeSimone CV
AD  - Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota.
LA  - eng
PT  - Journal Article
DEP - 20220315
PL  - United States
TA  - Heart Rhythm O2
JT  - Heart rhythm O2
JID - 101768511
PMC - PMC9207736
OTO - NOTNLM
OT  - Atrial fibrillation
OT  - Atrial fibrillation recurrence
OT  - Catheter ablation
OT  - Pulmonary vein isolation
OT  - Rheumatoid arthritis
OT  - Safety
EDAT- 2022/06/24 06:00
MHDA- 2022/06/24 06:01
PMCR- 2022/03/15
CRDT- 2022/06/23 02:38
PHST- 2022/06/23 02:38 [entrez]
PHST- 2022/06/24 06:00 [pubmed]
PHST- 2022/06/24 06:01 [medline]
PHST- 2022/03/15 00:00 [pmc-release]
AID - S2666-5018(22)00062-9 [pii]
AID - 10.1016/j.hroo.2022.03.001 [doi]
PST - epublish
SO  - Heart Rhythm O2. 2022 Mar 15;3(3):261-268. doi: 10.1016/j.hroo.2022.03.001. 
      eCollection 2022 Jun.

PMID- 35729718
OWN - NLM
STAT- MEDLINE
DCOM- 20221021
LR  - 20230203
IS  - 1538-4667 (Electronic)
IS  - 0196-0202 (Print)
IS  - 0196-0202 (Linking)
VI  - 43
IP  - 6
DP  - 2022 Nov-Dec 01
TI  - Factors Associated With the Development of Tinnitus and With the Degree of 
      Annoyance Caused by Newly Developed Tinnitus.
PG  - 1807-1815
LID - 10.1097/AUD.0000000000001250 [doi]
AB  - OBJECTIVES: Tinnitus is highly prevalent, but only a few risk factors for 
      developing tinnitus are known and little is known about factors associated with 
      the degree of annoyance of new-onset tinnitus. Longitudinal analysis can reveal 
      risk factors associated with the development of tinnitus and might lead to 
      targeted prevention. The aim of this study is twofold. (1) To identify risk 
      factors that are longitudinally associated with the odds of developing tinnitus 5 
      years later. (2) To identify factors that are cross-sectionally associated with 
      tinnitus annoyance in adults with new-onset tinnitus. METHODS: Baseline, 5-year, 
      and 10-year follow-up data of participants in the Netherlands Longitudinal Study 
      on Hearing (NL-SH) were used. The NL-SH is a web-based prospective cohort study, 
      which started in 2006 and includes both normal hearing and hearing-impaired 
      adults aged 18 to 70 years at baseline. The NL-SH uses an online digit-triplet 
      speech-in-noise test to asses speech recognition ability in noise, and online 
      questionnaires on various aspects of life. At follow-up, participants are asked 
      (1) if they suffer from tinnitus and (2) to rate tinnitus annoyance on a 0 to 100 
      numeric rating scale. We investigated whether demographic (age, sex, living 
      arrangement, educational level), lifestyle (history of tobacco smoking, alcohol 
      use), health (asthma, severe heart disease, hypertension, history of stroke, 
      osteoarthritis, rheumatoid arthritis, epilepsy, multiple sclerosis, and 
      migraine), hearing (speech recognition ability in noise, hyperacusis, and 
      occupational noise exposure), and psychological variables (distress, 
      somatization, depression, and anxiety) were potential risk factors for new-onset 
      tinnitus, or associated with annoyance caused by new-onset tinnitus. Generalized 
      estimating equations were used to longitudinally analyze the association between 
      potential risk factors and new-onset tinnitus measured 5 years later. A 
      multivariable association model was constructed using a forward selection 
      procedure with p < 0.05 for model entry. Linear regression analysis was used to 
      cross-sectionally analyze the association between potential factors and tinnitus 
      annoyance in new-onset tinnitus. For this purpose, a multivariable association 
      model was constructed using a forward selection procedure with p <0.05 for model 
      entry. RESULTS: In total, 734 participants without tinnitus at baseline were 
      included, from which 137 participants reported to suffer from new-onset tinnitus 
      5 or 10 years later. Risk factors for new-onset tinnitus were history of smoking 
      (odds ratio 1.5, 95% confidence interval [CI] 1.0 to 2.2, p = 0.027) and higher 
      levels of somatization (odds ratio 2.0, 95% CI 1.2 to 3.3, overall p = 0.024). 
      Factors associated with the degree of tinnitus annoyance were increased levels of 
      anxiety (β = 11.6, 95% CI 2.3-20.8, overall p = 0.035) and poor speech 
      recognition ability in noise (β = 13.5, 95% CI, 4.4 to 22.6, overall p = 0.014). 
      CONCLUSIONS: Higher levels of somatization and a history of smoking were found to 
      be risk factors for new-onset tinnitus 5 years later. Anxiety and poor speech 
      recognition ability in noise were associated with higher degrees of tinnitus 
      annoyance in new-onset tinnitus. Somatization deserves to be addressed in future 
      research and clinical practice as it might provide part of a model for the 
      development of chronic tinnitus.
CI  - Copyright © 2022 The Authors. Ear & Hearing is published on behalf of the 
      American Auditory Society, by Wolters Kluwer Health, Inc.
FAU - Goderie, Thadé
AU  - Goderie T
AD  - Amsterdam UMC location Vrije Universiteit Amsterdam, Otolaryngology-Head and Neck 
      Surgery, Section Ear and Hearing, Amsterdam, The Netherlands.
AD  - Amsterdam Public Health, Quality of Care, Amsterdam, The Netherlands.
FAU - van Wier, Marieke F
AU  - van Wier MF
AD  - Amsterdam UMC location Vrije Universiteit Amsterdam, Otolaryngology-Head and Neck 
      Surgery, Section Ear and Hearing, Amsterdam, The Netherlands.
AD  - Amsterdam Public Health, Quality of Care, Amsterdam, The Netherlands.
FAU - Lissenberg-Witte, Birgit I
AU  - Lissenberg-Witte BI
AD  - Amsterdam UMC location Vrije Universiteit Amsterdam, Epidemiology and Data 
      Science, Amsterdam, The Netherlands.
FAU - Merkus, Paul
AU  - Merkus P
AD  - Amsterdam UMC location Vrije Universiteit Amsterdam, Otolaryngology-Head and Neck 
      Surgery, Section Ear and Hearing, Amsterdam, The Netherlands.
AD  - Amsterdam Public Health, Quality of Care, Amsterdam, The Netherlands.
FAU - Smits, Cas
AU  - Smits C
AD  - Amsterdam Public Health, Quality of Care, Amsterdam, The Netherlands.
AD  - Amsterdam UMC location University of Amsterdam, Otolaryngology-Head and Neck 
      Surgery, Ear and Hearing, Amsterdam, The Netherlands.
FAU - Leemans, C René
AU  - Leemans CR
AD  - Amsterdam UMC location Vrije Universiteit Amsterdam, Otolaryngology-Head and Neck 
      Surgery, Section Ear and Hearing, Amsterdam, The Netherlands.
FAU - Kramer, Sophia E
AU  - Kramer SE
AD  - Amsterdam UMC location Vrije Universiteit Amsterdam, Otolaryngology-Head and Neck 
      Surgery, Section Ear and Hearing, Amsterdam, The Netherlands.
AD  - Amsterdam Public Health, Quality of Care, Amsterdam, The Netherlands.
LA  - eng
PT  - Journal Article
DEP - 20221018
PL  - United States
TA  - Ear Hear
JT  - Ear and hearing
JID - 8005585
SB  - IM
MH  - Adult
MH  - Humans
MH  - *Tinnitus/epidemiology
MH  - Longitudinal Studies
MH  - Prospective Studies
MH  - Hyperacusis/epidemiology
MH  - *Hearing Loss/psychology
PMC - PMC9592178
COIS- The authors have no conflicts of interest to disclose.
EDAT- 2022/06/23 06:00
MHDA- 2022/10/22 06:00
PMCR- 2022/10/24
CRDT- 2022/06/22 00:03
PHST- 2022/06/23 06:00 [pubmed]
PHST- 2022/10/22 06:00 [medline]
PHST- 2022/06/22 00:03 [entrez]
PHST- 2022/10/24 00:00 [pmc-release]
AID - 00003446-202211000-00020 [pii]
AID - 10.1097/AUD.0000000000001250 [doi]
PST - ppublish
SO  - Ear Hear. 2022 Nov-Dec 01;43(6):1807-1815. doi: 10.1097/AUD.0000000000001250. 
      Epub 2022 Oct 18.

PMID- 35728447
OWN - NLM
STAT- MEDLINE
DCOM- 20220908
LR  - 20230322
IS  - 1532-866X (Electronic)
IS  - 0049-0172 (Linking)
VI  - 56
DP  - 2022 Oct
TI  - Development and external validation of prediction models for adverse health 
      outcomes in rheumatoid arthritis: A multinational real-world cohort analysis.
PG  - 152050
LID - S0049-0172(22)00101-9 [pii]
LID - 10.1016/j.semarthrit.2022.152050 [doi]
AB  - BACKGROUND: Identification of rheumatoid arthritis (RA) patients at high risk of 
      adverse health outcomes remains a major challenge. We aimed to develop and 
      validate prediction models for a variety of adverse health outcomes in RA 
      patients initiating first-line methotrexate (MTX) monotherapy. METHODS: Data from 
      15 claims and electronic health record databases across 9 countries were used. 
      Models were developed and internally validated on Optum® De-identified 
      Clinformatics® Data Mart Database using L1-regularized logistic regression to 
      estimate the risk of adverse health outcomes within 3 months (leukopenia, 
      pancytopenia, infection), 2 years (myocardial infarction (MI) and stroke), and 5 
      years (cancers [colorectal, breast, uterine] after treatment initiation. 
      Candidate predictors included demographic variables and past medical history. 
      Models were externally validated on all other databases. Performance was assessed 
      using the area under the receiver operator characteristic curve (AUC) and 
      calibration plots. FINDINGS: Models were developed and internally validated on 
      21,547 RA patients and externally validated on 131,928 RA patients. Models for 
      serious infection (AUC: internal 0.74, external ranging from 0.62 to 0.83), MI 
      (AUC: internal 0.76, external ranging from 0.56 to 0.82), and stroke (AUC: 
      internal 0.77, external ranging from 0.63 to 0.95), showed good discrimination 
      and adequate calibration. Models for the other outcomes showed modest internal 
      discrimination (AUC < 0.65) and were not externally validated. INTERPRETATION: We 
      developed and validated prediction models for a variety of adverse health 
      outcomes in RA patients initiating first-line MTX monotherapy. Final models for 
      serious infection, MI, and stroke demonstrated good performance across multiple 
      databases and can be studied for clinical use. FUNDING: This activity under the 
      European Health Data & Evidence Network (EHDEN) has received funding from the 
      Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 
      806968. This Joint Undertaking receives support from the European Union's Horizon 
      2020 research and innovation programme and EFPIA.
CI  - Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.
FAU - Yang, Cynthia
AU  - Yang C
AD  - Department of Medical Informatics, Erasmus University Medical Center, Rotterdam, 
      The Netherlands. Electronic address: c.yang@erasmusmc.nl.
FAU - Williams, Ross D
AU  - Williams RD
AD  - Department of Medical Informatics, Erasmus University Medical Center, Rotterdam, 
      The Netherlands.
FAU - Swerdel, Joel N
AU  - Swerdel JN
AD  - Janssen Research and Development, Titusville, NJ, United States.
FAU - Almeida, João Rafael
AU  - Almeida JR
AD  - DETI/IEETA, University of Aveiro, Aveiro, Portugal.
FAU - Brouwer, Emily S
AU  - Brouwer ES
AD  - Janssen Research and Development, Titusville, NJ, United States.
FAU - Burn, Edward
AU  - Burn E
AD  - Nuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, 
      University of Oxford, Oxford, United Kingdom; Fundació Institut Universitari per 
      a la recerca a l'Atenció Primària de Salut Jordi Gol i Gurina (IDIAPJGol), 
      Barcelona, Spain.
FAU - Carmona, Loreto
AU  - Carmona L
AD  - Instituto de Salud Musculoesquelética, Madrid, Spain.
FAU - Chatzidionysiou, Katerina
AU  - Chatzidionysiou K
AD  - Department of Medicine, Solna, Rheumatology Unit, Karolinska Institute, 
      Stockholm, Sweden.
FAU - Duarte-Salles, Talita
AU  - Duarte-Salles T
AD  - Fundació Institut Universitari per a la recerca a l'Atenció Primària de Salut 
      Jordi Gol i Gurina (IDIAPJGol), Barcelona, Spain.
FAU - Fakhouri, Walid
AU  - Fakhouri W
AD  - Eli Lilly and Company, Windlesham, Surrey, United Kingdom.
FAU - Hottgenroth, Antje
AU  - Hottgenroth A
AD  - Lilly Deutschland GmbH, Bad Homburg, Germany.
FAU - Jani, Meghna
AU  - Jani M
AD  - Centre for Epidemiology Versus Arthritis, University of Manchester, Manchester, 
      United Kingdom.
FAU - Kolde, Raivo
AU  - Kolde R
AD  - Institute of Computer Science, University of Tartu, Tartu, Estonia.
FAU - Kors, Jan A
AU  - Kors JA
AD  - Department of Medical Informatics, Erasmus University Medical Center, Rotterdam, 
      The Netherlands.
FAU - Kullamaa, Lembe
AU  - Kullamaa L
AD  - Department of Epidemiology and Biostatistics, National Institute for Health 
      Development, Tallinn, Estonia; Institute of Family Medicine and Public Health, 
      University of Tartu, Tartu, Estonia; European Patients' Forum, Brussels, Belgium.
FAU - Lane, Jennifer
AU  - Lane J
AD  - Nuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, 
      University of Oxford, Oxford, United Kingdom.
FAU - Marinier, Karine
AU  - Marinier K
AD  - Servier, Suresnes, France.
FAU - Michel, Alexander
AU  - Michel A
AD  - Epidemiology, Bayer Basel, Basel, Switzerland.
FAU - Stewart, Henry Morgan
AU  - Stewart HM
AD  - Real-World Solutions, IQVIA, Brighton, United Kingdom.
FAU - Prats-Uribe, Albert
AU  - Prats-Uribe A
AD  - Nuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, 
      University of Oxford, Oxford, United Kingdom.
FAU - Reisberg, Sulev
AU  - Reisberg S
AD  - Institute of Computer Science, University of Tartu, Tartu, Estonia; STACC, Tartu, 
      Estonia; Quretec, Tartu, Estonia.
FAU - Sena, Anthony G
AU  - Sena AG
AD  - Department of Medical Informatics, Erasmus University Medical Center, Rotterdam, 
      The Netherlands; Janssen Research and Development, Titusville, NJ, United States.
FAU - Torre, Carmen O
AU  - Torre CO
AD  - Real-World Solutions, IQVIA, Brighton, United Kingdom.
FAU - Verhamme, Katia
AU  - Verhamme K
AD  - Department of Medical Informatics, Erasmus University Medical Center, Rotterdam, 
      The Netherlands.
FAU - Vizcaya, David
AU  - Vizcaya D
AD  - Bayer Pharmaceuticals, Barcelona, Spain.
FAU - Weaver, James
AU  - Weaver J
AD  - Janssen Research and Development, Titusville, NJ, United States; Observational 
      Health Data Sciences and Informatics, New York, NY, United States.
FAU - Ryan, Patrick
AU  - Ryan P
AD  - Janssen Research and Development, Titusville, NJ, United States; Observational 
      Health Data Sciences and Informatics, New York, NY, United States.
FAU - Prieto-Alhambra, Daniel
AU  - Prieto-Alhambra D
AD  - Nuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, 
      University of Oxford, Oxford, United Kingdom.
FAU - Rijnbeek, Peter R
AU  - Rijnbeek PR
AD  - Department of Medical Informatics, Erasmus University Medical Center, Rotterdam, 
      The Netherlands.
LA  - eng
GR  - 21605/VAC_/Versus Arthritis/United Kingdom
GR  - DH_/Department of Health/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220615
PL  - United States
TA  - Semin Arthritis Rheum
JT  - Seminars in arthritis and rheumatism
JID - 1306053
RN  - 0 (Antirheumatic Agents)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - *Antirheumatic Agents/therapeutic use
MH  - *Arthritis, Rheumatoid/drug therapy
MH  - Cohort Studies
MH  - Humans
MH  - Methotrexate/therapeutic use
MH  - Outcome Assessment, Health Care
MH  - *Stroke/etiology
OTO - NOTNLM
OT  - Cardiovascular diseases
OT  - Infections
OT  - Methotrexate
OT  - Prediction models
OT  - Rheumatoid arthritis
COIS- Declaration of Competing Interest CY, RDW, JRA, EB, TDS, MJ, RK, JAK, LK, APU, 
      SR, HMS, and COT report no competing interests related to this work. JNS, AGS, 
      JW, and PR are employees of Janssen Research & Development, a pharmaceutical 
      company of Johnson & Johnson, and shareholders of Johnson & Johnson. At the time 
      the study was conducted, ESB was an employee of Janssen Research & Development, a 
      pharmaceutical company of Johnson & Johnson, shareholder of Johnson & Johnson, 
      and shareholder of Takeda Pharmaceuticals. LC reports her institute has been 
      hired for methodological consultancy by AbbVie Spain, S.L.U., Astellas Pharma, 
      SA, Bristol-Myers Squibb, S.A.U. (BMS), Daiichi-Sankyo España, S.A., Dentsply 
      Sirona Iberia, S.A.U., Eisai Farmacéutica, SA, Fresenius Kabi España, S. A. U., 
      Laboratorios Gebro Pharma, SA, Lilly, S.A., Merck Sharp & Dohme España, S.A., 
      Novartis Farmaceutica, SA, Pfizer, S.L.U., Roche Farma, S.A, Sanofi Aventis, UCB 
      Pharma, S.A., outside the submitted work. KC reports consultancy fees from Eli 
      Lilly, AbbVie, and Pfizer, outside the submitted work. WF is an employee and 
      shareholder of Eli Lilly. AHO is an employee of Lilly Deutschland GmbH. JL 
      reports grants from Versus Arthritis, grants from Medical Research Council, 
      outside the submitted work. AM is an employee of Bayer AG. At the time the study 
      was conducted, KM was an employee of Servier. KV works for a research institute 
      which receives/received unconditional research grants from Yamanouchi, 
      Pfizer/Boehringer Ingelheim, Novartis, GSK, UCB, Amgen, Chiesi, none of these are 
      related to the content of this paper. DV reports personal fees from Bayer, during 
      the conduct of the study and outside the submitted work. DPA reports grants and 
      other (DPA's department has received fees for speaker services and advisory board 
      membership) from AMGEN, grants, non-financial support and other (DPA's department 
      has received fees for consultancy services) from UCB Biopharma, grants from Les 
      Laboratoires Servier, outside the submitted work; and Janssen, on behalf of 
      IMI-funded EHDEN and EMIF consortiums, and Synapse Management Partners have 
      supported training programmes organised by DPA's department and open for external 
      participants. PRR works for a research institute who receives/received 
      unconditional research grants from Yamanouchi, Pfizer-Boehringer Ingelheim, GSK, 
      Amgen, UCB, Novartis, AstraZeneca, Chiesi, Janssen Research and Development, none 
      of which relate to the content of this work.
EDAT- 2022/06/22 06:00
MHDA- 2022/09/09 06:00
CRDT- 2022/06/21 18:25
PHST- 2022/02/21 00:00 [received]
PHST- 2022/05/11 00:00 [revised]
PHST- 2022/06/10 00:00 [accepted]
PHST- 2022/06/22 06:00 [pubmed]
PHST- 2022/09/09 06:00 [medline]
PHST- 2022/06/21 18:25 [entrez]
AID - S0049-0172(22)00101-9 [pii]
AID - 10.1016/j.semarthrit.2022.152050 [doi]
PST - ppublish
SO  - Semin Arthritis Rheum. 2022 Oct;56:152050. doi: 10.1016/j.semarthrit.2022.152050. 
      Epub 2022 Jun 15.

PMID- 35711877
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220716
IS  - 2000-9666 (Print)
IS  - 2000-9666 (Electronic)
IS  - 2000-9666 (Linking)
VI  - 12
IP  - 1
DP  - 2022
TI  - Ruptured Sinus of Valsalva Aneurysm in Apert Syndrome: Case report.
PG  - 68-72
LID - 10.55729/2000-9666.1013 [doi]
AB  - BACKGROUND: Sinus of Valsalva aneurysm (SOVA) is a rare anomaly of the aorta that 
      can be congenital or acquired. It can be associated with syndromes such as Marfan 
      syndrome and Ehlers-Danlos syndrome. However, to our knowledge, it has never been 
      described in a patient with Apert syndrome. Although it often presents as an 
      incidental finding on imaging, SOVA is associated with the risk of serious 
      complications, including rupture. A possible connection between the conditions 
      might be the FGFR2 gene mutation in Apert syndrome and the influence of a 
      mutation in fibroblast growth factor 2 (FGF2) on heart development. Here we 
      report a case of acute heart failure secondary to rupture of SOVA into the right 
      atrium in a patient with Apert syndrome. CASE PRESENTATION: A 47-year-old 
      Caucasian woman with a history of Apert syndrome and rheumatoid arthritis 
      presented with shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, and 
      progressive bilateral lower extremity edema for 2 weeks. She was diagnosed with 
      acute right heart failure due to ruptured SOVA. The patient underwent surgical 
      repair of the ruptured SOVA. Unfortunately, her postoperative course was 
      complicated by a stroke leading to brain death. CONCLUSION: Ruptured SOVA is a 
      quite rare but serious condition that can cause life-threatening complications. 
      In this case, SOVA occurred in a patient with Apert syndrome. The case may 
      suggest that these two conditions may be related through the FGFR2 gene mutation 
      associated with Apert syndrome and the related growth factor FGF2 involved in 
      heart development.
CI  - © 2022 Greater Baltimore Medical Center.
FAU - Aldabain, Louay
AU  - Aldabain L
AD  - Department of Medicine, Medstar Good Samaritan Hospital, USA.
FAU - Haddaden, Metri
AU  - Haddaden M
AD  - Department of Medicine, MedStar Health Union Memorial Hospital, Baltimore, MD, 
      USA.
FAU - Bandaru, Sumanth
AU  - Bandaru S
AD  - Department of Medicine, MedStar Health Union Memorial Hospital, Baltimore, MD, 
      USA.
FAU - Camire, Lyn
AU  - Camire L
AD  - Department of Medicine, MedStar Health Union Memorial Hospital, Baltimore, MD, 
      USA.
FAU - Weisman, David S
AU  - Weisman DS
AD  - Department of Medicine, MedStar Health Union Memorial Hospital, Baltimore, MD, 
      USA.
AD  - Georgetown University School of Medicine, Washington, DC, USA.
LA  - eng
PT  - Case Reports
DEP - 20220131
PL  - United States
TA  - J Community Hosp Intern Med Perspect
JT  - Journal of community hospital internal medicine perspectives
JID - 101601396
PMC - PMC9195107
OTO - NOTNLM
OT  - Apert syndrome
OT  - Case report
OT  - Right heart failure
OT  - Rupture of sinus of Valsalva aneurysm
OT  - Sinus of Valsalva aneurysm
COIS- Conflict of interest The authors declare that they have no competing interests.
EDAT- 2022/06/18 06:00
MHDA- 2022/06/18 06:01
PMCR- 2022/01/31
CRDT- 2022/06/17 02:34
PHST- 2021/07/20 00:00 [received]
PHST- 2021/10/06 00:00 [revised]
PHST- 2021/10/25 00:00 [accepted]
PHST- 2022/06/17 02:34 [entrez]
PHST- 2022/06/18 06:00 [pubmed]
PHST- 2022/06/18 06:01 [medline]
PHST- 2022/01/31 00:00 [pmc-release]
AID - jchimp-12-01-068 [pii]
AID - 10.55729/2000-9666.1013 [doi]
PST - epublish
SO  - J Community Hosp Intern Med Perspect. 2022 Jan 31;12(1):68-72. doi: 
      10.55729/2000-9666.1013. eCollection 2022.

PMID- 35658786
OWN - NLM
STAT- MEDLINE
DCOM- 20230614
LR  - 20230615
IS  - 1502-7732 (Electronic)
IS  - 0300-9742 (Linking)
VI  - 52
IP  - 4
DP  - 2023 Jul
TI  - Rheumatoid arthritis and the risk of major cardiometabolic diseases: a Mendelian 
      randomization study.
PG  - 335-341
LID - 10.1080/03009742.2022.2070988 [doi]
AB  - OBJECTIVE: Rheumatoid arthritis (RA) is suggested to be implicated in the 
      development of cardiometabolic diseases. We conducted a Mendelian randomization 
      (MR) study to assess potential causality for associations of RA with the risk of 
      cardiometabolic diseases, including type 2 diabetes (T2D), coronary artery 
      disease (CAD), and ischaemic stroke. METHOD: Seventy independent 
      single-nucleotide polymorphisms (SNPs) associated with RA were identified as 
      instrumental variables from a genome-wide association study (GWAS) of 58 284 
      European subjects. Summary-level data for the associations of the 70 genetic 
      variants with T2D, CAD, and ischaemic stroke were taken from three GWASs with a 
      total of 1 529 131 participants. Inverse-variance weighted (IVW) MR was used in 
      the main analyses. RESULTS: The main IVW MR analysis showed that genetically 
      determined RA was associated with higher risks of T2D [odds ratio (OR): 1.04, 95% 
      confidence interval (CI) 1.02-1.05; p < 0.001] and CAD (OR: 1.02, 95% CI 
      1.00-1.03; p = 0.012), but not ischaemic stroke (OR: 1.00, 95% CI 0.99-1.02; p 
      = 0.961). Sensitivity analyses with multiple MR methods confirmed these 
      associations. MR-Egger regression showed no evidence of pleiotropy in the 
      association between genetically determined RA and the risk of T2D, CAD, and 
      ischaemic stroke. Leave-one-out sensitivity analysis showed that the association 
      between genetically determined RA and the risk of T2D, CAD, and ischaemic stroke 
      was not driven by any individual SNP. CONCLUSION: Genetically determined RA was 
      associated with increased risks of T2D and CAD, suggesting that RA plays a 
      crucial role in the pathogenesis of T2D and CAD.
FAU - Zhang, K
AU  - Zhang K
AUID- ORCID: 0000-0002-1351-4348
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Medical College of 
      Soochow University, Suzhou, Jiangsu, P.R. China.
FAU - Jia, Y
AU  - Jia Y
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Medical College of 
      Soochow University, Suzhou, Jiangsu, P.R. China.
FAU - Wang, R
AU  - Wang R
AD  - Department of Dermatology, The First Affiliated Hospital of Soochow University, 
      Suzhou, Jiangsu, P.R. China.
FAU - Guo, D
AU  - Guo D
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Medical College of 
      Soochow University, Suzhou, Jiangsu, P.R. China.
AD  - School of Nursing, Medical College of Soochow University, Suzhou, Jiangsu, P.R. 
      China.
FAU - Yang, P
AU  - Yang P
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Medical College of 
      Soochow University, Suzhou, Jiangsu, P.R. China.
FAU - Sun, L
AU  - Sun L
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Medical College of 
      Soochow University, Suzhou, Jiangsu, P.R. China.
FAU - Wang, Y
AU  - Wang Y
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Medical College of 
      Soochow University, Suzhou, Jiangsu, P.R. China.
FAU - Liu, F
AU  - Liu F
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Medical College of 
      Soochow University, Suzhou, Jiangsu, P.R. China.
FAU - Zang, Y
AU  - Zang Y
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Medical College of 
      Soochow University, Suzhou, Jiangsu, P.R. China.
FAU - Shi, M
AU  - Shi M
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Medical College of 
      Soochow University, Suzhou, Jiangsu, P.R. China.
FAU - Zhang, Y
AU  - Zhang Y
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Medical College of 
      Soochow University, Suzhou, Jiangsu, P.R. China.
FAU - Zhu, Z
AU  - Zhu Z
AD  - Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of 
      Preventive and Translational Medicine for Geriatric Diseases, Medical College of 
      Soochow University, Suzhou, Jiangsu, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20220606
PL  - England
TA  - Scand J Rheumatol
JT  - Scandinavian journal of rheumatology
JID - 0321213
SB  - IM
MH  - Humans
MH  - *Diabetes Mellitus, Type 2
MH  - Genome-Wide Association Study
MH  - Mendelian Randomization Analysis/methods
MH  - *Arthritis, Rheumatoid/etiology
MH  - Polymorphism, Single Nucleotide
MH  - *Cardiovascular Diseases
EDAT- 2022/06/07 06:00
MHDA- 2023/06/14 06:42
CRDT- 2022/06/06 09:57
PHST- 2023/06/14 06:42 [medline]
PHST- 2022/06/07 06:00 [pubmed]
PHST- 2022/06/06 09:57 [entrez]
AID - 10.1080/03009742.2022.2070988 [doi]
PST - ppublish
SO  - Scand J Rheumatol. 2023 Jul;52(4):335-341. doi: 10.1080/03009742.2022.2070988. 
      Epub 2022 Jun 6.

PMID- 35657933
OWN - NLM
STAT- MEDLINE
DCOM- 20220608
LR  - 20230413
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 17
IP  - 6
DP  - 2022
TI  - Association of atherogenic indices with C-reactive protein and risk factors to 
      assess cardiovascular risk in rheumatoid arthritis patient at Tikur Anbessa 
      Specialized Hospital, Addis Ababa.
PG  - e0269431
LID - 10.1371/journal.pone.0269431 [doi]
LID - e0269431
AB  - BACKGROUND: Rheumatoid arthritis (RA) is an autoimmune systemic chronic 
      inflammatory disorder, which is characterized by joint stiffness, damage, and 
      destruction of bone. In RA patients, the risk of cardiovascular disease is 
      increased by 2-3 folds as compared to the general population. The major burden of 
      RA is the development of cardiovascular diseases, including congestive heart 
      failure, stroke, and myocardial infarction. OBJECTIVES: Assessment of the 
      association of atherogenic indices with C-reactive protein to evaluate CVD risk 
      was one of the purposes of this study. In addition, the association of 
      atherogenic indices with elevated levels of cardiovascular risk factors (LDL-C 
      and TG) was another aim of this study. METHODS: The preferred study design for 
      this study was a hospital based comparative cross-sectional study method. Data 
      were cleaned, coded, and entered into Epi Data version 4.6 software, and exported 
      to SPSS version 20 for further analysis of atherogenic indices, C-reactive 
      protein, and risk factors. The comparison of atherogenic indices and other 
      variables among the case and control groups was estimated by the independent 
      t-test statistical analysis method. All variables with a p-value less than 0.2 
      during binary linear regression analysis were selected for multinomial logistic 
      regression analysis. The association of atherogenic indices with C-reactive 
      protein and risk factors was computed using multiple logistic regressions. The 
      data were presented using tables and figures for clarification of the study. 
      RESULTS: The levels of atherogenic indices were computed for both RA patients and 
      the control group. The values of atherogenic indices were significantly 
      associated with cardiovascular risk factor (CRP ≥ 2mg/L). Atherogenic index of 
      plasma (AIP) and TC/HDL-C ratio had a statistically significant association with 
      an elevated levels of triglycerides (P<0.01). The TC/HDL-Cratio value of the 
      patient had 2.38 folds more likely to have an elevated low density lipoprotein 
      level. In addition, AIP of RA patients had 57.51 and 23.65 folds more to have 
      elevated low density lipoprotein and triglycerides respectively. CONCLUSIONS: The 
      result of this study showed that TC/HDL-C, LDL/HDL-C ratio values, and 
      atherogenic index of plasma had a statistically significant association with 
      elevated level of low density lipoprotein and triglycerides. In addition to this, 
      they have a statistically significant association with the level of C-reactive 
      protein. There was a highly significant statistical association between 
      atherogenic indices, elevated low density lipoprotein, and triglycerides values. 
      Therefore, the result of this finding confirmed that atherogenic indices have a 
      potential role in the prediction and management of CVD risk in RA patients.
FAU - Dessie, Gashaw
AU  - Dessie G
AUID- ORCID: 0000-0003-2311-6180
AD  - Department of Biochemistry, School of Medicine, College of Medicine and Health 
      Sciences, University of Gondar, Gondar, Ethiopia.
LA  - eng
PT  - Journal Article
DEP - 20220603
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Cholesterol, HDL)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Triglycerides)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - *Arthritis, Rheumatoid
MH  - C-Reactive Protein/metabolism
MH  - *Cardiovascular Diseases/complications/diagnosis/epidemiology
MH  - Cholesterol, HDL
MH  - Cross-Sectional Studies
MH  - Ethiopia
MH  - Heart Disease Risk Factors
MH  - Hospitals
MH  - Humans
MH  - Lipoproteins, LDL
MH  - Risk Factors
MH  - Triglycerides
PMC - PMC9165848
COIS- The author declared that no competing interests exist.
EDAT- 2022/06/04 06:00
MHDA- 2022/06/09 06:00
PMCR- 2022/06/03
CRDT- 2022/06/03 13:46
PHST- 2021/11/11 00:00 [received]
PHST- 2022/05/21 00:00 [accepted]
PHST- 2022/06/03 13:46 [entrez]
PHST- 2022/06/04 06:00 [pubmed]
PHST- 2022/06/09 06:00 [medline]
PHST- 2022/06/03 00:00 [pmc-release]
AID - PONE-D-21-35743 [pii]
AID - 10.1371/journal.pone.0269431 [doi]
PST - epublish
SO  - PLoS One. 2022 Jun 3;17(6):e0269431. doi: 10.1371/journal.pone.0269431. 
      eCollection 2022.

PMID- 35610408
OWN - NLM
STAT- MEDLINE
DCOM- 20220916
LR  - 20220916
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 41
IP  - 9
DP  - 2022 Sep
TI  - Association of rheumatoid arthritis with mortality in chronic kidney disease: a 
      cohort study.
PG  - 2669-2676
LID - 10.1007/s10067-022-06223-x [doi]
AB  - BACKGROUND: Rheumatoid arthritis (RA) is associated with an increased risk of 
      cardiovascular disease (CVD) as well as with an increased risk of chronic kidney 
      disease (CKD), also a known cardiovascular risk factor. However, it is not known 
      if RA is a predictor of adverse outcomes in patients with CKD. We hypothesized 
      that among a cohort of patients with CKD, RA would be associated with an 
      increased risk of mortality. MATERIALS AND METHODS: We conducted a retrospective 
      study of 3939 participants with CKD from the prospective Chronic Renal 
      Insufficiency Cohort (CRIC) study. The primary outcome of interest was all-cause 
      mortality. Secondary outcomes included CKD progression (defined as end-stage 
      kidney disease or 50% decline in estimated glomerular filtration rate), 
      cardiovascular endpoints, and composite of myocardial infarction, cerebrovascular 
      accident, heart failure, or death. Multivariable Cox proportional hazards 
      regression was utilized, adjusting for potential confounders including age, sex, 
      race/ethnicity, body mass index, current smoker, and education. RESULTS: The 
      study cohort included 83 participants with RA on a disease modifying 
      anti-rheumatic drug (DMARD). In the adjusted analysis, CKD-RA status was 
      significantly associated with an increased risk of death (adjusted HR, aHR, 1.73 
      (1.27, 2.35)) and composite outcome (aHR 1.65 (1.27-2.15)) even after adjusting 
      for traditional risk factors. Similar statistically significant associations were 
      observed between CKD-RA and other secondary outcomes except for CKD progression. 
      CONCLUSION: RA was associated with higher mortality among individuals with CKD 
      but not progressive renal decline. Further studies evaluating the mechanisms 
      behind this association are needed. Key Points • Rheumatoid arthritis (RA) is 
      associated with an increased risk of cardiovascular disease (CVD) as well as with 
      an increased risk of chronic kidney disease (CKD), also a known cardiovascular 
      risk factor. However, it is not known if RA is an independent predictor of 
      adverse outcomes in patients with CKD • In this study, we observed that CKD 
      patients with RA experience higher mortality as well as an increased risk of CVD 
      compared to patients with CKD without comorbid RA • These data provide rationale 
      for more aggressive monitoring for CVD in patients with CKD and RA. They also 
      underscore the need for determining which interventions can help decrease the 
      burden of mortality in these patients.
CI  - © 2022. The Author(s), under exclusive licence to International League of 
      Associations for Rheumatology (ILAR).
FAU - Ezeanuna, Mary N
AU  - Ezeanuna MN
AD  - Division of Rheumatology, University of Washington, 1959 NE Pacific Street, 
      Seattle, WA, 98195, USA.
FAU - Prince, David K
AU  - Prince DK
AD  - Division of Nephrology, Kidney Research Institute, University of Washington, 
      Seattle, WA, USA.
FAU - Alexander, Swetha Ann
AU  - Alexander SA
AD  - Department of Internal Medicine, University of Connecticut, Farmington, CT, USA.
FAU - Richards, John S
AU  - Richards JS
AD  - Rheumatology Section, Medicine Service Line, Veterans Affairs Pittsburgh 
      Healthcare System, Pittsburgh, PA, USA.
AD  - Division of Rheumatology and Clinical Immunology, Department of Medicine, 
      University of Pittsburgh, Pittsburgh, PA, USA.
FAU - Kerr, Gail S
AU  - Kerr GS
AD  - Rheumatology Section, Washington, DC Veterans Affairs, Division of Rheumatology, 
      Georgetown and Howard University Hospitals, Washington, DC, USA.
FAU - Jalal, Diana
AU  - Jalal D
AD  - Division of Nephrology, University of Iowa Hospitals and Clinics and Iowa City VA 
      Medical Center, Iowa City, IA, USA.
FAU - Bansal, Nisha
AU  - Bansal N
AD  - Division of Nephrology, Kidney Research Institute, University of Washington, 
      Seattle, WA, USA.
FAU - Liew, Jean W
AU  - Liew JW
AUID- ORCID: 0000-0002-8104-2450
AD  - Section of Rheumatology, Boston University School of Medicine, Boston, MA, USA.
FAU - Singh, Namrata
AU  - Singh N
AUID- ORCID: 0000-0001-7149-363X
AD  - Division of Rheumatology, University of Washington, 1959 NE Pacific Street, 
      Seattle, WA, 98195, USA. nasingh@uw.edu.
LA  - eng
PT  - Journal Article
DEP - 20220525
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - *Antirheumatic Agents
MH  - *Arthritis, Rheumatoid/complications/drug therapy
MH  - *Cardiovascular Diseases/complications/epidemiology
MH  - Cohort Studies
MH  - Disease Progression
MH  - Humans
MH  - Prospective Studies
MH  - *Renal Insufficiency, Chronic/complications
MH  - Retrospective Studies
MH  - Risk Factors
OTO - NOTNLM
OT  - Chronic kidney disease
OT  - Mortality
OT  - Rheumatoid arthritis
EDAT- 2022/05/25 06:00
MHDA- 2022/09/17 06:00
CRDT- 2022/05/24 23:27
PHST- 2022/04/20 00:00 [received]
PHST- 2022/05/19 00:00 [accepted]
PHST- 2022/04/20 00:00 [revised]
PHST- 2022/05/25 06:00 [pubmed]
PHST- 2022/09/17 06:00 [medline]
PHST- 2022/05/24 23:27 [entrez]
AID - 10.1007/s10067-022-06223-x [pii]
AID - 10.1007/s10067-022-06223-x [doi]
PST - ppublish
SO  - Clin Rheumatol. 2022 Sep;41(9):2669-2676. doi: 10.1007/s10067-022-06223-x. Epub 
      2022 May 25.

PMID- 35583917
OWN - NLM
STAT- MEDLINE
DCOM- 20221028
LR  - 20230801
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Print)
IS  - 2326-5191 (Linking)
VI  - 74
IP  - 10
DP  - 2022 Oct
TI  - Genetic Liability to Rheumatoid Arthritis in Relation to Coronary Artery Disease 
      and Stroke Risk.
PG  - 1638-1647
LID - 10.1002/art.42239 [doi]
AB  - OBJECTIVE: To assess the causality of the associations of rheumatoid arthritis 
      (RA) with coronary artery disease (CAD) and stroke using the Mendelian 
      randomization approach. METHODS: Independent single-nucleotide polymorphisms 
      strongly associated with RA (n = 70) were selected as instrumental variables from 
      a genome-wide association meta-analysis including 14,361 RA patients and 43,923 
      controls of European ancestry. Summary-level data for CAD, all stroke, any 
      ischemic stroke and its subtypes, intracerebral hemorrhage (ICH), and 
      subarachnoid hemorrhage were obtained from meta-analyses of genetic studies, 
      international genetic consortia, the UK Biobank, and the FinnGen consortium. We 
      obtained summary-level data for common cardiovascular risk factors and related 
      inflammatory biomarkers to assess possible mechanisms. RESULTS: Genetic liability 
      to RA was associated with an increased risk of CAD and ICH. For a 1-unit increase 
      in log odds of RA, the combined odds ratios were 1.02 (95% confidence interval 
      [1.01, 1.03]; P = 0.003) for CAD and 1.05 (95% confidence interval [1.02, 1.08]; 
      P = 0.001) for ICH. Genetic liability to RA was associated with increased levels 
      of tumor necrosis factor and C-reactive protein (CRP). The association with CAD 
      was attenuated after adjustment for genetically predicted CRP levels. There were 
      no associations of genetic liability to RA with the other studied outcomes. 
      CONCLUSION: This study found that genetic liability to RA was associated with an 
      increased risk of CAD and ICH and that the association with CAD might be mediated 
      by CRP. The heightened cardiovascular risk should be actively monitored and 
      managed in RA patients, and this may include dampening systemic inflammation.
CI  - © 2022 The Authors. Arthritis & Rheumatology published by Wiley Periodicals LLC 
      on behalf of American College of Rheumatology.
FAU - Yuan, Shuai
AU  - Yuan S
AUID- ORCID: 0000-0001-5055-5627
AD  - Karolinska Institutet, Stockholm, Sweden.
FAU - Carter, Paul
AU  - Carter P
AD  - University of Cambridge, Cambridge, UK.
FAU - Mason, Amy M
AU  - Mason AM
AD  - University of Cambridge, Cambridge, UK.
FAU - Yang, Fangkun
AU  - Yang F
AD  - Ningbo First Hospital and Zhejiang University, Ningbo, China.
FAU - Burgess, Stephen
AU  - Burgess S
AD  - University of Cambridge, Cambridge, UK.
FAU - Larsson, Susanna C
AU  - Larsson SC
AUID- ORCID: 0000-0003-0118-0341
AD  - Karolinska Institutet, Stockholm, Sweden, and Uppsala University, Uppsala, 
      Sweden.
LA  - eng
GR  - 204623/Z/16/Z/WT_/Wellcome Trust/United Kingdom
GR  - MC_PC_17228/MRC_/Medical Research Council/United Kingdom
GR  - RG/13/13/30194/BHF_/British Heart Foundation/United Kingdom
GR  - DH_/Department of Health/United Kingdom
GR  - MC_UU_00002/7/MRC_/Medical Research Council/United Kingdom
GR  - RG/18/13/33946/BHF_/British Heart Foundation/United Kingdom
GR  - MC_QA137853/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
DEP - 20220817
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Biomarkers)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - 0 (Tumor Necrosis Factors)
SB  - IM
CIN - Arthritis Rheumatol. 2022 Oct;74(10):1612-1614. doi: 10.1002/art.42236. PMID: 
      35583794
CIN - Arthritis Rheumatol. 2023 Aug;75(8):1496. doi: 10.1002/art.42468. PMID: 36716118
MH  - Humans
MH  - *Arthritis, Rheumatoid/genetics
MH  - Biomarkers
MH  - C-Reactive Protein/genetics
MH  - *Coronary Artery Disease/epidemiology/genetics
MH  - Genetic Predisposition to Disease
MH  - Genome-Wide Association Study
MH  - Mendelian Randomization Analysis
MH  - Polymorphism, Single Nucleotide
MH  - Risk Factors
MH  - *Stroke/epidemiology/genetics
MH  - Tumor Necrosis Factors
PMC - PMC9804931
EDAT- 2022/05/19 06:00
MHDA- 2022/10/05 06:00
PMCR- 2022/12/31
CRDT- 2022/05/18 11:52
PHST- 2022/04/30 00:00 [revised]
PHST- 2021/12/09 00:00 [received]
PHST- 2022/05/12 00:00 [accepted]
PHST- 2022/05/19 06:00 [pubmed]
PHST- 2022/10/05 06:00 [medline]
PHST- 2022/05/18 11:52 [entrez]
PHST- 2022/12/31 00:00 [pmc-release]
AID - ART42239 [pii]
AID - 10.1002/art.42239 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2022 Oct;74(10):1638-1647. doi: 10.1002/art.42239. Epub 2022 
      Aug 17.

PMID- 35573508
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230314
IS  - 2168-8184 (Print)
IS  - 2168-8184 (Electronic)
IS  - 2168-8184 (Linking)
VI  - 14
IP  - 4
DP  - 2022 Apr
TI  - Mortality Rate of Ischemic Stroke Patients Undergoing Decompressive 
      Hemicraniectomy With Obesity.
PG  - e24069
LID - 10.7759/cureus.24069 [doi]
LID - e24069
AB  - Background Obesity has been shown to have a positive mortality benefit in 
      patients undergoing percutaneous coronary intervention and dialysis and those 
      with rheumatoid arthritis, chronic obstructive pulmonary disease, and various 
      wasting diseases. Studies for this mortality benefit in ischemic stroke patients 
      are conflicting and have not been well studied in hemicraniectomy patients. We 
      sought to determine the impact of obesity on outcomes of hemicraniectomy 
      patients. Methods We performed a retrospective case-control database analysis 
      using a multi-institutional database (TriNetX) looking at obese versus non-obese 
      patients with ischemic stroke undergoing hemicraniectomy. Our primary endpoint 
      was mortality. Secondary endpoints included seizure, pulmonary embolism, 
      myocardial infarction (MI), cerebral infarction, deep vein thrombosis, 
      tracheostomy, and percutaneous endoscopic gastrostomy. Cohorts were 
      propensity-score matched for confounders. Results After propensity score matching 
      for basic demographics and common comorbidities, as well as indicators of stroke 
      severity, 646 patients were identified that were obese and had an ischemic stroke 
      with subsequent hemicraniectomy (cohort 1), and 646 patients were identified who 
      were non-obese with ischemic stroke and hemicraniectomy (cohort 2). Thirty-day 
      survival rate was 98.142% in the obese vs. 87.771% in the non-obese cohorts, 
      90-day survival was 85.15% vs. 79.35%, 180-day survival was 96.44% vs. 84.52%, 
      365-day survival was 94.272% vs. 81.734%, and five-year survival was 81.889% vs. 
      75.077%, respectively. At five years, risk difference was -7.276% (95% CI: 
      -11.757, -2.794) and odds ratio was 0.666 (95% CI: 0.510, 0.871) (p = 0.0029). 
      Despite a higher mortality rate, obese patients had a statistically significant 
      increase in pulmonary embolism (11.61% vs. 5.108, p < 0.0001), deep venous 
      thrombosis (16.873% vs. 9.133%, p < 0.0001), and MI (8.824% vs. 5.882%, p = 
      0.0428). There was no significant difference in intensive care unit length of 
      stay, ventilator dependence, tracheostomy placement, percutaneous endoscopic 
      gastrostomy placement, or intracerebral hemorrhage. Conclusions Despite the 
      increased risk of ischemic stroke, obese patients who undergo hemicraniectomy 
      have decreased mortality rates compared to their non-obese counterparts.
CI  - Copyright © 2022, Hallan et al.
FAU - Hallan, David R
AU  - Hallan DR
AD  - Neurosurgery, Penn State Health Milton S. Hershey Medical Center, Hershey, USA.
FAU - Freedman, Zachary
AU  - Freedman Z
AD  - Neurosurgery, Penn State Health Milton S. Hershey Medical Center, Hershey, USA.
FAU - Rizk, Elias
AU  - Rizk E
AD  - Neurosurgery, Penn State Health Milton S. Hershey Medical Center, Hershey, USA.
LA  - eng
GR  - UL1 TR002014/TR/NCATS NIH HHS/United States
PT  - Journal Article
DEP - 20220412
PL  - United States
TA  - Cureus
JT  - Cureus
JID - 101596737
PMC - PMC9097930
OTO - NOTNLM
OT  - craniectomy
OT  - decompression
OT  - hemicraniectomy
OT  - ischemic stroke
OT  - mortality rate
OT  - neurosurgery
OT  - obesity
OT  - obesity paradox
OT  - outcomes
OT  - survival
COIS- The authors have declared that no competing interests exist.
EDAT- 2022/05/17 06:00
MHDA- 2022/05/17 06:01
PMCR- 2022/04/12
CRDT- 2022/05/16 04:28
PHST- 2022/03/24 00:00 [received]
PHST- 2022/04/12 00:00 [accepted]
PHST- 2022/05/16 04:28 [entrez]
PHST- 2022/05/17 06:00 [pubmed]
PHST- 2022/05/17 06:01 [medline]
PHST- 2022/04/12 00:00 [pmc-release]
AID - 10.7759/cureus.24069 [doi]
PST - epublish
SO  - Cureus. 2022 Apr 12;14(4):e24069. doi: 10.7759/cureus.24069. eCollection 2022 
      Apr.

PMID- 35565842
OWN - NLM
STAT- MEDLINE
DCOM- 20220517
LR  - 20220716
IS  - 2072-6643 (Electronic)
IS  - 2072-6643 (Linking)
VI  - 14
IP  - 9
DP  - 2022 Apr 29
TI  - The Potential Impact of Inducing a Restriction in Reimbursement Criteria on 
      Vitamin D Supplementation in Osteoporotic Patients with or without Fractures.
LID - 10.3390/nu14091877 [doi]
LID - 1877
AB  - In October 2019, the Italian Drug Agency (AIFA) restricted reimbursement criteria 
      for vitamin D (VD) use outside the osteoporosis setting (Note 96). However, 
      whether this restriction could also have involved patients at risk for or with 
      osteoporotic fractures has not yet been investigated. We retrospectively analyzed 
      databases from five Italian Local Health Units. Patients aged ≥50 years with 
      either at least one prescription for osteoporosis treatment or with fragility 
      fractures and evidence of osteoporosis from 2011 to 2020 were included. The 
      proportion of subjects with an interruption in VD treatment before and after the 
      introduction of the new reimbursement criteria and predictors of this 
      interruption were analyzed. A total of 94,505 patients (aged 69.4 years) were 
      included. Following the introduction of Note 96, a 2-fold (OR 1.98, 95% CI: 
      1.92-2.04) increased risk of VD discontinuation was observed. These findings were 
      independent of seasonal variation, osteoporosis treatment patterns, as well as 
      other confounding variables. However, a higher rate of interruption was observed 
      in patients without vertebral/femur fracture (37.8%) vs. those with fracture 
      (32.9%). Rheumatoid arthritis, dyslipidemia and previous fracture were associated 
      with a lower risk of VD interruption, while stroke increased the risk of VD 
      interruption. Our results highlight that a possible misinterpretation of newly 
      introduced criteria for reimbursement restrictions in VD outside of osteoporosis 
      have resulted in an inadequate level of VD supplementation in patients with 
      osteoporosis. This undertreatment could reduce the effect of osteoporosis 
      therapies leading to increased risk of negative outcome.
FAU - Esposti, Luca Degli
AU  - Esposti LD
AD  - CliCon Srl Società Benefit Health Economics and Outcome Research, 40137 Bologna, 
      Italy.
FAU - Perrone, Valentina
AU  - Perrone V
AD  - CliCon Srl Società Benefit Health Economics and Outcome Research, 40137 Bologna, 
      Italy.
FAU - Sella, Stefania
AU  - Sella S
AD  - Clinica Medica 1, Department of Medicine, University of Padova, 35128 Padova, 
      Italy.
FAU - Arcidiacono, Gaetano
AU  - Arcidiacono G
AUID- ORCID: 0000-0003-0409-4449
AD  - Clinica Medica 1, Department of Medicine, University of Padova, 35128 Padova, 
      Italy.
FAU - Bertoldo, Francesco
AU  - Bertoldo F
AD  - Internal Medicine, Department of Medicine, University Hospital AOUI, 37134 
      Verona, Italy.
FAU - Giustina, Andrea
AU  - Giustina A
AD  - Institute of Endocrine and Metabolic Sciences, Instituto di Ricovero e Cura a 
      Carattere Scientifico (IRCSS) San Raffaele Hospital, San Raffaele Vita-Salute 
      University, 20132 Milan, Italy.
FAU - Minisola, Salvatore
AU  - Minisola S
AUID- ORCID: 0000-0001-6525-0439
AD  - Department of Clinical, Internal, Anaesthesiology, and Cardiovascular Sciences 
      Sapienza University of Rome, 00185 Rome, Italy.
FAU - Napoli, Nicola
AU  - Napoli N
AD  - Division of Endocrinology and Diabetes, Università Campus Bio-Medico di Roma, 
      00128 Rome, Italy.
FAU - Passeri, Giovanni
AU  - Passeri G
AUID- ORCID: 0000-0002-4039-1160
AD  - Unit of Clinica e Terapia Medica, Department of Medicine and Surgery, University 
      of Parma, 43126 Parma, Italy.
FAU - Rossini, Maurizio
AU  - Rossini M
AUID- ORCID: 0000-0001-9692-2293
AD  - Rheumatology Unit, Department of Medicine, University of Verona, 37134 Verona, 
      Italy.
FAU - Giannini, Sandro
AU  - Giannini S
AUID- ORCID: 0000-0003-0796-9749
AD  - Clinica Medica 1, Department of Medicine, University of Padova, 35128 Padova, 
      Italy.
CN  - LHU Study Group
LA  - eng
PT  - Journal Article
DEP - 20220429
PL  - Switzerland
TA  - Nutrients
JT  - Nutrients
JID - 101521595
RN  - 0 (Bone Density Conservation Agents)
RN  - 0 (Vitamins)
RN  - 1406-16-2 (Vitamin D)
SB  - IM
MH  - *Bone Density Conservation Agents/therapeutic use
MH  - Dietary Supplements
MH  - Humans
MH  - *Osteoporosis/etiology
MH  - *Osteoporotic Fractures/epidemiology/prevention & control
MH  - Retrospective Studies
MH  - *Spinal Fractures/complications
MH  - Vitamin D/therapeutic use
MH  - Vitamins/therapeutic use
PMC - PMC9105449
OTO - NOTNLM
OT  - clinical setting
OT  - osteoporosis
OT  - refracture risk
OT  - regulatory restriction
OT  - vitamin D supplementation
COIS- The authors declare no conflict of interest.
EDAT- 2022/05/15 06:00
MHDA- 2022/05/18 06:00
PMCR- 2022/04/29
CRDT- 2022/05/14 01:21
PHST- 2022/04/13 00:00 [received]
PHST- 2022/04/27 00:00 [revised]
PHST- 2022/04/28 00:00 [accepted]
PHST- 2022/05/14 01:21 [entrez]
PHST- 2022/05/15 06:00 [pubmed]
PHST- 2022/05/18 06:00 [medline]
PHST- 2022/04/29 00:00 [pmc-release]
AID - nu14091877 [pii]
AID - nutrients-14-01877 [pii]
AID - 10.3390/nu14091877 [doi]
PST - epublish
SO  - Nutrients. 2022 Apr 29;14(9):1877. doi: 10.3390/nu14091877.

PMID- 35554562
OWN - NLM
STAT- MEDLINE
DCOM- 20230417
LR  - 20230417
IS  - 1439-7609 (Electronic)
IS  - 1439-7595 (Linking)
VI  - 33
IP  - 3
DP  - 2023 Apr 13
TI  - Systemic chronic diseases coexist with and affect locomotive syndrome: The 
      Nagahama Study.
PG  - 608-616
LID - 10.1093/mr/roac039 [doi]
AB  - OBJECTIVES: The concept of locomotive syndrome was proposed to highlight older 
      adults who require nursing care services due to the malfunctioning of their 
      locomotive organs. With the coming of a super-ageing society, there is a growing 
      need to understand the relation between systemic chronic diseases and locomotive 
      syndrome. METHODS: We analysed the second-visit dataset of the Nagahama Study. 
      The association analysis was performed to identify the chronic diseases that were 
      risk factors associated with the occurrence and the progression of locomotive 
      syndrome in both the cross-sectional and longitudinal studies. RESULTS: 
      Hypertension, stroke, coronary heart disease, rheumatoid arthritis, chronic renal 
      failure, osteoporosis, anaemia, and gastroesophageal reflux disease were 
      independently correlated with locomotive syndrome through the deterioration of 
      body pain, social activity, and cognitive function in the cross-sectional study. 
      Multiple chronic diseases had additive effects and significantly increased the 
      risk of locomotive syndrome. In the longitudinal study, osteoporosis and kidney 
      disease were significantly correlated with the worsening of the total GLFS-25 
      score. CONCLUSIONS: Locomotive syndrome coexisted with various systemic chronic 
      diseases, especially cardiovascular diseases. Osteoporosis and kidney disease 
      were significantly correlated with the progression of locomotive dysfunction. The 
      management of various chronic diseases may be useful to prevent locomotive 
      syndrome and vice versa.
CI  - © Japan College of Rheumatology 2022. Published by Oxford University Press. All 
      rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
FAU - Morita, Yugo
AU  - Morita Y
AD  - Department of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, 
      Kyoto, Japan.
AD  - Center for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, 
      Japan.
FAU - Ito, Hiromu
AU  - Ito H
AUID- ORCID: 0000-0002-1827-382X
AD  - Department of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, 
      Kyoto, Japan.
AD  - Department of Orthopaedic Surgery, Kurashiki Central Hospital, Kurashiki, Japan.
FAU - Kawaguchi, Shuji
AU  - Kawaguchi S
AD  - Center for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, 
      Japan.
FAU - Nishitani, Kohei
AU  - Nishitani K
AD  - Department of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, 
      Kyoto, Japan.
FAU - Nakamura, Shinichiro
AU  - Nakamura S
AD  - Department of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, 
      Kyoto, Japan.
FAU - Kuriyama, Shinichi
AU  - Kuriyama S
AD  - Department of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, 
      Kyoto, Japan.
FAU - Ikezoe, Tome
AU  - Ikezoe T
AD  - Department of Physical Therapy, Human Health Sciences, Graduate School of 
      Medicine, Kyoto University, Kyoto, Japan.
FAU - Tsuboyama, Tadao
AU  - Tsuboyama T
AD  - Department of Physical Therapy, Human Health Sciences, Graduate School of 
      Medicine, Kyoto University, Kyoto, Japan.
AD  - Department of Physical Therapy, School of Health Sciences, Bukkyo University, 
      Kyoto, Japan.
FAU - Ichihashi, Noriaki
AU  - Ichihashi N
AD  - Department of Physical Therapy, Human Health Sciences, Graduate School of 
      Medicine, Kyoto University, Kyoto, Japan.
FAU - Tabara, Yasuharu
AU  - Tabara Y
AD  - Center for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, 
      Japan.
AD  - Graduate School of Public Health, Shizuoka Graduate University of Public Health, 
      Shizuoka, Japan.
FAU - Matsuda, Fumihiko
AU  - Matsuda F
AD  - Center for Genomic Medicine, Kyoto University Graduate School of Medicine, Kyoto, 
      Japan.
FAU - Matsuda, Shuichi
AU  - Matsuda S
AD  - Department of Orthopaedic Surgery, Kyoto University Graduate School of Medicine, 
      Kyoto, Japan.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Mod Rheumatol
JT  - Modern rheumatology
JID - 100959226
SB  - IM
MH  - Humans
MH  - Aged
MH  - Cross-Sectional Studies
MH  - Longitudinal Studies
MH  - *Locomotion
MH  - *Osteoporosis/complications/epidemiology
MH  - Chronic Disease
OTO - NOTNLM
OT  - Locomotive syndrome
OT  - cardiovascular disease
OT  - life-style disease
OT  - pain
OT  - walking ability
EDAT- 2022/05/14 06:00
MHDA- 2023/04/17 06:41
CRDT- 2022/05/13 15:52
PHST- 2022/01/17 00:00 [received]
PHST- 2022/04/04 00:00 [revised]
PHST- 2022/04/18 00:00 [accepted]
PHST- 2023/04/17 06:41 [medline]
PHST- 2022/05/14 06:00 [pubmed]
PHST- 2022/05/13 15:52 [entrez]
AID - 6584647 [pii]
AID - 10.1093/mr/roac039 [doi]
PST - ppublish
SO  - Mod Rheumatol. 2023 Apr 13;33(3):608-616. doi: 10.1093/mr/roac039.

PMID- 35453162
OWN - NLM
STAT- MEDLINE
DCOM- 20240202
LR  - 20240206
IS  - 2193-6323 (Electronic)
IS  - 2193-6315 (Linking)
VI  - 85
IP  - 2
DP  - 2024 Mar
TI  - Diagnostic Value of Vessel Wall Imaging to Determine the Timing of 
      Extracranial‒Intracranial Bypass for Moyamoya Syndrome Associated with Active 
      Sjögren's Syndrome: A Case Report.
PG  - 227-232
LID - 10.1055/a-1832-3269 [doi]
AB  - BACKGROUND:  Sjögren's syndrome is a chronic autoimmune disorder that 
      predominantly affects exocrine organs. It is characterized by an organ-specific 
      infiltration of lymphocytes. The involvement of the major cerebral arteries in 
      Sjögren's syndrome has rarely been reported. A recent study reported a case of 
      successful extracranial-intracranial (EC-IC) bypass without complications, even 
      in the active inflammatory state, although the optimal timing of such a bypass 
      remains unclear. CASE DESCRIPTION: We here report the case of a 43-year-old woman 
      presenting with acute ischemic stroke due to progressive middle cerebral artery 
      (MCA) occlusion and signs of primary Sjögren's syndrome. During intensive 
      immunosuppressive therapy for active Sjögren's syndrome, the patient was 
      monitored using contrast-enhanced magnetic resonance vessel wall imaging 
      (MR-VWI). A couple of intravenous cyclophosphamide injections combined with a 
      methylprednisolone pulse and antiplatelet therapy resulted in clear resolution of 
      vessel wall enhancement, which suggested remission of inflammatory vasculitis. 
      Nevertheless, she still experienced a transient ischemic attack (TIA) due to 
      decreased regional cerebral blood flow by MCA occlusion, as demonstrated by the 
      conventional time-of-flight MR angiography and single-photon emission computed 
      tomography. Considering the increased risk of further stroke, the decision was 
      made to perform an EC-IC bypass as a treatment for medically uncontrollable 
      hemodynamic impairment. Her postoperative course was uneventful without further 
      repeated TIAs, and continued immunosuppressive therapy for Sjögren's syndrome 
      provided effective management. CONCLUSIONS:  Our findings emphasize the 
      diagnostic value of contrast-enhanced MR-VWI in monitoring the effect of 
      immunosuppressive therapy for the major cerebral artery vasculitis and in 
      determining the timing of EC-IC bypass as a "rescue" treatment for moyamoya 
      syndrome associated with active Sjögren's syndrome.
CI  - Thieme. All rights reserved.
FAU - Shindo, Takafumi
AU  - Shindo T
AD  - Department of Neurosurgery, Hokkaido University Hospital, Sapporo, Japan.
FAU - Ito, Masaki
AU  - Ito M
AUID- ORCID: 0000-0002-8032-7198
AD  - Department of Neurosurgery, Hokkaido University Hospital, Sapporo, Japan.
FAU - Sugiyama, Taku
AU  - Sugiyama T
AUID- ORCID: 0000-0003-0398-225X
AD  - Department of Neurosurgery, Hokkaido University Hospital, Sapporo, Japan.
FAU - Okuyama, Tomohiro
AU  - Okuyama T
AD  - Department of Neurosurgery, Hokkaido University Hospital, Sapporo, Japan.
FAU - Kono, Michihito
AU  - Kono M
AD  - Department of Rheumatology, Endocrinology, and Nephrology, Hokkaido University 
      Hospital, Sapporo, Japan.
FAU - Atsumi, Tatsuya
AU  - Atsumi T
AD  - Department of Rheumatology, Endocrinology, and Nephrology, Hokkaido University 
      Hospital, Sapporo, Japan.
FAU - Fujimura, Miki
AU  - Fujimura M
AD  - Department of Neurosurgery, Hokkaido University Hospital, Sapporo, Japan.
LA  - eng
PT  - Case Reports
PT  - Journal Article
DEP - 20220422
PL  - Germany
TA  - J Neurol Surg A Cent Eur Neurosurg
JT  - Journal of neurological surgery. Part A, Central European neurosurgery
JID - 101580767
SB  - IM
MH  - Humans
MH  - Female
MH  - Adult
MH  - *Moyamoya Disease/complications/diagnostic imaging/surgery
MH  - *Sjogren's Syndrome/complications/diagnostic imaging
MH  - *Ischemic Stroke/complications
MH  - *Ischemic Attack, Transient/etiology/pathology/surgery
MH  - Infarction, Middle Cerebral Artery
MH  - *Vasculitis/complications
COIS- None declared.
EDAT- 2022/04/23 06:00
MHDA- 2024/02/02 06:43
CRDT- 2022/04/22 20:16
PHST- 2024/02/02 06:43 [medline]
PHST- 2022/04/23 06:00 [pubmed]
PHST- 2022/04/22 20:16 [entrez]
AID - 10.1055/a-1832-3269 [doi]
PST - ppublish
SO  - J Neurol Surg A Cent Eur Neurosurg. 2024 Mar;85(2):227-232. doi: 
      10.1055/a-1832-3269. Epub 2022 Apr 22.

PMID- 35389771
OWN - NLM
STAT- MEDLINE
DCOM- 20231002
LR  - 20231002
IS  - 1563-5279 (Electronic)
IS  - 0020-7454 (Linking)
VI  - 133
IP  - 10
DP  - 2023 Dec
TI  - Multiple dissecting intracranial and extracranial aneurysms in rheumatoid 
      arthritis: a rare case.
PG  - 1193-1195
LID - 10.1080/00207454.2022.2059367 [doi]
AB  - A 52 year old female with a history of rheumatoid arthritis (RA) and persistently 
      raised levels of serum rheumatoid factor and cyclic citrunillated peptide, 
      presented with dissecting aneurysms at the right internal carotid artery, and 
      intact aneurysms at the supraclinoid segment and opening of the right opthalmic 
      artery. Coil embolization was performed. The patient developed an ischaemic 
      stroke two days later.Intra and extra-cranial large vessel aneurysms in RA have 
      rarely been reported in the literature. RA patients with persistent systemic 
      inflammation are at increased risk of developing vascular complications and 
      ischaemic stroke. Here, high levels of tissue-deposited immune complexes may have 
      resulted in cerebral artery vasculopathy. Risk stratification for the development 
      of vascular complications, including cranial aneurysms and ischaemic stroke, in 
      RA patients with poorly controlled systemic inflammation, is important; 
      especially when we consider the neurological sequelae associated with dissecting 
      cerebral aneurysms, cerebral infarction and surgical intervention.
FAU - Ozen, Selin
AU  - Ozen S
AUID- ORCID: 0000-0002-7290-8558
AD  - Başkent University Faculty of Medicine, Department of Physical Medicine and 
      Rehabilitation, Ankara, Turkey.
FAU - Guzel, Sukran
AU  - Guzel S
AUID- ORCID: 0000-0001-9852-0917
AD  - Başkent University Faculty of Medicine, Department of Physical Medicine and 
      Rehabilitation, Ankara, Turkey.
LA  - eng
PT  - Case Reports
PT  - Journal Article
DEP - 20220407
PL  - England
TA  - Int J Neurosci
JT  - The International journal of neuroscience
JID - 0270707
SB  - IM
MH  - Female
MH  - Humans
MH  - Middle Aged
MH  - *Brain Ischemia
MH  - *Stroke
MH  - *Intracranial Aneurysm/complications/diagnostic imaging
MH  - *Ischemic Stroke
MH  - *Arthritis, Rheumatoid/complications
MH  - Inflammation
MH  - Carotid Artery, Internal
OTO - NOTNLM
OT  - Intracranial aneurysm
OT  - cerebral arteries
OT  - rheumatoid arthritis
OT  - vasculitis
EDAT- 2022/04/08 06:00
MHDA- 2023/10/02 06:42
CRDT- 2022/04/07 17:12
PHST- 2023/10/02 06:42 [medline]
PHST- 2022/04/08 06:00 [pubmed]
PHST- 2022/04/07 17:12 [entrez]
AID - 10.1080/00207454.2022.2059367 [doi]
PST - ppublish
SO  - Int J Neurosci. 2023 Dec;133(10):1193-1195. doi: 10.1080/00207454.2022.2059367. 
      Epub 2022 Apr 7.

PMID- 35385337
OWN - NLM
STAT- MEDLINE
DCOM- 20220408
LR  - 20230502
IS  - 1946-6242 (Electronic)
IS  - 1946-6234 (Linking)
VI  - 14
IP  - 639
DP  - 2022 Apr 6
TI  - A proteomic surrogate for cardiovascular outcomes that is sensitive to multiple 
      mechanisms of change in risk.
PG  - eabj9625
LID - 10.1126/scitranslmed.abj9625 [doi]
AB  - A reliable, individualized, and dynamic surrogate of cardiovascular risk, 
      synoptic for key biologic mechanisms, could shorten the path for drug 
      development, enhance drug cost-effectiveness and improve patient outcomes. We 
      used highly multiplexed proteomics to address these objectives, measuring about 
      5000 proteins in each of 32,130 archived plasma samples from 22,849 participants 
      in nine clinical studies. We used machine learning to derive a 27-protein model 
      predicting 4-year likelihood of myocardial infarction, stroke, heart failure, or 
      death. The 27 proteins encompassed 10 biologic systems, and 12 were associated 
      with relevant causal genetic traits. We independently validated results in 11,609 
      participants. Compared to a clinical model, the ratio of observed events in 
      quintile 5 to quintile 1 was 6.7 for proteins versus 2.9 for the clinical model, 
      AUCs (95% CI) were 0.73 (0.72 to 0.74) versus 0.64 (0.62 to 0.65), c-statistics 
      were 0.71 (0.69 to 0.72) versus 0.62 (0.60 to 0.63), and the net reclassification 
      index was +0.43. Adding the clinical model to the proteins only improved 
      discrimination metrics by 0.01 to 0.02. Event rates in four predefined protein 
      risk categories were 5.6, 11.2, 20.0, and 43.4% within 4 years; median time to 
      event was 1.71 years. Protein predictions were directionally concordant with 
      changed outcomes. Adverse risks were predicted for aging, approaching an event, 
      anthracycline chemotherapy, diabetes, smoking, rheumatoid arthritis, cancer 
      history, cardiovascular disease, high systolic blood pressure, and lipids. 
      Reduced risks were predicted for weight loss and exenatide. The 27-protein model 
      has potential as a "universal" surrogate end point for cardiovascular risk.
FAU - Williams, Stephen A
AU  - Williams SA
AUID- ORCID: 0000-0002-8661-4315
AD  - SomaLogic Inc., Boulder, CO 80301, USA.
FAU - Ostroff, Rachel
AU  - Ostroff R
AUID- ORCID: 0000-0002-6867-5464
AD  - SomaLogic Inc., Boulder, CO 80301, USA.
FAU - Hinterberg, Michael A
AU  - Hinterberg MA
AUID- ORCID: 0000-0003-0693-7075
AD  - SomaLogic Inc., Boulder, CO 80301, USA.
FAU - Coresh, Josef
AU  - Coresh J
AD  - Johns Hopkins University, Baltimore, MD 21218, USA.
FAU - Ballantyne, Christie M
AU  - Ballantyne CM
AUID- ORCID: 0000-0002-6432-1730
AD  - Baylor College of Medicine, Houston, TX 77030, USA.
FAU - Matsushita, Kunihiro
AU  - Matsushita K
AUID- ORCID: 0000-0002-7179-718X
AD  - Johns Hopkins University, Baltimore, MD 21218, USA.
FAU - Mueller, Christian E
AU  - Mueller CE
AUID- ORCID: 0000-0002-1120-6405
AD  - Cardiovascular Research Institute, University of Basel, Basel 4001, Switzerland.
FAU - Walter, Joan
AU  - Walter J
AUID- ORCID: 0000-0001-6077-6941
AD  - Cardiovascular Research Institute, University of Basel, Basel 4001, Switzerland.
AD  - Institute of Diagnostic and Interventional Radiology, University Hospital Zürich, 
      University of Zürich, Zürich 7491, Switzerland.
FAU - Jonasson, Christian
AU  - Jonasson C
AUID- ORCID: 0000-0002-7694-6025
AD  - Jebsen Centre for Genetic Epidemiology, Department of Public Health and Nursing, 
      Norwegian University of Science and Technology, Trondheim 7491, Norway.
FAU - Holman, Rury R
AU  - Holman RR
AUID- ORCID: 0000-0002-1256-874X
AD  - Diabetes Trials Unit, Radcliffe Department of Medicine, University of Oxford, 
      Oxford OX3 9DU, UK.
FAU - Shah, Svati H
AU  - Shah SH
AD  - Division of Cardiology, Duke Department of Medicine, and Duke Molecular 
      Physiology Institute, Duke University, Durham, NC 27710, USA.
FAU - Sattar, Naveed
AU  - Sattar N
AUID- ORCID: 0000-0002-1604-2593
AD  - Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow 
      G12 8QQ, UK.
FAU - Taylor, Roy
AU  - Taylor R
AD  - Newcastle Magnetic Resonance Centre, University of Newcastle upon Tyne, Newcastle 
      upon Tyne NE1 7RU, UK.
FAU - Lean, Michael E
AU  - Lean ME
AUID- ORCID: 0000-0003-2216-0083
AD  - School of Medicine, Nursing and Dentistry, University of Glasgow, Glasgow G12 
      8QQ, UK.
FAU - Kato, Shintaro
AU  - Kato S
AD  - NEC Solution Innovators Ltd., Tokyo 136-0082, Japan.
FAU - Shimokawa, Hiroaki
AU  - Shimokawa H
AUID- ORCID: 0000-0001-7534-4826
AD  - Tohoku University Graduate School of Medicine, Sendai 980-8576, Japan.
AD  - Graduate School, International University of Health and Welfare, Narita 286-8686, 
      Japan.
FAU - Sakata, Yasuhiko
AU  - Sakata Y
AD  - Tohoku University Graduate School of Medicine, Sendai 980-8576, Japan.
FAU - Nochioka, Kotaro
AU  - Nochioka K
AUID- ORCID: 0000-0001-8297-8624
AD  - Tohoku University Graduate School of Medicine, Sendai 980-8576, Japan.
FAU - Parikh, Chirag R
AU  - Parikh CR
AUID- ORCID: 0000-0001-9051-7385
AD  - Johns Hopkins University, Baltimore, MD 21218, USA.
FAU - Coca, Steven G
AU  - Coca SG
AUID- ORCID: 0000-0002-0928-9168
AD  - Mt Sinai Clinical and Translational Science Research Unit, Icahn School of 
      Medicine at Mount Sinai, New York, NY 11766, USA.
FAU - Omland, Torbjørn
AU  - Omland T
AD  - Department of Cardiology, Akershus University Hospital and University of Oslo, 
      Oslo 1478, Norway.
FAU - Chadwick, Jessica
AU  - Chadwick J
AUID- ORCID: 0000-0002-2017-3094
AD  - SomaLogic Inc., Boulder, CO 80301, USA.
FAU - Astling, David
AU  - Astling D
AUID- ORCID: 0000-0001-8179-0304
AD  - SomaLogic Inc., Boulder, CO 80301, USA.
FAU - Hagar, Yolanda
AU  - Hagar Y
AD  - SomaLogic Inc., Boulder, CO 80301, USA.
FAU - Kureshi, Natasha
AU  - Kureshi N
AUID- ORCID: 0000-0001-8118-9068
AD  - SomaLogic Inc., Boulder, CO 80301, USA.
FAU - Loupy, Kelsey
AU  - Loupy K
AUID- ORCID: 0000-0002-7338-9104
AD  - SomaLogic Inc., Boulder, CO 80301, USA.
FAU - Paterson, Clare
AU  - Paterson C
AD  - SomaLogic Inc., Boulder, CO 80301, USA.
FAU - Primus, Jeremy
AU  - Primus J
AUID- ORCID: 0000-0001-7402-277X
AD  - SomaLogic Inc., Boulder, CO 80301, USA.
FAU - Simpson, Missy
AU  - Simpson M
AUID- ORCID: 0000-0002-9757-4427
AD  - SomaLogic Inc., Boulder, CO 80301, USA.
FAU - Trujillo, Nelson P
AU  - Trujillo NP
AD  - Boulder Community Hospital, Boulder, CO 80301, USA.
FAU - Ganz, Peter
AU  - Ganz P
AUID- ORCID: 0000-0002-0437-8882
AD  - Zuckerberg San Francisco General Hospital, University of California, San 
      Francisco, San Francisco, CA 94110, USA.
LA  - eng
GR  - R01 HL086694/HL/NHLBI NIH HHS/United States
GR  - HHSN268201700004I/HL/NHLBI NIH HHS/United States
GR  - HHSN268201700002I/HL/NHLBI NIH HHS/United States
GR  - HHSN268201700005I/HL/NHLBI NIH HHS/United States
GR  - HHSN268201700003I/HL/NHLBI NIH HHS/United States
GR  - R01 HL085757/HL/NHLBI NIH HHS/United States
GR  - U01 DK106962/DK/NIDDK NIH HHS/United States
GR  - U01 DK108809/DK/NIDDK NIH HHS/United States
GR  - HHSN268201700001I/HL/NHLBI NIH HHS/United States
GR  - U01 HG004402/HG/NHGRI NIH HHS/United States
GR  - R01 AG052964/AG/NIA NIH HHS/United States
GR  - R01 HL087641/HL/NHLBI NIH HHS/United States
GR  - R01 HL129856/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20220406
PL  - United States
TA  - Sci Transl Med
JT  - Science translational medicine
JID - 101505086
RN  - 0 (Biomarkers)
SB  - IM
CIN - Nat Rev Cardiol. 2022 Jun;19(6):352. doi: 10.1038/s41569-022-00716-7. PMID: 
      35444299
CIN - Sci Transl Med. 2022 Oct 5;14(665):eabq4810. doi: 10.1126/scitranslmed.abq4810. 
      PMID: 36197964
CIN - Sci Transl Med. 2022 Oct 5;14(665):eadd1355. doi: 10.1126/scitranslmed.add1355. 
      PMID: 36197965
MH  - Biomarkers
MH  - *Cardiovascular Diseases
MH  - *Heart Failure/drug therapy
MH  - Humans
MH  - *Myocardial Infarction/drug therapy
MH  - Proteomics
MH  - *Stroke/complications
EDAT- 2022/04/07 06:00
MHDA- 2022/04/09 06:00
CRDT- 2022/04/06 17:11
PHST- 2022/04/06 17:11 [entrez]
PHST- 2022/04/07 06:00 [pubmed]
PHST- 2022/04/09 06:00 [medline]
AID - 10.1126/scitranslmed.abj9625 [doi]
PST - ppublish
SO  - Sci Transl Med. 2022 Apr 6;14(639):eabj9625. doi: 10.1126/scitranslmed.abj9625. 
      Epub 2022 Apr 6.

PMID- 35313088
OWN - NLM
STAT- MEDLINE
DCOM- 20230828
LR  - 20240402
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Print)
IS  - 2151-464X (Linking)
VI  - 75
IP  - 4
DP  - 2023 Apr
TI  - Circulating Adipokines and Associations With Incident Cardiovascular Disease in 
      Rheumatoid Arthritis.
PG  - 768-777
LID - 10.1002/acr.24885 [doi]
AB  - OBJECTIVE: To assess whether circulating levels of adiponectin, leptin, and 
      fibroblast growth factor 21 (FGF-21) are associated with incident cardiovascular 
      disease (CVD) in rheumatoid arthritis (RA). METHODS: Adipokines were measured 
      using banked enrollment serum from patients with RA and dichotomized above/below 
      the median value. Incident CVD events (coronary artery disease [CAD], stroke, 
      heart failure [HF] hospitalization, venous thromboembolism, CVD-related deaths) 
      were identified using administrative data and the National Death Index. 
      Covariates were derived from medical record, biorepository, and registry 
      databases. Multivariable Cox models were generated to quantify associations 
      between adipokine concentrations and CVD incidence. Five-year incidence rates 
      were predicted. RESULTS: Among 2,598 participants, 639 (25%) had at least 1 CVD 
      event over 19,585 patient-years of follow-up. High adiponectin levels were 
      independently associated with HF hospitalization (hazard ratio [HR] 1.39 [95% 
      confidence interval (95% CI) 1.07-1.79], P = 0.01) and CVD-related death (HR 1.49 
      [95% CI 1.16-1.92], P = 0.002) but not with other CVD events. High leptin was 
      independently associated with CVD-related death (HR 1.44 [95% CI 1.05-1.97], 
      P = 0.02). High FGF-21 levels were independently associated with lower rates of 
      CAD (HR 0.75 [95% CI 0.58-0.97], P = 0.03). In subgroup analyses, associations 
      between high adiponectin and leptin levels with CVD-related death were driven by 
      strong associations in nonobese patients. CONCLUSION: Adipokines are associated 
      with HF hospitalization and CVD-related death in patients with RA, with stronger 
      associations in nonobese participants. These findings suggest that adipokines 
      effectively predict clinically important outcomes in RA perhaps through an 
      association with body composition and metabolic health. Further study is needed 
      to determine whether adipokine measures might augment existing tools to identify 
      RA patients at increased risk of CVD.
CI  - © 2022 American College of Rheumatology. This article has been contributed to by 
      U.S. Government employees and their work is in the public domain in the USA.
FAU - Federico, Lydia E
AU  - Federico LE
AUID- ORCID: 0000-0003-2607-9581
AD  - University of Pennsylvania, Philadelphia.
FAU - Johnson, Tate M
AU  - Johnson TM
AUID- ORCID: 0000-0003-0335-4157
AD  - Veterans Affairs Nebraska-Western Iowa Health Care System and University of 
      Nebraska Medical Center, Omaha, Nebraska.
FAU - England, Bryant R
AU  - England BR
AUID- ORCID: 0000-0002-9649-3588
AD  - Veterans Affairs Nebraska-Western Iowa Health Care System and University of 
      Nebraska Medical Center, Omaha, Nebraska.
FAU - Wysham, Katherine D
AU  - Wysham KD
AUID- ORCID: 0000-0001-8707-7649
AD  - Veterans Affairs Puget Sound Healthcare System and University of Washington, 
      Seattle.
FAU - George, Michael D
AU  - George MD
AUID- ORCID: 0000-0002-0398-2308
AD  - University of Pennsylvania, Philadelphia.
FAU - Sauer, Brian
AU  - Sauer B
AUID- ORCID: 0000-0002-3546-3051
AD  - University of Utah Medical Center and Veterans Affairs Salt Lake City Health Care 
      System, Salt Lake City.
FAU - Hamilton, Bartlett C
AU  - Hamilton BC
AD  - University of Nebraska Medical Center, Omaha.
FAU - Hunter, Carlos D
AU  - Hunter CD
AD  - University of Nebraska Medical Center, Omaha.
FAU - Duryee, Michael J
AU  - Duryee MJ
AD  - University of Nebraska Medical Center, Omaha.
FAU - Thiele, Geoffrey M
AU  - Thiele GM
AD  - Veterans Affairs Nebraska-Western Iowa Health Care System and University of 
      Nebraska Medical Center, Omaha, Nebraska.
FAU - Mikuls, Ted R
AU  - Mikuls TR
AUID- ORCID: 0000-0002-0897-2272
AD  - Veterans Affairs Nebraska-Western Iowa Health Care System and University of 
      Nebraska Medical Center, Omaha, Nebraska.
FAU - Baker, Joshua F
AU  - Baker JF
AD  - University of Pennsylvania and Corporal Michael J. Crescenz Veterans Affairs 
      Medical Center, Philadelphia.
LA  - eng
GR  - P50AR60772/AR/NIAMS NIH HHS/United States
GR  - U54 GM115458/GM/NIGMS NIH HHS/United States
GR  - IK2 CX002203/CX/CSRD VA/United States
GR  - I01 RX003644/RX/RRD VA/United States
GR  - R25AA020818/AA/NIAAA NIH HHS/United States
GR  - P50 AR060772/AR/NIAMS NIH HHS/United States
GR  - U54GM115458/GM/NIGMS NIH HHS/United States
GR  - I01 CX001703/CX/CSRD VA/United States
GR  - K23 AR073931/AR/NIAMS NIH HHS/United States
GR  - R25 AA020818/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20221111
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 0 (Adipokines)
RN  - 0 (Adiponectin)
RN  - 0 (Leptin)
SB  - IM
MH  - Humans
MH  - *Adipokines/blood
MH  - Adiponectin
MH  - *Arthritis, Rheumatoid/blood/diagnosis/epidemiology
MH  - *Cardiovascular Diseases/blood/diagnosis/epidemiology
MH  - Coronary Artery Disease
MH  - Leptin
MH  - Risk Factors
PMC - PMC10588673
MID - NIHMS1931606
EDAT- 2022/03/22 06:00
MHDA- 2023/03/29 06:05
PMCR- 2024/04/01
CRDT- 2022/03/21 17:20
PHST- 2022/03/09 00:00 [revised]
PHST- 2021/12/29 00:00 [received]
PHST- 2022/03/17 00:00 [accepted]
PHST- 2023/03/29 06:05 [medline]
PHST- 2022/03/22 06:00 [pubmed]
PHST- 2022/03/21 17:20 [entrez]
PHST- 2024/04/01 00:00 [pmc-release]
AID - 10.1002/acr.24885 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2023 Apr;75(4):768-777. doi: 10.1002/acr.24885. 
      Epub 2022 Nov 11.

PMID- 35244076
OWN - NLM
STAT- MEDLINE
DCOM- 20220322
LR  - 20230103
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 101
IP  - 9
DP  - 2022 Mar 4
TI  - Internal carotid artery occlusion related to poorly controlled rheumatoid 
      arthritis presenting with continuous hand shaking: A case report and literature 
      review.
PG  - e29001
LID - 10.1097/MD.0000000000029001 [doi]
LID - e29001
AB  - RATIONALE: Limb-shaking syndrome is a special manifestation of transient ischemic 
      attack, resulting from internal carotid artery (ICA) occlusion. Extra-articular 
      manifestations of rheumatoid arthritis (RA) are likely to occur in patients with 
      severe or active RA. RA may accelerate atherosclerotic processes through 
      inflammation. Here, we present a case of ICA occlusion related to poorly 
      controlled RA that presented with continuous hand shaking. PATIENT CONCERNS: A 
      73-year-old man with a history of poorly controlled RA developed total occlusion 
      of the right ICA in recent 4 months. He presented with 2 days of continuous and 
      rhythmic left-hand shaking before admission. DIAGNOSIS: The patient was suspected 
      to have transient ischemic attack resulting from ICA occlusion. INTERVENTIONS: 
      Antiplatelets and antiepileptic drugs were used for continuous nonepileptic focal 
      myoclonus. A disease-modifying antirheumatic drug-based regimen for RA was 
      developed to prevent further atherosclerosis. OUTCOMES: Following the initial 
      intervention, continuous hand shaking subsided on hospital day 7. Prednisolone 
      was titrated as an active RA control. At the 6-month follow-up visit, neither 
      painful wrist swelling nor recurrent shaking of the hand was noted. LESSONS: 
      Continuous hand shaking (nonepileptic focal myoclonus) can be the initial 
      presentation of ICA occlusion in patients with poorly controlled RA. Every 
      patient with RA should be treated aggressively with anti-rheumatic agents since 
      RA is an independent risk factor for stroke. Additionally, every patient with RA 
      should be surveyed for ICA stenosis, especially in those with poor control.
CI  - Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.
FAU - Chien, Ching-Fang
AU  - Chien CF
AD  - Department of Neurology, Kaohsiung Medical University Hospital, Kaohsiung Medical 
      University, Kaohsiung, Taiwan.
AD  - Department of Neurology, School of Medicine, College of Medicine, Kaohsiung 
      Medical University, Kaohsiung, Taiwan.
FAU - Tsai, Chun-Yi
AU  - Tsai CY
AD  - Department of Neurology, Kaohsiung Medical University Hospital, Kaohsiung Medical 
      University, Kaohsiung, Taiwan.
AD  - Department of Neurology, School of Medicine, College of Medicine, Kaohsiung 
      Medical University, Kaohsiung, Taiwan.
FAU - Wu, Meng-Ni
AU  - Wu MN
AD  - Department of Neurology, Kaohsiung Medical University Hospital, Kaohsiung Medical 
      University, Kaohsiung, Taiwan.
AD  - Department of Neurology, School of Medicine, College of Medicine, Kaohsiung 
      Medical University, Kaohsiung, Taiwan.
FAU - Lai, Chiou-Lian
AU  - Lai CL
AD  - Department of Neurology, Kaohsiung Medical University Hospital, Kaohsiung Medical 
      University, Kaohsiung, Taiwan.
AD  - Department of Neurology, School of Medicine, College of Medicine, Kaohsiung 
      Medical University, Kaohsiung, Taiwan.
FAU - Liou, Li-Min
AU  - Liou LM
AD  - Department of Neurology, Kaohsiung Medical University Hospital, Kaohsiung Medical 
      University, Kaohsiung, Taiwan.
AD  - Department of Neurology, School of Medicine, College of Medicine, Kaohsiung 
      Medical University, Kaohsiung, Taiwan.
LA  - eng
PT  - Case Reports
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
SB  - IM
MH  - Aged
MH  - Arterial Occlusive Diseases/*complications/diagnosis
MH  - Arthritis, Rheumatoid/*complications/drug therapy
MH  - Carotid Artery Diseases/*complications/diagnosis
MH  - Carotid Artery, Internal/*diagnostic imaging
MH  - Humans
MH  - Ischemic Attack, Transient/complications
MH  - Male
MH  - Myoclonus
MH  - Tremor/*etiology
MH  - Ultrasonography
PMC - PMC8896453
COIS- The authors report no conflicts of interest.
EDAT- 2022/03/05 06:00
MHDA- 2022/03/23 06:00
PMCR- 2022/03/04
CRDT- 2022/03/04 08:50
PHST- 2022/01/16 00:00 [received]
PHST- 2022/02/16 00:00 [accepted]
PHST- 2022/03/04 08:50 [entrez]
PHST- 2022/03/05 06:00 [pubmed]
PHST- 2022/03/23 06:00 [medline]
PHST- 2022/03/04 00:00 [pmc-release]
AID - 00005792-202203040-00043 [pii]
AID - MD-D-22-00283 [pii]
AID - 10.1097/MD.0000000000029001 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2022 Mar 4;101(9):e29001. doi: 10.1097/MD.0000000000029001.

PMID- 35209936
OWN - NLM
STAT- MEDLINE
DCOM- 20220310
LR  - 20220311
IS  - 1478-6362 (Electronic)
IS  - 1478-6354 (Print)
IS  - 1478-6354 (Linking)
VI  - 24
IP  - 1
DP  - 2022 Feb 24
TI  - Rheumatoid arthritis, as a clinical disease, but not rheumatoid 
      arthritis-associated autoimmunity, is linked to cardiovascular events.
PG  - 56
LID - 10.1186/s13075-022-02722-z [doi]
LID - 56
AB  - BACKGROUND: Rheumatoid arthritis (RA) is characterized by increased 
      cardiovascular (CV) mortality. CV events are particularly high in patients with 
      RA-specific autoimmunity, including rheumatoid factor (RF) and anti-citrullinated 
      protein antibodies (ACPA), raising the question whether RA-specific autoimmunity 
      itself is associated with CV events. METHODS: New CV events (myocardial 
      infarction, stroke or death by CV cause) were recorded in 20,625 subjects of the 
      Electricité de France - Gaz de France (GAZEL) cohort. Self-reported RA cases in 
      the GAZEL cohort were validated by phone interview on the basis of a specific 
      questionnaire. In 1618 subjects, in whom plasma was available, RF and ACPA were 
      measured. A piecewise exponential Poisson regression was used to analyze the 
      association of CV events with presence of RA as well as RA-specific autoimmunity 
      (without RA). RESULTS: CV events in GAZEL were associated with age, male sex, 
      smoking, hypertension, hyperlipidemia, and diabetes mellitus (HR from 1.06 to 
      1.87, p < 0.05). Forty-two confirmed RA cases were identified. Confirmed RA was 
      significantly associated with CV risk increase (HR of 3.03; 95% CI: 1.13-8.11, 
      p = 0.03) independently of conventional CV risk factors. One hundred 
      seventy-eight subjects showed RF or ACPA positivity without presence of RA. CV 
      events were not associated with ACPA positivity (HR: 1.52, 95% CI: 0.47-4.84, 
      p = 0.48) or RF positivity (HR: 1.15, 95% CI: 0.55-2.40, p = 0.70) in the absence 
      of RA. CONCLUSIONS: RA, as a clinical chronic inflammatory disease, but not mere 
      positivity for RF or ACPA in the absence of clinical disease is associated with 
      increased CV risk.
CI  - © 2022. The Author(s).
FAU - Gouze, Hélène
AU  - Gouze H
AUID- ORCID: 0000-0002-5333-0316
AD  - Infection & Inflammation, UMR 1173, Inserm, UVSQ/Paris Saclay, 78180, 
      Montigny-le-Bretonneux, France. helene.gouze@aphp.fr.
AD  - Service de Rhumatologie, Hôpital Ambroise Paré, AP-HP-Paris Saclay, 92100, 
      Boulogne, France. helene.gouze@aphp.fr.
AD  - Laboratoire d'Excellence Inflamex, Université Paris Descartes, Sorbonne Paris 
      Cité, Paris, France. helene.gouze@aphp.fr.
FAU - Aegerter, Philippe
AU  - Aegerter P
AD  - Inserm U1018 - Center for Research in Epidemiology and Population Health (CESP), 
      Integrative Respiratory Epidemiology Team, Paris Saclay University, Villejuif, 
      France.
FAU - Said-Nahal, Roula
AU  - Said-Nahal R
AD  - Infection & Inflammation, UMR 1173, Inserm, UVSQ/Paris Saclay, 78180, 
      Montigny-le-Bretonneux, France.
AD  - Service de Rhumatologie, Hôpital Ambroise Paré, AP-HP-Paris Saclay, 92100, 
      Boulogne, France.
AD  - Laboratoire d'Excellence Inflamex, Université Paris Descartes, Sorbonne Paris 
      Cité, Paris, France.
FAU - Zins, Marie
AU  - Zins M
AD  - Population-based Cohorts Unit-UMS 011, Paris University, Villejuif, France.
FAU - Goldberg, Marcel
AU  - Goldberg M
AD  - Population-based Cohorts Unit-UMS 011, Paris University, Villejuif, France.
FAU - Morelle, Guillaume
AU  - Morelle G
AD  - Service de Rhumatologie, Hôpital Ambroise Paré, AP-HP-Paris Saclay, 92100, 
      Boulogne, France.
FAU - Schett, Georg
AU  - Schett G
AD  - Department of Internal Medicine 3 - Rheumatology and Immunology, 
      Friedrich-Alexander University (FAU), Erlangen-Nuremberg and Universitätsklinikum 
      Erlangen, Erlangen, Germany.
AD  - Deutsches Zentrum für Immuntherapie, Friedrich-Alexander University (FAU), 
      Erlangen-Nuremberg and Universitätsklinikum Erlangen, Erlangen, Germany.
FAU - Breban, Maxime
AU  - Breban M
AD  - Infection & Inflammation, UMR 1173, Inserm, UVSQ/Paris Saclay, 78180, 
      Montigny-le-Bretonneux, France.
AD  - Service de Rhumatologie, Hôpital Ambroise Paré, AP-HP-Paris Saclay, 92100, 
      Boulogne, France.
AD  - Laboratoire d'Excellence Inflamex, Université Paris Descartes, Sorbonne Paris 
      Cité, Paris, France.
FAU - D'Agostino, Maria Antonietta
AU  - D'Agostino MA
AD  - Infection & Inflammation, UMR 1173, Inserm, UVSQ/Paris Saclay, 78180, 
      Montigny-le-Bretonneux, France.
AD  - Service de Rhumatologie, Hôpital Ambroise Paré, AP-HP-Paris Saclay, 92100, 
      Boulogne, France.
AD  - Laboratoire d'Excellence Inflamex, Université Paris Descartes, Sorbonne Paris 
      Cité, Paris, France.
AD  - Istituto di Reumatologia, Università Cattolica del Sacro Cuore, Fondazione 
      Policlinico Universitario Agostino Gemelli IRCSS, Rome, Italy.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220224
PL  - England
TA  - Arthritis Res Ther
JT  - Arthritis research & therapy
JID - 101154438
RN  - 0 (Anti-Citrullinated Protein Antibodies)
RN  - 0 (Autoantibodies)
RN  - 9009-79-4 (Rheumatoid Factor)
SB  - IM
MH  - Anti-Citrullinated Protein Antibodies
MH  - *Arthritis, Rheumatoid/complications/epidemiology
MH  - Autoantibodies
MH  - Autoimmunity
MH  - *Cardiovascular Diseases/complications/diagnosis/epidemiology
MH  - Humans
MH  - Male
MH  - Rheumatoid Factor
PMC - PMC8867622
OTO - NOTNLM
OT  - Anti-citrullinated protein autoantibody
OT  - Autoimmunity
OT  - Cardiovascular diseases
OT  - Cardiovascular risk
OT  - Rheumatoid arthritis
COIS- The authors declare no competing interests.
EDAT- 2022/02/26 06:00
MHDA- 2022/03/11 06:00
PMCR- 2022/02/24
CRDT- 2022/02/25 05:30
PHST- 2021/07/26 00:00 [received]
PHST- 2022/01/13 00:00 [accepted]
PHST- 2022/02/25 05:30 [entrez]
PHST- 2022/02/26 06:00 [pubmed]
PHST- 2022/03/11 06:00 [medline]
PHST- 2022/02/24 00:00 [pmc-release]
AID - 10.1186/s13075-022-02722-z [pii]
AID - 2722 [pii]
AID - 10.1186/s13075-022-02722-z [doi]
PST - epublish
SO  - Arthritis Res Ther. 2022 Feb 24;24(1):56. doi: 10.1186/s13075-022-02722-z.

PMID- 35191418
OWN - NLM
STAT- MEDLINE
DCOM- 20220428
LR  - 20230222
IS  - 2542-5641 (Electronic)
IS  - 0366-6999 (Print)
IS  - 0366-6999 (Linking)
VI  - 135
IP  - 6
DP  - 2022 Mar 20
TI  - Multimorbidity patterns and association with mortality in 0.5 million Chinese 
      adults.
PG  - 648-657
LID - 10.1097/CM9.0000000000001985 [doi]
AB  - BACKGROUND: Few studies have assessed the relationship between multimorbidity 
      patterns and mortality risk in the Chinese population. We aimed to identify 
      multimorbidity patterns and examined the associations of multimorbidity patterns 
      and the number of chronic diseases with the risk of mortality among Chinese 
      middle-aged and older adults. METHODS: We used data from the China Kadoorie 
      Biobank and included 512,723 participants aged 30 to 79 years. Multimorbidity was 
      defined as the presence of two or more of the 15 chronic diseases collected by 
      self-report or physical examination at baseline. Multimorbidity patterns were 
      identified using hierarchical cluster analysis. Cox regression was used to 
      estimate the associations of multimorbidity patterns and the number of chronic 
      diseases with all-cause and cause-specific mortality. RESULTS: Overall, 15.8% of 
      participants had multimorbidity. The prevalence of multimorbidity increased with 
      age and was higher in urban than rural participants. Four multimorbidity patterns 
      were identified, including cardiometabolic multimorbidity (diabetes, coronary 
      heart disease, stroke, and hypertension), respiratory multimorbidity 
      (tuberculosis, asthma, and chronic obstructive pulmonary disease), 
      gastrointestinal and hepatorenal multimorbidity (gallstone disease, chronic 
      kidney disease, cirrhosis, peptic ulcer, and cancer), and mental and arthritis 
      multimorbidity (neurasthenia, psychiatric disorder, and rheumatoid arthritis). 
      During a median of 10.8 years of follow-up, 49,371 deaths occurred. Compared with 
      participants without multimorbidity, cardiometabolic multimorbidity (hazard 
      ratios [HR] = 2.20, 95% confidence intervals [CI]: 2.14 - 2.26) and respiratory 
      multimorbidity (HR = 2.13, 95% CI:1.97 - 2.31) demonstrated relatively higher 
      risks of mortality, followed by gastrointestinal and hepatorenal multimorbidity 
      (HR = 1.33, 95% CI:1.22 - 1.46). The mortality risk increased by 36% (HR = 1.36, 
      95% CI: 1.35 - 1.37) with every additional disease. CONCLUSION: Cardiometabolic 
      multimorbidity and respiratory multimorbidity posed the highest threat on 
      mortality risk and deserved particular attention in Chinese adults.
CI  - Copyright © 2022 The Chinese Medical Association, produced by Wolters Kluwer, 
      Inc. under the CC-BY-NC-ND license.
FAU - Fan, Junning
AU  - Fan J
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing 100191, China.
FAU - Sun, Zhijia
AU  - Sun Z
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing 100191, China.
FAU - Yu, Canqing
AU  - Yu C
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing 100191, China.
AD  - Peking University Center for Public Health and Epidemic Preparedness and 
      Response, Peking University, Beijing 100191, China.
FAU - Guo, Yu
AU  - Guo Y
AD  - National Clinical Research Center of Cardiovascular Diseases, National Center for 
      Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and 
      Peking Union Medical College, Beijing 100037, China.
FAU - Pei, Pei
AU  - Pei P
AD  - China Kadoorie Biobank National Coordination Centre, Chinese Academy of Medical 
      Sciences, Beijing 100730, China.
FAU - Yang, Ling
AU  - Yang L
AD  - Nuffield Department of Population Health, Medical Research Council Population 
      Health Research Unit, University of Oxford, Oxford OX3 7LF, United Kingdom.
AD  - Nuffield Department of Population Health, University of Oxford, Clinical Trial 
      Service Unit and Epidemiological Studies Unit (CTSU), Oxford OX3 7LF, United 
      Kingdom.
FAU - Chen, Yiping
AU  - Chen Y
AD  - Nuffield Department of Population Health, Medical Research Council Population 
      Health Research Unit, University of Oxford, Oxford OX3 7LF, United Kingdom.
AD  - Nuffield Department of Population Health, University of Oxford, Clinical Trial 
      Service Unit and Epidemiological Studies Unit (CTSU), Oxford OX3 7LF, United 
      Kingdom.
FAU - Du, Huaidong
AU  - Du H
AD  - Nuffield Department of Population Health, Medical Research Council Population 
      Health Research Unit, University of Oxford, Oxford OX3 7LF, United Kingdom.
AD  - Nuffield Department of Population Health, University of Oxford, Clinical Trial 
      Service Unit and Epidemiological Studies Unit (CTSU), Oxford OX3 7LF, United 
      Kingdom.
FAU - Sun, Dianjianyi
AU  - Sun D
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing 100191, China.
FAU - Pang, Yuanjie
AU  - Pang Y
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing 100191, China.
FAU - Zhang, Jun
AU  - Zhang J
AD  - Suzhou Center for Disease Control and Prevention, Suzhou, Jiangsu 215004, China.
FAU - Gilbert, Simon
AU  - Gilbert S
AD  - Nuffield Department of Population Health, University of Oxford, Clinical Trial 
      Service Unit and Epidemiological Studies Unit (CTSU), Oxford OX3 7LF, United 
      Kingdom.
FAU - Avery, Daniel
AU  - Avery D
AD  - Nuffield Department of Population Health, University of Oxford, Clinical Trial 
      Service Unit and Epidemiological Studies Unit (CTSU), Oxford OX3 7LF, United 
      Kingdom.
FAU - Chen, Junshi
AU  - Chen J
AD  - China National Center for Food Safety Risk Assessment, Beijing 100022, China.
FAU - Chen, Zhengming
AU  - Chen Z
AD  - Nuffield Department of Population Health, University of Oxford, Clinical Trial 
      Service Unit and Epidemiological Studies Unit (CTSU), Oxford OX3 7LF, United 
      Kingdom.
FAU - Lyu, Jun
AU  - Lyu J
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing 100191, China.
AD  - Peking University Center for Public Health and Epidemic Preparedness and 
      Response, Peking University, Beijing 100191, China.
AD  - Key Laboratory of Molecular Cardiovascular Sciences, Peking University, Ministry 
      of Education, Beijing 100191, China.
FAU - Li, Liming
AU  - Li L
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Peking 
      University, Beijing 100191, China.
AD  - Peking University Center for Public Health and Epidemic Preparedness and 
      Response, Peking University, Beijing 100191, China.
CN  - China Kadoorie Biobank Collaborative Group
LA  - eng
GR  - MC_U137686851/MRC_/Medical Research Council/United Kingdom
GR  - MC_UU_00017/1/MRC_/Medical Research Council/United Kingdom
GR  - MC_UU_12026/2/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
DEP - 20220320
PL  - China
TA  - Chin Med J (Engl)
JT  - Chinese medical journal
JID - 7513795
SB  - IM
MH  - Aged
MH  - *Arthritis, Rheumatoid
MH  - Asian People
MH  - China/epidemiology
MH  - Humans
MH  - *Hypertension
MH  - Middle Aged
MH  - Multimorbidity
PMC - PMC9276333
COIS- None.
EDAT- 2022/02/23 06:00
MHDA- 2022/04/29 06:00
PMCR- 2022/03/20
CRDT- 2022/02/22 08:40
PHST- 2021/09/13 00:00 [received]
PHST- 2022/02/23 06:00 [pubmed]
PHST- 2022/04/29 06:00 [medline]
PHST- 2022/02/22 08:40 [entrez]
PHST- 2022/03/20 00:00 [pmc-release]
AID - 00029330-202203200-00004 [pii]
AID - CMJ-2021-2970 [pii]
AID - 10.1097/CM9.0000000000001985 [doi]
PST - epublish
SO  - Chin Med J (Engl). 2022 Mar 20;135(6):648-657. doi: 10.1097/CM9.0000000000001985.

PMID- 35171444
OWN - NLM
STAT- MEDLINE
DCOM- 20220406
LR  - 20220516
IS  - 1534-3170 (Electronic)
IS  - 1523-3782 (Linking)
VI  - 24
IP  - 4
DP  - 2022 Apr
TI  - Updates in the Impact of Chronic Systemic Inflammation on Vascular Inflammation 
      by Positron Emission Tomography (PET).
PG  - 317-326
LID - 10.1007/s11886-022-01651-2 [doi]
AB  - PURPOSE OF REVIEW: In this review, we focus on the clinical and epidemiological 
      studies pertaining to systemic and vascular inflammation by positron emission 
      tomography (PET) in patients with chronic inflammatory conditions such as 
      rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), human 
      immunodeficiency virus (HIV), and psoriasis to highlight the importance of 
      chronic systemic inflammation on vascular inflammation by PET in these disease 
      states. RECENT FINDINGS: Recent clinical and translation advancements have 
      demonstrated the durable relationship between chronic systemic inflammation and 
      cardiovascular disease (CVD). In chronic inflammatory states, this relationship 
      is robustly evident in the form of increased vascular inflammation, yet 
      traditional risk estimates often underestimate the subclinical cardiovascular 
      risk conferred by chronic inflammation. PET has emerged as a novel, non-invasive 
      imaging modality capable of both quantifying the degree of systemic and vascular 
      inflammation and detecting residual inflammation prior to cardiovascular events. 
      We begin by demonstrating the role of inflammation in the pathogenesis of 
      atherosclerosis, discussing how PET has been utilized to measure systemic and 
      vascular inflammation and their effect on subclinical atherosclerosis, and 
      finally reviewing recent applications of PET in constructing improved risk 
      stratification for patients at high risk for stroke and CVD.
CI  - © 2022. This is a U.S. government work and not under copyright protection in the 
      U.S.; foreign copyright protection may apply.
FAU - Parel, Philip M
AU  - Parel PM
AD  - Inflammation and Cardiometabolic Diseases, Clinical Research Center, National 
      Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, 
      Bethesda, MD, USA.
FAU - Berg, Alexander R
AU  - Berg AR
AD  - Inflammation and Cardiometabolic Diseases, Clinical Research Center, National 
      Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, 
      Bethesda, MD, USA.
FAU - Hong, Christin G
AU  - Hong CG
AD  - Inflammation and Cardiometabolic Diseases, Clinical Research Center, National 
      Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, 
      Bethesda, MD, USA.
FAU - Florida, Elizabeth M
AU  - Florida EM
AD  - Inflammation and Cardiometabolic Diseases, Clinical Research Center, National 
      Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, 
      Bethesda, MD, USA.
FAU - O'Hagan, Ross
AU  - O'Hagan R
AD  - Inflammation and Cardiometabolic Diseases, Clinical Research Center, National 
      Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, 
      Bethesda, MD, USA.
FAU - Sorokin, Alexander V
AU  - Sorokin AV
AD  - Inflammation and Cardiometabolic Diseases, Clinical Research Center, National 
      Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, 
      Bethesda, MD, USA.
FAU - Mehta, Nehal N
AU  - Mehta NN
AD  - Inflammation and Cardiometabolic Diseases, Clinical Research Center, National 
      Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, 
      Bethesda, MD, USA. nehal.mehta@nih.gov.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220216
PL  - United States
TA  - Curr Cardiol Rep
JT  - Current cardiology reports
JID - 100888969
SB  - IM
MH  - *Arthritis, Rheumatoid/complications
MH  - *Atherosclerosis/etiology
MH  - Humans
MH  - Inflammation/complications/diagnostic imaging
MH  - *Lupus Erythematosus, Systemic/complications/diagnostic imaging
MH  - Positron-Emission Tomography
MH  - Risk Factors
OTO - NOTNLM
OT  - Atherosclerosis
OT  - Cardiovascular disease
OT  - Coronary artery disease
OT  - Imaging
OT  - Inflammation
OT  - PET
EDAT- 2022/02/17 06:00
MHDA- 2022/04/07 06:00
CRDT- 2022/02/16 12:17
PHST- 2021/12/17 00:00 [accepted]
PHST- 2022/02/17 06:00 [pubmed]
PHST- 2022/04/07 06:00 [medline]
PHST- 2022/02/16 12:17 [entrez]
AID - 10.1007/s11886-022-01651-2 [pii]
AID - 10.1007/s11886-022-01651-2 [doi]
PST - ppublish
SO  - Curr Cardiol Rep. 2022 Apr;24(4):317-326. doi: 10.1007/s11886-022-01651-2. Epub 
      2022 Feb 16.

PMID- 35119769
OWN - NLM
STAT- MEDLINE
DCOM- 20230224
LR  - 20230228
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Linking)
VI  - 75
IP  - 3
DP  - 2023 Mar
TI  - Reduction of Cardiovascular Disease and Mortality Versus Risk of New-Onset 
      Diabetes Mellitus With Statin Use in Patients With Rheumatoid Arthritis.
PG  - 597-607
LID - 10.1002/acr.24866 [doi]
AB  - OBJECTIVE: To assess the effect of statin use on the risk of cardiovascular 
      disease (CVD), all-cause mortality, and type 2 diabetes mellitus (DM) in patients 
      with rheumatoid arthritis (RA). METHODS: We identified a cohort of patients with 
      RA between 1989 and 2018, within the UK Clinical Practice Research Datalink. We 
      employed a prevalent new-user cohort design by which patients initiating statins 
      were each matched to 2 concurrent nonusers by the time-conditional propensity 
      score (TCPS). Patients were followed until the occurrence of the composite end 
      point of myocardial infarction, stroke, hospitalized heart failure or CVD 
      mortality, all-cause mortality, and incident type 2 DM. The Cox proportional 
      hazards model was used to estimate the hazard ratio (HR) of each outcome 
      associated with as-treated statin use, with adjustment for TCPS deciles and 
      imbalanced covariables. RESULTS: Among 1,768 statin initiators and 3,528 
      nonusers, 63 versus 340 CVD (3.0 per 100 person-years versus 2.7 per 100 
      person-years) and 62 versus 525 deaths (2.8 per 100 person-years versus 4.1 per 
      100 person-years) occurred. Incident type 2 DM was noted in 128 of 3,608 statin 
      initiators (3.0 per 100 person-years) and 518 of 7,208 nonusers (2.0 per 100 
      person-years). Statin initiation was associated with 32% (HR 0.68 [95% confidence 
      interval (95% CI) 0.51-0.90]) reduction in CVD, 54% (HR 0.46 [95% CI 0.35-0.60]) 
      reduction in all-cause mortality, and 33% increase in type 2 DM (HR 1.33 [95% CI 
      1.09-1.63]). The number needed to treat/number needed to harm to prevent a CVD or 
      all-cause mortality or to cause type 2 DM in 1 year was 102, 42, and 127, 
      respectively. CONCLUSION: Statins are associated with important reductions in CVD 
      and mortality that outweigh the modest increase in type 2 DM risk in RA patients.
CI  - © 2022 American College of Rheumatology.
FAU - Ozen, Gulsen
AU  - Ozen G
AUID- ORCID: 0000-0002-5423-393X
AD  - University of Nebraska Medical Center, Omaha.
FAU - Dell'Aniello, Sophie
AU  - Dell'Aniello S
AD  - Jewish General Hospital, Montreal, Quebec, Canada.
FAU - Pedro, Sofia
AU  - Pedro S
AD  - FORWARD, The National Databank for Rheumatic Diseases, Wichita, Kansas.
FAU - Michaud, Kaleb
AU  - Michaud K
AUID- ORCID: 0000-0002-5350-3934
AD  - University of Nebraska Medical Center, Omaha, and FORWARD, The National Databank 
      for Rheumatic Diseases, Wichita, Kansas.
FAU - Suissa, Samy
AU  - Suissa S
AUID- ORCID: 0000-0002-1281-5296
AD  - Jewish General Hospital and McGill University, Montreal, Quebec, Canada.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20221117
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
SB  - IM
MH  - Humans
MH  - *Cardiovascular Diseases/epidemiology
MH  - *Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use
MH  - *Diabetes Mellitus, Type 2/epidemiology
MH  - *Arthritis, Rheumatoid/drug therapy
MH  - *Myocardial Infarction
EDAT- 2022/02/05 06:00
MHDA- 2023/02/25 06:00
CRDT- 2022/02/04 12:14
PHST- 2022/01/17 00:00 [revised]
PHST- 2021/10/27 00:00 [received]
PHST- 2022/01/17 00:00 [accepted]
PHST- 2022/02/05 06:00 [pubmed]
PHST- 2023/02/25 06:00 [medline]
PHST- 2022/02/04 12:14 [entrez]
AID - 10.1002/acr.24866 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2023 Mar;75(3):597-607. doi: 10.1002/acr.24866. 
      Epub 2022 Nov 17.

PMID- 35096568
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220201
IS  - 2234-943X (Print)
IS  - 2234-943X (Electronic)
IS  - 2234-943X (Linking)
VI  - 11
DP  - 2021
TI  - Knockdown of NAA25 Suppresses Breast Cancer Progression by Regulating Apoptosis 
      and Cell Cycle.
PG  - 755267
LID - 10.3389/fonc.2021.755267 [doi]
LID - 755267
AB  - NAA25 gene variants were reported as risk factors for type 1 diabetes, rheumatoid 
      arthritis and acute arterial stroke. But it's unknown whether it could contribute 
      to breast cancer. We identified rs11066150 in lncHSAT164, which contributes to 
      breast cancer, in our earlier genome-wide long non-coding RNA association study 
      on Han Chinese women. However, rs11066150 A/G variant is also located in NAA25 
      intron. Based on the public database, such as TCGA and Curtis dataset, NAA25 gene 
      is highly expressed in breast cancer tissues and this result has also been proved 
      in our samples and cell lines through RT-qPCR and western blot analysis. To 
      better understand the function of NAA25 in breast cancer, we knocked down the 
      expression of NAA25 in breast cancer cell lines, FACS was used to detect cell 
      apoptosis and cell cycle and colony formation assay was used to detect cell 
      proliferation. We found that NAA25-deficient cells could increase cell apoptosis, 
      delay G2/M phase cell and decrease cell clone formation. RNA sequencing was then 
      applied to analyze the molecular profiles of NAA25-deficient cells, and compared 
      to the control group, NAA25 knockdown could activate apoptosis-related pathways, 
      reduce the activation of tumor-associated signaling pathways and decrease immune 
      response-associated pathways. Additionally, RT-qPCR was employed to validate 
      these results. Taken together, our results revealed that NAA25 was highly 
      expressed in breast cancer, and NAA25 knockdown might serve as a therapeutic 
      target in breast cancer.
CI  - Copyright © 2022 Xu, Li, Zuo, Li, Zhang, Zhang and Cui.
FAU - Xu, Jingkai
AU  - Xu J
AD  - Department of Dermatology, China-Japan Friendship Hospital, Beijing, China.
FAU - Li, Zhi
AU  - Li Z
AD  - Department of Dermatology, Jiangsu Province Hospital, Nanjing, China.
FAU - Zuo, Xianbo
AU  - Zuo X
AD  - Department of Dermatology, China-Japan Friendship Hospital, Beijing, China.
FAU - Li, Guozheng
AU  - Li G
AD  - School of Life Sciences, Anhui Medical University, Hefei, China.
AD  - Department of Oncology, No. 2 Hospital, Anhui Medical University, Hefei, China.
FAU - Zhang, Xuejun
AU  - Zhang X
AD  - Department of Dermatology, The First Affiliated Hospital of Anhui Medical 
      University, Hefei, China.
FAU - Zhang, Bo
AU  - Zhang B
AD  - School of Life Sciences, Anhui Medical University, Hefei, China.
AD  - Department of Oncology, No. 2 Hospital, Anhui Medical University, Hefei, China.
FAU - Cui, Yong
AU  - Cui Y
AD  - Department of Dermatology, China-Japan Friendship Hospital, Beijing, China.
LA  - eng
PT  - Journal Article
DEP - 20220113
PL  - Switzerland
TA  - Front Oncol
JT  - Frontiers in oncology
JID - 101568867
PMC - PMC8792228
OTO - NOTNLM
OT  - NAA25
OT  - RNA sequencing
OT  - apoptosis
OT  - breast cancer
OT  - cell cycle
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest. The reviewer, H-FZ, declared a past co-authorship with one 
      of the authors, XJZ, to the handling editor.
EDAT- 2022/02/01 06:00
MHDA- 2022/02/01 06:01
PMCR- 2021/01/01
CRDT- 2022/01/31 05:59
PHST- 2021/09/07 00:00 [received]
PHST- 2021/12/21 00:00 [accepted]
PHST- 2022/01/31 05:59 [entrez]
PHST- 2022/02/01 06:00 [pubmed]
PHST- 2022/02/01 06:01 [medline]
PHST- 2021/01/01 00:00 [pmc-release]
AID - 10.3389/fonc.2021.755267 [doi]
PST - epublish
SO  - Front Oncol. 2022 Jan 13;11:755267. doi: 10.3389/fonc.2021.755267. eCollection 
      2021.

PMID- 35074047
OWN - NLM
STAT- MEDLINE
DCOM- 20220304
LR  - 20240923
IS  - 2050-084X (Electronic)
IS  - 2050-084X (Linking)
VI  - 11
DP  - 2022 Jan 25
TI  - Disease consequences of higher adiposity uncoupled from its adverse metabolic 
      effects using Mendelian randomisation.
LID - 10.7554/eLife.72452 [doi]
LID - e72452
AB  - BACKGROUND: Some individuals living with obesity may be relatively metabolically 
      healthy, whilst others suffer from multiple conditions that may be linked to 
      adverse metabolic effects or other factors. The extent to which the adverse 
      metabolic component of obesity contributes to disease compared to the 
      non-metabolic components is often uncertain. We aimed to use Mendelian 
      randomisation (MR) and specific genetic variants to separately test the causal 
      roles of higher adiposity with and without its adverse metabolic effects on 
      diseases. METHODS: We selected 37 chronic diseases associated with obesity and 
      genetic variants associated with different aspects of excess weight. These 
      genetic variants included those associated with metabolically 'favourable 
      adiposity' (FA) and 'unfavourable adiposity' (UFA) that are both associated with 
      higher adiposity but with opposite effects on metabolic risk. We used these 
      variants and two sample MR to test the effects on the chronic diseases. RESULTS: 
      MR identified two sets of diseases. First, 11 conditions where the metabolic 
      effect of higher adiposity is the likely primary cause of the disease. Here, MR 
      with the FA and UFA genetics showed opposing effects on risk of disease: coronary 
      artery disease, peripheral artery disease, hypertension, stroke, type 2 diabetes, 
      polycystic ovary syndrome, heart failure, atrial fibrillation, chronic kidney 
      disease, renal cancer, and gout. Second, 9 conditions where the non-metabolic 
      effects of excess weight (e.g. mechanical effect) are likely a cause. Here, MR 
      with the FA genetics, despite leading to lower metabolic risk, and MR with the 
      UFA genetics, both indicated higher disease risk: osteoarthritis, rheumatoid 
      arthritis, osteoporosis, gastro-oesophageal reflux disease, gallstones, 
      adult-onset asthma, psoriasis, deep vein thrombosis, and venous thromboembolism. 
      CONCLUSIONS: Our results assist in understanding the consequences of higher 
      adiposity uncoupled from its adverse metabolic effects, including the risks to 
      individuals with high body mass index who may be relatively metabolically 
      healthy. FUNDING: Diabetes UK, UK Medical Research Council, World Cancer Research 
      Fund, National Cancer Institute.
CI  - © 2022, Martin et al.
FAU - Martin, Susan
AU  - Martin S
AUID- ORCID: 0000-0001-8746-0947
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical 
      School, Research, Innovation, Learning and Development building, Royal Devon & 
      Exeter Hospital, Exeter, United Kingdom.
FAU - Tyrrell, Jessica
AU  - Tyrrell J
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical 
      School, Research, Innovation, Learning and Development building, Royal Devon & 
      Exeter Hospital, Exeter, United Kingdom.
FAU - Thomas, E Louise
AU  - Thomas EL
AUID- ORCID: 0000-0003-4235-4694
AD  - Research Centre for Optimal Health, School of Life Sciences, University of 
      Westminster, London, United Kingdom.
FAU - Bown, Matthew J
AU  - Bown MJ
AD  - Department of Cardiovascular Sciences, University of Leicester, Leicester, United 
      Kingdom.
AD  - NIHR Leicester Biomedical Research Centre, Leicester, United Kingdom.
FAU - Wood, Andrew R
AU  - Wood AR
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical 
      School, Research, Innovation, Learning and Development building, Royal Devon & 
      Exeter Hospital, Exeter, United Kingdom.
FAU - Beaumont, Robin N
AU  - Beaumont RN
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical 
      School, Research, Innovation, Learning and Development building, Royal Devon & 
      Exeter Hospital, Exeter, United Kingdom.
FAU - Tsoi, Lam C
AU  - Tsoi LC
AD  - Department of Dermatology, University of Michigan, Ann Arbor, United States.
FAU - Stuart, Philip E
AU  - Stuart PE
AD  - Department of Dermatology, University of Michigan, Ann Arbor, United States.
FAU - Elder, James T
AU  - Elder JT
AD  - Department of Dermatology, University of Michigan, Ann Arbor, United States.
AD  - Ann Arbor Veterans Affairs Hospital, Ann Arbor, United States.
FAU - Law, Philip
AU  - Law P
AD  - The Institute of Cancer Research, London, United Kingdom.
FAU - Houlston, Richard
AU  - Houlston R
AD  - The Institute of Cancer Research, London, United Kingdom.
FAU - Kabrhel, Christopher
AU  - Kabrhel C
AD  - Department of Emergency Medicine, Massachusetts General Hospital, Boston, United 
      States.
AD  - Department of Emergency Medicine, Harvard Medical School, Boston, United States.
FAU - Papadimitriou, Nikos
AU  - Papadimitriou N
AD  - Nutrition and Metabolism Branch, International Agency for Research on Cancer, 
      Lyon, France.
FAU - Gunter, Marc J
AU  - Gunter MJ
AD  - Nutrition and Metabolism Branch, International Agency for Research on Cancer, 
      Lyon, France.
FAU - Bull, Caroline J
AU  - Bull CJ
AD  - MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, United 
      Kingdom.
AD  - Population Health Sciences, Bristol Medical School, University of Bristol, 
      Bristol, United Kingdom.
AD  - School of Cellular and Molecular Medicine, University of Bristol, Bristol, United 
      Kingdom.
FAU - Bell, Joshua A
AU  - Bell JA
AD  - MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, United 
      Kingdom.
AD  - Population Health Sciences, Bristol Medical School, University of Bristol, 
      Bristol, United Kingdom.
FAU - Vincent, Emma E
AU  - Vincent EE
AD  - MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, United 
      Kingdom.
AD  - Population Health Sciences, Bristol Medical School, University of Bristol, 
      Bristol, United Kingdom.
AD  - School of Cellular and Molecular Medicine, University of Bristol, Bristol, United 
      Kingdom.
FAU - Sattar, Naveed
AU  - Sattar N
AUID- ORCID: 0000-0002-1604-2593
AD  - Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, 
      United Kingdom.
FAU - Dunlop, Malcolm G
AU  - Dunlop MG
AD  - University of Edinburgh, Edinburgh, United Kingdom.
AD  - Western General Hospital, Edinburgh, United Kingdom.
FAU - Tomlinson, Ian P M
AU  - Tomlinson IPM
AD  - Edinburgh Cancer Research Centre, IGMM, University of Edinburgh, Edinburgh, 
      United Kingdom.
FAU - Lindström, Sara
AU  - Lindström S
AD  - Department of Epidemiology, University of Washington, Seattle, United States.
AD  - Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 
      Seattle, United States.
CN  - INVENT consortium
FAU - Bell, Jimmy D
AU  - Bell JD
AUID- ORCID: 0000-0003-3804-1281
AD  - Research Centre for Optimal Health, School of Life Sciences, University of 
      Westminster, London, United Kingdom.
FAU - Frayling, Timothy M
AU  - Frayling TM
AUID- ORCID: 0000-0001-8362-2603
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical 
      School, Research, Innovation, Learning and Development building, Royal Devon & 
      Exeter Hospital, Exeter, United Kingdom.
FAU - Yaghootkar, Hanieh
AU  - Yaghootkar H
AUID- ORCID: 0000-0001-9672-9477
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical 
      School, Research, Innovation, Learning and Development building, Royal Devon & 
      Exeter Hospital, Exeter, United Kingdom.
AD  - Research Centre for Optimal Health, School of Life Sciences, University of 
      Westminster, London, United Kingdom.
AD  - Centre for Inflammation Research and Translational Medicine (CIRTM), Department 
      of Life Sciences, Brunel University London, Uxbridge, United Kingdom.
LA  - eng
GR  - U01 HG004446/HG/NHGRI NIH HHS/United States
GR  - U10 CA037429/CA/NCI NIH HHS/United States
GR  - P01 CA196569/CA/NCI NIH HHS/United States
GR  - 12076/CRUK_/Cancer Research UK/United Kingdom
GR  - R01 CA067941/CA/NCI NIH HHS/United States
GR  - U01 CA067941/CA/NCI NIH HHS/United States
GR  - R01 CA059045/CA/NCI NIH HHS/United States
GR  - HHSN268201100001I/HL/NHLBI NIH HHS/United States
GR  - R01 CA197350/CA/NCI NIH HHS/United States
GR  - RG/18/10/33842/BHF_/British Heart Foundation/United Kingdom
GR  - R01 CA076366/CA/NCI NIH HHS/United States
GR  - R35 CA197735/CA/NCI NIH HHS/United States
GR  - MR/T002239/1/MRC_/Medical Research Council/United Kingdom
GR  - C8221/A19170/CRUK_/Cancer Research UK/United Kingdom
GR  - U01 HG004438/HG/NHGRI NIH HHS/United States
GR  - R01 CA072520/CA/NCI NIH HHS/United States
GR  - 25514/CRUK_/Cancer Research UK/United Kingdom
GR  - P01 CA087969/CA/NCI NIH HHS/United States
GR  - CS/14/2/30841/BHF_/British Heart Foundation/United Kingdom
GR  - P30 CA015704/CA/NCI NIH HHS/United States
GR  - HHSN268201100004I/HL/NHLBI NIH HHS/United States
GR  - P30 CA006973/CA/NCI NIH HHS/United States
GR  - MC-UU_12015/1/MRC_/Medical Research Council/United Kingdom
GR  - K05 CA154337/CA/NCI NIH HHS/United States
GR  - P01 CA055075/CA/NCI NIH HHS/United States
GR  - S10 OD028685/OD/NIH HHS/United States
GR  - R01 CA151993/CA/NCI NIH HHS/United States
GR  - MC_U127527198/MRC_/Medical Research Council/United Kingdom
GR  - HHSN268201100046C/HL/NHLBI NIH HHS/United States
GR  - P30 DK034987/DK/NIDDK NIH HHS/United States
GR  - DH_/Department of Health/United Kingdom
GR  - R01 CA048998/CA/NCI NIH HHS/United States
GR  - U01 CA137088/CA/NCI NIH HHS/United States
GR  - R01 CA189184/CA/NCI NIH HHS/United States
GR  - U01 CA167552/CA/NCI NIH HHS/United States
GR  - HHSN268201100003C/WH/WHI NIH HHS/United States
GR  - Z01 CP010200/ImNIH/Intramural NIH HHS/United States
GR  - U24 CA074794/CA/NCI NIH HHS/United States
GR  - U01 CA164930/CA/NCI NIH HHS/United States
GR  - MC_UU_00011/1/MRC_/Medical Research Council/United Kingdom
GR  - C864/A14136/CRUK_/Cancer Research UK/United Kingdom
GR  - R01 CA066635/CA/NCI NIH HHS/United States
GR  - U01 CA206110/CA/NCI NIH HHS/United States
GR  - 1000143/MRC_/Medical Research Council/United Kingdom
GR  - C490/A16561/CRUK_/Cancer Research UK/United Kingdom
GR  - R21 CA191312/CA/NCI NIH HHS/United States
GR  - HHSN268201200008C/HL/NHLBI NIH HHS/United States
GR  - R01 CA137178/CA/NCI NIH HHS/United States
GR  - U01 CA074794/CA/NCI NIH HHS/United States
GR  - U01 CA167551/CA/NCI NIH HHS/United States
GR  - MR/N003284/1/MRC_/Medical Research Council/United Kingdom
GR  - P30 CA076292/CA/NCI NIH HHS/United States
GR  - 29019/CRUK_/Cancer Research UK/United Kingdom
GR  - P30 CA014089/CA/NCI NIH HHS/United States
GR  - G0401527/MRC_/Medical Research Council/United Kingdom
GR  - C570/A16491/CRUK_/Cancer Research UK/United Kingdom
GR  - 18927/CRUK_/Cancer Research UK/United Kingdom
GR  - R01 CA081488/CA/NCI NIH HHS/United States
GR  - MR/L00002/1/MRC_/Medical Research Council/United Kingdom
GR  - HHSN271201100004C/AG/NIA NIH HHS/United States
GR  - R01 CA201407/CA/NCI NIH HHS/United States
GR  - R01 CA063464/CA/NCI NIH HHS/United States
GR  - P01 CA033619/CA/NCI NIH HHS/United States
GR  - U01 CA086308/CA/NCI NIH HHS/United States
GR  - UM1 CA186107/CA/NCI NIH HHS/United States
GR  - MR/M012190/1/MRC_/Medical Research Council/United Kingdom
GR  - HHSN268201100002C/WH/WHI NIH HHS/United States
GR  - R01 CA207371/CA/NCI NIH HHS/United States
GR  - R03 CA153323/CA/NCI NIH HHS/United States
GR  - G1000143/MRC_/Medical Research Council/United Kingdom
GR  - 27327/CRUK_/Cancer Research UK/United Kingdom
GR  - R01 CA042182/CA/NCI NIH HHS/United States
GR  - C588/A19167/CRUK_/Cancer Research UK/United Kingdom
GR  - T32 ES013678/ES/NIEHS NIH HHS/United States
GR  - R01 CA136726/CA/NCI NIH HHS/United States
GR  - P30 CA016058/CA/NCI NIH HHS/United States
GR  - 14136/CRUK_/Cancer Research UK/United Kingdom
GR  - UM1 CA167552/CA/NCI NIH HHS/United States
GR  - K05 CA152715/CA/NCI NIH HHS/United States
GR  - U01 CA122839/CA/NCI NIH HHS/United States
GR  - R01 AR063611/AR/NIAMS NIH HHS/United States
GR  - MR/M008924/1/MRC_/Medical Research Council/United Kingdom
GR  - HHSN268201100003I/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100002I/HL/NHLBI NIH HHS/United States
GR  - U01 CA074783/CA/NCI NIH HHS/United States
GR  - U01 CA084968/CA/NCI NIH HHS/United States
GR  - KL2 TR000421/TR/NCATS NIH HHS/United States
GR  - PG/17/21/32844/BHF_/British Heart Foundation/United Kingdom
GR  - MC_UU_00007/1/MRC_/Medical Research Council/United Kingdom
GR  - 001/WHO_/World Health Organization/International
GR  - P50 CA127003/CA/NCI NIH HHS/United States
GR  - MC_PC_13048/MRC_/Medical Research Council/United Kingdom
GR  - UM1 CA182883/CA/NCI NIH HHS/United States
GR  - K07 CA190673/CA/NCI NIH HHS/United States
GR  - HHSN268201200008I/HL/NHLBI NIH HHS/United States
GR  - MC_PC_U127527198/MRC_/Medical Research Council/United Kingdom
GR  - U01 CA164973/CA/NCI NIH HHS/United States
GR  - R37 CA054281/CA/NCI NIH HHS/United States
GR  - HHSN268201100001C/WH/WHI NIH HHS/United States
GR  - HHSN268201100004C/WH/WHI NIH HHS/United States
GR  - R01 CA097325/CA/NCI NIH HHS/United States
GR  - HHSN268201700006C/HL/NHLBI NIH HHS/United States
GR  - C18281/A29019/CRUK_/Cancer Research UK/United Kingdom
GR  - U19 CA148107/CA/NCI NIH HHS/United States
GR  - U01 AG018033/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, N.I.H., Intramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20220125
PL  - England
TA  - Elife
JT  - eLife
JID - 101579614
SB  - IM
EIN - Elife. 2022 May 18;11:e80233. doi: 10.7554/eLife.80233. PMID: 35583923
MH  - Adiposity/*genetics
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Body Mass Index
MH  - Cardiometabolic Risk Factors
MH  - Female
MH  - Genome-Wide Association Study
MH  - Humans
MH  - Male
MH  - Mendelian Randomization Analysis/*methods
MH  - Middle Aged
MH  - Obesity/*genetics
PMC - PMC8789289
OTO - NOTNLM
OT  - Mendelian randomisation
OT  - cancer
OT  - cardiovascular disease
OT  - epidemiology
OT  - favourable adiposity
OT  - genetics
OT  - genomics
OT  - global health
OT  - human
OT  - obesity
COIS- SM, JT, ET, MB, AW, RB, LT, PS, JE, PL, RH, CK, NP, MG, CB, JB, EV, MD, IT, JB, 
      HY No competing interests declared, NS Naveed Sattar has consulted for Afimmune, 
      Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, Hanmi Pharmaceuticals, Merck 
      Sharp &amp; Dohme, Novartis, Novo Nordisk, Pfizer, and Sanofi; and received grant 
      support paid to his University from AstraZeneca, Boehringer Ingelheim and Roche 
      Diagnostics outside the submitted work, TF Tim Frayling has consulted for 
      Boehringer Ingelheim and Sanofi and has a student supported by GSK
EDAT- 2022/01/26 06:00
MHDA- 2022/03/05 06:00
PMCR- 2022/01/25
CRDT- 2022/01/25 05:37
PHST- 2021/07/23 00:00 [received]
PHST- 2021/12/21 00:00 [accepted]
PHST- 2022/01/25 05:37 [entrez]
PHST- 2022/01/26 06:00 [pubmed]
PHST- 2022/03/05 06:00 [medline]
PHST- 2022/01/25 00:00 [pmc-release]
AID - 72452 [pii]
AID - 10.7554/eLife.72452 [doi]
PST - epublish
SO  - Elife. 2022 Jan 25;11:e72452. doi: 10.7554/eLife.72452.

PMID- 35029902
OWN - NLM
STAT- MEDLINE
DCOM- 20220124
LR  - 20240405
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 101
IP  - 1
DP  - 2022 Jan 7
TI  - Hypothyroidism risk associated with rheumatoid arthritis: A population-based 
      retrospective cohort study.
PG  - e28487
LID - 10.1097/MD.0000000000028487 [doi]
LID - e28487
AB  - Studies on the thyroid disease risk in patients with rheumatoid arthritis (RA) 
      associated with comorbidities are limited. This population-based retrospective 
      cohort study investigated the hypothyroidism risk in patients with RA and the 
      role of comorbidities.We used Taiwan National Health Insurance Research Database 
      to identify 16,714 RA patients newly diagnosed in 2000 to 2008 and 66,856 control 
      persons without RA, frequency matched by sex, age, and index year. Incidence and 
      the RA group to controls hazard ratio of hypothyroidism were estimated.The 
      hypothyroidism incidence was 1.74-fold higher in the RA group than in controls 
      (16.6 vs 9.52 per 10,000 person-years), with the Cox method estimated adjusted 
      hazard ratio of 1.67 (95% confidence interval = 1.39-2.00) after controlling for 
      covariates. Near 75% of the study population were women, with the incidence 
      3.6-time higher than men in both groups. The hypothyroidism incidence increased 
      with age, from 12.1 per 1000 person-years in 20 to 39 years to 20.0 per 1000 
      person-years in 60+ years in RA patients, higher than that in controls (7.17 vs 
      10.0 per 1000 person-years, respectively by age). Each comorbidity was related to 
      an increased incidence and higher in the RA group than in controls. Among all 
      comorbidities, stroke exerted the greatest impact in the RA group with an 
      adjusted hazard ratio of 3.85 (95% confidence interval = 1.24-12.0).RA patients 
      have an increased risk of developing hypothyroidism; this risk was pronounced in 
      women and the elderly. RA patients should be closely monitored to prevent the 
      development of hypothyroidism.
CI  - Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.
FAU - Huang, Chung-Ming
AU  - Huang CM
AUID- ORCID: 0000-0003-4323-7115
AD  - Division of Immunology and Rheumatology, Department of Internal Medicine, China 
      Medical University Hospital, Taichung, Taiwan.
AD  - Graduate Institute of Integrated Medicine, China Medical University College of 
      Chinese Medicine, Taichung, Taiwan.
FAU - Sung, Fung-Chang
AU  - Sung FC
AD  - Management Office for Health Data, China Medical University Hospital, Taichung, 
      Taiwan.
AD  - Department of Health Services Administration, China Medical University College of 
      Public Health, Taichung, Taiwan.
AD  - Department of Food Nutrition and Health Biotechnology, Asia University, Taichung, 
      Taiwan.
FAU - Chen, Hsuan-Ju
AU  - Chen HJ
AD  - Management Office for Health Data, China Medical University Hospital, Taichung, 
      Taiwan.
FAU - Lin, Che-Chen
AU  - Lin CC
AD  - Management Office for Health Data, China Medical University Hospital, Taichung, 
      Taiwan.
AD  - China Medical University College of Medicine, Taichung, Taiwan.
FAU - Lin, Cheng-Li
AU  - Lin CL
AD  - Management Office for Health Data, China Medical University Hospital, Taichung, 
      Taiwan.
FAU - Huang, Po-Hao
AU  - Huang PH
AD  - Division of Immunology and Rheumatology, Department of Internal Medicine, China 
      Medical University Hospital, Taichung, Taiwan.
LA  - eng
GR  - MOHW109-TDU-B-212-114004/Health Promotion Administration, Ministry of Health and 
      Welfare/
GR  - DMR-108-045/Clinical Trial Center, China Medical University Hospital/
GR  - DMR-109-027, DMR-109-175/Clinical Trial Center, China Medical University 
      Hospital/
GR  - DMR-110-023/Clinical Trial Center, China Medical University Hospital/
GR  - BM10701010021/Academia Sinica/
GR  - (MOST 107-2321-B-039 -004)/National Center of Excellence for Clinical Trial and 
      Research/
PT  - Journal Article
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*complications/epidemiology
MH  - Cohort Studies
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Hypothyroidism/*epidemiology
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Taiwan/epidemiology
PMC - PMC8735800
COIS- The authors have no conflicts of interest to disclose.
EDAT- 2022/01/15 06:00
MHDA- 2022/01/27 06:00
PMCR- 2022/01/07
CRDT- 2022/01/14 15:33
PHST- 2020/11/25 00:00 [received]
PHST- 2021/12/16 00:00 [accepted]
PHST- 2022/01/14 15:33 [entrez]
PHST- 2022/01/15 06:00 [pubmed]
PHST- 2022/01/27 06:00 [medline]
PHST- 2022/01/07 00:00 [pmc-release]
AID - 00005792-202201070-00033 [pii]
AID - MD-D-20-11714 [pii]
AID - 10.1097/MD.0000000000028487 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2022 Jan 7;101(1):e28487. doi: 10.1097/MD.0000000000028487.

PMID- 35029702
OWN - NLM
STAT- MEDLINE
DCOM- 20220207
LR  - 20220218
IS  - 1432-1289 (Electronic)
IS  - 0020-9554 (Print)
IS  - 0020-9554 (Linking)
VI  - 63
IP  - 2
DP  - 2022 Feb
TI  - [Treatment of rheumatoid arthritis and spondylarthritis with biologics].
PG  - 135-142
LID - 10.1007/s00108-021-01248-x [doi]
AB  - Biologics are an integral part of modern strategies for treatment of rheumatoid 
      arthritis (RA) and spondylarthritis (SpA), including psoriatic arthritis (PsA). 
      Biologics are biotechnologically produced proteins that have inhibiting effects 
      on humoral and cellular components of rheumatic inflammation. Substance classes 
      used in rheumatology are tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, 
      IL‑6, IL-12, IL-17 and IL-23 inhibitors effective against cytokines as well as 
      the T lymphocyte activation inhibitor abatacept and the B lymphocyte-depleting 
      rituximab. There are clear recommendations for the use of biologics for RA 
      patients inadequately responding to one or more conventional synthetic 
      disease-modifying antirheumatic drugs and for ankylosing spondylitis (AS) and 
      nonradiographical axial SpA patients with an inadequate response to at least two 
      nonsteroidal antirheumatic drugs. For PsA the recommended use depends on the most 
      prominent manifestations in each case. Treatment with biologics should follow the 
      treat to target principle, with a defined and validated treatment target. 
      Treatment in cases of RA and SpA should target remission or at least a low or 
      minimum disease activity. The safety of treatment with biologics has been 
      intensively investigated. There are very specific contraindications for 
      individual substance classes with a focus on an increased risk of infections. The 
      standard procedure before starting treatment with biologics includes the 
      exclusion of latent tuberculosis and hepatitis B. The TNF-alpha inhibitors have a 
      protective effect with respect to myocardial infarction, stroke and venous 
      thromboembolism.
CI  - © 2022. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, 
      ein Teil von Springer Nature.
FAU - Fiehn, Christoph
AU  - Fiehn C
AD  - Rheumatologie Baden-Baden, Tätigkeitsschwerpunkt Klinische Immunologie und 
      Belegarzteinheit Rheumatologie an den ViDia-Kliniken Karlsruhe, Beethovenstr. 2, 
      76530, Baden-Baden, Deutschland. c.fiehn@rheuma-badenbaden.de.
LA  - ger
PT  - Journal Article
PT  - Review
TT  - Biologikatherapie von rheumatoider Arthritis und Spondyloarthritiden.
DEP - 20220114
PL  - Germany
TA  - Internist (Berl)
JT  - Der Internist
JID - 0264620
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - *Antirheumatic Agents/adverse effects
MH  - *Arthritis, Psoriatic/drug therapy
MH  - *Arthritis, Rheumatoid/diagnosis/drug therapy
MH  - *Biological Products/adverse effects
MH  - Humans
MH  - *Spondylarthritis/diagnosis/drug therapy
MH  - *Spondylitis, Ankylosing
MH  - Tumor Necrosis Factor-alpha/therapeutic use
PMC - PMC8759427
OTO - NOTNLM
OT  - Antirheumatic agents
OT  - Arthritis, psoriatic
OT  - Interleukin inhibitors
OT  - Spondylitis, ankylosing
OT  - Tumor necrosis factor inhibitors
EDAT- 2022/01/15 06:00
MHDA- 2022/02/08 06:00
PMCR- 2022/01/14
CRDT- 2022/01/14 12:17
PHST- 2021/12/16 00:00 [accepted]
PHST- 2022/01/15 06:00 [pubmed]
PHST- 2022/02/08 06:00 [medline]
PHST- 2022/01/14 12:17 [entrez]
PHST- 2022/01/14 00:00 [pmc-release]
AID - 10.1007/s00108-021-01248-x [pii]
AID - 1248 [pii]
AID - 10.1007/s00108-021-01248-x [doi]
PST - ppublish
SO  - Internist (Berl). 2022 Feb;63(2):135-142. doi: 10.1007/s00108-021-01248-x. Epub 
      2022 Jan 14.

PMID- 35027405
OWN - NLM
STAT- MEDLINE
DCOM- 20220519
LR  - 20240827
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Print)
IS  - 0003-4967 (Linking)
VI  - 81
IP  - 6
DP  - 2022 Jun
TI  - Tofacitinib and risk of cardiovascular outcomes: results from the Safety of 
      TofAcitinib in Routine care patients with Rheumatoid Arthritis (STAR-RA) study.
PG  - 798-804
LID - 10.1136/annrheumdis-2021-221915 [doi]
AB  - OBJECTIVES: Recent results from 'ORAL Surveillance' trial have raised concerns 
      regarding the cardiovascular safety of tofacitinib in patients with rheumatoid 
      arthritis (RA). We further examined this safety concern in the real-world 
      setting. METHODS: We created two cohorts of patients with RA initiating treatment 
      with tofacitinib or tumour necrosis factor inhibitors (TNFI) using deidentified 
      data from Optum Clinformatics (2012-2020), IBM MarketScan (2012-2018) and 
      Medicare (parts A, B and D, 2012-2017) claims databases: (1) A 'real-world 
      evidence (RWE) cohort' consisting of routine care patients and (2) A 'randomised 
      controlled trial (RCT)-duplicate cohort' mimicking inclusion and exclusion 
      criteria of the ORAL surveillance trial to calibrate results against the trial 
      findings. Cox proportional hazards models with propensity score fine 
      stratification weighting were used to estimate HR and 95% CIs for composite 
      outcome of myocardial infarction and stroke and accounting for 76 potential 
      confounders. Database-specific effect estimates were pooled using fixed effects 
      models with inverse-variance weighting. RESULTS: In the RWE cohort, 102 263 
      patients were identified of whom 12 852 (12.6%) initiated tofacitinib. The pooled 
      weighted HR (95% CI) comparing tofacitinib with TNFI was 1.01 (0.83 to 1.23) in 
      RWE cohort and 1.24 (0.90 to 1.69) in RCT-duplicate cohort which aligned closely 
      with ORAL-surveillance results (HR: 1.33, 95% CI 0.91 to 1.94). CONCLUSIONS: We 
      did not find evidence for an increased risk of cardiovascular outcomes with 
      tofacitinib in patients with RA treated in the real-world setting; however, 
      tofacitinib was associated with an increased risk of cardiovascular outcomes, 
      although statistically non-significant, in patients with RA with cardiovascular 
      risk factors. TRIAL REGISTRATION NUMBER: NCT04772248.
CI  - © Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and 
      permissions. Published by BMJ.
FAU - Khosrow-Khavar, Farzin
AU  - Khosrow-Khavar F
AUID- ORCID: 0000-0003-3636-8918
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Boston, Massachusetts, USA.
FAU - Kim, Seoyoung C
AU  - Kim SC
AUID- ORCID: 0000-0002-2517-3579
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Boston, Massachusetts, USA.
AD  - Division of Rheumatology, Inflammation, and Immunity, Brigham and Women's 
      Hospital, Boston, Massachusetts, USA.
FAU - Lee, Hemin
AU  - Lee H
AUID- ORCID: 0000-0003-4389-4924
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Boston, Massachusetts, USA.
FAU - Lee, Su Been
AU  - Lee SB
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Boston, Massachusetts, USA.
FAU - Desai, Rishi J
AU  - Desai RJ
AUID- ORCID: 0000-0003-0299-7273
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Boston, Massachusetts, USA RDESAI@BWH.HARVARD.EDU.
LA  - eng
SI  - ClinicalTrials.gov/NCT04772248
GR  - K24 AR078959/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20220113
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Piperidines)
RN  - 0 (Pyrimidines)
RN  - 0 (Pyrroles)
RN  - 0 (Tumor Necrosis Factor Inhibitors)
RN  - 87LA6FU830 (tofacitinib)
SB  - IM
MH  - *Antirheumatic Agents/adverse effects
MH  - *Arthritis, Rheumatoid/epidemiology
MH  - Humans
MH  - Piperidines/adverse effects
MH  - Pyrimidines/adverse effects
MH  - Pyrroles/adverse effects
MH  - Treatment Outcome
MH  - Tumor Necrosis Factor Inhibitors
PMC - PMC9117457
MID - NIHMS1792413
OTO - NOTNLM
OT  - antirheumatic agents
OT  - arthritis
OT  - epidemiology
OT  - rheumatoid
OT  - rheumatoid arthritis
COIS- Competing interests: RJD has received research grants to the Brigham and Women’s 
      Hospital from Bayer, Novartis, and Vertex for unrelated projects. SCK has 
      received research grants to the Brigham and Women’s Hospital from 
      Roche/Genentech, Pfizer, Bristol-Myers Squibb, Roche, and AbbVie for unrelated 
      studies. All other authors have no conflict of interests to disclose.
EDAT- 2022/01/15 06:00
MHDA- 2022/05/20 06:00
PMCR- 2023/06/01
CRDT- 2022/01/14 05:43
PHST- 2021/11/24 00:00 [received]
PHST- 2021/12/30 00:00 [accepted]
PHST- 2022/01/15 06:00 [pubmed]
PHST- 2022/05/20 06:00 [medline]
PHST- 2022/01/14 05:43 [entrez]
PHST- 2023/06/01 00:00 [pmc-release]
AID - annrheumdis-2021-221915 [pii]
AID - 10.1136/annrheumdis-2021-221915 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2022 Jun;81(6):798-804. doi: 10.1136/annrheumdis-2021-221915. Epub 
      2022 Jan 13.

PMID- 35023833
OWN - NLM
STAT- MEDLINE
DCOM- 20220317
LR  - 20241012
IS  - 2050-084X (Electronic)
IS  - 2050-084X (Linking)
VI  - 11
DP  - 2022 Jan 13
TI  - Epigenetic scores for the circulating proteome as tools for disease prediction.
LID - 10.7554/eLife.71802 [doi]
LID - e71802
AB  - Protein biomarkers have been identified across many age-related morbidities. 
      However, characterising epigenetic influences could further inform disease 
      predictions. Here, we leverage epigenome-wide data to study links between the DNA 
      methylation (DNAm) signatures of the circulating proteome and incident diseases. 
      Using data from four cohorts, we trained and tested epigenetic scores (EpiScores) 
      for 953 plasma proteins, identifying 109 scores that explained between 1% and 58% 
      of the variance in protein levels after adjusting for known protein quantitative 
      trait loci (pQTL) genetic effects. By projecting these EpiScores into an 
      independent sample (Generation Scotland; n = 9537) and relating them to incident 
      morbidities over a follow-up of 14 years, we uncovered 137 EpiScore-disease 
      associations. These associations were largely independent of immune cell 
      proportions, common lifestyle and health factors, and biological aging. Notably, 
      we found that our diabetes-associated EpiScores highlighted previous top 
      biomarker associations from proteome-wide assessments of diabetes. These 
      EpiScores for protein levels can therefore be a valuable resource for disease 
      prediction and risk stratification.
CI  - © 2022, Gadd et al.
FAU - Gadd, Danni A
AU  - Gadd DA
AUID- ORCID: 0000-0001-6398-5407
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
FAU - Hillary, Robert F
AU  - Hillary RF
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
FAU - McCartney, Daniel L
AU  - McCartney DL
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
FAU - Zaghlool, Shaza B
AU  - Zaghlool SB
AD  - Department of Physiology and Biophysics, Weill Cornell Medicine-Qatar, Education 
      City, Doha, Qatar.
AD  - Computer Engineering Department, Virginia Tech, Blacksburg, United States.
FAU - Stevenson, Anna J
AU  - Stevenson AJ
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
FAU - Cheng, Yipeng
AU  - Cheng Y
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
FAU - Fawns-Ritchie, Chloe
AU  - Fawns-Ritchie C
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
AD  - Department of Psychology, University of Edinburgh, Edinburgh, United Kingdom.
FAU - Nangle, Cliff
AU  - Nangle C
AUID- ORCID: 0000-0001-5432-1158
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
FAU - Campbell, Archie
AU  - Campbell A
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
FAU - Flaig, Robin
AU  - Flaig R
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
FAU - Harris, Sarah E
AU  - Harris SE
AUID- ORCID: 0000-0002-4941-5106
AD  - Department of Psychology, University of Edinburgh, Edinburgh, United Kingdom.
AD  - Lothian Birth Cohorts, University of Edinburgh, Edinburgh, United Kingdom.
FAU - Walker, Rosie M
AU  - Walker RM
AD  - Centre for Clinical Brain Sciences, Chancellor's Building, University of 
      Edinburgh, Edinburgh, United Kingdom.
FAU - Shi, Liu
AU  - Shi L
AD  - Department of Psychiatry, University of Oxford, Oxford, United Kingdom.
FAU - Tucker-Drob, Elliot M
AU  - Tucker-Drob EM
AD  - Department of Psychology, The University of Texas at Austin, Austin, United 
      States.
AD  - Population Research Center, The University of Texas at Austin, Austin, United 
      States.
FAU - Gieger, Christian
AU  - Gieger C
AD  - Research Unit Molecular Epidemiology, Helmholtz Zentrum München, German Research 
      Center for Environmental Health, Neuherberg, Germany.
AD  - Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for 
      Environmental Health, Neuherberg, Germany.
AD  - German Center for Cardiovascular Research (DZHK), partner site Munich Heart 
      Alliance, Munich, Germany.
AD  - German Center for Diabetes Research (DZD), Neuherberg, Germany.
FAU - Peters, Annette
AU  - Peters A
AD  - Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for 
      Environmental Health, Neuherberg, Germany.
AD  - German Center for Cardiovascular Research (DZHK), partner site Munich Heart 
      Alliance, Munich, Germany.
AD  - German Center for Diabetes Research (DZD), Neuherberg, Germany.
FAU - Waldenberger, Melanie
AU  - Waldenberger M
AD  - Research Unit Molecular Epidemiology, Helmholtz Zentrum München, German Research 
      Center for Environmental Health, Neuherberg, Germany.
AD  - Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for 
      Environmental Health, Neuherberg, Germany.
AD  - German Center for Cardiovascular Research (DZHK), partner site Munich Heart 
      Alliance, Munich, Germany.
FAU - Graumann, Johannes
AU  - Graumann J
AD  - Scientific Service Group Biomolecular Mass Spectrometry, Max Planck Institute for 
      Heart and Lung Research, W.G. Kerckhoff Institute, Bad Nauheim, Germany.
AD  - German Centre for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Max 
      Planck Institute of Heart and Lung Research, Bad Nauheim, Germany.
FAU - McRae, Allan F
AU  - McRae AF
AD  - Institute for Molecular Bioscience, University of Queensland, Brisbane, 
      Australia.
FAU - Deary, Ian J
AU  - Deary IJ
AD  - Department of Psychology, University of Edinburgh, Edinburgh, United Kingdom.
AD  - Lothian Birth Cohorts, University of Edinburgh, Edinburgh, United Kingdom.
FAU - Porteous, David J
AU  - Porteous DJ
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
FAU - Hayward, Caroline
AU  - Hayward C
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
AD  - Medical Research Council Human Genetics Unit, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
FAU - Visscher, Peter M
AU  - Visscher PM
AD  - Institute for Molecular Bioscience, University of Queensland, Brisbane, 
      Australia.
FAU - Cox, Simon R
AU  - Cox SR
AD  - Department of Psychology, University of Edinburgh, Edinburgh, United Kingdom.
AD  - Lothian Birth Cohorts, University of Edinburgh, Edinburgh, United Kingdom.
FAU - Evans, Kathryn L
AU  - Evans KL
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
FAU - McIntosh, Andrew M
AU  - McIntosh AM
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
AD  - Division of Psychiatry, University of Edinburgh, Royal Edinburgh Hospital, 
      Edinburgh, United Kingdom.
FAU - Suhre, Karsten
AU  - Suhre K
AUID- ORCID: 0000-0001-9638-3912
AD  - Department of Physiology and Biophysics, Weill Cornell Medicine-Qatar, Education 
      City, Doha, Qatar.
FAU - Marioni, Riccardo E
AU  - Marioni RE
AUID- ORCID: 0000-0003-4430-4260
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, 
      University of Edinburgh, Edinburgh, United Kingdom.
LA  - eng
GR  - BB/F019394/1/BB_/Biotechnology and Biological Sciences Research Council/United 
      Kingdom
GR  - 216767/Z/19/Z/WT_/Wellcome Trust/United Kingdom
GR  - 221890/Z/20/Z/WT_/Wellcome Trust/United Kingdom
GR  - G0700704/MRC_/Medical Research Council/United Kingdom
GR  - P2C HD042849/HD/NICHD NIH HHS/United States
GR  - MR/R024065/1/MRC_/Medical Research Council/United Kingdom
GR  - MC_UU_00007/10/MRC_/Medical Research Council/United Kingdom
GR  - WT_/Wellcome Trust/United Kingdom
GR  - MR/L023784/2/MRC_/Medical Research Council/United Kingdom
GR  - MR/M013111/1/MRC_/Medical Research Council/United Kingdom
GR  - RF1 AG073593/AG/NIA NIH HHS/United States
GR  - 104036/Z/14/Z/WT_/Wellcome Trust/United Kingdom
GR  - 220857/Z/20/Z/WT_/Wellcome Trust/United Kingdom
GR  - 203771/Z/16/Z/WT_/Wellcome Trust/United Kingdom
GR  - 108890/Z/15/Z/WT_/Wellcome Trust/United Kingdom
GR  - DH_/Department of Health/United Kingdom
GR  - R01 AG054628/AG/NIA NIH HHS/United States
GR  - P30 AG066614/AG/NIA NIH HHS/United States
GR  - G1001245/MRC_/Medical Research Council/United Kingdom
GR  - G0701120/MRC_/Medical Research Council/United Kingdom
GR  - MR/K026992/1/MRC_/Medical Research Council/United Kingdom
GR  - CZD/16/6/CSO_/Chief Scientist Office/United Kingdom
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20220113
PL  - England
TA  - Elife
JT  - eLife
JID - 101579614
RN  - 0 (Biomarkers)
RN  - 0 (Proteome)
SB  - IM
CIN - Elife. 2022 Feb 25;11:e77180. doi: 10.7554/eLife.77180. PMID: 35212264
EIN - Elife. 2023 Nov 20;12:e94481. doi: 10.7554/eLife.94481. PMID: 37982710
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Aging
MH  - Biomarkers
MH  - Cardiovascular Diseases/*diagnosis
MH  - DNA Methylation/*genetics
MH  - Diabetes Mellitus/*diagnosis
MH  - Epigenesis, Genetic
MH  - Epigenomics/*methods
MH  - Female
MH  - Humans
MH  - Life Style
MH  - Male
MH  - Middle Aged
MH  - Neoplasms/*diagnosis
MH  - Proteome/*genetics
MH  - Risk Factors
MH  - Scotland
MH  - Young Adult
PMC - PMC8880990
OAB - Although our genetic code does not change throughout our lives, our genes can be 
      turned on and off as a result of epigenetics. Epigenetics can track how the 
      environment and even certain behaviors add or remove small chemical markers to 
      the DNA that makes up the genome. The type and location of these markers may 
      affect whether genes are active or silent, this is, whether the protein coded for 
      by that gene is being produced or not. One common epigenetic marker is known as 
      DNA methylation. DNA methylation has been linked to the levels of a range of 
      proteins in our cells and the risk people have of developing chronic diseases. 
      Blood samples can be used to determine the epigenetic markers a person has on 
      their genome and to study the abundance of many proteins. Gadd, Hillary, 
      McCartney, Zaghlool et al. studied the relationships between DNA methylation and 
      the abundance of 953 different proteins in blood samples from individuals in the 
      German KORA cohort and the Scottish Lothian Birth Cohort 1936. They then used 
      machine learning to analyze the relationship between epigenetic markers found in 
      people’s blood and the abundance of proteins, obtaining epigenetic scores or 
      ‘EpiScores’ for each protein. They found 109 proteins for which DNA methylation 
      patterns explained between at least 1% and up to 58% of the variation in protein 
      levels. Integrating the ‘EpiScores’ with 14 years of medical records for more 
      than 9000 individuals from the Generation Scotland study revealed 130 connections 
      between EpiScores for proteins and a future diagnosis of common adverse health 
      outcomes. These included diabetes, stroke, depression, various cancers, and 
      inflammatory conditions such as rheumatoid arthritis and inflammatory bowel 
      disease. Age-related chronic diseases are a growing issue worldwide and place 
      pressure on healthcare systems. They also severely reduce quality of life for 
      individuals over many years. This work shows how epigenetic scores based on 
      protein levels in the blood could predict a person’s risk of several of these 
      diseases. In the case of type 2 diabetes, the EpiScore results replicated 
      previous research linking protein levels in the blood to future diagnosis of 
      diabetes. Protein EpiScores could therefore allow researchers to identify people 
      with the highest risk of disease, making it possible to intervene early and 
      prevent these people from developing chronic conditions as they age.
OABL- eng
OTO - NOTNLM
OT  - aging
OT  - biomarker
OT  - epidemiology
OT  - epigenetic
OT  - genetics
OT  - genomics
OT  - global health
OT  - human
OT  - morbiditiy
OT  - prediction
OT  - proteomics
COIS- DG, DM, SZ, AS, YC, CF, CN, AC, RF, SH, RW, LS, ET, CG, AP, MW, JG, AM, ID, DP, 
      CH, PV, SC, KE, AM, KS No competing interests declared, RH has received 
      consultant fees from Illumina, RM has received speaker fees from Illumina and is 
      an advisor to the Epigenetic Clock Development Foundation
EDAT- 2022/01/14 06:00
MHDA- 2022/03/18 06:00
PMCR- 2022/01/13
CRDT- 2022/01/13 12:22
PHST- 2021/06/30 00:00 [received]
PHST- 2022/01/11 00:00 [accepted]
PHST- 2022/01/14 06:00 [pubmed]
PHST- 2022/03/18 06:00 [medline]
PHST- 2022/01/13 12:22 [entrez]
PHST- 2022/01/13 00:00 [pmc-release]
AID - 71802 [pii]
AID - 10.7554/eLife.71802 [doi]
PST - epublish
SO  - Elife. 2022 Jan 13;11:e71802. doi: 10.7554/eLife.71802.

PMID- 35013839
OWN - NLM
STAT- MEDLINE
DCOM- 20220228
LR  - 20220429
IS  - 1437-160X (Electronic)
IS  - 0172-8172 (Linking)
VI  - 42
IP  - 2
DP  - 2022 Feb
TI  - Cardiovascular disease detection using machine learning and carotid/femoral 
      arterial imaging frameworks in rheumatoid arthritis patients.
PG  - 215-239
LID - 10.1007/s00296-021-05062-4 [doi]
AB  - The study proposes a novel machine learning (ML) paradigm for cardiovascular 
      disease (CVD) detection in individuals at medium to high cardiovascular risk 
      using data from a Greek cohort of 542 individuals with rheumatoid arthritis, or 
      diabetes mellitus, and/or arterial hypertension, using conventional or 
      office-based, laboratory-based blood biomarkers and carotid/femoral ultrasound 
      image-based phenotypes. Two kinds of data (CVD risk factors and presence of 
      CVD-defined as stroke, or myocardial infarction, or coronary artery syndrome, or 
      peripheral artery disease, or coronary heart disease) as ground truth, were 
      collected at two-time points: (i) at visit 1 and (ii) at visit 2 after 3 years. 
      The CVD risk factors were divided into three clusters (conventional or 
      office-based, laboratory-based blood biomarkers, carotid ultrasound image-based 
      phenotypes) to study their effect on the ML classifiers. Three kinds of ML 
      classifiers (Random Forest, Support Vector Machine, and Linear Discriminant 
      Analysis) were applied in a two-fold cross-validation framework using the data 
      augmented by synthetic minority over-sampling technique (SMOTE) strategy. The 
      performance of the ML classifiers was recorded. In this cohort with overall 46 
      CVD risk factors (covariates) implemented in an online cardiovascular framework, 
      that requires calculation time less than 1 s per patient, a mean accuracy and 
      area-under-the-curve (AUC) of 98.40% and 0.98 (p < 0.0001) for CVD presence 
      detection at visit 1, and 98.39% and 0.98 (p < 0.0001) at visit 2, respectively. 
      The performance of the cardiovascular framework was significantly better than the 
      classical CVD risk score. The ML paradigm proved to be powerful for CVD 
      prediction in individuals at medium to high cardiovascular risk.
CI  - © 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, 
      part of Springer Nature.
FAU - Konstantonis, George
AU  - Konstantonis G
AD  - Rheumatology Unit, National Kapodistrian University of Athens, Athens, Greece.
FAU - Singh, Krishna V
AU  - Singh KV
AUID- ORCID: 0000-0003-4311-8730
AD  - Research Intern, AtheroPoint™, Roseville, CA, USA.
FAU - Sfikakis, Petros P
AU  - Sfikakis PP
AUID- ORCID: 0000-0001-5484-2930
AD  - Rheumatology Unit, National Kapodistrian University of Athens, Athens, Greece.
FAU - Jamthikar, Ankush D
AU  - Jamthikar AD
AUID- ORCID: 0000-0002-3030-7236
AD  - Research Scientist, AtheroPoint™, USA, Roseville, CA, USA.
AD  - Visvesvaraya National Institute of Technology, Nagpur, India.
FAU - Kitas, George D
AU  - Kitas GD
AUID- ORCID: 0000-0002-0828-6176
AD  - Academic Affairs, Dudley Group NHS Foundation Trust, Dudley, UK.
AD  - Arthritis Research UK Epidemiology Unit, Manchester University, Manchester, M13, 
      UK.
FAU - Gupta, Suneet K
AU  - Gupta SK
AUID- ORCID: 0000-0001-7935-8598
AD  - Department of Computer Science, Bennett University, Gr. Noida, India.
FAU - Saba, Luca
AU  - Saba L
AUID- ORCID: 0000-0003-2870-3771
AD  - Department of Radiology, University of Cagliari, Cagliari, Italy.
FAU - Verrou, Kleio
AU  - Verrou K
AD  - Department of Medicine, National and Kapodistrian University of Athens, Athens, 
      Greece.
FAU - Khanna, Narendra N
AU  - Khanna NN
AUID- ORCID: 0000-0002-6935-0039
AD  - Department of Cardiology, Indraprastha Apollo Hospitals, New Delhi, India.
FAU - Ruzsa, Zoltan
AU  - Ruzsa Z
AUID- ORCID: 0000-0002-2474-5723
AD  - Department of Internal Medicines, Invasive Cardiology Division, University of 
      Szeged, Szeged, Hungary.
FAU - Sharma, Aditya M
AU  - Sharma AM
AUID- ORCID: 0000-0003-1756-2504
AD  - Division of Cardiovascular Medicine, University of Virginia, Charlottesville, VA, 
      USA.
FAU - Laird, John R
AU  - Laird JR
AUID- ORCID: 0000-0003-2095-2191
AD  - Heart and Vascular Institute, Adventist Health St. Helena, St Helena, CA, USA.
FAU - Johri, Amer M
AU  - Johri AM
AUID- ORCID: 0000-0001-7044-8212
AD  - Department of Medicine, Division of Cardiology, Queen's University, Kingston, ON, 
      Canada.
FAU - Kalra, Manudeep
AU  - Kalra M
AUID- ORCID: 0000-0001-9938-7476
AD  - Department of Radiology, Massachusetts General Hospital, 55 Fruit Street, Boston, 
      MA, USA.
FAU - Protogerou, Athanasios
AU  - Protogerou A
AUID- ORCID: 0000-0002-3825-532X
AD  - Cardiovascular Prevention Unit, Department of Pathophysiology, National 
      Kapodistrian University of Athens, Athens, Greece.
FAU - Suri, Jasjit S
AU  - Suri JS
AD  - Stroke Monitoring and Diagnostic Division, AtheroPoint™, Roseville, CA, 95661, 
      USA. jasjit.suri@atheropoint.com.
LA  - eng
PT  - Journal Article
PT  - Validation Study
DEP - 20220111
PL  - Germany
TA  - Rheumatol Int
JT  - Rheumatology international
JID - 8206885
SB  - IM
MH  - Arthritis, Rheumatoid/*complications
MH  - Cardiovascular Diseases/*diagnosis
MH  - Carotid Arteries/diagnostic imaging
MH  - Cross-Sectional Studies
MH  - Female
MH  - Femoral Artery/diagnostic imaging
MH  - Heart Disease Risk Factors
MH  - Humans
MH  - *Machine Learning
MH  - Male
MH  - Pilot Projects
MH  - Plaque, Atherosclerotic/*diagnostic imaging
MH  - Reproducibility of Results
OTO - NOTNLM
OT  - And machine learning
OT  - Cardiovascular disease
OT  - Cardiovascular risk estimation
OT  - Conventional risk factors
OT  - Three-year follow-up
OT  - Ultrasound
EDAT- 2022/01/12 06:00
MHDA- 2022/03/01 06:00
CRDT- 2022/01/11 06:56
PHST- 2021/10/25 00:00 [received]
PHST- 2021/11/29 00:00 [accepted]
PHST- 2022/01/12 06:00 [pubmed]
PHST- 2022/03/01 06:00 [medline]
PHST- 2022/01/11 06:56 [entrez]
AID - 10.1007/s00296-021-05062-4 [pii]
AID - 10.1007/s00296-021-05062-4 [doi]
PST - ppublish
SO  - Rheumatol Int. 2022 Feb;42(2):215-239. doi: 10.1007/s00296-021-05062-4. Epub 2022 
      Jan 11.

PMID- 34941008
OWN - NLM
STAT- MEDLINE
DCOM- 20230329
LR  - 20240923
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Print)
IS  - 2151-464X (Linking)
VI  - 75
IP  - 4
DP  - 2023 Apr
TI  - Hydroxychloroquine Use and Cardiovascular Events Among Patients With Systemic 
      Lupus Erythematosus and Rheumatoid Arthritis.
PG  - 743-748
LID - 10.1002/acr.24850 [doi]
AB  - OBJECTIVE: We evaluated the potential temporal association between 
      hydroxychloroquine (HCQ) use and cardiovascular (CV) events among patients with 
      systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA). METHODS: We 
      conducted a nested case-control study within inception cohorts of SLE and RA 
      patients using administrative health databases including the entire population of 
      British Columbia, Canada. We identified cases with incident CV events, including 
      myocardial infarction (MI), stroke, or venous thromboembolism (VTE). We matched 
      each case with up to 3 controls on age, sex, and rheumatic disease. HCQ exposure 
      was categorized by the time between the last HCQ prescription date covered and 
      the index date as current use, recent use, remote use, or never used. We used 
      conditional logistic regression to assess the association between HCQ exposure 
      and CV events, using remote use as the reference group. RESULTS: We identified 
      10,268 cases and 29,969 controls. Adjusted conditional odd ratios (cORs) and 95% 
      confidence intervals (95% CIs) for current HCQ use relative to remote use were 
      0.86 (0.77-0.97) for combined CV events, 0.88 (0.74-1.05) for MI, 0.87 
      (0.74-1.03) for stroke, and 0.74 (0.59-0.94) for VTE. Recent HCQ users and 
      nonusers had similar odds of combined CV events as remote users (cORs 0.93, 95% 
      CI 0.77-1.13 and 0.96, 95% CI 0.88-1.04, respectively). CONCLUSION: In this 
      nested case-control study of patients with SLE and RA, we found a reduced risk of 
      overall CV events associated with current HCQ use, including reductions in VTE 
      and trends toward reductions in MI and stroke. These findings suggest a possible 
      cardiovascular preventative benefit of HCQ use.
CI  - © 2021 American College of Rheumatology.
FAU - Jorge, April
AU  - Jorge A
AUID- ORCID: 0000-0001-6935-880X
AD  - Massachusetts General Hospital, Boston.
FAU - Lu, Na
AU  - Lu N
AD  - Massachusetts General Hospital, Boston, and Arthritis Research Canada, Richmond, 
      British Columbia, Canada.
FAU - Choi, Hyon
AU  - Choi H
AD  - Massachusetts General Hospital, Boston.
FAU - Esdaile, John M
AU  - Esdaile JM
AD  - Arthritis Research Canada and University of British Columbia, Vancouver, British 
      Columbia, Canada.
FAU - Lacaille, Diane
AU  - Lacaille D
AUID- ORCID: 0000-0002-4065-4151
AD  - Arthritis Research Canada and University of British Columbia, Vancouver, British 
      Columbia, Canada.
FAU - Avina-Zubieta, J Antonio
AU  - Avina-Zubieta JA
AUID- ORCID: 0000-0001-5526-663X
AD  - Arthritis Research Canada and University of British Columbia, Vancouver, British 
      Columbia, Canada.
LA  - eng
GR  - K23 AR079040/AR/NIAMS NIH HHS/United States
GR  - L30 AR076110/AR/NIAMS NIH HHS/United States
GR  - P50 AR060772/AR/NIAMS NIH HHS/United States
GR  - P50-AR-060772/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20221217
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 4QWG6N8QKH (Hydroxychloroquine)
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Humans
MH  - Hydroxychloroquine/adverse effects
MH  - *Antirheumatic Agents/adverse effects
MH  - Case-Control Studies
MH  - *Venous Thromboembolism/drug therapy
MH  - *Lupus Erythematosus, Systemic/diagnosis/drug therapy/epidemiology
MH  - *Arthritis, Rheumatoid/diagnosis/drug therapy/epidemiology
MH  - *Myocardial Infarction/chemically induced/epidemiology
MH  - *Stroke/diagnosis/epidemiology/prevention & control
MH  - British Columbia/epidemiology
PMC - PMC9218009
MID - NIHMS1766515
COIS- Declaration of Interest: None
EDAT- 2021/12/24 06:00
MHDA- 2023/03/29 06:04
PMCR- 2024/04/01
CRDT- 2021/12/23 12:58
PHST- 2021/12/14 00:00 [revised]
PHST- 2021/05/18 00:00 [received]
PHST- 2021/12/21 00:00 [accepted]
PHST- 2023/03/29 06:04 [medline]
PHST- 2021/12/24 06:00 [pubmed]
PHST- 2021/12/23 12:58 [entrez]
PHST- 2024/04/01 00:00 [pmc-release]
AID - 10.1002/acr.24850 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2023 Apr;75(4):743-748. doi: 10.1002/acr.24850. 
      Epub 2022 Dec 17.

PMID- 34931349
OWN - NLM
STAT- MEDLINE
DCOM- 20220517
LR  - 20220731
IS  - 1365-2125 (Electronic)
IS  - 0306-5251 (Print)
IS  - 0306-5251 (Linking)
VI  - 88
IP  - 6
DP  - 2022 Jun
TI  - Dissecting the IL-6 pathway in cardiometabolic disease: A Mendelian randomization 
      study on both IL6 and IL6R.
PG  - 2875-2884
LID - 10.1111/bcp.15191 [doi]
AB  - AIMS: Chronic inflammation is a risk factor for cardiovascular disease (CVD). 
      IL-6 signalling perturbation through IL-6 or IL-6R blockade may have potential 
      benefit on cardiovascular risk. It is unknown whether targeting either IL-6 or 
      IL-6 receptor may result in similar effects on CVD and adverse events. We 
      compared the anticipated effects of targeting IL-6 and IL-6 receptor on 
      cardiometabolic risk and potential side effects. METHODS: We constructed four 
      instruments: two main instruments with genetic variants in the IL6 and IL6R loci 
      weighted for their association with CRP, and two after firstly filtering variants 
      for their association with IL-6 or IL-6R expression. Analyses were performed for 
      coronary artery disease (CAD), ischemic stroke, atrial fibrillation (AF), heart 
      failure, type 2 diabetes (T2D), rheumatoid arthritis (RA), infection endpoints, 
      and quantitative haematological, metabolic and anthropometric parameters. 
      RESULTS: A 1 mg/L lower CRP by the IL6 instrument was associated with lower CAD 
      (odds ratio [OR] 0.86, 95% confidence interval [CI] 0.77;0.96), AF and T2D risk. 
      A 1 mg/L lower CRP by the IL6R instrument was associated with lower CAD (OR 0.90, 
      95% CI 0.86;0.95), any stroke and ischemic stroke, AF, RA risk and higher 
      pneumonia risk. The eQTL-filtered results were in concordance with the main 
      results, but with wider confidence intervals. CONCLUSIONS: IL-6 signalling 
      perturbation by either IL6 or IL6R genetic instruments is associated with a 
      similar risk reduction for multiple cardiometabolic diseases, suggesting that 
      both IL-6 and IL-6R are potential therapeutic targets to lower CVD. Moreover, 
      IL-6 rather than IL-6R inhibition might have a more favourable pneumonia risk.
CI  - © 2021 The Authors. British Journal of Clinical Pharmacology published by John 
      Wiley & Sons Ltd on behalf of British Pharmacological Society.
FAU - Cupido, Arjen J
AU  - Cupido AJ
AUID- ORCID: 0000-0003-3300-8124
AD  - Department of Vascular Medicine, Amsterdam University Medical Centers, location 
      AMC, University of Amsterdam, Amsterdam, Netherlands.
AD  - Department of Cardiology, Division Heart & Lungs, University Medical Center 
      Utrecht, Utrecht University, Utrecht, the Netherlands.
FAU - Asselbergs, Folkert W
AU  - Asselbergs FW
AUID- ORCID: 0000-0002-1692-8669
AD  - Department of Cardiology, Division Heart & Lungs, University Medical Center 
      Utrecht, Utrecht University, Utrecht, the Netherlands.
AD  - Institute of Cardiovascular Science, Faculty of Population Health Sciences, 
      University College London, London, UK.
AD  - Health Data Research UK and Institute of Health Informatics, University College 
      London, London, UK.
FAU - Natarajan, Pradeep
AU  - Natarajan P
AUID- ORCID: 0000-0001-8402-7435
AD  - Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical 
      School, Boston, MA, USA.
AD  - Program in Medical and Population Genetics and Cardiovascular Disease Initiative, 
      Broad Institute of Harvard and MIT, Cambridge, MA, USA.
CN  - CHARGE Inflammation Working Group
FAU - Ridker, Paul M
AU  - Ridker PM
AUID- ORCID: 0000-0003-1249-4522
AD  - Divisions of Preventive Medicine and Cardiovascular Medicine, Department of 
      Medicine, Center for Cardiovascular Disease Prevention, Brigham and Women's 
      Hospital, Harvard Medical School, Boston, MA, USA.
FAU - Hovingh, G Kees
AU  - Hovingh GK
AUID- ORCID: 0000-0002-8145-1676
AD  - Department of Vascular Medicine, Amsterdam University Medical Centers, location 
      AMC, University of Amsterdam, Amsterdam, Netherlands.
FAU - Schmidt, A Floriaan
AU  - Schmidt AF
AUID- ORCID: 0000-0003-1327-0424
AD  - Department of Cardiology, Division Heart & Lungs, University Medical Center 
      Utrecht, Utrecht University, Utrecht, the Netherlands.
AD  - Institute of Cardiovascular Science, Faculty of Population Health Sciences, 
      University College London, London, UK.
LA  - eng
GR  - R01 HL151283/HL/NHLBI NIH HHS/United States
GR  - R01 HL148565/HL/NHLBI NIH HHS/United States
GR  - R01 HL142711/HL/NHLBI NIH HHS/United States
GR  - PG/18/50/33837/BHF_/British Heart Foundation/United Kingdom
GR  - R01 HL148050/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20220128
PL  - England
TA  - Br J Clin Pharmacol
JT  - British journal of clinical pharmacology
JID - 7503323
RN  - 0 (IL6R protein, human)
RN  - 0 (Interleukin-6)
RN  - 0 (Receptors, Interleukin-6)
SB  - IM
MH  - Arthritis, Rheumatoid/drug therapy
MH  - Atrial Fibrillation
MH  - *Coronary Artery Disease/genetics
MH  - *Diabetes Mellitus, Type 2/genetics
MH  - Genome-Wide Association Study
MH  - Humans
MH  - *Interleukin-6/genetics/metabolism
MH  - *Ischemic Stroke
MH  - Mendelian Randomization Analysis
MH  - Polymorphism, Single Nucleotide
MH  - *Receptors, Interleukin-6/genetics/metabolism
MH  - Risk Factors
PMC - PMC9303316
OTO - NOTNLM
OT  - IL-6
OT  - cardiovascular disease
OT  - classical signalling
OT  - trans-signalling
COIS- A.J.C. has nothing to disclose. F.W.A. and A.F.S. have received Servier funding 
      for unrelated work. P.N. has received research support from Apple, Amgen and 
      Boston Scientific, personal fees from Apple, Genentech, Novartis and Blackstone 
      Life Sciences, and spousal employment at Vertex, all unrelated to the present 
      work. P.M.R. has served as a consultant to Flame, Agepha, Corvidia, Inflammazome, 
      Novartis, Amgen, Merck and Civi Bio and is listed as co‐inventor on patents 
      related to the use of inflammatory biomarkers in CVD and diabetes that are no 
      longer active. G.K.H. has received funding from Regeneron, Aegerion, Amgen, 
      AstraZeneca, Eli Lilly, Genzyme, Kowa, Pfizer, Regeneron Pharmaceuticals, Roche, 
      Sanofi, The Medicines Company, Ionis and personal fees from Novo Nordisk.
EDAT- 2021/12/22 06:00
MHDA- 2022/05/18 06:00
PMCR- 2022/01/28
CRDT- 2021/12/21 06:55
PHST- 2021/10/07 00:00 [revised]
PHST- 2021/07/09 00:00 [received]
PHST- 2021/10/28 00:00 [accepted]
PHST- 2021/12/22 06:00 [pubmed]
PHST- 2022/05/18 06:00 [medline]
PHST- 2021/12/21 06:55 [entrez]
PHST- 2022/01/28 00:00 [pmc-release]
AID - BCP15191 [pii]
AID - 10.1111/bcp.15191 [doi]
PST - ppublish
SO  - Br J Clin Pharmacol. 2022 Jun;88(6):2875-2884. doi: 10.1111/bcp.15191. Epub 2022 
      Jan 28.

PMID- 34676228
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211023
IS  - 2296-858X (Print)
IS  - 2296-858X (Electronic)
IS  - 2296-858X (Linking)
VI  - 8
DP  - 2021
TI  - Rheumatoid Arthritis and Cardiovascular Risk: Retrospective Matched-Cohort 
      Analysis Based on the RECORD Study of the Italian Society for Rheumatology.
PG  - 745601
LID - 10.3389/fmed.2021.745601 [doi]
LID - 745601
AB  - Background: Rheumatoid arthritis (RA) is associated with an increase in 
      cardiovascular (CV) risk. This issue maybe not only explained by a genetic 
      component, as well as by the traditional CV risk factors, but also by an 
      underestimation and undertreatment of concomitant CV comorbidities. Method: This 
      was a retrospective matched-cohort analysis in the Italian RA real-world 
      population based on the healthcare-administrative databases to assess the CV risk 
      factors and incidence of CV events in comparison with the general population. 
      Persistence and adherence to the CV therapy were also evaluated in both groups. 
      Results: In a RA cohort (N = 21,201), there was a greater prevalence of 
      hypertension and diabetes with respect to the non-RA subjects (N = 249,156) (36.9 
      vs. 33.4% and 10.2 vs. 9.6%, respectively), while dyslipidemia was more frequent 
      in the non-RA group (15.4 vs. 16.5%). Compared with a non-RA cohort, the patients 
      with RA had a higher incidence of atrial fibrillation (incidence rate ratio, IRR 
      1.28), heart failure (IRR 1.53), stroke (IRR 1.19), and myocardial infarction 
      (IRR 1.48). The patients with RA presented a significantly lower persistence rate 
      to glucose-lowering and lipid-lowering therapies than the controls (odds ratio, 
      OR 0.73 [95% CI 0.6-0.8] and OR 0.82 [0.8-0.9], respectively). The difference in 
      the adherence to glucose-lowering therapy was significant (OR 0.7 [0.6-0.8]), 
      conversely no statistically significant differences emerged regarding the 
      adherence to lipid-lowering therapy (OR 0.89 [95% CI 0.8-1.0]) and 
      anti-hypertensive therapy (OR 0.96 [95% CI 0.9-1.0]). Conclusion: The patients 
      with RA have a higher risk of developing CV events compared with the general 
      population, partially explained by the excess and undertreatment of CV risk 
      factors.
CI  - Copyright © 2021 Argnani, Zanetti, Carrara, Silvagni, Guerrini, Zambon and Scirè.
FAU - Argnani, Lisa
AU  - Argnani L
AD  - Department of Experimental, Diagnostic and Specialty Medicine, University of 
      Bologna, Bologna, Italy.
FAU - Zanetti, Anna
AU  - Zanetti A
AD  - Epidemiology Unit, Italian Society for Rheumatology, Milan, Italy.
AD  - Department of Statistics and Quantitative Methods, Division of Biostatistics, 
      Epidemiology and Public Health, University of Milano-Bicocca, Milan, Italy.
FAU - Carrara, Greta
AU  - Carrara G
AD  - Epidemiology Unit, Italian Society for Rheumatology, Milan, Italy.
FAU - Silvagni, Ettore
AU  - Silvagni E
AD  - Rheumatology Unit, Department of Medical Sciences, University of Ferrara and 
      Azienda Ospedaliero-Universitaria S.Anna, Cona, Italy.
FAU - Guerrini, Giulio
AU  - Guerrini G
AD  - Biomedical and Biotechnological Science at Department of Life Sciences and 
      Biotechnology, University of Ferrara, Ferrara, Italy.
AD  - Internal Medicine, State Hospital, Borgo Maggiore, San Marino.
FAU - Zambon, Antonella
AU  - Zambon A
AD  - Department of Statistics and Quantitative Methods, Division of Biostatistics, 
      Epidemiology and Public Health, University of Milano-Bicocca, Milan, Italy.
FAU - Scirè, Carlo Alberto
AU  - Scirè CA
AD  - Epidemiology Unit, Italian Society for Rheumatology, Milan, Italy.
AD  - School of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy.
LA  - eng
PT  - Journal Article
DEP - 20211005
PL  - Switzerland
TA  - Front Med (Lausanne)
JT  - Frontiers in medicine
JID - 101648047
PMC - PMC8523847
OTO - NOTNLM
OT  - cardiovascular events
OT  - cardiovascular risk
OT  - prevalence
OT  - real-world population
OT  - rheumatoid arthritis
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/10/23 06:00
MHDA- 2021/10/23 06:01
PMCR- 2021/10/05
CRDT- 2021/10/22 06:53
PHST- 2021/07/22 00:00 [received]
PHST- 2021/09/06 00:00 [accepted]
PHST- 2021/10/22 06:53 [entrez]
PHST- 2021/10/23 06:00 [pubmed]
PHST- 2021/10/23 06:01 [medline]
PHST- 2021/10/05 00:00 [pmc-release]
AID - 10.3389/fmed.2021.745601 [doi]
PST - epublish
SO  - Front Med (Lausanne). 2021 Oct 5;8:745601. doi: 10.3389/fmed.2021.745601. 
      eCollection 2021.

PMID- 34655002
OWN - NLM
STAT- MEDLINE
DCOM- 20220228
LR  - 20220228
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 41
IP  - 3
DP  - 2022 Mar
TI  - Metabolic syndrome and its effect on the outcomes of rheumatoid arthritis in a 
      multi-ethnic cohort in Singapore.
PG  - 649-660
LID - 10.1007/s10067-021-05945-8 [doi]
AB  - INTRODUCTION: Over-expression of common inflammatory mediators in the metabolic 
      syndrome (MetS) and in rheumatoid arthritis (RA) may lead to mutually adverse 
      outcomes. AIM: We investigate the prevalence of MetS in a multi-ethnic population 
      of RA patients and its effect on clinical and patient-reported outcomes. METHOD: 
      Six hundred sixty RA (561 women) patients from a public-sector specialist clinic 
      in a hospital in Singapore were assessed for MetS according to the 2009 Joint 
      Consensus (JC) and the 2004 National Cholesterol Education Program Adult 
      Treatment Panel III (NCEP ATP III) definitions. Univariable and multivariable 
      regression modelling were used to investigate the associations between patients' 
      demographics with MetS and MetS with RA outcomes. RESULTS: The prevalence of MetS 
      in our RA cohort was 49.4% and 44.9% according to the JC and NCEP ATP III 
      definitions, respectively. The diagnosis of MetS was largely due to 
      hypertriglyceridemia, hypertension, and obesity. MetS was associated with older 
      age (OR 1.06 [95% CI 1.04-1.08]), Malay ethnicity (OR 1.78 [95% CI 1.02-3.09]), 
      or Indian ethnicity (OR 3.07 [95% CI 1.68-5.59]). No significant associations 
      between MetS and RA outcomes were observed. RA patients with MetS are more likely 
      to suffer from stroke and ischemic heart disease. CONCLUSION: The prevalence of 
      MetS in RA patients in Singapore was almost double that in the general 
      population. MetS does not adversely affect RA outcomes but raises the risks of 
      stroke and heart disease. RA patients, especially those older and of Indian and 
      Malay ethnicities, should be routinely screened for MetS. Any MetS-defining 
      condition should be actively controlled. Key Points • Approximately half of the 
      RA sample from the Singapore RA population can be diagnosed with MetS. • Older 
      patients, and patients of Malay and Indian ethnicities have higher odds of MetS. 
      • MetS does not adversely affect RA outcomes but raises the risks of stroke and 
      heart disease.
CI  - © 2021. International League of Associations for Rheumatology (ILAR).
FAU - Hee, Jia Yi
AU  - Hee JY
AUID- ORCID: 0000-0002-5863-4458
AD  - School of Public Health, The University of Queensland, 288 Herston Road, 
      Brisbane, Queensland, 4006, Australia. J.hee@uqconnect.edu.au.
FAU - Protani, Melinda M
AU  - Protani MM
AUID- ORCID: 0000-0001-6452-7571
AD  - School of Public Health, The University of Queensland, 288 Herston Road, 
      Brisbane, Queensland, 4006, Australia.
FAU - Koh, Ee Tzun
AU  - Koh ET
AUID- ORCID: 0000-0002-0329-4257
AD  - Department of Rheumatology, Allergy and Immunology, Tan Tock Seng Hospital, 11 
      Jalan Tan Tock Seng, Singapore, 308433, Singapore.
FAU - Leong, Khai Pang
AU  - Leong KP
AUID- ORCID: 0000-0003-4060-5525
AD  - Department of Rheumatology, Allergy and Immunology, Tan Tock Seng Hospital, 11 
      Jalan Tan Tock Seng, Singapore, 308433, Singapore.
CN  - Tan Tock Seng Hospital Rheumatoid Arthritis Study Group
LA  - eng
PT  - Journal Article
DEP - 20211015
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
SB  - IM
MH  - Adult
MH  - *Arthritis, Rheumatoid/complications/diagnosis/epidemiology
MH  - Cross-Sectional Studies
MH  - Ethnicity
MH  - Female
MH  - Humans
MH  - *Metabolic Syndrome/complications/epidemiology
MH  - Prevalence
MH  - Risk Factors
MH  - Singapore/epidemiology
OTO - NOTNLM
OT  - Disease outcomes
OT  - Metabolic syndrome
OT  - Multi-ethnic
OT  - Rheumatoid arthritis
OT  - Singapore
FIR - Ang, Andrea Ee Ling
IR  - Ang AEL
FIR - Chan, Grace Yin Lai
IR  - Chan GYL
FIR - Chan, Madelynn Tsu-Li
IR  - Chan MT
FIR - Chia, Faith Li-Ann
IR  - Chia FL
FIR - Chng, Hiok Hee
IR  - Chng HH
FIR - Chua, Choon Guan
IR  - Chua CG
FIR - Howe, Hwee Siew
IR  - Howe HS
FIR - Koh, Ee Tzun
IR  - Koh ET
FIR - Koh, Li Wearn
IR  - Koh LW
FIR - Kong, Kok Ooi
IR  - Kong KO
FIR - Law, Weng Giap
IR  - Law WG
FIR - Lee, Samuel Shang Ming
IR  - Lee SSM
FIR - Leong, Khai Pang
IR  - Leong KP
FIR - Lian, Tsui Yee
IR  - Lian TY
FIR - Lim, Xin Rong
IR  - Lim XR
FIR - Loh, Jess Mung Ee
IR  - Loh JME
FIR - Manghani, Mona
IR  - Manghani M
FIR - Tan, Justina Wei Lynn
IR  - Tan JWL
FIR - Tan, Sze-Chin
IR  - Tan SC
FIR - Teo, Claire Min-Li
IR  - Teo CM
FIR - Thong, Bernard Yu-Hor
IR  - Thong BY
FIR - Tjokrosaputro, Paula Permatasari
IR  - Tjokrosaputro PP
FIR - Xu, Chuanhui
IR  - Xu C
EDAT- 2021/10/17 06:00
MHDA- 2022/03/01 06:00
CRDT- 2021/10/16 06:03
PHST- 2021/08/25 00:00 [received]
PHST- 2021/09/25 00:00 [accepted]
PHST- 2021/09/22 00:00 [revised]
PHST- 2021/10/17 06:00 [pubmed]
PHST- 2022/03/01 06:00 [medline]
PHST- 2021/10/16 06:03 [entrez]
AID - 10.1007/s10067-021-05945-8 [pii]
AID - 10.1007/s10067-021-05945-8 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2022 Mar;41(3):649-660. doi: 10.1007/s10067-021-05945-8. Epub 
      2021 Oct 15.

PMID- 34593286
OWN - NLM
STAT- MEDLINE
DCOM- 20230109
LR  - 20230111
IS  - 1436-2023 (Electronic)
IS  - 0949-2658 (Linking)
VI  - 28
IP  - 1
DP  - 2023 Jan
TI  - Predictors of preoperative deep vein thrombosis in hip fractures: A systematic 
      review and meta-analysis.
PG  - 222-232
LID - S0949-2658(21)00285-2 [pii]
LID - 10.1016/j.jos.2021.08.013 [doi]
AB  - BACKGROUND: The predictors of preoperative deep vein thrombosis (DVT) in patients 
      with hip fractures remain unclear. Therefore, this study describes the results of 
      a systematic review and meta-analysis of relevant peer-reviewed literature on 
      this topic. METHODS: We searched PubMed, Google Scholar, Cochrane Library, Web of 
      Science, and MEDLINE for articles published in English on the predictors of 
      preoperative DVT in hip fractures. We calculated pooled odds ratios (OR) or mean 
      differences (MD) for the DVT groups as compared with the non-DVT groups for each 
      variable, including gender, age, body mass index, injury side, current smoking 
      status, time from injury to admission, time from injury to surgery, fracture 
      type, hypertension, arrhythmia, coronary artery disease, diabetes, stroke, kidney 
      disease, liver disease, lung disease, malignancy, rheumatoid arthritis, D-dimer, 
      fibrinogen, activated partial thromboplastin time, prothrombin time, thrombin 
      time, hemoglobin, albumin, total cholesterol, and triglycerides. RESULTS: We 
      included 9 studies involving 3,123 Asian patients with hip fractures (DVT, 
      n = 570; non-DVT, n = 2,553). Being female (OR = 1.27; 95% confidence interval 
      [CI] 1.04-1.56; p = 0.02), being of advanced age (MD = 1.63; 95% CI 0.80-2.47; 
      p = 0.0001), having a longer time from injury to admission (MD = 0.80; 95% CI 
      0.48-1.12; p < 0.00001), having a longer time from injury to surgery (MD = 2.20; 
      95% CI 1.53-2.88; p < 0.00001), and the presence of kidney disease (OR = 1.76; 
      95% CI 1.04-2.96; p = 0.03) were correlated with a high risk of DVT. However, we 
      found no significant differences between the two groups in the other predictors. 
      CONCLUSIONS: Evidence indicates that being female, being of advanced age, having 
      a longer time from injury to admission, having a longer time from injury to 
      surgery, and having kidney disease are significantly correlated with a high risk 
      of preoperative DVT in Asian patients with hip fracture. Further investigations 
      with patients of other ethnicities are required.
CI  - Copyright © 2021 The Japanese Orthopaedic Association. Published by Elsevier B.V. 
      All rights reserved.
FAU - Kobayashi, Takaomi
AU  - Kobayashi T
AD  - Department of Orthopaedic Surgery, Imari-Arita Kyoritsu Hospital, 860 Ninosekou 
      Arita-Town Nishimatsuura-Gun, Saga 849-4141, Japan; Department of Orthopaedic 
      Surgery, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga 849-8501, 
      Japan. Electronic address: takaomi_920@yahoo.co.jp.
FAU - Akiyama, Takayuki
AU  - Akiyama T
AD  - Department of Orthopaedic Surgery, Imari-Arita Kyoritsu Hospital, 860 Ninosekou 
      Arita-Town Nishimatsuura-Gun, Saga 849-4141, Japan; Department of Orthopaedic 
      Surgery, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga 849-8501, 
      Japan.
FAU - Mawatari, Masaaki
AU  - Mawatari M
AD  - Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, 5-1-1 
      Nabeshima, Saga 849-8501, Japan.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Systematic Review
DEP - 20210927
PL  - Japan
TA  - J Orthop Sci
JT  - Journal of orthopaedic science : official journal of the Japanese Orthopaedic 
      Association
JID - 9604934
SB  - IM
MH  - Humans
MH  - Female
MH  - Male
MH  - *Venous Thrombosis/etiology
MH  - *Hip Fractures/surgery
MH  - Hospitalization
MH  - Risk Factors
MH  - Retrospective Studies
COIS- Declaration of competing interest The authors declare that they have no conflict 
      of interest.
EDAT- 2021/10/02 06:00
MHDA- 2023/01/10 06:00
CRDT- 2021/10/01 05:53
PHST- 2021/07/27 00:00 [received]
PHST- 2021/08/25 00:00 [revised]
PHST- 2021/08/27 00:00 [accepted]
PHST- 2021/10/02 06:00 [pubmed]
PHST- 2023/01/10 06:00 [medline]
PHST- 2021/10/01 05:53 [entrez]
AID - S0949-2658(21)00285-2 [pii]
AID - 10.1016/j.jos.2021.08.013 [doi]
PST - ppublish
SO  - J Orthop Sci. 2023 Jan;28(1):222-232. doi: 10.1016/j.jos.2021.08.013. Epub 2021 
      Sep 27.

PMID- 34583328
OWN - NLM
STAT- MEDLINE
DCOM- 20220215
LR  - 20220215
IS  - 1476-1645 (Electronic)
IS  - 0002-9637 (Print)
IS  - 0002-9637 (Linking)
VI  - 105
IP  - 6
DP  - 2021 Sep 27
TI  - A Population-Based Cohort Study on Chronic Comorbidity Risk Factors for Adverse 
      Dengue Outcomes.
PG  - 1544-1551
LID - tpmd210716 [pii]
LID - 10.4269/ajtmh.21-0716 [doi]
AB  - The global burden of dengue is increasing against a background of rising global 
      prevalence of chronic noncommunicable diseases (NCDs) and an epidemiological 
      shift of dengue toward older age groups. The contribution of NCDs toward risk for 
      adverse clinical and healthcare utilization outcomes was assessed in a national 
      linked-database study. About 51,433 adult dengue cases between 2014 and 2015 were 
      assessed for outpatient and inpatient claims data in Taiwan's National Health 
      Insurance Research Database for the 30 days after their dengue diagnosis. A 
      multivariable logistic regression with generalized estimating equations was used 
      to estimate the probability of adverse dengue outcomes in patients with NCDs 
      compared with dengue patients without underlying diseases. Rheumatoid arthritis 
      and related disease were associated with the highest risk of hospitalization 
      after dengue diagnosis (odds ratio: 1.78; 95% CI: 1.37-2.30), followed by stroke, 
      chronic kidney disease (CKD), liver cirrhosis, asthma, coronary artery disease, 
      chronic obstructive pulmonary disease, diabetes, congestive heart failure, 
      hypertension, and malignancy. Chronic kidney disease and diabetes were associated 
      with higher risks of hospitalization, intensive care unit (ICU) use, and 
      all-cause mortality. After adjusting for socioeconomic status and other 
      variables, the number of coexisting chronic diseases was associated with 
      increasing risk of adverse dengue outcomes. Specific NCDs were associated with 
      longer hospitalizations, ICU admission, and higher healthcare costs. Quantifying 
      the risks of adverse dengue outcomes and health expenditures among dengue 
      patients with preexisting NCDs provides insights for improved clinical management 
      and essential inputs for health economic analyses on the cost-benefit of 
      risk-based routine or catch-up immunization programs.
FAU - Lien, Chia-En
AU  - Lien CE
AD  - Research Center for Epidemic Prevention, National Yang Ming Chiao Tung 
      University, Taipei, Taiwan.
FAU - Chou, Yiing-Jenq
AU  - Chou YJ
AD  - Institute of Public Health, School of Medicine, National Yang Ming Chiao Tung 
      University, Taipei, Taiwan.
AD  - Office of the Deputy Superintendent, National Yang Ming Chiao Tung University 
      Hospital, Yilan County, Taiwan.
FAU - Shen, Yi-Jung
AU  - Shen YJ
AD  - Institute of Hospital and Health Care Administration, National Yang Ming Chiao 
      Tung University, Taipei, Taiwan.
FAU - Tsai, Theodore
AU  - Tsai T
AD  - Takeda Vaccines, Cambridge, Massachusetts.
FAU - Huang, Nicole
AU  - Huang N
AD  - Institute of Hospital and Health Care Administration, National Yang Ming Chiao 
      Tung University, Taipei, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210927
PL  - United States
TA  - Am J Trop Med Hyg
JT  - The American journal of tropical medicine and hygiene
JID - 0370507
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/complications
MH  - Asthma/complications
MH  - Chronic Disease
MH  - Cohort Studies
MH  - Comorbidity
MH  - Dengue/*complications/*mortality
MH  - Female
MH  - Fibrosis/complications
MH  - Heart Failure/complications
MH  - Hematologic Diseases/complications
MH  - Hospitalization/economics
MH  - Humans
MH  - Intensive Care Units/economics
MH  - Length of Stay/economics
MH  - Male
MH  - Middle Aged
MH  - Neoplasms/complications
MH  - Pulmonary Disease, Chronic Obstructive/complications
MH  - Renal Insufficiency, Chronic/complications
MH  - Risk Factors
MH  - Stroke/complications
PMC - PMC8641312
EDAT- 2021/09/29 06:00
MHDA- 2022/02/16 06:00
PMCR- 2021/09/27
CRDT- 2021/09/28 20:31
PHST- 2021/06/24 00:00 [received]
PHST- 2021/07/23 00:00 [accepted]
PHST- 2021/09/29 06:00 [pubmed]
PHST- 2022/02/16 06:00 [medline]
PHST- 2021/09/28 20:31 [entrez]
PHST- 2021/09/27 00:00 [pmc-release]
AID - tpmd210716 [pii]
AID - 10.4269/ajtmh.21-0716 [doi]
PST - epublish
SO  - Am J Trop Med Hyg. 2021 Sep 27;105(6):1544-1551. doi: 10.4269/ajtmh.21-0716.

PMID- 34504395
OWN - NLM
STAT- MEDLINE
DCOM- 20220222
LR  - 20220426
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 2021
DP  - 2021
TI  - The Biological Disease-Modifying Antirheumatic Drugs and the Risk of 
      Cardiovascular Events: A Systematic Review and Meta-Analysis.
PG  - 7712587
LID - 10.1155/2021/7712587 [doi]
LID - 7712587
AB  - OBJECTIVE: To assess the association between the use of biological 
      disease-modifying antirheumatic drugs (bDMARDs) and the risk of cardiovascular 
      events in patients with systemic inflammatory conditions. METHODS: Eligible 
      cohort studies or randomized controlled trials (RCTs) from inception to January 
      2021 were included. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) 
      for cardiovascular outcomes were calculated in the fixed- and random-effects 
      model accordingly. Associated factors with risks of cardiovascular events were 
      also studied in sensitivity analyses and metaregression analyses. RESULTS: 
      Compared with non-bDMARD users, the risks of myocardial infarction (MI) (OR = 
      0.74, 95% CI, 0.63 to 0.87), heart failure (OR = 0.84, 95% CI, 0.74 to 0.95), 
      cardiovascular (CV) death (OR = 0.62, 95% CI, 0.40 to 0.95), all-cause mortality 
      (OR = 0.64, 95% CI, 0.58 to 0.70), and 3P-MACE (composite endpoint of MI, stroke, 
      and CV death) (OR = 0.69, 95% CI, 0.53 to 0.89) were significantly reduced in 
      bDMARD users, which were mainly driven by the risk reduction in patients with 
      rheumatoid arthritis (RA). TNF-α inhibitors exhibited consistent benefits in 
      reducing the risks of MI, heart failure, CV death, all-cause mortality, and 
      3P-MACE. Moreover, the risks of heart failure, CV death, all-cause mortality, and 
      3P-MACE were significantly reduced in bDMARD users with follow-up over one year. 
      CONCLUSIONS: The use of bDMARDs might be associated with the reduced risks of CV 
      events, especially in patients with RA. The CV events might be less frequent in 
      bDMARD users with TNF-α inhibitors or follow-up over one year. More 
      investigations are needed to validate conclusions.
CI  - Copyright © 2021 Suiyuan Hu et al.
FAU - Hu, Suiyuan
AU  - Hu S
AD  - Department of Endocrinology and Metabolism, Peking University People's Hospital, 
      Beijing, China.
FAU - Lin, Chu
AU  - Lin C
AUID- ORCID: 0000-0002-2365-9831
AD  - Department of Endocrinology and Metabolism, Peking University People's Hospital, 
      Beijing, China.
FAU - Cai, Xiaoling
AU  - Cai X
AUID- ORCID: 0000-0002-7881-0543
AD  - Department of Endocrinology and Metabolism, Peking University People's Hospital, 
      Beijing, China.
FAU - Zhu, Xingyun
AU  - Zhu X
AD  - Department of Endocrinology and Metabolism, Peking University People's Hospital, 
      Beijing, China.
FAU - Lv, Fang
AU  - Lv F
AD  - Department of Endocrinology and Metabolism, Peking University People's Hospital, 
      Beijing, China.
FAU - Nie, Lin
AU  - Nie L
AD  - Department of Endocrinology and Metabolism, Beijing Airport Hospital, Beijing, 
      China.
FAU - Ji, Linong
AU  - Ji L
AUID- ORCID: 0000-0002-3262-2168
AD  - Department of Endocrinology and Metabolism, Peking University People's Hospital, 
      Beijing, China.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Systematic Review
DEP - 20210831
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Antirheumatic Agents/*pharmacology
MH  - Arthritis, Rheumatoid/complications/drug therapy
MH  - Cardiovascular Diseases/*prevention & control
MH  - Cardiovascular System
MH  - Heart Failure/prevention & control
MH  - Humans
MH  - Inflammation
MH  - Lupus Erythematosus, Systemic/complications/drug therapy
MH  - Myocardial Infarction/prevention & control
MH  - Odds Ratio
MH  - Psoriasis/complications/drug therapy
MH  - Randomized Controlled Trials as Topic
MH  - Research Design
MH  - Risk
MH  - Risk Factors
MH  - Stroke/prevention & control
MH  - Treatment Outcome
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
PMC - PMC8423578
COIS- LJ has received fees for lecture presentations and for consulting from 
      AstraZeneca, Merck, Metabasis, MSD, Novartis, Eli Lilly, Roche, Sanofi-Aventis, 
      and Takeda. There is no other support from any organization for the submitted 
      work other than that described above.
EDAT- 2021/09/11 06:00
MHDA- 2022/02/23 06:00
PMCR- 2021/08/31
CRDT- 2021/09/10 06:58
PHST- 2021/07/06 00:00 [received]
PHST- 2021/08/18 00:00 [accepted]
PHST- 2021/09/10 06:58 [entrez]
PHST- 2021/09/11 06:00 [pubmed]
PHST- 2022/02/23 06:00 [medline]
PHST- 2021/08/31 00:00 [pmc-release]
AID - 10.1155/2021/7712587 [doi]
PST - epublish
SO  - Mediators Inflamm. 2021 Aug 31;2021:7712587. doi: 10.1155/2021/7712587. 
      eCollection 2021.

PMID- 34450504
OWN - NLM
STAT- MEDLINE
DCOM- 20210929
LR  - 20221221
IS  - 1532-866X (Electronic)
IS  - 0049-0172 (Print)
IS  - 0049-0172 (Linking)
VI  - 51
IP  - 5
DP  - 2021 Oct
TI  - Outcomes of COVID-19 in patients with rheumatoid arthritis: A multicenter 
      research network study in the United States.
PG  - 1057-1066
LID - S0049-0172(21)00164-5 [pii]
LID - 10.1016/j.semarthrit.2021.08.010 [doi]
AB  - OBJECTIVES: To investigate outcomes of Coronavirus Disease-2019 (COVID-19) in 
      patients with rheumatoid arthritis (RA) as compared to the general population. 
      Additionally, outcomes were explored among RA patients stratified by sex, race, 
      and medications use through sub-cohort analyses. METHODS: This comparative cohort 
      study used a US multicenter research network (TriNetX) to extract data on all 
      adult RA patients who were diagnosed with COVID-19, and adults without RA who 
      were diagnosed with COVID-19 (comparative cohort) anytime from January 20, 2020 
      to April 11, 2021. COVID-19 outcomes were assessed within 30 days after its 
      diagnosis. Baseline characteristics that included demographics and comorbidities 
      were controlled in propensity score matching. RESULTS: A total of 9730 RA 
      patients with COVID-19 and 656,979 non-RA with COVID-19 were identified. Before 
      matching, the risk of all outcomes including mortality (RR: 2.11, 95%CI: 1.90 to 
      2.34), hospitalization (RR: 1.60, 1.55 to 1.66), intensive care unit-ICU 
      admission (RR: 1.86, 1.71 to 2.05), mechanical ventilation (RR: 1.62, 1.44 to 
      1.82), severe COVID-19 (RR: 1.89, 1.74 to 2.06), acute kidney injury (RR: 2.13, 
      1.99 to 2.29), kidney replacement therapy/hemodialysis (RR: 1.40, 1.03 to 1.89), 
      acute respiratory distress syndrome-ARDS (RR: 1.76, 1.53 to 2.02), ischemic 
      stroke (RR: 2.62, 2.24 to 3.07), venous thromboembolism-VTE (RR: 2.30, 2.07 to 
      2.56), and sepsis (RR: 1.97, 1.81 to 2.13) was higher in RA compared to non-RA. 
      After matching, the risks did not differ in both cohorts except for VTE (RR: 
      1.18, 1.01 to 1.38) and sepsis (RR: 1.27, 1.12 to 1.43), which were higher in the 
      RA cohort. Male sex, black race, and glucocorticoid use increased the risk of 
      adverse outcomes. The risk of hospitalization was higher in rituximab or 
      interleukin 6 inhibitors (IL-6i) users compared to tumor necrosis factor 
      inhibitors (TNFi) users, with no significant difference between Janus kinase 
      inhibitors (JAKi) or abatacept users and TNFi users. CONCLUSION: This large 
      cohort study of RA-COVID-19 found that the risk of all outcomes was higher in the 
      RA compared to the non-RA cohort before matching, with no difference in the 
      majority of outcomes after matching, implying the risk being attributed to 
      adjusted factors. However, the risk of VTE and sepsis was higher in RA cohort 
      even after matching, indicating RA as an independent risk factor. Male sex, black 
      race, and glucocorticoid use were associated with adverse outcomes in RA with 
      COVID-19. Rituximab or IL-6i users were associated with an increased risk of 
      hospitalization compared to TNFi users.
CI  - Copyright © 2021 Elsevier Inc. All rights reserved.
FAU - Raiker, Rahul
AU  - Raiker R
AD  - West Virginia University School of Medicine, Morgantown, WV, USA.
FAU - DeYoung, Charles
AU  - DeYoung C
AD  - Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA, 
      USA.
FAU - Pakhchanian, Haig
AU  - Pakhchanian H
AD  - George Washington University School of Medicine and Health Sciences, Washington, 
      D.C., USA.
FAU - Ahmed, Sakir
AU  - Ahmed S
AD  - Department of Clinical Immunology and Rheumatology, Kalinga Institute of Medical 
      Sciences (KIMS), KIIT University, Bhubaneswar, India.
FAU - Kavadichanda, Chengappa
AU  - Kavadichanda C
AD  - Department of Clinical Immunology, Jawaharlal Institute of Postgraduate Medical 
      Education and Research (JIPMER), Puducherry, India.
FAU - Gupta, Latika
AU  - Gupta L
AD  - Department of Clinical Immunology and Rheumatology, Sanjay Gandhi Postgraduate 
      Institute of Medical Sciences (SGPGI), Lucknow, Uttar Pradesh, India.
FAU - Kardeş, Sinan
AU  - Kardeş S
AD  - Department of Medical Ecology and Hydroclimatology, Istanbul Faculty of Medicine, 
      Istanbul University, Istanbul, Turkey. Electronic address: 
      sinan.kardes@istanbul.edu.tr.
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
DEP - 20210820
PL  - United States
TA  - Semin Arthritis Rheum
JT  - Seminars in arthritis and rheumatism
JID - 1306053
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor Inhibitors)
SB  - IM
MH  - Adult
MH  - *Antirheumatic Agents/therapeutic use
MH  - *Arthritis, Rheumatoid/complications/drug therapy
MH  - *COVID-19
MH  - Cohort Studies
MH  - Humans
MH  - Male
MH  - SARS-CoV-2
MH  - Tumor Necrosis Factor Inhibitors
MH  - United States/epidemiology
PMC - PMC8376523
OTO - NOTNLM
OT  - COVID-19
OT  - Epidemiology
OT  - Rheumatoid arthritis
OT  - Risk
OT  - SARS-CoV-2
COIS- Declaration of Competing Interest SA has received honorarium as speaker for 
      Pfizer (unrelated to the current study), and has no other potential conflicts of 
      interest. SK has received congress travel, accommodation, and participation fee 
      support (12th Anatolian Rheumatology Days) from Abbvie. All other authors declare 
      no competing interests.
EDAT- 2021/08/28 06:00
MHDA- 2021/09/30 06:00
PMCR- 2021/08/20
CRDT- 2021/08/27 20:25
PHST- 2021/06/04 00:00 [received]
PHST- 2021/07/31 00:00 [revised]
PHST- 2021/08/17 00:00 [accepted]
PHST- 2021/08/28 06:00 [pubmed]
PHST- 2021/09/30 06:00 [medline]
PHST- 2021/08/27 20:25 [entrez]
PHST- 2021/08/20 00:00 [pmc-release]
AID - S0049-0172(21)00164-5 [pii]
AID - 10.1016/j.semarthrit.2021.08.010 [doi]
PST - ppublish
SO  - Semin Arthritis Rheum. 2021 Oct;51(5):1057-1066. doi: 
      10.1016/j.semarthrit.2021.08.010. Epub 2021 Aug 20.

PMID- 34373923
OWN - NLM
STAT- MEDLINE
DCOM- 20220509
LR  - 20220525
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 61
IP  - 5
DP  - 2022 May 5
TI  - The impact of statins on coronary atherosclerosis progression and long-term 
      cardiovascular disease risk in rheumatoid arthritis.
PG  - 1857-1866
LID - 10.1093/rheumatology/keab642 [doi]
AB  - OBJECTIVES: To evaluate whether statins lower cardiovascular disease (CVD) risk 
      in RA and if tentative benefits are related to changes in coronary plaque burden 
      or composition. METHODS: In an observational cohort study, 150 patients without 
      CVD underwent coronary atherosclerosis evaluation (total, noncalcified, partially 
      and fully calcified plaque) with CT angiography. Prespecified cardiovascular 
      events including cardiac death, myocardial infarction, unstable angina, 
      revascularization, stroke, claudication and heart failure were prospectively 
      recorded. Change in plaque burden and composition was re-assessed in 102 patients 
      within 6.9 (0.3) years. RESULTS: Time-varying statin therapy, modeled using 
      inverse probability treatment and censoring weights, did not significantly 
      attenuate CVD risk in RA overall [adjusted odds ratio (OR) = 0.39 (95% CI: 0.15, 
      1.07), P =0.067]. However, statins associated with lower CVD risk in patients 
      with baseline CRP > 0.5 mg/dl [adjusted OR = 0.09 (95%CI: 0.03, 0.30), P <0.001] 
      but not in those with CRP < 0.5 mg/dl (P-interaction = 0.023), after controlling 
      for Framingham-CVD score and time-varying bDMARD use. In patients treated with 
      statin >50% of follow-up time, CRP did not associate with new plaque formation 
      [adjusted OR = 0.42 (95% CI: 0.09, 1.94)], in contrast to statin-naïve [adjusted 
      OR = 1.89 (95% CI:1.41, 2.54)] and statin-treated <50% time [adjusted-OR = 1.41 
      (95% CI: 1.03, 1.95), P-interaction = 0.029]. Statin therapy >50% follow-up time 
      predicted dissipation [adjusted-OR = 5.84 (95% CI: 1.29, 26.55)] and 
      calcification of prevalent noncalcified lesions [adjusted-OR = 4.16 (95% CI: 
      1.11, 15.54)], as well as new calcified plaque formation in segments without 
      baseline plaque [adjusted-OR = 2.84 (95% CI:1.09, 7.41)]. CONCLUSION: Statin 
      therapy associated with lower long-term cardiovascular risk in RA patients with 
      higher inflammation. Moreover, statin therapy modified the impact of inflammation 
      on new coronary plaque formation and predicted both regression and calcification 
      of prevalent noncalcified lesions.
CI  - © The Author(s) 2021. Published by Oxford University Press on behalf of the 
      British Society for Rheumatology. All rights reserved. For permissions, please 
      email: journals.permissions@oup.com.
FAU - Karpouzas, George A
AU  - Karpouzas GA
AUID- ORCID: 0000-0003-1065-1563
AD  - Division of Rheumatology.
FAU - Ormseth, Sarah R
AU  - Ormseth SR
AD  - Division of Rheumatology.
FAU - Hernandez, Elizabeth
AU  - Hernandez E
AD  - Division of Rheumatology.
FAU - Budoff, Matthew J
AU  - Budoff MJ
AD  - Division of Cardiology, Harbor-UCLA Medical Center and Lundquist Institute for 
      Biomedical Innovation, Torrance, CA, USA.
LA  - eng
PT  - Journal Article
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
SB  - IM
MH  - *Arthritis, Rheumatoid/chemically induced/complications/drug therapy
MH  - *Calcinosis/complications
MH  - *Cardiovascular Diseases/chemically induced/prevention & control
MH  - Coronary Angiography
MH  - *Coronary Artery Disease/etiology
MH  - Disease Progression
MH  - Humans
MH  - *Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use
MH  - Inflammation/complications
MH  - *Plaque, Atherosclerotic/complications/diagnostic imaging
MH  - Risk Factors
OTO - NOTNLM
OT  - atherosclerosis progression
OT  - cardiovascular disease
OT  - computed tomography
OT  - rheumatoid arthritis
OT  - statins
EDAT- 2021/08/11 06:00
MHDA- 2022/05/10 06:00
CRDT- 2021/08/10 06:43
PHST- 2021/05/05 00:00 [received]
PHST- 2021/08/04 00:00 [revised]
PHST- 2021/08/11 06:00 [pubmed]
PHST- 2022/05/10 06:00 [medline]
PHST- 2021/08/10 06:43 [entrez]
AID - 6346999 [pii]
AID - 10.1093/rheumatology/keab642 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2022 May 5;61(5):1857-1866. doi: 
      10.1093/rheumatology/keab642.

PMID- 34311770
OWN - NLM
STAT- MEDLINE
DCOM- 20210813
LR  - 20210813
IS  - 1478-6362 (Electronic)
IS  - 1478-6354 (Print)
IS  - 1478-6354 (Linking)
VI  - 23
IP  - 1
DP  - 2021 Jul 27
TI  - Higher levels of anti-phosphorylcholine autoantibodies in early rheumatoid 
      arthritis indicate lower risk of incident cardiovascular events.
PG  - 201
LID - 10.1186/s13075-021-02581-0 [doi]
LID - 201
AB  - BACKGROUND: The increased risk of cardiovascular events (CVE) in rheumatoid 
      arthritis (RA) is not fully explained by traditional risk factors. 
      Immuno-inflammatory mechanisms and autoantibodies could be involved in the 
      pathogenesis of atherosclerotic disease. It has been suggested that 
      anti-phosphorylcholine antibodies (anti-PC) of the IgM subclass may have 
      atheroprotective effects. Here, we aimed to investigate the association between 
      levels of IgM anti-PC antibodies with CVE in patients with early RA. METHODS: The 
      study population was derived from the BARFOT early RA cohort, recruited in 
      1994-1999. The outcome of incident CVE (AMI, angina pectoris, coronary 
      intervention, ischemic stroke, TIA) was tracked through the Swedish Hospital 
      Discharge and the National Cause of Death Registries. Sera collected at inclusion 
      and the 2-year visit were analyzed with ELISA to determine levels of anti-PC IgM. 
      The Kaplan-Meier estimates and Cox proportional hazards regression models were 
      used to compare CV outcome in the groups categorized by baseline median level of 
      IgM anti-PC. RESULTS: In all, 653 patients with early RA, 68% women, mean (SD) 
      age 54.8 (14.7) years, DAS28 5.2 (1.3), 68% seropositive, and without prevalent 
      CVD, were included. During the follow-up of mean 11.7 years, 141 incident CVE 
      were recorded. Baseline IgM anti-PC above median was associated with a reduction 
      in risk of incident CVE in patients aged below 55 years at inclusion, HR 0.360 
      (95% CI, 0.142-0.916); in males, HR 0.558 (0.325-0.958); in patients with BMI 
      above 30 kg/m(2), HR 0.235 (0.065-0.842); and in those who did not achieve DAS28 
      remission at 1 year, HR 0.592 (0.379-0.924). The pattern of associations was 
      confirmed in the models with AUC IgM anti-PC over 2 years. CONCLUSION: Protective 
      effects of higher levels of innate IgM anti-PC autoantibodies on CVE were 
      detected in younger patients with RA and those at high risk of CVE: males, 
      presence of obesity, and non-remission at 1 year.
CI  - © 2021. The Author(s).
FAU - Ajeganova, Sofia
AU  - Ajeganova S
AUID- ORCID: 0000-0001-9162-9717
AD  - Division of Gastroenterology and Rheumatology, Department of Medicine Huddinge, 
      Karolinska Institutet, 171 77, Stockholm, Sweden. sofia.ajeganova@ki.se.
AD  - Department of Clinical Sciences, Rheumatology Division, Universitair Ziekenhuis 
      Brussel, Vrije Universiteit Brussel, Brussels, Belgium. sofia.ajeganova@ki.se.
FAU - Andersson, Maria L E
AU  - Andersson MLE
AD  - Faculty of Medicine, Department of Rheumatology, Lund University, Lund and 
      Spenshult Research and Development Centre, Halmstad, Sweden.
FAU - Frostegård, Johan
AU  - Frostegård J
AD  - Section of Immunology and Chronic disease, Institute of Environmental Medicine, 
      Karolinska Institutet, Stockholm, Sweden.
FAU - Hafström, Ingiäld
AU  - Hafström I
AD  - Division of Gastroenterology and Rheumatology, Department of Medicine Huddinge, 
      Karolinska Institutet, 171 77, Stockholm, Sweden.
AD  - Rheumatology Unit, Karolinska University Hospital, Stockholm, Sweden.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210727
PL  - England
TA  - Arthritis Res Ther
JT  - Arthritis research & therapy
JID - 101154438
RN  - 0 (Autoantibodies)
RN  - 0 (Immunoglobulin M)
RN  - 107-73-3 (Phosphorylcholine)
SB  - IM
MH  - Aged
MH  - *Arthritis, Rheumatoid/diagnosis/epidemiology
MH  - *Atherosclerosis
MH  - Autoantibodies
MH  - *Cardiovascular Diseases/diagnosis/epidemiology
MH  - Female
MH  - Humans
MH  - Immunoglobulin M
MH  - Male
MH  - Middle Aged
MH  - Phosphorylcholine
MH  - Risk Factors
PMC - PMC8314464
OTO - NOTNLM
OT  - Cardiovascular events
OT  - Innate immunity
OT  - Phosphorylcholine autoantibodies
OT  - Rheumatoid arthritis
COIS- J.F. is named as an inventor on patents of anti-PC.
EDAT- 2021/07/28 06:00
MHDA- 2021/08/14 06:00
PMCR- 2021/07/27
CRDT- 2021/07/27 05:45
PHST- 2021/05/04 00:00 [received]
PHST- 2021/07/15 00:00 [accepted]
PHST- 2021/07/27 05:45 [entrez]
PHST- 2021/07/28 06:00 [pubmed]
PHST- 2021/08/14 06:00 [medline]
PHST- 2021/07/27 00:00 [pmc-release]
AID - 10.1186/s13075-021-02581-0 [pii]
AID - 2581 [pii]
AID - 10.1186/s13075-021-02581-0 [doi]
PST - epublish
SO  - Arthritis Res Ther. 2021 Jul 27;23(1):201. doi: 10.1186/s13075-021-02581-0.

PMID- 34238587
OWN - NLM
STAT- MEDLINE
DCOM- 20211124
LR  - 20220531
IS  - 1879-114X (Electronic)
IS  - 0149-2918 (Linking)
VI  - 43
IP  - 8
DP  - 2021 Aug
TI  - Risk of Thromboembolic Events and Associated Risk Factors, Including Treatments, 
      in Patients with Immune-mediated Diseases.
PG  - 1392-1407.e1
LID - S0149-2918(21)00239-3 [pii]
LID - 10.1016/j.clinthera.2021.06.008 [doi]
AB  - PURPOSE: This study assessed the association between thromboembolic events (TEs) 
      and immune-mediated diseases (IMDs) and characterized the risk profile of TEs 
      among patients with IMDs. METHODS: An administrative claims database (2014-2018) 
      was used to identify adults with ≥2 diagnoses on different dates for ≥1 IMD (IMD 
      cohort; ankylosing spondylitis, atopic dermatitis, inflammatory bowel disease, 
      multiple sclerosis, psoriasis, psoriatic arthritis, rheumatoid arthritis, and 
      systemic lupus erythematosus); patients without an IMD diagnosis were assigned to 
      the non-IMD cohort. Patients in the IMD cohort were matched 1:1 to patients in 
      the non-IMD cohort on age, sex, and index date. Incremental risk of TE (ie, deep 
      vein thrombosis [DVT], pulmonary embolism [PE], myocardial infarction [MI], and 
      ischemic stroke [IS]) was assessed using adjusted incidence rate ratios (aIRRs) 
      to control for covariates in both cohorts. Risk factors for TEs were assessed in 
      the IMD cohort and included age, female sex, comorbidities, baseline TEs, non-IMD 
      treatments, and IMD treatments. FINDINGS: A total of 182,431 patients were 
      included in each cohort (mean age, [51.3] years; 64.3% female). A higher 
      proportion of patients in the IMD cohort versus the non-IMD cohort had ≥1 
      baseline TE (4.1% vs 2.7%; P < 0.0001). The IMD cohort had a 1.80 (95% CI, 
      1.68-1.92; P < 0.0001) times higher rate of TEs versus patients in the non-IMD 
      cohort. After adjustments, patients in the IMD cohort had a 1.49 (95% CI, 
      1.40-1.59; P < 0.0001) times higher rate of TEs versus patients in the non-IMD 
      cohort. Similar results were observed across individual TEs (DVT: aIRR = 1.78; 
      PE: aIRR = 1.66; MI: aIRR = 1.17; IS: aIRR = 1.35; all P < 0.05). Risk factor 
      profiles varied by TE. The greatest risk factor was respective TE during baseline 
      (eg, patients with baseline DVT had 41.1 times the rate of DVT during the study 
      period vs patients without baseline DVT; P < 0.001). Comorbidities, such as 
      cardiovascular diseases, type 2 diabetes, and peripheral vascular disease, were 
      associated with increased rates of MI (IRR = 2.60, 1.30, and 1.54, respectively; 
      all P < 0.05) and IS (IRR = 1.53, 1.54, and 1.24, respectively; all P < 0.05). 
      Janus kinase inhibitors were associated with an increased rate of PE (IRR = 2.52; 
      P < 0.05) and nonsignificant, numerically higher rates of DVT (IRR = 1.23; 
      P = NS) and IS (IRR = 1.82; P = NS). Sphingosine 1-phosphate receptor modulators 
      were associated with decreased rates of TEs (DVT: IRR = 0.61, P = NS; PE: 
      IRR = 0.30, P = NS; MI: IRR = 0.54, P = NS; IS: IRR = 0.33, P < 0.05). 
      IMPLICATIONS: The risk of TEs was higher among patients with IMD versus patients 
      without IMD; several factors may affect this risk.
CI  - Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
FAU - Setyawan, Juliana
AU  - Setyawan J
AD  - Arena Pharmaceuticals, San Diego, California.
FAU - Mu, Fan
AU  - Mu F
AD  - Analysis Group Inc, Boston, Massachusetts. Electronic address: 
      Fan.Mu@analysisgroup.com.
FAU - Yarur, Andres
AU  - Yarur A
AD  - Division of Gastroenterology and Hepatology, Medical College of Wisconsin, 
      Milwaukee, Wisconsin.
FAU - Zichlin, Miriam L
AU  - Zichlin ML
AD  - Analysis Group Inc, Boston, Massachusetts.
FAU - Yang, Hongbo
AU  - Yang H
AD  - Analysis Group Inc, Boston, Massachusetts.
FAU - Fernan, Catherine
AU  - Fernan C
AD  - Analysis Group Inc, Boston, Massachusetts.
FAU - Billmyer, Emma
AU  - Billmyer E
AD  - Analysis Group Inc, Boston, Massachusetts.
FAU - Downes, Nathaniel
AU  - Downes N
AD  - Analysis Group Inc, Boston, Massachusetts.
FAU - Azimi, Nassir
AU  - Azimi N
AD  - Sharp Grossmont Hospital, La Mesa, California.
FAU - Strand, Vibeke
AU  - Strand V
AD  - Division of Immunology and Rheumatology, Stanford University School of Medicine, 
      Palo Alto, California.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210706
PL  - United States
TA  - Clin Ther
JT  - Clinical therapeutics
JID - 7706726
SB  - IM
MH  - Adult
MH  - Female
MH  - Humans
MH  - Immune System Diseases/*epidemiology
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - *Pulmonary Embolism/epidemiology
MH  - Risk Factors
MH  - *Thromboembolism/epidemiology
MH  - *Venous Thrombosis/epidemiology
OTO - NOTNLM
OT  - Janus kinase inhibitors
OT  - arterial thromboembolic events
OT  - immune-mediated diseases
OT  - risk profile
OT  - thromboembolic events
OT  - venous thromboembolic events
EDAT- 2021/07/10 06:00
MHDA- 2021/11/25 06:00
CRDT- 2021/07/09 05:53
PHST- 2021/03/19 00:00 [received]
PHST- 2021/06/07 00:00 [revised]
PHST- 2021/06/13 00:00 [accepted]
PHST- 2021/07/10 06:00 [pubmed]
PHST- 2021/11/25 06:00 [medline]
PHST- 2021/07/09 05:53 [entrez]
AID - S0149-2918(21)00239-3 [pii]
AID - 10.1016/j.clinthera.2021.06.008 [doi]
PST - ppublish
SO  - Clin Ther. 2021 Aug;43(8):1392-1407.e1. doi: 10.1016/j.clinthera.2021.06.008. 
      Epub 2021 Jul 6.

PMID- 34215644
OWN - NLM
STAT- MEDLINE
DCOM- 20211206
LR  - 20220504
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 80
IP  - 12
DP  - 2021 Dec
TI  - Short-term dose and duration-dependent glucocorticoid risk for cardiovascular 
      events in glucocorticoid-naive patients with rheumatoid arthritis.
PG  - 1522-1529
LID - 10.1136/annrheumdis-2021-220577 [doi]
AB  - OBJECTIVES: Rheumatoid arthritis (RA), along with glucocorticoid use, is 
      associated with cardiovascular disease. Cardiovascular safety of glucocorticoids 
      in RA is controversial and may be related to dose and duration of use. We 
      determined if initiating glucocorticoids in steroid-naive RA patients would 
      increase cardiovascular event (CVE) risk in a dose and duration-dependent manner 
      over short-term intervals. METHODS: Patients enrolled in CorEvitas (formerly 
      Corrona) RA registry. Cox proportional-hazards models estimated adjusted HRs 
      (aHR) for incident CVE in patients who initiated glucocorticoid treatment, 
      adjusting for RA duration, traditional cardiovascular risk factors and 
      time-varying covariates: Clinical Disease activity Index, disease-modifying 
      antirheumatic drugs use and prednisone-equivalent use. Glucocorticoid use 
      assessed current daily dose, cumulative dose and duration of use over rolling 
      intervals of preceding 6 months and 1 year. RESULTS: 19 902 patients met 
      criteria. 1106 CVE occurred (1.66/100 person-years). Increased aHR occurred at 
      current doses of ≥5-9 mg 1.56 (1.18-2.06) and ≥10 mg 1.91 (1.31-2.79), without 
      increased risk at 0-4 mg 1.04 (0.55-1.59). Cumulative dose over preceding 
      6 months showed increased aHR at 751-1100 mg 1.43 (1.04-1.98) and >1100 mg 2.05 
      (1.42-2.94), without increased risk at lower doses; duration of use over 
      preceding 6 months exhibited increased aHR for >81 days of use 1.54 (1.08-2.32), 
      without increased risk at shorter durations. One-year analyses were consistent. 
      CONCLUSIONS: Over preceding 6-month and 1-year intervals, initiating 
      glucocorticoids in steroid-naïve RA patients is associated with increased risk of 
      CVE at daily doses ≥5 mg and increased cumulative dose and duration of use. No 
      association with risk for CVE was found with daily prednisone of ≤4 mg or shorter 
      cumulative doses and durations.
CI  - © Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and 
      permissions. Published by BMJ.
FAU - Ocon, Anthony James
AU  - Ocon AJ
AUID- ORCID: 0000-0003-2903-5429
AD  - Medicine and Allergy, Immunology, Rheumatology, University of Rochester Medical 
      Center, Rochester, New York, USA anthony.ocon@gmail.com.
FAU - Reed, George
AU  - Reed G
AD  - Medicine, Preventative and Behavioral Medicine, University of Massachusetts 
      Medical School, Worcester, Massachusetts, USA.
AD  - Corrona Research Foundation, LLC, Waltham, MA, USA.
FAU - Pappas, Dimitrios A
AU  - Pappas DA
AUID- ORCID: 0000-0001-8338-027X
AD  - Corrona Research Foundation, LLC, Waltham, MA, USA.
AD  - Medicine and Rheumatology, Columbia University, New York, New York, USA.
AD  - CorEvitas (formerly CORRONA), LCC, Waltham, Massachusetts, USA.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AUID- ORCID: 0000-0002-8907-8976
AD  - Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, 
      USA.
FAU - Kremer, Joel M
AU  - Kremer JM
AD  - Corrona Research Foundation, LLC, Waltham, MA, USA.
AD  - CorEvitas (formerly CORRONA), LCC, Waltham, Massachusetts, USA.
AD  - Medicine and Rheumatology, Albany Medical College, The Center for Rheumatology, 
      LLC, Albany, New York, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210702
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Glucocorticoids)
RN  - VB0R961HZT (Prednisone)
SB  - IM
CIN - Ocul Immunol Inflamm. 2022 Feb 17;30(2):479-480. doi: 
      10.1080/09273948.2022.2027467. PMID: 35050828
MH  - Acute Coronary Syndrome/epidemiology
MH  - Adult
MH  - Aged
MH  - Angina, Unstable/epidemiology
MH  - Antirheumatic Agents/therapeutic use
MH  - Arrhythmias, Cardiac/epidemiology
MH  - Arthritis, Rheumatoid/*drug therapy/physiopathology
MH  - Cardiovascular Diseases/*epidemiology/mortality
MH  - Dose-Response Relationship, Drug
MH  - *Duration of Therapy
MH  - Female
MH  - Glucocorticoids/*therapeutic use
MH  - Heart Disease Risk Factors
MH  - Heart Failure/epidemiology
MH  - Hospitalization/statistics & numerical data
MH  - Humans
MH  - Hypertension/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology
MH  - Myocardial Revascularization/statistics & numerical data
MH  - Peripheral Arterial Disease/epidemiology
MH  - Prednisone/*therapeutic use
MH  - Proportional Hazards Models
MH  - Pulmonary Embolism/epidemiology
MH  - Stroke/epidemiology
MH  - Thromboembolism/epidemiology
MH  - Venous Thrombosis/epidemiology
OTO - NOTNLM
OT  - Arthritis
OT  - Cardiovascular Diseases
OT  - Glucocorticoids
OT  - Rheumatoid
COIS- Competing interests: AJO has no financial conflicts of interest. GR and JMK are 
      consultants for Corrona, LLC. GR is a consultant for the Corrona Research 
      Foundation (CRF), while JMK is an officer of the CRF who serves without any form 
      of remuneration. The CRF is a not for profit, 501(C)(3) independent charitable 
      foundation, with no industry financial ties. DAP is an employee and shareholder 
      of Corrona, and a consultant for Regeneron, Novartis and Roche (unrelated work), 
      and is a member of the board of directors for CFR. JRC has research grants and/or 
      consulting from Abbvie, Amgen, Corrona, Janssen, Lilly, Pfizer, Sanofi (for 
      unrelated work).
EDAT- 2021/07/04 06:00
MHDA- 2021/12/15 06:00
CRDT- 2021/07/03 05:37
PHST- 2021/04/16 00:00 [received]
PHST- 2021/06/22 00:00 [accepted]
PHST- 2021/07/04 06:00 [pubmed]
PHST- 2021/12/15 06:00 [medline]
PHST- 2021/07/03 05:37 [entrez]
AID - annrheumdis-2021-220577 [pii]
AID - 10.1136/annrheumdis-2021-220577 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2021 Dec;80(12):1522-1529. doi: 10.1136/annrheumdis-2021-220577. 
      Epub 2021 Jul 2.

PMID- 34193517
OWN - NLM
STAT- MEDLINE
DCOM- 20210831
LR  - 20210831
IS  - 2056-5933 (Electronic)
IS  - 2056-5933 (Linking)
VI  - 7
IP  - 2
DP  - 2021 Jun
TI  - Risk factors for venous thromboembolism and atherosclerotic cardiovascular 
      disease: do they differ in patients with rheumatoid arthritis?
LID - 10.1136/rmdopen-2021-001618 [doi]
LID - e001618
AB  - OBJECTIVE: Venous thromboembolism (VTE) is an increasing concern in rheumatoid 
      arthritis (RA) with little known about risk factors. We aimed to compare risk 
      factors for unprovoked VTE and atherosclerotic cardiovascular disease (ASCVD) in 
      patients with RA and to assess subsequent ASCVD risk after an unprovoked VTE. 
      METHODS: People with RA participating in a US-wide longitudinal observational 
      registry from 1998 to 2018 were assessed for incident unprovoked VTE (deep venous 
      thrombosis and pulmonary emboli not associated with cancer, recent surgery, 
      hospitalisation, fracture and pregnancy) and ASCVD (myocardial infarction and 
      stroke) validated from hospital/death records. Risk factors for VTE and ASCVD and 
      the risk of ASCVD after an unprovoked VTE were determined using Cox proportional 
      hazards models. RESULTS: During median (IQR) 4 (1.5-7) years of follow-up in 31 
      366 patients with RA, 539 unprovoked VTE and 1648 ASCVD events were identified. 
      The adjusted models showed increased VTE and ASCVD risk with older age, male sex, 
      comorbidities, prior fracture, worse disability, higher disease activity and 
      glucocorticoids. Traditional cardiovascular disease risk factors were common in 
      both ASCVD and VTE but only increased ASCVD risk with obesity as the exception 
      (VTE HR (95% CI), 1.46 (1.13-1.87)) and ASCVD, 0.58 (0.50-0.68)). ASCVD risk 
      doubled after an unprovoked VTE (HR (95% CI), 2.05 (1.43-2.95)). CONCLUSION: Our 
      findings suggest that unprovoked VTE is mediated by inflammation of RA and may be 
      considered a spectrum of pan-cardiovascular syndrome.
CI  - © Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No 
      commercial re-use. See rights and permissions. Published by BMJ.
FAU - Ozen, Gulsen
AU  - Ozen G
AUID- ORCID: 0000-0002-5423-393X
AD  - Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA.
FAU - Pedro, Sofia
AU  - Pedro S
AD  - FORWARD, The National Databank for Rheumatic Diseases, Wichita, Kansas, USA.
FAU - Schumacher, Rebecca
AU  - Schumacher R
AD  - FORWARD, The National Databank for Rheumatic Diseases, Wichita, Kansas, USA.
FAU - Simon, Teresa
AU  - Simon T
AUID- ORCID: 0000-0003-4042-0715
AD  - Physicians Research Center, LLC, Toms River, New Jersey, USA.
FAU - Michaud, Kaleb
AU  - Michaud K
AUID- ORCID: 0000-0002-5350-3934
AD  - Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA 
      kmichaud@unmc.edu.
AD  - FORWARD, The National Databank for Rheumatic Diseases, Wichita, Kansas, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - RMD Open
JT  - RMD open
JID - 101662038
SB  - IM
MH  - Aged
MH  - *Arthritis, Rheumatoid/complications/epidemiology
MH  - *Cardiovascular Diseases/epidemiology
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Pregnancy
MH  - Risk Factors
MH  - *Venous Thromboembolism/epidemiology/etiology
PMC - PMC8246357
OTO - NOTNLM
OT  - arthritis
OT  - cardiovascular diseases
OT  - epidemiology
OT  - inflammation
OT  - rheumatoid
COIS- Competing interests: None declared.
EDAT- 2021/07/02 06:00
MHDA- 2021/09/01 06:00
PMCR- 2021/06/30
CRDT- 2021/07/01 06:13
PHST- 2021/02/04 00:00 [received]
PHST- 2021/06/14 00:00 [accepted]
PHST- 2021/07/01 06:13 [entrez]
PHST- 2021/07/02 06:00 [pubmed]
PHST- 2021/09/01 06:00 [medline]
PHST- 2021/06/30 00:00 [pmc-release]
AID - rmdopen-2021-001618 [pii]
AID - 10.1136/rmdopen-2021-001618 [doi]
PST - ppublish
SO  - RMD Open. 2021 Jun;7(2):e001618. doi: 10.1136/rmdopen-2021-001618.

PMID- 34154556
OWN - NLM
STAT- MEDLINE
DCOM- 20210628
LR  - 20210628
IS  - 1471-2318 (Electronic)
IS  - 1471-2318 (Linking)
VI  - 21
IP  - 1
DP  - 2021 Jun 21
TI  - Factors associated with long-term care certification in older adults: a 
      cross-sectional study based on a nationally representative survey in Japan.
PG  - 374
LID - 10.1186/s12877-021-02308-5 [doi]
LID - 374
AB  - BACKGROUND: Long-term care (LTC) prevention is a pressing concern in ageing 
      societies. To understand the risk factors of LTC, it is vital to consider 
      psychological and social factors in addition to physical factors. Owing to a lack 
      of relevant data, we aimed to investigate the social, physical and psychological 
      factors associated with LTC using large-scale, nationally representative data to 
      identify a high-risk population for LTC in terms of multidimensional frailty. 
      METHODS: We performed a cross-sectional study using anonymised data from the 2013 
      Comprehensive Survey of Living Conditions conducted by the Ministry of Health, 
      Labour and Welfare of Japan. Among the 23,730 eligible people aged 65 years or 
      older and those who were not in hospitals or care facilities during the survey, 
      1718 stated that they had LTC certification. Univariate and multivariate logistic 
      regression analyses were performed to determine the factors associated with LTC 
      certification. RESULTS: Factors positively associated with LTC certification in 
      the multivariate analyses included older age, the interaction term between sex 
      and age group at age 85-89 years, limb movement difficulties, swollen/heavy feet, 
      incontinence, severe psychological distress (indicated by a Kessler Psychological 
      Distress Scale [K6] score ≥ 13), regular hospital visits for dementia, stroke, 
      Parkinson's disease, chronic obstructive pulmonary disease, fracture, rheumatoid 
      arthritis, kidney disease, diabetes and osteoporosis. Factors negatively 
      associated with LTC certification included the presence of a spouse, regular 
      hospital visits for hypertension and consulting with friends or acquaintances 
      about worries and stress. CONCLUSIONS: In summary, we identified the physical, 
      psychological and social factors associated with LTC certification using 
      nationally representative data. Our findings highlight the importance of the 
      establishment of multidimensional approaches for LTC prevention in older adults.
FAU - Momose, Akira
AU  - Momose A
AD  - Department of Prevention of Diabetes and Lifestyle-Related Diseases, Graduate 
      School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 
      113-8655, Japan.
AD  - Asahi Mutual Life Insurance Company, Tokyo, Japan.
FAU - Yamaguchi, Satoko
AU  - Yamaguchi S
AD  - Department of Prevention of Diabetes and Lifestyle-Related Diseases, Graduate 
      School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 
      113-8655, Japan. syamaguc-tky@umin.ac.jp.
FAU - Okada, Akira
AU  - Okada A
AD  - Department of Prevention of Diabetes and Lifestyle-Related Diseases, Graduate 
      School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 
      113-8655, Japan.
FAU - Ikeda-Kurakawa, Kayo
AU  - Ikeda-Kurakawa K
AD  - Department of Prevention of Diabetes and Lifestyle-Related Diseases, Graduate 
      School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 
      113-8655, Japan.
AD  - Asahi Mutual Life Insurance Company, Tokyo, Japan.
FAU - Namiki, Daisuke
AU  - Namiki D
AD  - Department of Prevention of Diabetes and Lifestyle-Related Diseases, Graduate 
      School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 
      113-8655, Japan.
AD  - Asahi Mutual Life Insurance Company, Tokyo, Japan.
FAU - Nannya, Yasuhito
AU  - Nannya Y
AD  - Department of Pathology and Tumor Biology, Kyoto University, Kyoto, Japan.
FAU - Kato, Hideki
AU  - Kato H
AD  - Department of Prevention of Diabetes and Lifestyle-Related Diseases, Graduate 
      School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 
      113-8655, Japan.
AD  - Division of Nephrology and Endocrinology, Graduate School of Medicine, The 
      University of Tokyo, Tokyo, Japan.
FAU - Yamauchi, Toshimasa
AU  - Yamauchi T
AD  - Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, The 
      University of Tokyo, Tokyo, Japan.
FAU - Nangaku, Masaomi
AU  - Nangaku M
AD  - Division of Nephrology and Endocrinology, Graduate School of Medicine, The 
      University of Tokyo, Tokyo, Japan.
FAU - Kadowaki, Takashi
AU  - Kadowaki T
AD  - Department of Prevention of Diabetes and Lifestyle-Related Diseases, Graduate 
      School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 
      113-8655, Japan.
AD  - Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, The 
      University of Tokyo, Tokyo, Japan.
AD  - Toranomon Hospital, Tokyo, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210621
PL  - England
TA  - BMC Geriatr
JT  - BMC geriatrics
JID - 100968548
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - *Certification
MH  - Cross-Sectional Studies
MH  - Humans
MH  - Japan/epidemiology
MH  - *Long-Term Care
MH  - Surveys and Questionnaires
PMC - PMC8215807
OTO - NOTNLM
OT  - Frailty
OT  - Long-term care
OT  - Psychological distress
OT  - Social interaction
COIS- This study was conducted at the Department of Prevention of Diabetes and 
      Lifestyle-Related Diseases, which is engaged in a cooperative program between the 
      University of Tokyo and Asahi Mutual Life Insurance Company, which is the funding 
      organisation for the present study. AM, SY, AO, KIK, DN, HK and TK were members 
      of the department when the study was conducted. AM, KIK and DN are employees of 
      Asahi Mutual Life Insurance Company.
EDAT- 2021/06/23 06:00
MHDA- 2021/06/29 06:00
PMCR- 2021/06/21
CRDT- 2021/06/22 05:35
PHST- 2020/12/28 00:00 [received]
PHST- 2021/05/28 00:00 [accepted]
PHST- 2021/06/22 05:35 [entrez]
PHST- 2021/06/23 06:00 [pubmed]
PHST- 2021/06/29 06:00 [medline]
PHST- 2021/06/21 00:00 [pmc-release]
AID - 10.1186/s12877-021-02308-5 [pii]
AID - 2308 [pii]
AID - 10.1186/s12877-021-02308-5 [doi]
PST - epublish
SO  - BMC Geriatr. 2021 Jun 21;21(1):374. doi: 10.1186/s12877-021-02308-5.

PMID- 34081620
OWN - NLM
STAT- MEDLINE
DCOM- 20210721
LR  - 20210721
IS  - 1945-4589 (Electronic)
IS  - 1945-4589 (Linking)
VI  - 13
IP  - 11
DP  - 2021 Jun 3
TI  - Development and validation of a nomogram for predicting stroke risk in rheumatoid 
      arthritis patients.
PG  - 15061-15077
LID - 10.18632/aging.203071 [doi]
AB  - We developed and validated a nomogram to predict the risk of stroke in patients 
      with rheumatoid arthritis (RA) in northern China. Out of six machine learning 
      algorithms studied to improve diagnostic and prognostic accuracy of the 
      prediction model, the logistic regression algorithm showed high performance in 
      terms of calibration and decision curve analysis. The nomogram included 
      stratifications of sex, age, systolic blood pressure, C-reactive protein, 
      erythrocyte sedimentation rate, total cholesterol, and low-density lipoprotein 
      cholesterol along with the history of traditional risk factors such as 
      hypertensive, diabetes, atrial fibrillation, and coronary heart disease. The 
      nomogram exhibited a high Hosmer-Lemeshow goodness-for-fit and good calibration 
      (P > 0.05). The analysis, including the area under the receiver operating 
      characteristic curve, the net reclassification index, the integrated 
      discrimination improvement, and clinical use, showed that our prediction model 
      was more accurate than the Framingham risk model in predicting stroke risk in RA 
      patients. In conclusion, the nomogram can be used for individualized preoperative 
      prediction of stroke risk in RA patients.
FAU - Xin, Fangran
AU  - Xin F
AD  - Department of Clinical Epidemiology and Evidence-Based Medicine, The First 
      Affiliated Hospital, China Medical University, Shenyang, China.
FAU - Fu, Lingyu
AU  - Fu L
AD  - Department of Clinical Epidemiology and Evidence-Based Medicine, The First 
      Affiliated Hospital, China Medical University, Shenyang, China.
AD  - Department of Medical Record Management Center, The First Affiliated Hospital, 
      China Medical University, Shenyang, China.
FAU - Yang, Bowen
AU  - Yang B
AD  - Department of Medical Record Management Center, The First Affiliated Hospital, 
      China Medical University, Shenyang, China.
FAU - Liu, Haina
AU  - Liu H
AD  - Department of Rheumatology, The First Affiliated Hospital, China Medical 
      University, Shenyang, China.
FAU - Wei, Tingting
AU  - Wei T
AD  - Department of Clinical Epidemiology and Evidence-Based Medicine, The First 
      Affiliated Hospital, China Medical University, Shenyang, China.
FAU - Zou, Cunlu
AU  - Zou C
AD  - Neusoft Research of Intelligent Healthcare Technology, Co. Ltd., Shenyang, China.
FAU - Bai, Bingqing
AU  - Bai B
AD  - Department of Clinical Epidemiology and Evidence-Based Medicine, The First 
      Affiliated Hospital, China Medical University, Shenyang, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Validation Study
DEP - 20210603
PL  - United States
TA  - Aging (Albany NY)
JT  - Aging
JID - 101508617
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*complications
MH  - Calibration
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Models, Biological
MH  - *Nomograms
MH  - Reproducibility of Results
MH  - Risk Factors
MH  - Stroke/*epidemiology
MH  - Young Adult
PMC - PMC8221354
OTO - NOTNLM
OT  - development and validation nomogram
OT  - inflammatory markers
OT  - lipids
OT  - rheumatoid arthritis
OT  - stroke
COIS- CONFLICTS OF INTEREST: The authors declare no conflicts of interest related to 
      this study.
EDAT- 2021/06/04 06:00
MHDA- 2021/07/22 06:00
PMCR- 2021/06/15
CRDT- 2021/06/03 17:16
PHST- 2020/11/16 00:00 [received]
PHST- 2021/04/29 00:00 [accepted]
PHST- 2021/06/04 06:00 [pubmed]
PHST- 2021/07/22 06:00 [medline]
PHST- 2021/06/03 17:16 [entrez]
PHST- 2021/06/15 00:00 [pmc-release]
AID - 203071 [pii]
AID - 10.18632/aging.203071 [doi]
PST - ppublish
SO  - Aging (Albany NY). 2021 Jun 3;13(11):15061-15077. doi: 10.18632/aging.203071. 
      Epub 2021 Jun 3.

PMID- 34049859
OWN - NLM
STAT- MEDLINE
DCOM- 20211122
LR  - 20220503
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Print)
IS  - 0003-4967 (Linking)
VI  - 80
IP  - 11
DP  - 2021 Nov
TI  - Investigating changes in disease activity as a mediator of cardiovascular risk 
      reduction with methotrexate use in rheumatoid arthritis.
PG  - 1385-1392
LID - 10.1136/annrheumdis-2021-220125 [doi]
AB  - OBJECTIVE: Examine the association of methotrexate (MTX) use with cardiovascular 
      disease (CVD) in rheumatoid arthritis (RA) using marginal structural models (MSM) 
      and determine if CVD risk is mediated through modification of disease activity. 
      METHODS: We identified incident CVD events (coronary artery disease (CAD), 
      stroke, heart failure (HF) hospitalisation, CVD death) within a multicentre, 
      prospective cohort of US Veterans with RA. A 28-joint Disease Activity Score with 
      C-reactive protein (DAS28-CRP) was collected at regular visits and medication 
      exposures were determined by linking to pharmacy dispensing data. MSMs were used 
      to estimate the treatment effect of MTX on risk of incident CVD, accounting for 
      time-varying confounders between receiving MTX and CVD events. A mediation 
      analysis was performed to estimate the indirect effects of methotrexate on CVD 
      risk through modification of RA disease activity. RESULTS: Among 2044 RA patients 
      (90% male, mean age 63.9 years, baseline DAS28-CRP 3.6), there were 378 incident 
      CVD events. Using MSM, MTX use was associated with a 24% reduced risk of 
      composite CVD events (HR 0.76, 95% CI 0.58 to 0.99) including a 57% reduction in 
      HF hospitalisations (HR 0.43, 95% CI 0.24 to 0.77). Individual associations with 
      CAD, stroke and CVD death were not statistically significant. In mediation 
      analyses, there was no evidence of indirect effects of MTX on CVD risk through 
      disease activity modification (HR 1.03, 95% CI 0.80 to 1.32). CONCLUSIONS: MTX 
      use in RA was associated with a reduced risk of CVD events, particularly 
      HF-related hospitalisations. These associations were not mediated through 
      reductions in RA disease activity, suggesting alternative MTX-related mechanisms 
      may modify CVD risk in this population.
CI  - © Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and 
      permissions. Published by BMJ.
FAU - Johnson, Tate M
AU  - Johnson TM
AUID- ORCID: 0000-0003-0335-4157
AD  - Medicine & Research Service, VA Nebraska-Western Iowa Health Care System, Omaha, 
      Nebraska, USA.
AD  - Department of Internal Medicine, Division of Rheumatology, University of Nebraska 
      Medical Center, Omaha, Nebraska, USA.
FAU - Sayles, Harlan R
AU  - Sayles HR
AD  - Medicine & Research Service, VA Nebraska-Western Iowa Health Care System, Omaha, 
      Nebraska, USA.
AD  - Department of Biostatistics, University of Nebraska Medical Center, Omaha, 
      Nebraska, USA.
FAU - Baker, Joshua F
AU  - Baker JF
AD  - Department of Medicine, Division of Rheumatology, University of Pennsylvania 
      Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
AD  - Rheumatology, Corporal Michael J Crescenz VA Medical Center, Philadelphia, 
      Pennsylvania, USA.
FAU - George, Michael D
AU  - George MD
AD  - Department of Medicine, Division of Rheumatology, University of Pennsylvania 
      Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
AD  - Rheumatology, Corporal Michael J Crescenz VA Medical Center, Philadelphia, 
      Pennsylvania, USA.
FAU - Roul, Punyasha
AU  - Roul P
AD  - Medicine & Research Service, VA Nebraska-Western Iowa Health Care System, Omaha, 
      Nebraska, USA.
FAU - Zheng, Cheng
AU  - Zheng C
AD  - Department of Biostatistics, University of Nebraska Medical Center, Omaha, 
      Nebraska, USA.
FAU - Sauer, Brian
AU  - Sauer B
AD  - Rheumatology, VA Salt Lake City Health Care System, Salt Lake City, Utah, USA.
AD  - Department of Medicine, Division of Rheumatology, University of Utah Medical 
      Center, Salt Lake City, Utah, USA.
FAU - Liao, Katherine P
AU  - Liao KP
AD  - Rheumatology, VA Boston Healthcare System, West Roxbury, Massachusetts, USA.
FAU - Anderson, Daniel R
AU  - Anderson DR
AD  - Department of Internal Medicine, Division of Cardiology, University of Nebraska 
      Medical Center, Omaha, Nebraska, USA.
FAU - Mikuls, Ted R
AU  - Mikuls TR
AUID- ORCID: 0000-0002-0897-2272
AD  - Medicine & Research Service, VA Nebraska-Western Iowa Health Care System, Omaha, 
      Nebraska, USA.
AD  - Department of Internal Medicine, Division of Rheumatology, University of Nebraska 
      Medical Center, Omaha, Nebraska, USA.
FAU - England, Bryant R
AU  - England BR
AUID- ORCID: 0000-0002-9649-3588
AD  - Medicine & Research Service, VA Nebraska-Western Iowa Health Care System, Omaha, 
      Nebraska, USA bryant.england@unmc.edu.
AD  - Department of Internal Medicine, Division of Rheumatology, University of Nebraska 
      Medical Center, Omaha, Nebraska, USA.
LA  - eng
GR  - U54 GM115458/GM/NIGMS NIH HHS/United States
GR  - IK2 CX002203/CX/CSRD VA/United States
GR  - IK6 BX004600/BX/BLRD VA/United States
GR  - P50 AR060772/AR/NIAMS NIH HHS/United States
GR  - R25 AA020818/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20210528
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Antirheumatic Agents)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Aged
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy/epidemiology/physiopathology
MH  - Cardiovascular Diseases/mortality
MH  - Coronary Artery Disease/*epidemiology
MH  - Female
MH  - *Heart Disease Risk Factors
MH  - Heart Failure/*epidemiology
MH  - Hospitalization/*statistics & numerical data
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Methotrexate/*therapeutic use
MH  - Middle Aged
MH  - Proportional Hazards Models
MH  - Stroke/*epidemiology
PMC - PMC8516691
MID - NIHMS1720121
OTO - NOTNLM
OT  - cardiovascular disease
OT  - methotrexate
OT  - rheumatoid arthritis
COIS- Competing interests: MDG receives grant support from Bristol Myers Squibb for 
      unrelated work.
EDAT- 2021/05/30 06:00
MHDA- 2021/11/23 06:00
PMCR- 2022/05/01
CRDT- 2021/05/29 05:39
PHST- 2021/02/08 00:00 [received]
PHST- 2021/05/19 00:00 [accepted]
PHST- 2021/05/30 06:00 [pubmed]
PHST- 2021/11/23 06:00 [medline]
PHST- 2021/05/29 05:39 [entrez]
PHST- 2022/05/01 00:00 [pmc-release]
AID - annrheumdis-2021-220125 [pii]
AID - 10.1136/annrheumdis-2021-220125 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2021 Nov;80(11):1385-1392. doi: 10.1136/annrheumdis-2021-220125. 
      Epub 2021 May 28.

PMID- 34011089
OWN - NLM
STAT- MEDLINE
DCOM- 20210525
LR  - 20230103
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 100
IP  - 20
DP  - 2021 May 21
TI  - Clinical characteristics, triggering etiologies, and response of plasmapheresis 
      in thrombotic microangiopathy in Taiwan.
PG  - e25986
LID - 10.1097/MD.0000000000025986 [doi]
LID - e25986
AB  - Thrombotic microangiopathy (TMA) syndromes are extraordinarily diverse in 
      clinical presentations and etiologies. However, there are still a limited number 
      of large cohort studies focusing on the underlying causes, outcomes, and response 
      to plasmapheresis.A retrospective study was designed to understand trigger 
      etiologies, organ dysfunctions, clinical outcomes, and efficacy of plasmapheresis 
      in patients with TMA. The whole population of Taiwan was set up into 2 cohorts: 
      875 patients with TMA in the 2006 cohort (2006-2010) and 1352 patients with TMA 
      in the 2011 cohort (2011-2015). One hundred ninety-five patients in the 2006 
      cohort and 272 patients in the 2011 cohort were under plasmapheresis 
      treatment.The common underlying etiologies were pregnancy, followed by systemic 
      lupus erythematosus, rheumatoid arthritis, transplantation and drugs, which were 
      significantly higher than the control group. Stroke, seizure, arterial 
      thrombosis, vascular stenosis, hypertension, myocardial infarction, and 
      pancreatitis were the main clinical signs and extra-renal involvements. In the 
      multivariate regression analysis, stroke, arterial thrombosis, peripheral 
      arterial disease, and uremia were significantly higher compared with the control 
      group. The mortality rate in TMA under plasmapheresis was significantly higher 
      than all TMA cases (39.33% vs 15.39% in the 2006 cohort and 39.27% vs 15.06% in 
      the 2011 cohort).This study indicated the spectrum of underlying causes, 
      extra-renal characteristics, and the response to plasmapheresis of patients with 
      TMA in Taiwan. Of note, the poor clinical outcomes of plasmapheresis in patients 
      with TMA might highlight the masked underlying etiology or worse disease 
      condition that should be noticed.
CI  - Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.
FAU - Chung, Ching-Hu
AU  - Chung CH
AD  - Department of Medicine, Mackay Medical College, New Taipei City.
FAU - Tsai, I-Jung
AU  - Tsai IJ
AD  - Division of Nephrology, Department of Pediatrics, National Taiwan University 
      Children Hospital, Taipei.
FAU - Tseng, Min-Hua
AU  - Tseng MH
AD  - Division of Nephrology, Department of Pediatrics, Chang Gung Memorial Hospital, 
      Taoyuan, Taiwan.
AD  - Department of Pediatrics, Xiamen Chang Gung Hospital, Ximen, China.
FAU - Chou, Hsin-Hsu
AU  - Chou HH
AD  - Department of Pediatrics, Ditmanson Medical Foundation Chia-Yi Christian 
      Hospital, Chiayi.
AD  - Department of Bioinformatics and Medical Engineering, College of Information and 
      Electrical Engineering, Asia University, Taichung.
FAU - Tain, You-Lin
AU  - Tain YL
AD  - Division of Pediatric Nephrology, Chang Gung Memorial Hospital-Kaohsiung Medical 
      Center, Kaohsiung.
FAU - Tsai, Jeng-Daw
AU  - Tsai JD
AD  - Division of Nephrology, Department of Pediatrics, MacKay Children's Hospital, 
      Taipei.
FAU - Chiou, Yuan-Yow
AU  - Chiou YY
AD  - Departments of Pediatrics, Institute of Clinical Medicine, National Cheng Kung 
      University Medical College and Hospital, Tainan 704.
FAU - Chiou, Yee-Hsuan
AU  - Chiou YH
AD  - Department of Pediatrics, Kaohsiung Veterans General Hospital.
AD  - Department of Medical Technology, Fooyin University, Kaohsiung 831.
FAU - Lin, Ching-Yuang
AU  - Lin CY
AD  - Clinical Immunological Center, Children's Hospital, China Medical University, 
      Taichung, Taiwan.
LA  - eng
GR  - MMC-1072D02, MMC-1081B27, 1091B12, 1091E01 and 109-CF-G1-01/Mackay Medical 
      College/
PT  - Journal Article
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Glucocorticoids)
RN  - 0 (Immunosuppressive Agents)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Antihypertensive Agents/therapeutic use
MH  - Female
MH  - Glucocorticoids
MH  - Humans
MH  - Immunosuppressive Agents/therapeutic use
MH  - Kaplan-Meier Estimate
MH  - Male
MH  - Middle Aged
MH  - Plasmapheresis/*statistics & numerical data
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Survival Rate
MH  - Taiwan/epidemiology
MH  - Thrombotic Microangiopathies/diagnosis/*etiology/mortality/therapy
MH  - Treatment Outcome
MH  - Young Adult
PMC - PMC8137071
COIS- The authors have no conflicts of interest to disclose.
EDAT- 2021/05/21 06:00
MHDA- 2021/05/26 06:00
PMCR- 2021/05/21
CRDT- 2021/05/20 01:01
PHST- 2021/01/19 00:00 [received]
PHST- 2021/04/28 00:00 [accepted]
PHST- 2021/05/20 01:01 [entrez]
PHST- 2021/05/21 06:00 [pubmed]
PHST- 2021/05/26 06:00 [medline]
PHST- 2021/05/21 00:00 [pmc-release]
AID - 00005792-202105210-00070 [pii]
AID - MD-D-21-00426 [pii]
AID - 10.1097/MD.0000000000025986 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2021 May 21;100(20):e25986. doi: 
      10.1097/MD.0000000000025986.

PMID- 33999944
OWN - NLM
STAT- MEDLINE
DCOM- 20211019
LR  - 20211019
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 16
IP  - 5
DP  - 2021
TI  - Association between ischemic stroke and seropositive rheumatoid arthritis in 
      Korea: A nationwide longitudinal cohort study.
PG  - e0251851
LID - 10.1371/journal.pone.0251851 [doi]
LID - e0251851
AB  - The purpose of this longitudinal follow-up study was to investigate the risk of 
      ischemic stroke nationwide in patients with seropositive rheumatoid arthritis 
      (RA) and controls who were matched in age and sex. Patient data were collected 
      from the National Health Insurance Service (NHIS) Health Screening (HEALS) 
      cohort. Using the International Classification of Diseases code M05 (seropositive 
      RA), with a prescription of any disease-modifying anti-rheumatic drug (DMARD), RA 
      was identified. A total of 2,765 patients and 13,825 control subjects were 
      included in our study. The 12-year incidence of ischemic stroke in each group was 
      calculated using the Kaplan-Meier method. The risk ratio of ischemic stroke was 
      estimated using Cox proportional hazards regression. Sixty-four patients (2.31%) 
      in the seropositive RA group and 512 (3.70%) in the control group experienced 
      ischemic stroke (P < 0.001) during the follow-up period. The hazard ratio of 
      ischemic stroke in the seropositive RA group was 1.32 (95% confidence interval 
      (CI), 1.02-1.73) after adjusting for age and sex. The adjusted hazard ratio of 
      ischemic stroke in the seropositive RA group was 1.40 (95% CI, 1.07-1.82) after 
      adjusting for demographics and comorbid medical disorders. According to the 
      subgroup analysis, the hazard ratios of ischemic stroke risks in the female and 
      hypertensive subgroups were 1.44 (95% CI, 1.05-1.97) and 1.66 (95% CI, 
      1.16-2.38), respectively. In the non-diabetes and non-dyslipidemia subgroups, the 
      corresponding hazard ratios of ischemic stroke were 1.47 (95% CI, 1.11-1.95) and 
      1.43 (95% CI, 1.07-1.91). Seropositive RA patients have an increased risk of 
      ischemic stroke. In female, hypertension, non-diabetes, and non-dyslipidemia RA 
      subgroups, even without the traditional risk factors for stroke (except for 
      hypertension), increased the risk, which could be potentially attributed to RA.
FAU - Lee, Dong Hyun
AU  - Lee DH
AUID- ORCID: 0000-0002-8252-622X
AD  - Department of Neurosurgery, Spine Center, The Leon Wiltse Memorial Hospital, 
      Suwon, Gyeonggi-do, South Korea.
AD  - Department of Neurosurgery, CHA University, CHA Bundang Medical Center, Seongnam, 
      Gyeonggi-do, South Korea.
FAU - Sheen, Seung Hun
AU  - Sheen SH
AD  - Department of Neurosurgery, CHA University, CHA Bundang Medical Center, Seongnam, 
      Gyeonggi-do, South Korea.
FAU - Lee, Dong-Geun
AU  - Lee DG
AD  - Department of Neurosurgery, Spine Center, The Leon Wiltse Memorial Hospital, 
      Suwon, Gyeonggi-do, South Korea.
FAU - Jang, Jae-Won
AU  - Jang JW
AD  - Department of Neurosurgery, Spine Center, The Leon Wiltse Memorial Hospital, 
      Suwon, Gyeonggi-do, South Korea.
FAU - Lee, Dong Chan
AU  - Lee DC
AD  - Department of Neurosurgery, Spine Center, The Leon Wiltse Memorial Hospital, 
      Anyang, Gyeonggi-do, South Korea.
FAU - Shin, Seung-Ho
AU  - Shin SH
AD  - Department of Neurosurgery, Spine Center, The Leon Wiltse Memorial Hospital, 
      Anyang, Gyeonggi-do, South Korea.
FAU - Han, In-Bo
AU  - Han IB
AD  - Department of Neurosurgery, CHA University, CHA Bundang Medical Center, Seongnam, 
      Gyeonggi-do, South Korea.
FAU - Hong, Je Beom
AU  - Hong JB
AD  - Kangbuk Samsung Hospital, Sungkyunkwan University College of Medicine, Seoul, 
      Korea.
FAU - Kim, Hakyung
AU  - Kim H
AD  - Department of Public Health, Genome & Health Big Data Branch, Graduate School of 
      Public Health, Seoul National University, Seoul, Korea.
FAU - Sohn, Seil
AU  - Sohn S
AUID- ORCID: 0000-0001-5724-8099
AD  - Department of Neurosurgery, CHA University, CHA Bundang Medical Center, Seongnam, 
      Gyeonggi-do, South Korea.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210517
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antirheumatic Agents
MH  - Arthritis, Rheumatoid/blood/complications/*epidemiology/pathology
MH  - Brain Ischemia/blood/*epidemiology/pathology
MH  - Diabetes Mellitus/blood/*epidemiology/pathology
MH  - Dyslipidemias/blood/epidemiology/pathology
MH  - Female
MH  - Humans
MH  - Hypertension/blood/complications/epidemiology/pathology
MH  - Insurance, Health
MH  - Ischemic Stroke/blood/complications/*epidemiology/pathology
MH  - Kaplan-Meier Estimate
MH  - Korea/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Proportional Hazards Models
MH  - Risk Factors
PMC - PMC8128246
COIS- The authors have declared that no competing interests exist.
EDAT- 2021/05/18 06:00
MHDA- 2021/10/21 06:00
PMCR- 2021/05/17
CRDT- 2021/05/17 17:29
PHST- 2020/10/14 00:00 [received]
PHST- 2021/05/05 00:00 [accepted]
PHST- 2021/05/17 17:29 [entrez]
PHST- 2021/05/18 06:00 [pubmed]
PHST- 2021/10/21 06:00 [medline]
PHST- 2021/05/17 00:00 [pmc-release]
AID - PONE-D-20-30296 [pii]
AID - 10.1371/journal.pone.0251851 [doi]
PST - epublish
SO  - PLoS One. 2021 May 17;16(5):e0251851. doi: 10.1371/journal.pone.0251851. 
      eCollection 2021.

PMID- 33977741
OWN - NLM
STAT- MEDLINE
DCOM- 20210611
LR  - 20210611
IS  - 2224-5839 (Electronic)
IS  - 2224-5820 (Linking)
VI  - 10
IP  - 5
DP  - 2021 May
TI  - Patients with different types of arthritis may be at risk for major depression: 
      results from the National Health and Nutrition Examination Survey 2007-2018.
PG  - 5280-5288
LID - 10.21037/apm-21-279 [doi]
AB  - BACKGROUND: Arthritis is one of the common causes of physical pain and 
      disability, which often makes patients fall into major depression. However, the 
      correlation between arthritis and major depression, and how different types of 
      arthritis correspond to major depression remain to be explored. The purpose of 
      this study is to explore the relationship between arthritis and major depression. 
      METHODS: Arthritis status was reported by participants themselves, and the 
      Patient Health Questionnaire-9 in National Health and Nutrition Examination 
      Survey (NHANES) was used to evaluate major depression, logistic regression was 
      used to evaluate the relationship between arthritis and major depression. 
      RESULTS: We analyzed the data of 25,990 adults who participated in the NHANES 
      from 2007 to 2018. Participants with major depression were more likely to be 
      female, Hispanic, smoker, less educated, less recreational activities, 
      poverty-to-income ratio <5, coronary heart disease, stroke, cancer or malignant 
      tumor, diabetes, hypertension and higher body mass index (BMI). Arthritis was 
      significantly correlated with major depression (25.4% vs. 44.9%; P<0.001), even 
      after adjusting for gender, age, race, BMI, PIR, education, marriage, moderate 
      recreational activities, smoking, history of coronary heart disease, stroke, 
      cancer or malignant tumor, diabetes, and hypertension (OR =2.30, 95% CI, 
      2.06-2.56, P<0.001). Subgroup analysis showed that compared with degenerative 
      arthritis, rheumatoid arthritis (RA), or other arthritis, psoriatic arthritis 
      (PsA) had the greatest influence on major depression patients. CONCLUSIONS: All 
      patients with arthritis, especially PsA, may have the risk of major depression. 
      Psychological intervention necessary for patients with arthritis.
FAU - Wang, Mi-Yuan
AU  - Wang MY
AD  - Beijing University of Chinese Medicine, Beijing, China.
FAU - Li, Jie
AU  - Li J
AD  - College of Traditional Chinese Medicine, Shandong University of Traditional 
      Chinese Medicine, Jinan, China.
FAU - Peng, Hong-Ye
AU  - Peng HY
AD  - Beijing University of Chinese Medicine, Beijing, China.
FAU - Liu, Jia
AU  - Liu J
AD  - Beijing University of Chinese Medicine, Beijing, China.
FAU - Huang, Kai-Lin
AU  - Huang KL
AD  - Beijing University of Chinese Medicine, Beijing, China.
FAU - Li, Lei
AU  - Li L
AD  - Beijing University of Chinese Medicine, Beijing, China.
FAU - Yan, Zao-Fang
AU  - Yan ZF
AD  - Beijing University of Chinese Medicine, Beijing, China.
FAU - Zhao, Zhen-Hai
AU  - Zhao ZH
AD  - Dongzhimen Hospital of Beijing University of Chinese Medicine, Beijing, China.
LA  - eng
PT  - Journal Article
DEP - 20210422
PL  - China
TA  - Ann Palliat Med
JT  - Annals of palliative medicine
JID - 101585484
SB  - IM
MH  - Adult
MH  - *Arthritis, Rheumatoid
MH  - Cross-Sectional Studies
MH  - Depression
MH  - *Depressive Disorder, Major/epidemiology
MH  - *Diabetes Mellitus
MH  - Female
MH  - Humans
MH  - Male
MH  - Nutrition Surveys
OTO - NOTNLM
OT  - Major depression
OT  - National Health and Nutrition Examination Survey (NHANES)
OT  - arthritis
OT  - cross-sectional study
OT  - psoriatic arthritis (PsA)
EDAT- 2021/05/13 06:00
MHDA- 2021/06/12 06:00
CRDT- 2021/05/12 08:41
PHST- 2021/01/31 00:00 [received]
PHST- 2021/04/08 00:00 [accepted]
PHST- 2021/05/13 06:00 [pubmed]
PHST- 2021/06/12 06:00 [medline]
PHST- 2021/05/12 08:41 [entrez]
AID - apm-21-279 [pii]
AID - 10.21037/apm-21-279 [doi]
PST - ppublish
SO  - Ann Palliat Med. 2021 May;10(5):5280-5288. doi: 10.21037/apm-21-279. Epub 2021 
      Apr 22.

PMID- 33966169
OWN - NLM
STAT- MEDLINE
DCOM- 20210928
LR  - 20210928
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 40
IP  - 10
DP  - 2021 Oct
TI  - Systemic inflammatory response index as an independent risk factor for ischemic 
      stroke in patients with rheumatoid arthritis: a retrospective study based on 
      propensity score matching.
PG  - 3919-3927
LID - 10.1007/s10067-021-05762-z [doi]
AB  - OBJECTIVE: To investigate the relationship between systemic inflammatory response 
      index (SIRI) and ischemic stroke (IS) in rheumatoid arthritis (RA) patients. 
      METHODS: Fifty-two RA patients with IS, who were admitted to Wujin Hospital 
      Affiliated with Jiangsu University between 2015 and 2019, were selected as the 
      study group, and 236 RA patients without IS were selected as the control group. 
      Propensity score matching (PSM) function of SPSS 26.0 was used to carry out 1:1 
      propensity score matching for gender, age, blood pressure, blood glucose, blood 
      lipid, and smoking history of patients in the two groups, and the caliper value 
      was set as 0.02 to obtain covariate balanced samples between groups. When 
      performing blood tests, the following are determined: rheumatoid factor (RF), 
      erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), mean platelet 
      volume (MPV), calculated SIRI = (neutrophil × monocyte)/lymphocyte, and completed 
      28-joint disease activity score (DAS28-CRP). The differences in inflammatory 
      markers between the two groups were compared, the independent risk factors were 
      analyzed by logistic regression, and the auxiliary diagnostic value was evaluated 
      by the receiver operating characteristic (ROC) curve. RESULTS: A total of 48 
      pairs of patients were successfully matched. SIRI in the study group was higher 
      than that in the control group (p < 0.05), and the mean platelet volume (MPV) was 
      lower in the study group than in the control group (p < 0.05). SIRI, DAS28-CRP 
      (r = 0.508, p < 0.01), ESR (r = 0.359, p < 0.05), and CRP (r = 0.473, p < 0.01) 
      were positively correlated. Logistic regression analysis showed that SIRI was an 
      independent IS risk factor in RA patients (odds ratio, 1.30; 95% confidence 
      interval, approximately 1.008-1.678). The optimal threshold for SIRI-assisted 
      diagnosis of patients with RA and IS was 1.62, the area under the ROC curve was 
      0.721 (p < 0.01), sensitivity was 54.17%, and specificity was 83.33%. CONCLUSION: 
      SIRI was independently associated with the occurrence of ischemic stroke in 
      patients with RA. Thus, RA patients with elevated SIRI should be closely 
      monitored. Key points • RA patients with IS had fewer traditional risk factors 
      such as hypertension and diabetes, while inflammatory indicators were 
      significantly increased. • The SIRI have drawn attention in recent years as novel 
      non-specific inflammatory markers. However, only a few studies have been 
      conducted to investigate their value in RA. • This study completes the gaps in 
      the research on the relationship between SIRI and the risk of IS occurrence in RA 
      patients.
CI  - © 2021. International League of Associations for Rheumatology (ILAR).
FAU - Jin, Zihan
AU  - Jin Z
AD  - Department of Clinical Laboratory, The Affiliated Changzhou No. 2 People's 
      Hospital of Nanjing Medical University, Changzhou City, Jiangsu Province, China.
FAU - Hao, Dongli
AU  - Hao D
AD  - Department of Neurology, Wujin Hospital Affiliated with Jiangsu University, 
      Changzhou City, Jiangsu Province, China.
FAU - Song, Yuanjian
AU  - Song Y
AD  - School of Basic Medicine, Xuzhou Medical University, Xuzhou City, Jiangsu 
      Province, China.
FAU - Zhuang, Lin
AU  - Zhuang L
AD  - Department of Surgery, Wujin Hospital Affiliated with Jiangsu University, 
      Changzhou City, Jiangsu Province, China.
FAU - Wang, Qiang
AU  - Wang Q
AD  - Department of Surgery, Wujin Hospital Affiliated with Jiangsu University, 
      Changzhou City, Jiangsu Province, China.
FAU - Yu, Xiaolong
AU  - Yu X
AUID- ORCID: 0000-0003-4078-1350
AD  - Science and Education Section, Wujin Hospital Affiliated with Jiangsu University, 
      Changzhou City, Jiangsu Province, China. xllxl9999@126.com.
AD  - Department of Ultrasonics, The Wujin Clinical College of Xuzhou Medical 
      University, Changzhou City, Jiangsu Province, China. xllxl9999@126.com.
AD  - Jiangsu Key Laboratory of Immunology and Metabolism (Xuzhou Medical University), 
      Xuzhou City, Jiangsu Province, China. xllxl9999@126.com.
LA  - eng
GR  - CZQM2020120/Young Talent Development Plan of Changzhou Health Commission/
GR  - XZSYSKF2020018/Jiangsu Key Laboratory of Immunology and Metabolism/
PT  - Journal Article
DEP - 20210509
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
RN  - 0 (Biomarkers)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - *Arthritis, Rheumatoid/complications
MH  - Biomarkers
MH  - Blood Sedimentation
MH  - *Brain Ischemia/complications/epidemiology
MH  - C-Reactive Protein/analysis
MH  - Humans
MH  - *Ischemic Stroke
MH  - Propensity Score
MH  - Retrospective Studies
MH  - Risk Factors
MH  - *Stroke/epidemiology
MH  - Systemic Inflammatory Response Syndrome
OTO - NOTNLM
OT  - Ischemic stroke
OT  - Rheumatoid arthritis
OT  - Systemic inflammatory response index
EDAT- 2021/05/10 06:00
MHDA- 2021/09/29 06:00
CRDT- 2021/05/09 21:03
PHST- 2020/11/22 00:00 [received]
PHST- 2021/05/03 00:00 [accepted]
PHST- 2021/04/02 00:00 [revised]
PHST- 2021/05/10 06:00 [pubmed]
PHST- 2021/09/29 06:00 [medline]
PHST- 2021/05/09 21:03 [entrez]
AID - 10.1007/s10067-021-05762-z [pii]
AID - 10.1007/s10067-021-05762-z [doi]
PST - ppublish
SO  - Clin Rheumatol. 2021 Oct;40(10):3919-3927. doi: 10.1007/s10067-021-05762-z. Epub 
      2021 May 9.

PMID- 33884656
OWN - NLM
STAT- MEDLINE
DCOM- 20220207
LR  - 20220207
IS  - 1938-3673 (Electronic)
IS  - 0741-5400 (Linking)
VI  - 111
IP  - 2
DP  - 2022 Feb
TI  - Phenotypes, roles, and modulation of regulatory lymphocytes in periodontitis and 
      its associated systemic diseases.
PG  - 451-467
LID - 10.1002/JLB.3VMR0321-027RRR [doi]
AB  - Periodontitis is a common chronic inflammatory disease that can result in tooth 
      loss and poses a risk to systemic health. Lymphocytes play important roles in 
      periodontitis through multiple mechanisms. Regulatory lymphocytes including 
      regulatory B cells (Bregs) and T cells (Tregs) are the main immunosuppressive 
      cells that maintain immune homeostasis, and are critical to our understanding of 
      the pathogenesis of periodontitis and the development of effective treatments. In 
      this review, we discuss the phenotypes, roles, and modulating strategies of 
      regulatory lymphocytes including Bregs and Tregs in periodontitis and frequently 
      cooccurring inflammatory diseases such as rheumatoid arthritis, Alzheimer 
      disease, diabetes mellitus, and stroke. The current evidence suggests that 
      restoring immune balance through therapeutic targeting of regulatory lymphocytes 
      is a promising strategy for the treatment of periodontitis and other systemic 
      inflammatory diseases.
CI  - ©2021 Society for Leukocyte Biology.
FAU - Zou, Hang
AU  - Zou H
AD  - Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-Sen University, 
      Guangzhou, China.
AD  - Guangdong Provincial Key Laboratory of Stomatology, Guangzhou, China.
FAU - Zhou, Niu
AU  - Zhou N
AD  - Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-Sen University, 
      Guangzhou, China.
AD  - Guangdong Provincial Key Laboratory of Stomatology, Guangzhou, China.
AD  - Guangzhou Zoo, Guangzhou, China.
FAU - Huang, Yilian
AU  - Huang Y
AD  - School of Nursing, Guangdong Pharmaceutical University, Guangzhou, China.
FAU - Luo, Aoxiang
AU  - Luo A
AD  - School of Nursing, Guangdong Pharmaceutical University, Guangzhou, China.
FAU - Sun, Jianbo
AU  - Sun J
AD  - Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-Sen University, 
      Guangzhou, China.
AD  - Guangdong Provincial Key Laboratory of Stomatology, Guangzhou, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20210422
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
SB  - IM
MH  - Animals
MH  - B-Lymphocytes, Regulatory/*immunology
MH  - Humans
MH  - Metabolic Diseases/immunology/*pathology
MH  - Periodontitis/immunology/*pathology
MH  - Phenotype
MH  - T-Lymphocytes, Regulatory/*immunology
OTO - NOTNLM
OT  - Breg
OT  - Th17
OT  - Treg
OT  - immune imbalance
OT  - periodontitis
EDAT- 2021/04/23 06:00
MHDA- 2022/02/08 06:00
CRDT- 2021/04/22 06:58
PHST- 2021/04/23 06:00 [pubmed]
PHST- 2022/02/08 06:00 [medline]
PHST- 2021/04/22 06:58 [entrez]
AID - 10.1002/JLB.3VMR0321-027RRR [doi]
PST - ppublish
SO  - J Leukoc Biol. 2022 Feb;111(2):451-467. doi: 10.1002/JLB.3VMR0321-027RRR. Epub 
      2021 Apr 22.

PMID- 33860677
OWN - NLM
STAT- MEDLINE
DCOM- 20211026
LR  - 20230413
IS  - 2047-9980 (Electronic)
IS  - 2047-9980 (Linking)
VI  - 10
IP  - 8
DP  - 2021 Apr 20
TI  - Patients With Rheumatoid Arthritis With an Inadequate Response to 
      Disease-Modifying Antirheumatic Drugs at a Higher Risk of Acute Coronary 
      Syndrome.
PG  - e018290
LID - 10.1161/JAHA.120.018290 [doi]
LID - e018290
AB  - Background Cardiovascular disease is the most common cause of death in patients 
      with rheumatoid arthritis. It is believed that using disease-modifying 
      antirheumatic drugs (DMARDs) to control inflammation can reduce the risk of 
      cardiovascular disease. In this study, we investigated whether patients who 
      responded differently to DMARDs might sustain different cardiovascular events. 
      Methods and Results We designed a cohort study using the Chang Gung Research 
      Database. We identified 7114 patients diagnosed with rheumatoid arthritis. After 
      strict exclusion criteria, we collected 663 individuals as an inadequate response 
      to DMARDs group. Then, 2034 individuals were included as the control group. The 
      end point was composite vascular outcomes, including acute coronary syndrome or 
      ischemic stroke. We used the inverse probability of treatment weighting to keep 
      the covariates between these 2 groups well balanced. We compared the risk of 
      these outcomes using the Cox proportional hazards model. The mean follow-up time 
      was 4.7 years. During follow-up, there were 7.5% and 6.4% of patients with 
      composite vascular outcomes in the DMARD-inadequate response and control groups, 
      respectively. There was no significant difference in the risk of composite 
      vascular outcomes (95% CI, 0.94-1.41) and ischemic stroke (95% CI, 0.84-1.36). 
      The risk of acute coronary syndrome was significantly higher in the 
      DMARD-inadequate response group (hazard ratio, 1.45; 95% CI, 1.02-2.05). 
      Conclusions Patients with DMARD-inadequate response rheumatoid arthritis have a 
      higher risk of developing acute coronary syndrome than those whose disease can be 
      controlled by DMARDs.
FAU - Hsu, Chung-Yuan
AU  - Hsu CY
AD  - Division of Rheumatology, Allergy, and Immunology Department of Internal Medicine 
      Kaohsiung Chang Gung Memorial HospitalChang Gung University College of Medicine 
      Taiwan.
FAU - Su, Yu-Jih
AU  - Su YJ
AD  - Division of Rheumatology, Allergy, and Immunology Department of Internal Medicine 
      Kaohsiung Chang Gung Memorial HospitalChang Gung University College of Medicine 
      Taiwan.
FAU - Chen, Jia-Feng
AU  - Chen JF
AD  - Division of Rheumatology, Allergy, and Immunology Department of Internal Medicine 
      Kaohsiung Chang Gung Memorial HospitalChang Gung University College of Medicine 
      Taiwan.
FAU - Sun, Chi-Chin
AU  - Sun CC
AD  - Department of Ophthalmology Chang Gung Memorial Hospital Keelung Taiwan.
AD  - School of Medicine College of Medicine Chang Gung University Taoyuan Taiwan.
FAU - Cheng, Tien-Tsai
AU  - Cheng TT
AD  - Division of Rheumatology, Allergy, and Immunology Department of Internal Medicine 
      Kaohsiung Chang Gung Memorial HospitalChang Gung University College of Medicine 
      Taiwan.
FAU - Tsai, Tzu-Hsien
AU  - Tsai TH
AD  - Division of Cardiology Department of Internal Medicine Kaohsiung Chang Gung 
      Memorial HospitalChang Gung University College of Medicine Taiwan.
FAU - Lin, Shang-Hong
AU  - Lin SH
AD  - Department of Dermatology Kaohsiung Chang Gung Memorial HospitalChang Gung 
      University College of Medicine Taiwan.
FAU - Chang, Cheng-Chieh
AU  - Chang CC
AD  - Department of Chinese Medicine Chang Gung Memorial Hospital-Kaohsiung Medical 
      Center Taiwan.
FAU - Chen, Tien-Hsing
AU  - Chen TH
AD  - Division of Cardiology Department of Internal Medicine Chang Gung Memorial 
      Hospital Keelung Taiwan.
AD  - Department of Medical Research and Development Chang Gung Memorial Hospital 
      Keelung Taiwan.
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20210416
PL  - England
TA  - J Am Heart Assoc
JT  - Journal of the American Heart Association
JID - 101580524
RN  - 0 (Antirheumatic Agents)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Acute Coronary Syndrome/epidemiology/*etiology
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/complications/*drug therapy
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Methotrexate/*therapeutic use
MH  - Middle Aged
MH  - Prognosis
MH  - Retrospective Studies
MH  - Risk Assessment/*methods
MH  - Risk Factors
MH  - Taiwan/epidemiology
PMC - PMC8174161
OTO - NOTNLM
OT  - antirheumatic agents
OT  - cardiovascular disease
OT  - rheumatoid arthritis
COIS- None.
EDAT- 2021/04/17 06:00
MHDA- 2021/10/27 06:00
PMCR- 2021/04/20
CRDT- 2021/04/16 08:38
PHST- 2021/04/17 06:00 [pubmed]
PHST- 2021/10/27 06:00 [medline]
PHST- 2021/04/16 08:38 [entrez]
PHST- 2021/04/20 00:00 [pmc-release]
AID - JAH36114 [pii]
AID - 10.1161/JAHA.120.018290 [doi]
PST - ppublish
SO  - J Am Heart Assoc. 2021 Apr 20;10(8):e018290. doi: 10.1161/JAHA.120.018290. Epub 
      2021 Apr 16.

PMID- 33823727
OWN - NLM
STAT- MEDLINE
DCOM- 20211020
LR  - 20211020
IS  - 1369-1627 (Electronic)
IS  - 0954-0261 (Linking)
VI  - 33
IP  - 3
DP  - 2021 May
TI  - Depression in disabling medical conditions - current perspectives.
PG  - 312-325
LID - 10.1080/09540261.2021.1887823 [doi]
AB  - Chronic diseases commonly entail disability and are highly comorbid with mental 
      health problems, particularly depression. Prevalence of depression across 
      different disabling conditions affecting adult patients, as well as risk factors 
      for depression in these patient groups are reviewed in the current work, with a 
      particular focus on the literature published in the past 5 years. The prevalence 
      of depression in disabling conditions is higher than in the general population 
      and is associated with different factors. Examples of disease-specific factors 
      include neurological implications of stoke, diabetic related conditions (e.g. 
      amputation), limitations imposed by vision loss caused by age-related eye 
      diseases, fatigue in rheumatoid arthritis, and pain in cancer. Common factors 
      identified across different conditions include pre-morbid depression, history of 
      mental health problems, poor social support, disease-related disability, 
      multi-morbidity, and less adaptive coping strategies. We also reviewed studies 
      suggesting a potential bidirectional relationship between depression and chronic 
      disease, particularly for stroke, cardiovascular disease, diabetes, and potential 
      factors mediating that relationship. Current findings suggested that long-term 
      depression might be associated with an increased risk of subsequent physical 
      health problems, although the nature of that relationship and its underlying 
      mechanisms are still unclear.
FAU - Senra, Hugo
AU  - Senra H
AD  - Centre for Research in Neuropsychology and Cognitive and Behavioural Intervention 
      (CINEICC), University of Coimbra, Coimbra, Portugal.
AD  - School of Health and Social Care, University of Essex, Colchester, UK.
FAU - McPherson, Susan
AU  - McPherson S
AD  - School of Health and Social Care, University of Essex, Colchester, UK.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20210406
PL  - England
TA  - Int Rev Psychiatry
JT  - International review of psychiatry (Abingdon, England)
JID - 8918131
SB  - IM
MH  - Adaptation, Psychological
MH  - Chronic Disease/*epidemiology/*psychology
MH  - Depression/*epidemiology
MH  - Humans
MH  - Prevalence
MH  - Risk Factors
OTO - NOTNLM
OT  - Depression
OT  - chronic diseases
OT  - disability
EDAT- 2021/04/08 06:00
MHDA- 2021/10/21 06:00
CRDT- 2021/04/07 05:34
PHST- 2021/04/08 06:00 [pubmed]
PHST- 2021/10/21 06:00 [medline]
PHST- 2021/04/07 05:34 [entrez]
AID - 10.1080/09540261.2021.1887823 [doi]
PST - ppublish
SO  - Int Rev Psychiatry. 2021 May;33(3):312-325. doi: 10.1080/09540261.2021.1887823. 
      Epub 2021 Apr 6.

PMID- 33789293
OWN - NLM
STAT- MEDLINE
DCOM- 20211028
LR  - 20211028
IS  - 1423-0208 (Electronic)
IS  - 0251-5350 (Linking)
VI  - 55
IP  - 2
DP  - 2021
TI  - Increased Incidence of Stroke and Transient Ischemic Attack in Patients with 
      Rheumatoid Arthritis and Ankylosing Spondylitis in Germany.
PG  - 162-170
LID - 10.1159/000514889 [doi]
AB  - BACKGROUND: As chronic inflammatory diseases may be associated with an increased 
      risk of vascular events, the aim of the present study was to assess the incidence 
      of stroke and transient ischemic attack (TIA) in patients with rheumatoid 
      arthritis (RA) and ankylosing spondylitis (AS). METHODS: Patients diagnosed with 
      RA and AS in 1,262 general practices in Germany between 2000 and 2015 were 
      selected. RA and AS patients were matched to patients without RA or AS using 
      propensity scores based on age, sex, physician, co-diagnoses, and co-therapies. 
      The Kaplan-Meier curves and Cox regression models were used to study the 
      incidence of stroke and TIA as a function of RA and AS. RESULTS: In the study 
      population (N = 29,106; mean age 54.8 years; 65% women), 24,580 patients had RA 
      and 4,526 had AS. RA was significantly associated with the stroke (hazard ratio 
      [HR] = 1.42, confidence interval [CI]: 1.25-1.60) and TIA (HR = 1.69, CI: 
      1.46-1.95). The association between RA and stroke was strongest in the age group 
      18-40 years (HR = 3.45, CI: 1.30-9.18). The HR for stroke in AS was 1.41 (CI: 
      0.99-2.00) and for TIA 1.62 (1.08-2.44). CONCLUSION: RA was significantly 
      associated with stroke and TIA, with young patients being at a particularly 
      increased risk. AS was tendentially associated with stroke and TIA.
CI  - © 2021 S. Karger AG, Basel.
FAU - Trömmer, Kathleen
AU  - Trömmer K
AD  - Department of Neurology, Asklepios Hospital St. Georg, Hamburg, Germany.
FAU - Kostev, Karel
AU  - Kostev K
AD  - Epidemiology, IQVIA, Frankfurt am Main, Germany.
FAU - Jacob, Louis
AU  - Jacob L
AD  - Faculty of Medicine, University of Versailles Saint-Quentinen-Yvelines, 
      Versailles, France.
FAU - Tanislav, Christian
AU  - Tanislav C
AD  - Department of Geriatrics and Neurology, Diakonie Hospital Jung Stilling Siegen, 
      Siegen, Germany.
LA  - eng
PT  - Journal Article
DEP - 20210331
PL  - Switzerland
TA  - Neuroepidemiology
JT  - Neuroepidemiology
JID - 8218700
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - *Arthritis, Rheumatoid/complications/epidemiology
MH  - Female
MH  - Germany/epidemiology
MH  - Humans
MH  - Incidence
MH  - *Ischemic Attack, Transient/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - *Spondylitis, Ankylosing/complications/epidemiology
MH  - *Stroke/epidemiology
MH  - Young Adult
OTO - NOTNLM
OT  - Ankylosing spondylitis
OT  - Cohort studies
OT  - Rheumatoid arthritis
OT  - Stroke
OT  - Transient ischemic attack
EDAT- 2021/04/01 06:00
MHDA- 2021/10/29 06:00
CRDT- 2021/03/31 20:12
PHST- 2021/01/20 00:00 [received]
PHST- 2021/01/30 00:00 [accepted]
PHST- 2021/04/01 06:00 [pubmed]
PHST- 2021/10/29 06:00 [medline]
PHST- 2021/03/31 20:12 [entrez]
AID - 000514889 [pii]
AID - 10.1159/000514889 [doi]
PST - ppublish
SO  - Neuroepidemiology. 2021;55(2):162-170. doi: 10.1159/000514889. Epub 2021 Mar 31.

PMID- 33725018
OWN - NLM
STAT- MEDLINE
DCOM- 20211013
LR  - 20231104
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 16
IP  - 3
DP  - 2021
TI  - Stroke risk in arthritis: A systematic review and meta-analysis of cohort 
      studies.
PG  - e0248564
LID - 10.1371/journal.pone.0248564 [doi]
LID - e0248564
AB  - BACKGROUND AND OBJECTIVE: Stroke is a major contributor to the global burden of 
      disease. Although numerous modifiable risk factors (RF) for stroke have been 
      identified, some remain unexplained. Increasing studies have investigated stroke 
      risk in arthritis, but their results are inconsistent. We aimed to synthesize, 
      quantify, and compare the risk of stroke for the major types of arthritis in 
      cohort studies by using a systematic review and meta-analysis approach. METHODS: 
      We searched Chinese and English databases to identify relevant studies from 
      inception to April 30, 2020. Only studies adjusting at least for age and sex were 
      included. We calculated pooled effect estimates for relative risk (RR) and 95% 
      confidence interval (CI) and identified potential sources of heterogeneity and 
      publication bias. RESULTS: A total of 1,348 articles were retrieved, and after an 
      preliminary screening of titles and abstracts, 69 were reviewed for full text, 
      and finally, 32 met the criteria for meta-analysis. Stroke risk in arthritis was 
      significantly increased in studies adjusting for age and sex (RR = 1.36, 95% CI: 
      1.27-1.46) and for at least one traditional risk factor (RR = 1.40, 95% CI: 
      1.28-1.54). The results of studies stratified by stroke subtype were consistent 
      with the main finding (ischemic stroke: RR = 1.53, 95% CI: 1.32-1.78; hemorrhagic 
      stroke: RR = 1.45, 95% CI: 1.15-1.84). In subgroup analysis by arthritis type, 
      stroke risk was significantly increased in rheumatoid arthritis (RR = 1.38, 95% 
      CI: 1.29-1.48), ankylosing spondylitis (RR = 1.49, 95% CI: 1.25-1.77), psoriatic 
      arthritis (RR = 1.33, 95% CI: 1.22-1.45), and gout (RR = 1.40, 95% CI: 1.13-1.73) 
      but not osteoarthritis (RR = 1.03, 95% CI: 0.91-1.16). Age and sex subgroup 
      analyses indicated that stroke risk was similar by sex (women: RR = 1.47, 95% CI: 
      1.31-1.66; men: RR = 1.44, 95% CI: 1.28-1.61); risk was higher with younger age 
      (<45 years) (RR = 1.46, 95% CI: 1.17-1.82) than older age (≥65 years) (RR = 1.17, 
      95% CI: 1.08-1.26). CONCLUSIONS: Stroke risk was increased in multiple arthritis 
      and similar between ischemic and hemorrhagic stroke. Young patients with 
      arthritis had the highest risk.
FAU - Liu, Wei
AU  - Liu W
AD  - Institute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China.
FAU - Ma, Wei
AU  - Ma W
AD  - Institute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China.
FAU - Liu, Hua
AU  - Liu H
AD  - Department of Neurology, The Third People's Hospital of Chengdu & The Affiliated 
      Hospital of Southwest Jiaotong University, Chengdu, Sichuan, China.
FAU - Li, Chunyan
AU  - Li C
AD  - Institute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China.
FAU - Zhang, Yangwei
AU  - Zhang Y
AD  - Department of Neurology, Nanchong Central Hospital & The Second Clinical Medical 
      College, North Sichuan Medical College, Nanchong, Sichuan, China.
FAU - Liu, Jie
AU  - Liu J
AD  - Institute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China.
FAU - Liang, Yu
AU  - Liang Y
AD  - Institute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China.
FAU - Zhang, Sijia
AU  - Zhang S
AD  - Institute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China.
FAU - Wu, Zhen
AU  - Wu Z
AD  - Second Department of General Surgery, First People's Hospital of Yunnan Province, 
      Kunming, Yunnan, China.
FAU - Zang, Chenghao
AU  - Zang C
AD  - Second Department of General Surgery, First People's Hospital of Yunnan Province, 
      Kunming, Yunnan, China.
FAU - Guo, Jianhui
AU  - Guo J
AD  - Second Department of General Surgery, First People's Hospital of Yunnan Province, 
      Kunming, Yunnan, China.
FAU - Li, Liyan
AU  - Li L
AUID- ORCID: 0000-0002-2411-4235
AD  - Institute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Systematic Review
DEP - 20210316
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
SB  - IM
MH  - Adult
MH  - Age Factors
MH  - Aged
MH  - Arthritis, Psoriatic/complications/*epidemiology/immunology
MH  - Arthritis, Rheumatoid/complications/*epidemiology/immunology
MH  - Cohort Studies
MH  - Female
MH  - Gout/complications/*epidemiology/immunology
MH  - Humans
MH  - Male
MH  - Risk Factors
MH  - Sex Factors
MH  - Spondylitis, Ankylosing/complications/*epidemiology/immunology
MH  - Stroke/*epidemiology/immunology
PMC - PMC7963101
COIS- The authors have declared that no competing interests exist.
EDAT- 2021/03/17 06:00
MHDA- 2021/10/14 06:00
PMCR- 2021/03/16
CRDT- 2021/03/16 17:26
PHST- 2020/06/23 00:00 [received]
PHST- 2021/03/01 00:00 [accepted]
PHST- 2021/03/16 17:26 [entrez]
PHST- 2021/03/17 06:00 [pubmed]
PHST- 2021/10/14 06:00 [medline]
PHST- 2021/03/16 00:00 [pmc-release]
AID - PONE-D-20-19285 [pii]
AID - 10.1371/journal.pone.0248564 [doi]
PST - epublish
SO  - PLoS One. 2021 Mar 16;16(3):e0248564. doi: 10.1371/journal.pone.0248564. 
      eCollection 2021.

PMID- 33667301
OWN - NLM
STAT- MEDLINE
DCOM- 20211228
LR  - 20211228
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Print)
IS  - 1462-0324 (Linking)
VI  - 60
IP  - 11
DP  - 2021 Nov 3
TI  - Patients with rheumatoid arthritis have impaired long-term outcomes after 
      myocardial infarction: a nationwide case-control registry study.
PG  - 5205-5215
LID - 10.1093/rheumatology/keab204 [doi]
AB  - OBJECTIVE: To investigate the long-term outcomes of patients with RA after 
      myocardial infarction (MI). METHODS: All-comer, real-life MI patients with RA 
      (n = 1614, mean age 74 years) were retrospectively compared with propensity score 
      (1:5) matched MI patients without RA (n = 8070) in a multicentre, nationwide, 
      cohort register study in Finland. The impact of RA duration and the usage of 
      corticosteroids and antirheumatic drugs on RA patients' outcomes were also 
      studied. The median follow-up was 7.3 years. RESULTS: RA was associated with an 
      increased 14-year mortality risk after MI compared with patients without RA 
      [80.4% vs 72.3%; hazard ratio (HR) 1.25; CI: 1.16, 1.35; P <0.0001]. Patients 
      with RA were at higher risk of new MI (HR 1.22; CI: 1.09, 1.36; P =0.0001) and 
      revascularization (HR 1.28; CI: 1.10, 1.49; P =0.002) after discharge from index 
      MI. Cumulative stroke rate after MI did not differ between RA and non-RA patients 
      (P =0.322). RA duration and corticosteroid usage before MI, but not use of 
      methotrexate or biologic antirheumatic drugs, were independently associated with 
      higher mortality (P <0.001) and new MI (P =0.009). A higher dosage of 
      corticosteroids prior to MI was independently associated with higher long-term 
      mortality (P =0.002) and methotrexate usage with lower stroke rate (P =0.034). 
      Serological status of RA was not associated with outcomes. CONCLUSION: RA is 
      independently associated with poorer prognosis after MI. RA duration and 
      corticosteroid usage and dosage were independent predictors of mortality after MI 
      in RA. Special attention is needed for improvement of outcomes after MI in this 
      vulnerable population.
CI  - © The Author(s) 2021. Published by Oxford University Press on behalf of the 
      British Society for Rheumatology.
FAU - Palomäki, Antti
AU  - Palomäki A
AUID- ORCID: 0000-0002-8835-8116
AD  - Division of Medicine, Centre for Rheumatology and Clinical Immunology, Turku 
      University Hospital.
AD  - Department of Medicine, University of Turku, Turku.
AD  - Institute for Molecular Medicine Finland, FIMM, HiLIFE, University of Helsinki, 
      Helsinki, Finland.
FAU - Kerola, Anne M
AU  - Kerola AM
AD  - Division of Rheumatology and Research, Preventive Cardio-Rheuma Clinic, 
      Diakonhjemmet Hospital, Oslo, Norway.
AD  - Department of Rheumatology, Päijät-Häme Joint Authority for Health and Wellbeing, 
      Lahti.
FAU - Malmberg, Markus
AU  - Malmberg M
AUID- ORCID: 0000-0002-9955-6089
AD  - Heart Center, Turku University Hospital and University of Turku.
FAU - Rautava, Päivi
AU  - Rautava P
AUID- ORCID: 0000-0003-2795-1327
AD  - Department of Public Health, University of Turku.
AD  - Turku Clinical Research Centre, Turku University Hospital.
FAU - Kytö, Ville
AU  - Kytö V
AUID- ORCID: 0000-0002-4521-1093
AD  - Heart Center, Turku University Hospital and University of Turku.
AD  - Research Center of Applied and Preventive Cardiovascular Medicine, University of 
      Turku.
AD  - Center for Population Health Research, Turku University Hospital and University 
      of Turku.
AD  - Administrative Centre, Hospital District of Southwest Finland, Turku, Finland.
LA  - eng
GR  - Finnish Cultural Foundation/
GR  - Paulo Foundation/
GR  - Finnish Governmental VTR-funding/
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*complications
MH  - Female
MH  - Finland/epidemiology
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*complications/mortality/surgery
MH  - Myocardial Revascularization/statistics & numerical data
MH  - Recurrence
MH  - *Registries
MH  - Retrospective Studies
MH  - Stroke/epidemiology/etiology
PMC - PMC8566209
OTO - NOTNLM
OT  - Cohort study
OT  - coronary artery disease
OT  - myocardial infarction
OT  - outcomes
OT  - rheumatoid arthritis
EDAT- 2021/03/06 06:00
MHDA- 2021/12/29 06:00
PMCR- 2021/03/01
CRDT- 2021/03/05 17:08
PHST- 2020/12/22 00:00 [received]
PHST- 2021/02/14 00:00 [revised]
PHST- 2021/03/06 06:00 [pubmed]
PHST- 2021/12/29 06:00 [medline]
PHST- 2021/03/05 17:08 [entrez]
PHST- 2021/03/01 00:00 [pmc-release]
AID - 6154670 [pii]
AID - keab204 [pii]
AID - 10.1093/rheumatology/keab204 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2021 Nov 3;60(11):5205-5215. doi: 
      10.1093/rheumatology/keab204.

PMID- 33619316
OWN - NLM
STAT- MEDLINE
DCOM- 20211203
LR  - 20230919
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 11
IP  - 1
DP  - 2021 Feb 22
TI  - Genetically predicted education attainment in relation to somatic and mental 
      health.
PG  - 4296
LID - 10.1038/s41598-021-83801-0 [doi]
LID - 4296
AB  - A deeper understanding of the causal links from education level to health 
      outcomes may shed a light for disease prevention. In the present Mendelian 
      randomization study, we found that genetically higher education level was 
      associated with lower risk of major mental disorders and most somatic diseases, 
      independent of intelligence. Higher education level adjusted for intelligence was 
      associated with lower risk of suicide attempts, insomnia, major depressive 
      disorder, heart failure, stroke, coronary artery disease, lung cancer, breast 
      cancer, type 2 diabetes and rheumatoid arthritis but with higher risk of 
      obsessive-compulsive disorder, anorexia nervosa, anxiety, bipolar disorder and 
      prostate cancer. Higher education level was associated with reduced obesity and 
      smoking, which mediated quite an extent of the associations between education 
      level and health outcomes. These findings emphasize the importance of education 
      to reduce the burden of common diseases.
FAU - Yuan, Shuai
AU  - Yuan S
AD  - Unit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental 
      Medicine, Karolinska Institutet, Nobelsväg 13, 17177, Stockholm, Sweden.
FAU - Xiong, Ying
AU  - Xiong Y
AD  - Department of Public Health Sciences, Karolinska Institutet, Stockholm, Sweden.
FAU - Michaëlsson, Madeleine
AU  - Michaëlsson M
AD  - Department of Education, Health and Social Studies, Dalarna University, Falun, 
      Sweden.
FAU - Michaëlsson, Karl
AU  - Michaëlsson K
AD  - Unit of Medical Epidemiology, Department of Surgical Sciences, Uppsala 
      University, Dag Hammarskjölds Väg 14B, 75185, Uppsala, Sweden.
FAU - Larsson, Susanna C
AU  - Larsson SC
AD  - Unit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental 
      Medicine, Karolinska Institutet, Nobelsväg 13, 17177, Stockholm, Sweden. 
      susanna.larsson@surgsci.uu.se.
AD  - Unit of Medical Epidemiology, Department of Surgical Sciences, Uppsala 
      University, Dag Hammarskjölds Väg 14B, 75185, Uppsala, Sweden. 
      susanna.larsson@surgsci.uu.se.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Systematic Review
DEP - 20210222
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
SB  - IM
MH  - Body Mass Index
MH  - *Educational Status
MH  - *Genetic Background
MH  - Genetic Predisposition to Disease
MH  - Genome-Wide Association Study/methods
MH  - *Health Status
MH  - Humans
MH  - Intelligence
MH  - Mendelian Randomization Analysis/methods
MH  - *Mental Health
MH  - Odds Ratio
MH  - Risk Factors
PMC - PMC7900220
COIS- All authors declared no support from any organization for the submitted work; no 
      financial relationships with any organization that might have an interest in the 
      submitted work in the previous three years; no other relationships or activities 
      that could appear to have influenced the submitted work.
EDAT- 2021/02/24 06:00
MHDA- 2021/12/15 06:00
PMCR- 2021/02/22
CRDT- 2021/02/23 06:12
PHST- 2020/10/09 00:00 [received]
PHST- 2021/02/08 00:00 [accepted]
PHST- 2021/02/23 06:12 [entrez]
PHST- 2021/02/24 06:00 [pubmed]
PHST- 2021/12/15 06:00 [medline]
PHST- 2021/02/22 00:00 [pmc-release]
AID - 10.1038/s41598-021-83801-0 [pii]
AID - 83801 [pii]
AID - 10.1038/s41598-021-83801-0 [doi]
PST - epublish
SO  - Sci Rep. 2021 Feb 22;11(1):4296. doi: 10.1038/s41598-021-83801-0.

PMID- 33607787
OWN - NLM
STAT- MEDLINE
DCOM- 20210226
LR  - 20230103
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 100
IP  - 7
DP  - 2021 Feb 19
TI  - Methotrexate can prevent cardiovascular events in patients with rheumatoid 
      arthritis: An updated meta-analysis.
PG  - e24579
LID - 10.1097/MD.0000000000024579 [doi]
LID - e24579
AB  - AIMS: The incidence of cardiovascular events (CVEs) in patients with rheumatoid 
      arthritis (RA) is higher than that in people without RA. This may be because 
      inflammation promotes the progression of atherosclerosis. Anti-inflammatory drugs 
      might reduce the occurrence of CVEs in patients with RA. Methotrexate (MTX) is a 
      conventional synthetic anti-rheumatic drug that is widely used in the treatment 
      of RA. We performed a meta-analysis to determine whether MTX can prevent CVEs in 
      RA patients. Then, we discussed the possibility of using MTX to prevent recurred 
      CVEs in patients with coronary heart disease (CHD). METHODS: We searched PubMed, 
      Embase, Web of Science, and the Cochrane Library using the key words 
      "methotrexate," "cardiovascular," "acute coronary syndrome," "coronary heart 
      disease," "myocardial infarction," "angina pectoris," and "rheumatoid arthritis." 
      The efficacy outcome was defined as a composite of CVEs, including stable angina, 
      acute coronary syndrome, stroke, heart failure, and cardiac death. RESULTS: A 
      total of 10 studies and 195,416 RA patients were included in our meta-analysis, 
      and the effect size of relative risk (RR) was pooled using a fixed effect model. 
      The results showed that MTX prevented CVEs in RA patients (RR: 0.798, 95% CI 
      0.726-0.876, P = .001, I2 = 27. 9%). CONCLUSION: MTX can prevent CVEs in RA 
      patients, but there is not sufficient evidence for using MTX to treat patients 
      with CHD.
CI  - Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.
FAU - Sun, Kai-Jun
AU  - Sun KJ
AD  - Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South 
      University, 139 Middle Renmin Road, Changsha, Hunan, China.
FAU - Liu, Lei-Ling
AU  - Liu LL
FAU - Hu, Jia-Hui
AU  - Hu JH
FAU - Chen, Yan-Ying
AU  - Chen YY
FAU - Xu, Dan-Yan
AU  - Xu DY
AUID- ORCID: 0000-0003-2113-0800
LA  - eng
GR  - 81871858/Key Programme/
PT  - Journal Article
PT  - Meta-Analysis
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
RN  - 0 (Antirheumatic Agents)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Cardiovascular Diseases/*prevention & control
MH  - Humans
MH  - Methotrexate/*therapeutic use
PMC - PMC7899830
COIS- The authors declare no conflict of interest.
EDAT- 2021/02/21 06:00
MHDA- 2021/02/27 06:00
PMCR- 2021/02/19
CRDT- 2021/02/20 01:01
PHST- 2020/09/27 00:00 [received]
PHST- 2021/01/14 00:00 [accepted]
PHST- 2021/02/20 01:01 [entrez]
PHST- 2021/02/21 06:00 [pubmed]
PHST- 2021/02/27 06:00 [medline]
PHST- 2021/02/19 00:00 [pmc-release]
AID - 00005792-202102190-00026 [pii]
AID - MD-D-20-09442 [pii]
AID - 10.1097/MD.0000000000024579 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2021 Feb 19;100(7):e24579. doi: 
      10.1097/MD.0000000000024579.

PMID- 33604209
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210220
IS  - 2168-8184 (Print)
IS  - 2168-8184 (Electronic)
IS  - 2168-8184 (Linking)
VI  - 13
IP  - 1
DP  - 2021 Jan 13
TI  - Obesity and Mechanical Thrombectomy.
PG  - e12671
LID - 10.7759/cureus.12671 [doi]
LID - e12671
AB  - Background Obesity has been shown to have a positive mortality benefit in 
      patients undergoing percutaneous coronary intervention, dialysis, those with 
      rheumatoid arthritis, chronic obstructive pulmonary disease, and various wasting 
      diseases. Studies for this mortality benefit in ischemic stroke patients are 
      conflicting, and it has not been well studied in mechanical thrombectomy 
      patients. We sought to determine the impact of obesity on outcomes of mechanical 
      thrombectomy patients. Methodology We used a large global health research network 
      to gather clinical data extracted from the electronic medical records of ischemic 
      stroke patients who underwent mechanical thrombectomy, and then stratified these 
      patients into obese and non-obese cohorts. The primary endpoint was mortality. 
      Results After propensity score matching, obese patients who underwent mechanical 
      thrombectomy had decreased mortality (p = 0.0033, odds ratio = 0.81, 95% 
      confidence interval = 0.704,0.932) compared to non-obese patients. No 
      statistically significant difference was shown between these two cohorts for the 
      outcomes of ventilator dependence, hemicraniectomy, or post-procedure 
      intracerebral hemorrhage. Conclusion Despite increasing risk of ischemic stroke, 
      obese patients who undergo mechanical thrombectomy have decreased mortality rates 
      compared to their non-obese counterparts.
CI  - Copyright © 2021, Hallan et al.
FAU - Hallan, David R
AU  - Hallan DR
AD  - Neurosurgery, Penn State Health Milton S. Hershey Medical Center, Hershey, USA.
LA  - eng
PT  - Journal Article
DEP - 20210113
PL  - United States
TA  - Cureus
JT  - Cureus
JID - 101596737
PMC - PMC7880829
OTO - NOTNLM
OT  - bmi
OT  - cerebrovascular
OT  - hemorrhagic conversion
OT  - mortality
OT  - neurosurgery
OT  - obesity
OT  - outcomes
OT  - stroke
OT  - thrombectomy
OT  - trinetx
COIS- The authors have declared that no competing interests exist.
EDAT- 2021/02/20 06:00
MHDA- 2021/02/20 06:01
PMCR- 2021/01/13
CRDT- 2021/02/19 06:07
PHST- 2021/02/19 06:07 [entrez]
PHST- 2021/02/20 06:00 [pubmed]
PHST- 2021/02/20 06:01 [medline]
PHST- 2021/01/13 00:00 [pmc-release]
AID - 10.7759/cureus.12671 [doi]
PST - epublish
SO  - Cureus. 2021 Jan 13;13(1):e12671. doi: 10.7759/cureus.12671.

PMID- 33590984
OWN - NLM
STAT- MEDLINE
DCOM- 20210218
LR  - 20210218
IS  - 0374-9096 (Print)
IS  - 0374-9096 (Linking)
VI  - 55
IP  - 1
DP  - 2021 Jan
TI  - [A Rare Yeast: Cases of Rhodotorula mucilaginosa Infection Followed Up in a 
      Tertiary University Hospital].
PG  - 91-98
LID - 10.5578/mb.20188 [doi]
AB  - Rhodotorula species are yeasts that are common in the environment,but are not 
      frequently encountered as an infectious agent in humans. Rhodotorula 
      mucilaginosa, Rhodotorula glutinis and Rhodotorula minuta are the species that 
      cause disease in humans. Although its isolation from mucosa is doubtful in terms 
      of the presence of true infection, it is more frequently encountered in daily 
      practice due to the increasing number of invasive procedures, immune system 
      deficiencies caused by immunosuppressive drugs and diseases. R.mucilaginosa 
      growth isolated from various clinical samples between 2000 and 2018 in a tertiary 
      university hospital was presented in this case report. The first case was an 
      82-year-old man with chronic lung disease, hypertension, congestive heart failure 
      and acute leukemia causing severe immunosuppression. Use of broad spectrum 
      antibiotics, history of immunosuppressive therapy, presence of jugular catheter 
      were the risk factors in this patient. R.mucilaginosa was isolated from blood 
      culture while the patient was receiving fluconazole treatment for Candida 
      albicans grown in urine culture and the patient died before starting the 
      treatment. The second case was a 34-year-old female patient with congenital heart 
      disease. Discharge was observed at the intracardiac defibrillator site of the 
      patient, a temporary pacemaker was inserted, and she used broad spectrum 
      antibiotics for a long time. When the yeast growth was reported in the blood 
      culture, caspofungin treatment was initiated. Although the treatment was switched 
      to amphotericin B lipid complex after the culture result was reported as 
      R.mucilaginosa, the patient died after 12 hours. The third case was a 70-year-old 
      woman with hypertension, dementia, diabetes mellitus and rheumatoid arthritis 
      admitted to the intensive care unit due to cerebrovascular accident. She received 
      different immunosuppressive treatments and had invasive procedures. 
      R.mucilaginosa was isolated from the blood culture taken from the patient's 
      catheter, and there was no growth in the blood culture obtained from the 
      peripheral vein. Anidulafungin was started empirically, which was changed to 
      amphotericin B lipid complex after the identification of the yeast. The patient 
      died for various reasons 10 days after the antifungal treatment was stopped. Our 
      last case was a 55-year-old woman with metastatic ovarian cancer and secondary 
      ascites. Broad-spectrum multiple antibiotics were used and invasive procedures 
      were performed. R.mucilaginosa and C.albicans were isolated from the urine of the 
      patient who had a urinary catheter. No growth was detected from urine after 
      changing the urinary catheter. Therefore, growths were evaluated as colonization, 
      and fluconazole was administered for C.albicans due to the high risk of invasive 
      infection. The patient was lost for different reasons. The development and 
      diversity of the treatment methods lead to the emergence of some opportunistic 
      infectious agents that were not observed previously. Rhodotorula species are one 
      of the rare agents that have increased over the years. Rhodotorula species should 
      be considered as the cause of an infection if no clinical response is obtained 
      after echinocandin and/or fluconazole treatment in patients with long-term 
      immunosuppression and invasive procedures. Data on clinical pictures, treatment 
      responses, follow-up and treatment results of this rare yeast are still limited. 
      This case series was presented to draw attention to the risk factors related to 
      R.mucilaginosa infection/colonization, clinical characteristics of the patients, 
      follow-up results and treatment options and to contribute to the literature.
FAU - Ayaz, Çağlayan Merve
AU  - Ayaz ÇM
AD  - Hacettepe University Faculty of Medicine, Department of Infectious Diseases and 
      Clinical Microbiology, Ankara, Turkey.
FAU - Gülmez, Dolunay
AU  - Gülmez D
AD  - Hacettepe University Faculty of Medicine, Department of Medical Microbiology, 
      Ankara, Turkey.
FAU - Arıkan Akdağlı, Sevtap
AU  - Arıkan Akdağlı S
AD  - Hacettepe University Faculty of Medicine, Department of Medical Microbiology, 
      Ankara, Turkey.
FAU - Uzun, Ömrüm
AU  - Uzun Ö
AD  - Hacettepe University Faculty of Medicine, Department of Infectious Diseases and 
      Clinical Microbiology, Ankara, Turkey.
LA  - tur
PT  - Case Reports
PT  - Journal Article
TT  - Nadir Etken Bir Maya: Üçüncü Basamak Üniversite Hastanesinde İzlenen Rhodotorula 
      mucilaginosa Enfeksiyonu Olguları.
PL  - Turkey
TA  - Mikrobiyol Bul
JT  - Mikrobiyoloji bulteni
JID - 7503830
RN  - 0 (Antifungal Agents)
RN  - Rhodotorula mucilaginosa
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Antifungal Agents/therapeutic use
MH  - Fatal Outcome
MH  - Female
MH  - Fungemia/drug therapy/microbiology
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Mycoses/drug therapy/microbiology/urine
MH  - *Rhodotorula
MH  - Tertiary Care Centers
MH  - Turkey
EDAT- 2021/02/17 06:00
MHDA- 2021/02/20 06:00
CRDT- 2021/02/16 08:38
PHST- 2021/02/16 08:38 [entrez]
PHST- 2021/02/17 06:00 [pubmed]
PHST- 2021/02/20 06:00 [medline]
AID - 10.5578/mb.20188 [doi]
PST - ppublish
SO  - Mikrobiyol Bul. 2021 Jan;55(1):91-98. doi: 10.5578/mb.20188.

PMID- 33589553
OWN - NLM
STAT- MEDLINE
DCOM- 20211021
LR  - 20240928
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 48
IP  - 9
DP  - 2021 Sep
TI  - Improved Incidence of Cardiovascular Disease in Patients With Incident Rheumatoid 
      Arthritis in the 2000s: A Population-based Cohort Study.
PG  - 1379-1387
LID - 10.3899/jrheum.200842 [doi]
AB  - OBJECTIVE: To assess trends in incidence of cardiovascular disease (CVD) and 
      mortality following incident CVD events in patients with rheumatoid arthritis 
      (RA) onset in 1980-2009 vs non-RA subjects. METHODS: We studied Olmsted County, 
      Minnesota residents with incident RA (aged > 18 yrs, 1987 American College of 
      Rheumatology criteria met in 1980-2009) and non-RA subjects from the same source 
      population with similar age, sex, and calendar year of index. All subjects were 
      followed until death, migration, or December 31, 2016. Incident CVD events 
      included myocardial infarction and stroke. Patients with CVD before RA 
      incidence/index date were excluded. Cox models were used to compare incident CVD 
      events by decade, adjusting for age, sex, and CVD risk factors. RESULTS: The 
      study included 905 patients with RA and 904 non-RA subjects. Cumulative incidence 
      of any CVD event was lower in patients with incident RA in the 2000s vs the 
      1980s. The HR for any incident CVD in the 2000s vs 1980s was 0.53 (95% CI 
      0.31-0.93). The strength of association attenuated after adjustment for 
      anti-rheumatic medication use (HR 0.64, 95% CI 0.34-1.22). Patients with RA in 
      the 2000s had no excess in CVD over non-RA subjects (HR 0.71, 95% CI 0.42-1.19). 
      Risk of death after a CVD event was somewhat lower in patients with RA after the 
      1980s with an HR of 0.54 (95% CI 0.33-0.90) in the 1990s vs 1980s and 0.68 (95% 
      CI 0.33-1.41) in the 2000s vs 1980s. CONCLUSION: The incidence of major CVD 
      events in RA has declined in recent decades. The gap in CVD occurrence between 
      patients with RA and the general population is closing. Mortality after CVD 
      events in RA may be improving.
CI  - © 2021 The Journal of Rheumatology.
FAU - Myasoedova, Elena
AU  - Myasoedova E
AUID- ORCID: 0000-0003-2006-1436
AD  - E. Myasoedova, MD, PhD, Division of Rheumatology, Department of Internal 
      Medicine, and Division of Epidemiology, Department of Health Sciences Research, 
      Mayo Clinic; myasoedova.elena@mayo.edu.
FAU - Davis, John M
AU  - Davis JM
AUID- ORCID: 0000-0002-9710-8143
AD  - J.M. Davis III, MD, MS, Division of Rheumatology, Department of Internal 
      Medicine, Mayo Clinic.
FAU - Roger, Veronique L
AU  - Roger VL
AD  - V.L. Roger, MD, MPH, Division of Epidemiology, Department of Health Sciences 
      Research, and Division of Circulatory Failure, Department of Cardiovascular 
      Disease, Mayo Clinic.
FAU - Achenbach, Sara J
AU  - Achenbach SJ
AD  - S.J. Achenbach, MS, Division of Medical Statistics and Informatics, Department of 
      Health Sciences Research, Mayo Clinic.
FAU - Crowson, Cynthia S
AU  - Crowson CS
AUID- ORCID: 0000-0001-5847-7475
AD  - C.S. Crowson, PhD, Division of Rheumatology, Department of Internal Medicine, and 
      Division of Medical Statistics and Informatics, Department of Health Sciences 
      Research, Mayo Clinic, Rochester, Minnesota, USA.
LA  - eng
GR  - R01 AR046849/AR/NIAMS NIH HHS/United States
GR  - R01 AG034676/AG/NIA NIH HHS/United States
GR  - R33 AG058738/AG/NIA NIH HHS/United States
GR  - R01 HL120859/HL/NHLBI NIH HHS/United States
GR  - R01 AG068192/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20210215
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Antirheumatic Agents)
SB  - IM
CIN - J Rheumatol. 2021 Sep;48(9):1351-1353. doi: 10.3899/jrheum.210366. PMID: 34329190
MH  - *Antirheumatic Agents/therapeutic use
MH  - *Arthritis, Rheumatoid/drug therapy/epidemiology
MH  - *Cardiovascular Diseases/drug therapy/epidemiology
MH  - Cohort Studies
MH  - Humans
MH  - Incidence
PMC - PMC8364571
MID - NIHMS1668557
OTO - NOTNLM
OT  - cardiovascular diseases
OT  - epidemiology
OT  - rheumatoid arthritis
COIS- Conflict of interest: Authors declare no conflict of interest.
EDAT- 2021/02/17 06:00
MHDA- 2022/09/03 06:00
PMCR- 2022/09/01
CRDT- 2021/02/16 06:02
PHST- 2021/01/29 00:00 [accepted]
PHST- 2021/02/17 06:00 [pubmed]
PHST- 2022/09/03 06:00 [medline]
PHST- 2021/02/16 06:02 [entrez]
PHST- 2022/09/01 00:00 [pmc-release]
AID - jrheum.200842 [pii]
AID - 10.3899/jrheum.200842 [doi]
PST - ppublish
SO  - J Rheumatol. 2021 Sep;48(9):1379-1387. doi: 10.3899/jrheum.200842. Epub 2021 Feb 
      15.

PMID- 33563055
OWN - NLM
STAT- MEDLINE
DCOM- 20220602
LR  - 20220602
IS  - 1532-4311 (Electronic)
IS  - 0882-0139 (Linking)
VI  - 51
IP  - 4
DP  - 2022 May
TI  - The increased risk of atrial fibrillation in inflammatory arthritis: a systematic 
      review and meta-analysis of cohort studies.
PG  - 1095-1107
LID - 10.1080/08820139.2021.1884091 [doi]
AB  - BACKGROUND: Atrial fibrillation (AF) is the most common cardiac arrhythmia 
      contributing to stroke and sudden cardiac death. Numbers of studies indicated 
      that patients with inflammatory arthritis have an increased risk of AF. The 
      present study aims to assess the risk of AF in inflammatory arthritis patients. 
      METHODS: We systematically searched cohort studies regarding the risk of AF in 
      patients with rheumatoid arthritis, or spondyloarthritis through PubMed, Web of 
      Science, Cochrane Library, Clinical Trials Registry, and China National Knowledge 
      from inception to August 1, 2019. Meta-analysis was performed using fixed effect 
      model, estimating both crude and adjusted hazard ratios (HRs) with 95% confidence 
      intervals (CIs). Subgroup analysis and meta-regression based on geographic 
      characteristics, comorbidities, and medication use were conducted to explore the 
      source of heterogeneity. RESULTS: Literature search identified 388 potentially 
      relevant studies, and five studies containing seven cohorts of rheumatoid 
      arthritis or spondyloarthritis were included in the meta-analysis. The AF risk of 
      inflammatory arthritis patients was significantly increased compared with health 
      controls (HR = 1.42, 95% CI: 1.36 to 1.49, Z = 14.17, P < .001), and the pooled 
      HR of studies adjusted factor, like demographic characteristics, medications use, 
      and comorbidities, was 1.37 (95% CI: 1.29 to 1.46; Z = 9.82, P < .001). 
      CONCLUSION: Patients with inflammatory arthritis have increased risk of AF, 
      probably due to the underlying chronic inflammation. Although various confounders 
      have been adjusted like medications use and comorbidities, the risk of AF is 
      still significantly increased in inflammatory arthritis patients. ABBREVIATIONS: 
      AF: Atrial fibrillation; AS: Ankylosing spondylitis; CI: Confidence interval; HR: 
      Hazard ratio; NOS: Newcastle-Ottawa scale; NSAIDs: Non-steroid anti-inflammatory 
      drugs; PsA: Psoriatic arthritis; RA: Rheumatoid arthritis; SpA: 
      Spondyloarthritis; TNFi: Tumor necrosis factors inhibitor; uSpA: Undifferentiated 
      spondyloarthritis.
FAU - Ma, Yubo
AU  - Ma Y
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Anhui 
      Medical University, Hefei, Anhui, China.
AD  - The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, 
      Anhui, China.
FAU - Pan, Zhipeng
AU  - Pan Z
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Anhui 
      Medical University, Hefei, Anhui, China.
AD  - Department of Medical Oncology, First Affiliated Hospital of Anhui Medical 
      University, Hefei, Anhui, China.
FAU - Fan, Dazhi
AU  - Fan D
AUID- ORCID: 0000-0003-2773-9166
AD  - Foshan Institute of Fetal Medicine, Southern Medical University Affiliated 
      Maternal and Child Health Hospital of Foshan, Foshan, Guangdong, China.
FAU - Xu, Shanshan
AU  - Xu S
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Anhui 
      Medical University, Hefei, Anhui, China.
AD  - The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, 
      Anhui, China.
FAU - Pan, Faming
AU  - Pan F
AUID- ORCID: 0000-0003-4242-1025
AD  - Department of Epidemiology and Biostatistics, School of Public Health, Anhui 
      Medical University, Hefei, Anhui, China.
AD  - The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, Hefei, 
      Anhui, China.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Systematic Review
DEP - 20210210
PL  - England
TA  - Immunol Invest
JT  - Immunological investigations
JID - 8504629
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal
MH  - *Arthritis, Psoriatic
MH  - *Arthritis, Rheumatoid/complications/drug therapy
MH  - *Atrial Fibrillation/drug therapy/epidemiology
MH  - Cohort Studies
MH  - Humans
MH  - Risk Factors
MH  - *Spondylarthritis/complications/drug therapy/epidemiology
OTO - NOTNLM
OT  - Ankylosing spondylitis
OT  - atrial fibrillation
OT  - inflammatory arthritis
OT  - rheumatoid arthritis
EDAT- 2021/02/11 06:00
MHDA- 2022/06/03 06:00
CRDT- 2021/02/10 05:34
PHST- 2021/02/11 06:00 [pubmed]
PHST- 2022/06/03 06:00 [medline]
PHST- 2021/02/10 05:34 [entrez]
AID - 10.1080/08820139.2021.1884091 [doi]
PST - ppublish
SO  - Immunol Invest. 2022 May;51(4):1095-1107. doi: 10.1080/08820139.2021.1884091. 
      Epub 2021 Feb 10.

PMID- 28520369
STAT- Publisher
DRDT- 20210125
CTDT- 20160818
PB  - National Center for Biotechnology Information (US)
DP  - 2012
TI  - Celecoxib Therapy and CYP2C9 Genotype.
BTI - Medical Genetics Summaries
AB  - Celecoxib (brand name Celebrex) is a nonsteroidal anti-inflammatory drug (NSAID) 
      that is used to manage osteoarthritis, rheumatoid arthritis, menstrual symptoms, 
      and acute pain. Celecoxib is a “COX-2 inhibitor.” The cyclooxygenase (COX) 
      enzymes catalyze pathways that play a key role in the generation of the 
      inflammatory response. Most NSAIDs inhibit both types of cyclooxygenase, COX-1 
      and COX-2, while celecoxib selectively inhibits COX-2. Celecoxib is primarily 
      metabolized by CYP2C9. Individuals who lack CYP2C9 activity (“CYP2C9 poor 
      metabolizers”) have an increased exposure to celecoxib, and an increased risk of 
      side effects. Like all non-aspirin NSAIDs, celecoxib increases the risk of 
      serious cardiovascular events, including myocardial infarction and stroke, and 
      serious gastrointestinal (GI) adverse events such as bleeding, ulceration, and 
      perforation. The FDA-approved drug label states that in individuals “who are 
      known or suspected to be poor CYP2C9 metabolizers based on genotype or previous 
      history/experience with other CYP2C9 substrates (such as warfarin, phenytoin), 
      initiate treatment with half the lowest recommended dose” (Table 1)(1). 
      Recommendations from the Clinical Pharmacogenetics Implementation Consortium 
      (CPIC) include initiating celecoxib at 25–50% of the lowest recommended starting 
      dose. Titrate dose upward to clinical effect or 25–50% of the maximum recommended 
      dose with caution” (Table 2)(2).
FED - Pratt, Victoria M
ED  - Pratt VM
AD  - Adjunct Professor, Clinical Pharmacology, Indiana University School of Medicine, 
      Indianapolis, IN 46202
AD  - Director, Scientific Affairs Pharmacogenetics, Agena Bioscience, San Diego CA 
      92121
FED - Scott, Stuart A
ED  - Scott SA
AD  - Professor, Department of Pathology Stanford University, Palo Alto, CA 94305
AD  - Director, Stanford Medicine Clinical Genomics Laboratory, Stanford, CA 94305
FED - Pirmohamed, Munir
ED  - Pirmohamed M
AD  - David Weatherall Chair of Medicine and UK National Health Service Chair of 
      Pharmacogenetics, University of Liverpool, Liverpool, UK
AD  - Director, MRC Centre for Drug Safety Science and Wolfson Centre for Personalized 
      Medicine, University of Liverpool, Liverpool, UK
AD  - Director, Health Data Research UK North, Liverpool, UK
FED - Esquivel, Bernard
ED  - Esquivel B
AD  - CEO, GenXys, Vancouver, BC V6B 1B8, Canada
AD  - VP, Clinical Innovation, ixlayer, San Francisco, CA 94105
FED - Kattman, Brandi L
ED  - Kattman BL
AD  - Chief, Medical Genetics and Human Variation, National Center for Biotechnology 
      Information (NCBI), National Library of Medicine, National Institutes of Health, 
      Bethesda, MD 20894
FED - Malheiro, Adriana J
ED  - Malheiro AJ
AD  - Project Lead, Medical Genetics and Human Variation, National Center for 
      Biotechnology Information (NCBI), National Library of Medicine, National 
      Institutes of Health, Bethesda, MD 20894
FAU - Dean, Laura
AU  - Dean L
AD  - NCBI
FAU - Kane, Megan
AU  - Kane M
AD  - NCBI
LA  - eng
PT  - Review
PT  - Book Chapter
PL  - Bethesda (MD)
OTO - NLM
OT  - Celecoxib therapy
OT  - celecoxib response
OT  - Celebrex response
OT  - CYP2C9
OT  - CYP2C9*2
OT  - CYP2C9*3
EDAT- 2021/01/25 00:00
CRDT- 2021/01/25 00:00
AID - NBK379478 [bookaccession]

PMID- 33482567
OWN - NLM
STAT- MEDLINE
DCOM- 20210323
LR  - 20240103
IS  - 1532-8511 (Electronic)
IS  - 1052-3057 (Print)
IS  - 1052-3057 (Linking)
VI  - 30
IP  - 4
DP  - 2021 Apr
TI  - Association Between Chronic Inflammatory Diseases and Stroke-Associated Pneumonia 
      - An Epidemiological Study.
PG  - 105605
LID - S1052-3057(21)00007-0 [pii]
LID - 10.1016/j.jstrokecerebrovasdis.2021.105605 [doi]
AB  - BACKGROUND: Pneumonia, the most common post-acute ischemic stroke (AIS) 
      infection, accounts for up to 30% of deaths after a stroke. Multiple chronic 
      inflammatory diseases, such as rheumatoid arthritis, psoriasis, and inflammatory 
      bowel disease, are associated with increased risk of stroke and stroke morbidity. 
      This study assessed the relationship between chronic inflammatory diseases and 
      stroke-associated pneumonia (SAP). METHODS: Using data from the 2015-2017 
      National Inpatient Sample, we classified hospital discharges with a diagnosis of 
      AIS as having ulcerative colitis, Crohn's disease, rheumatoid arthritis, 
      psoriasis, systemic lupus erythematosus, other chronic inflammatory diseases, 
      multiple chronic inflammatory diseases, or none. With multivariable logistic 
      regression, we assessed for associations between chronic inflammatory disease and 
      in-hospital SAP or death. RESULTS: Among AIS discharges, there was a decreased 
      risk of SAP among those with psoriasis or other chronic inflammatory diseases 
      (adjusted odds ratio (aOR) 0.70, 95%CI 0.63-0.99; aOR 0.64, 95%CI, 0.46-0.89, 
      respectively), compared to those without psoriasis and without other chronic 
      inflammatory disease, respectively. Rheumatoid arthritis, psoriasis, and other 
      chronic inflammatory diseases were associated with reduced in-hospital mortality 
      (aOR 0.89, 95%CI 0.78-1.00; aOR 0.77, 95%CI 0.59-1.00; aOR 0.69, 95%CI 0.50-0.94, 
      respectively). CONCLUSIONS: The risk of SAP and in-hospital mortality varies by 
      chronic inflammatory disease - psoriasis and other chronic inflammatory diseases 
      are associate with reduced rates of SAP, whereas rheumatoid arthritis, psoriasis 
      and other chronic inflammatory disease were associated with reduced in-hospital 
      mortality. Further investigations are needed to determine a relationship between 
      the potential role of immunomodulation and the reduction in SAP and mortality in 
      chronic inflammatory diseases.
CI  - Copyright © 2021 Elsevier Inc. All rights reserved.
FAU - Dylla, Layne
AU  - Dylla L
AD  - Department of Emergency Medicine, University of Colorado School of Medicine, 
      12401 E. 17th Ave., B215, Aurora, CO 80045, United States. Electronic address: 
      Layne.Dylla@cuanschutz.edu.
FAU - Herson, Paco S
AU  - Herson PS
AD  - Department of Anesthesiology, University of Colorado School of Medicine, United 
      States.
FAU - Poisson, Sharon N
AU  - Poisson SN
AD  - Department of Neurology, University of Colorado School of Medicine, United 
      States.
FAU - Rice, John D
AU  - Rice JD
AD  - Department of Biostatistics and Informatics, Colorado School of Public Health, 
      United States.
FAU - Ginde, Adit A
AU  - Ginde AA
AD  - Department of Emergency Medicine, University of Colorado School of Medicine, 
      12401 E. 17th Ave., B215, Aurora, CO 80045, United States.
LA  - eng
GR  - K12 AR084226/AR/NIAMS NIH HHS/United States
GR  - K12 HD057022/HD/NICHD NIH HHS/United States
PT  - Journal Article
DEP - 20210119
PL  - United States
TA  - J Stroke Cerebrovasc Dis
JT  - Journal of stroke and cerebrovascular diseases : the official journal of National 
      Stroke Association
JID - 9111633
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Chronic Disease
MH  - Databases, Factual
MH  - Female
MH  - Hospital Mortality
MH  - Humans
MH  - Inflammation/diagnosis/*epidemiology/mortality
MH  - Inpatients
MH  - Male
MH  - Middle Aged
MH  - Pneumonia/diagnosis/*epidemiology/mortality
MH  - Retrospective Studies
MH  - Risk Assessment
MH  - Risk Factors
MH  - Stroke/diagnosis/*epidemiology/mortality
MH  - United States/epidemiology
MH  - Young Adult
PMC - PMC7946738
MID - NIHMS1660902
OTO - NOTNLM
OT  - Acute Ischemic Stroke
OT  - Cerebrovascular infarction
OT  - Stroke
OT  - Stroke complications
OT  - Stroke-associated Pneumonia
EDAT- 2021/01/23 06:00
MHDA- 2021/03/24 06:00
PMCR- 2022/04/01
CRDT- 2021/01/22 20:14
PHST- 2020/10/06 00:00 [received]
PHST- 2020/12/23 00:00 [revised]
PHST- 2021/01/02 00:00 [accepted]
PHST- 2021/01/23 06:00 [pubmed]
PHST- 2021/03/24 06:00 [medline]
PHST- 2021/01/22 20:14 [entrez]
PHST- 2022/04/01 00:00 [pmc-release]
AID - S1052-3057(21)00007-0 [pii]
AID - 10.1016/j.jstrokecerebrovasdis.2021.105605 [doi]
PST - ppublish
SO  - J Stroke Cerebrovasc Dis. 2021 Apr;30(4):105605. doi: 
      10.1016/j.jstrokecerebrovasdis.2021.105605. Epub 2021 Jan 19.

PMID- 33386606
OWN - NLM
STAT- MEDLINE
DCOM- 20211026
LR  - 20211026
IS  - 1970-9366 (Electronic)
IS  - 1828-0447 (Linking)
VI  - 16
IP  - 6
DP  - 2021 Sep
TI  - Temporal trends from 2005 to 2018 in deaths and cardiovascular events in subjects 
      with newly diagnosed rheumatoid arthritis.
PG  - 1467-1475
LID - 10.1007/s11739-020-02581-z [doi]
AB  - Although rheumatoid arthritis (RA) is associated with an increased risk of death 
      and cardiovascular (CV) disease, the excess of these risks is expected to have 
      diminished over time, in more recent incident cohorts with RA. We analysed the 
      risk of all-cause death, stroke, and myocardial infarction as primary outcomes 
      and all CV events as secondary outcomes in RA subjects compared to the general 
      population, from 2005 to 2018. The risk outcomes were also evaluated in relation 
      to the time since RA diagnosis. We conducted a cohort study using linkable 
      administrative healthcare databases of the Lombardy Region, Northern Italy. 
      Analyses included subjects newly diagnosed RA subjects and a random sample of 
      No-RA subjects. An adjusted Cox proportional hazard regression model was used to 
      calculate hazard ratios and 95% CIs for all outcomes. The study population 
      comprised 16,047 RA subjects and 500,000 without RA. The risks of dying (HR 1.22, 
      95% CI 1.15-1.30), stroke (HR 1.39, 95% CI 1.22-1.58), myocardial infarction (HR 
      2.00, 95% CI 1.78-2.26) were significantly higher in the RA cohort, as were those 
      that for secondary outcomes. Differences between RA and No-RA already emerged 
      during the first five years after diagnosis. Risk patterns remained statistically 
      significant during the next 5 years or more. Subjects with RA still have a higher 
      risk of death and worse CV outcomes than the general population, appearing early 
      and not decreasing with time. Preventive interventions are urgently needed.
CI  - © 2021. Società Italiana di Medicina Interna (SIMI).
FAU - Baviera, Marta
AU  - Baviera M
AUID- ORCID: 0000-0002-0264-151X
AD  - Laboratory of Cardiovascular Prevention, Istituto di Ricerche Farmacologiche 
      Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy. 
      marta.baviera@marionegri.it.
FAU - Cioffi, Giovanni
AU  - Cioffi G
AD  - Rheumatology Section, Department of Medicine, University of Verona and Azienda 
      Ospedaliera Universitaria Integrata of Verona, Verona, Italy.
AD  - Division of Cardiac Rehabilitation, S. Pancrazio Hospital, Arco, Trento, Italy.
FAU - Colacioppo, Pierluca
AU  - Colacioppo P
AD  - Laboratory of Cardiovascular Prevention, Istituto di Ricerche Farmacologiche 
      Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy.
FAU - Tettamanti, Mauro
AU  - Tettamanti M
AD  - Laboratory of Geriatric Neuropsychiatry, Istituto di Ricerche Farmacologiche 
      Mario Negri IRCCS, Milan, Italy.
FAU - Fortino, Ida
AU  - Fortino I
AD  - Regional Health Ministry, Lombardy Region, Milan, Italy.
FAU - Roncaglioni, Maria Carla
AU  - Roncaglioni MC
AD  - Laboratory of Cardiovascular Prevention, Istituto di Ricerche Farmacologiche 
      Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210102
PL  - Italy
TA  - Intern Emerg Med
JT  - Internal and emergency medicine
JID - 101263418
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications/epidemiology/mortality
MH  - Cardiovascular Diseases/epidemiology/*mortality
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Italy/epidemiology
MH  - Kaplan-Meier Estimate
MH  - Male
MH  - Middle Aged
MH  - Mortality/*trends
MH  - Proportional Hazards Models
MH  - *Time Factors
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - Death
OT  - Myocardial infarction
OT  - Rheumatoid arthritis
OT  - Stroke
EDAT- 2021/01/03 06:00
MHDA- 2021/10/27 06:00
CRDT- 2021/01/02 05:20
PHST- 2020/07/10 00:00 [received]
PHST- 2020/11/20 00:00 [accepted]
PHST- 2021/01/03 06:00 [pubmed]
PHST- 2021/10/27 06:00 [medline]
PHST- 2021/01/02 05:20 [entrez]
AID - 10.1007/s11739-020-02581-z [pii]
AID - 10.1007/s11739-020-02581-z [doi]
PST - ppublish
SO  - Intern Emerg Med. 2021 Sep;16(6):1467-1475. doi: 10.1007/s11739-020-02581-z. Epub 
      2021 Jan 2.

PMID- 33343726
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220419
IS  - 1759-720X (Print)
IS  - 1759-7218 (Electronic)
IS  - 1759-720X (Linking)
VI  - 12
DP  - 2020
TI  - Higher depression rates and similar cardiovascular comorbidity in psoriatic 
      arthritis compared with rheumatoid arthritis and diabetes mellitus.
PG  - 1759720X20976975
LID - 10.1177/1759720X20976975 [doi]
LID - 1759720X20976975
AB  - BACKGROUND: We explore the spectrum of comorbidities in psoriatic arthritis (PsA) 
      patients in comparison with other high comorbidity-burden diseases like 
      rheumatoid arthritis (RA) and diabetes mellitus (DM). METHODS: Two hundred and 
      fifteen PsA patients, cross-sectionally collected from two tertiary hospitals, 
      were compared with 215 RA and 215 DM patients (age/sex-matched, similar disease 
      duration). Cardiovascular risk factors [hypertension, current smoking, 
      hyperlipidaemia, obesity (body mass index (BMI) ⩾30)], coronary artery disease 
      (CAD), stroke, major adverse cardiac events (MACEs; combined CAD and stroke), 
      depression, osteoporosis and malignancies were recorded. Odds ratios (ORs) for 
      stroke, CAD and MACE were adjusted for age, sex, hypertension, smoking, 
      hyperlipidaemia, BMI, glucocorticoids use and those for depression were adjusted 
      for age, sex, disease duration, skin involvement and smoking. Within the PsA 
      group, associations between comorbidities and demographic/clinical features were 
      assessed. RESULTS: Depression [OR (95% confidence interval (CI)): 3.02 
      (1.57-5.81)], obesity [OR (95% CI): 2.83, (1.65-4.86)] and hyperlipidaemia [OR 
      (95% CI): 1.96 (1.32-2.90)] were more prevalent in PsA compared with RA, while no 
      differences were observed for CAD, stroke, MACE and malignancies. Depression [OR 
      (95% CI): 4.85 (2.37-9.93)] and osteoporosis [OR (95% CI): 6.22 (1.33-29.2)] were 
      more common in PsA than in DM. Hypertension, but not the other cardiovascular 
      risk factors, was more frequent in DM [OR (95% CI) 0.49 (0.33-0.74)]. However, 
      prevalence of stroke, CAD and MACE did not differ between PsA and DM. Within PsA 
      group, depression was associated with age [OR (95% CI): 1.03 (0.99-1.06)], female 
      sex [OR (95% CI): 3.47 (1.51-7.99)] and smoking [OR (95% CI): 2.78 (1.31-5.88)] 
      while MACEs were associated with age [OR (95% CI): 1.08 (1.00-1.17)], male sex 
      [OR (95% CI) for females: 0.26 (0.06-1.23) and hypertension [OR (95% CI): 6.07 
      (1.12-33.0)]. No differences were recorded in comorbidities between the different 
      PsA phenotypes. CONCLUSION: Depression was more prevalent in PsA compared with RA 
      and DM, while cardiovascular comorbidity was comparable to both groups, 
      supporting the need for their assessment and management.
CI  - © The Author(s), 2020.
FAU - Fragoulis, George E
AU  - Fragoulis GE
AUID- ORCID: 0000-0003-4932-7023
AD  - Rheumatology Unit, Joint Rheumatology Program, Medical School, First Department 
      of Propaedeutic Internal Medicine, National and Kapodistrian University of 
      Athens, "Laiko" General Hospital, 75 Mikras Asias Str., Athens, 115 27, Greece.
FAU - Evangelatos, Gerasimos
AU  - Evangelatos G
AD  - Rheumatology Department, 417 Army Shared Fund Hospital "NIMTS", Athens, Greece.
FAU - Tentolouris, Nikolaos
AU  - Tentolouris N
AD  - Diabetology Unit, First Department of Propaedeutic Internal Medicine, Medical 
      School, National and Kapodistrian University of Athens, "Laiko" General Hospital, 
      Athens, Greece.
FAU - Fragkiadaki, Kalliopi
AU  - Fragkiadaki K
AD  - Rheumatology Unit, First Department of Propaedeutic Internal Medicine, Joint 
      Rheumatology Program, Medical School, National and Kapodistrian University of 
      Athens, "Laiko" General Hospital, Athens, Greece.
FAU - Panopoulos, Stylianos
AU  - Panopoulos S
AD  - Rheumatology Unit, First Department of Propaedeutic Internal Medicine, Joint 
      Rheumatology Program, Medical School, National and Kapodistrian University of 
      Athens, "Laiko" General Hospital, Athens, Greece.
FAU - Konstantonis, George
AU  - Konstantonis G
AD  - Rheumatology Unit, First Department of Propaedeutic Internal Medicine, Joint 
      Rheumatology Program, Medical School, National and Kapodistrian University of 
      Athens, "Laiko" General Hospital, Athens, Greece.
FAU - Iliopoulos, Alexios
AU  - Iliopoulos A
AD  - Rheumatology Department, 417 Army Shared Fund Hospital "NIMTS", Athens, Greece.
FAU - Chatzidionysiou, Katerina
AU  - Chatzidionysiou K
AD  - Rheumatology Unit, First Department of Propaedeutic Internal Medicine, Joint 
      Rheumatology Program, Medical School, National and Kapodistrian University of 
      Athens, "Laiko" General Hospital, Athens, Greece.
FAU - Sfikakis, Petros P
AU  - Sfikakis PP
AD  - Rheumatology Unit, First Department of Propaedeutic Internal Medicine, Joint 
      Rheumatology Program, Medical School, National and Kapodistrian University of 
      Athens, "Laiko" General Hospital, Athens, Greece.
FAU - Tektonidou, Maria G
AU  - Tektonidou MG
AUID- ORCID: 0000-0003-2238-0975
AD  - Rheumatology Unit, First Department of Propaedeutic Internal Medicine, Joint 
      Rheumatology Program, Medical School, National and Kapodistrian University of 
      Athens, "Laiko" General Hospital, Athens, Greece.
LA  - eng
PT  - Journal Article
DEP - 20201208
PL  - England
TA  - Ther Adv Musculoskelet Dis
JT  - Therapeutic advances in musculoskeletal disease
JID - 101517322
PMC - PMC7727079
OTO - NOTNLM
OT  - cardiovascular disease
OT  - comorbidities
OT  - depression
OT  - diabetes mellitus
OT  - psoriatic arthritis
OT  - rheumatoid arthritis
COIS- Conflict of interest statement: George E Fragoulis: has received speaker 
      honoraria from Janssen, travelling grants from AbbVie and MSD. Gerasimos 
      Evangelatos: does not have conflicts of interest related to this work. Nikolaos 
      Tentolouris: does not have conflicts of interest related to this work. Kalliopi G 
      Fragkiadaki: does not have conflicts of interest related to this work. Stylianos 
      Panopoulos: does not have conflicts of interest related to this work. Alexios 
      Iliopoulos: does not have conflicts of interest related to this work. Katerina 
      Chatzidionysiou: has received consultant fees from AbbVie, Pfizer, Lilly. Petros 
      P Sfikakis: has received consultant fees and unrestricted grants from AbbVie, 
      Pfizer, MSD, Roche, UCB, GSK, Novartis deposited to the Special Account for 
      Research Funding (ELKE) of the National and Kapodistrian University of Athens 
      Medical School. Maria G Tektonidou: has received consultant fees and unrestricted 
      grants from AbbVie, GSK, Genesis, MSD, Novartis, Pfizer and UCB deposited to 
      the Special Account for Research Funding (ELKE) of the National and Kapodistrian 
      University of Athens Medical School.
EDAT- 2020/12/22 06:00
MHDA- 2020/12/22 06:01
PMCR- 2020/12/08
CRDT- 2020/12/21 06:05
PHST- 2020/07/27 00:00 [received]
PHST- 2020/11/05 00:00 [accepted]
PHST- 2020/12/21 06:05 [entrez]
PHST- 2020/12/22 06:00 [pubmed]
PHST- 2020/12/22 06:01 [medline]
PHST- 2020/12/08 00:00 [pmc-release]
AID - 10.1177_1759720X20976975 [pii]
AID - 10.1177/1759720X20976975 [doi]
PST - epublish
SO  - Ther Adv Musculoskelet Dis. 2020 Dec 8;12:1759720X20976975. doi: 
      10.1177/1759720X20976975. eCollection 2020.

PMID- 33307184
OWN - NLM
STAT- MEDLINE
DCOM- 20220316
LR  - 20230402
IS  - 1542-7714 (Electronic)
IS  - 1542-3565 (Print)
IS  - 1542-3565 (Linking)
VI  - 20
IP  - 4
DP  - 2022 Apr
TI  - Long-term Outcomes Following Multiply Recurrent Clostridioides difficile 
      Infection and Fecal Microbiota Transplantation.
PG  - 806-816.e6
LID - S1542-3565(20)31642-6 [pii]
LID - 10.1016/j.cgh.2020.12.004 [doi]
AB  - BACKGROUND AND AIMS: Fecal microbiota transplantation (FMT) is a commonly used 
      therapy for multiply recurrent Clostridioides difficile (mrCDI). By altering the 
      gut microbiota, there is the potential for FMT to impact the risk for 
      cardiometabolic, intestinal or immune-mediated conditions. Likewise, the 
      microbiota disturbance associated with mrCDI could potentially lead to these 
      conditions. We aimed to assess the associations of mrCDI and FMT with 
      cardiometabolic, immune-mediated diseases, and irritable bowel syndrome. METHODS: 
      This retrospective cohort study using a United States commercial claims database 
      included persons diagnosed with CDI or undergoing FMT. We created 2 pairwise 
      comparisons: mrCDI vs non-mrCDI, and non-mrCDI or mrCDI treated with FMT vs mrCDI 
      without FMT. RESULTS: We found no significant association between mrCDI (vs 
      non-mrCDI) and inflammatory bowel disease (adjusted hazard ratio (aHR) = 1.65; 
      95% confidence interval, 0.67-4.04), rheumatoid arthritis (HR = 0.86; 0.47-1.56), 
      psoriasis (HR = 0.72; 0.23-2.27), diabetes (aHR = 0.97; 0.67-1.40), hypertension 
      (aHR = 1.05; 0.76-1.44), myocardial infarction (aHR = 0.82; 0.63-1.06), stroke 
      (aHR = 0.83; 0.62-1.12), or irritable bowel syndrome (HR = 0.94; 0.61-1.45). 
      Similarly, we found no association of CDI with FMT (vs mrCDI without FMT) and 
      diabetes (aHR = 0.92; 0.27-3.11), hypertension (aHR = 1.41; 0.64-3.15), stroke 
      (aHR = 1.27; 0.69-2.34) or inflammatory bowel syndrome (aHR = 0.80; 0.26-2.46). 
      However, the incidence of myocardial infarction was increased following FMT (aHR 
      = 1.68; 1.01-2.81). CONCLUSION: Relative to those with CDI, persons with mrCDI do 
      not appear to be intrinsically at higher risk of cardiometabolic, immune-mediated 
      diseases, or irritable bowel syndrome. However, those who underwent FMT for CDI 
      had a higher incidence of myocardial infarction. Future studies should assess 
      this association to assess reproducibility.
CI  - Copyright © 2022 AGA Institute. Published by Elsevier Inc. All rights reserved.
FAU - Dawwas, Ghadeer K
AU  - Dawwas GK
AD  - Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, 
      Philadelphia, Pennsylvania.
FAU - Brensinger, Colleen M
AU  - Brensinger CM
AD  - Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, 
      Philadelphia, Pennsylvania.
FAU - Vajravelu, Ravy K
AU  - Vajravelu RK
AD  - Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, 
      Philadelphia, Pennsylvania; Division of Gastroenterology and Hepatology, Perelman 
      School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
FAU - Wu, Qufei
AU  - Wu Q
AD  - Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, 
      Philadelphia, Pennsylvania.
FAU - Kelly, Colleen R
AU  - Kelly CR
AD  - Division of Gastroenterology, Warren Alpert Medical School, Brown University, 
      Providence, Rhode Island.
FAU - Laine, Loren
AU  - Laine L
AD  - Section of Digestive Diseases, Yale School of Medicine, New Haven, Connecticut; 
      VA Connecticut Healthcare System, West Haven, Connecticut.
FAU - Wu, Gary D
AU  - Wu GD
AD  - Division of Gastroenterology and Hepatology, Perelman School of Medicine, 
      University of Pennsylvania, Philadelphia, Pennsylvania.
FAU - Lewis, James D
AU  - Lewis JD
AD  - Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, 
      Philadelphia, Pennsylvania; Division of Gastroenterology and Hepatology, Perelman 
      School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. 
      Electronic address: lewisjd@pennmedicine.upenn.edu.
LA  - eng
GR  - R24 AI118629/AI/NIAID NIH HHS/United States
GR  - UL1 TR001863/TR/NCATS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20201208
PL  - United States
TA  - Clin Gastroenterol Hepatol
JT  - Clinical gastroenterology and hepatology : the official clinical practice journal 
      of the American Gastroenterological Association
JID - 101160775
SB  - IM
MH  - *Clostridioides difficile
MH  - *Clostridium Infections/complications/therapy
MH  - Fecal Microbiota Transplantation/adverse effects
MH  - Humans
MH  - Recurrence
MH  - Reproducibility of Results
MH  - Retrospective Studies
PMC - PMC8184854
MID - NIHMS1653466
OTO - NOTNLM
OT  - Clostridioides difficile
OT  - Diabetes
OT  - Fecal Microbiota Transplantation
OT  - Hypertension
OT  - Inflammatory Bowel Disease
OT  - Irritable Bowel Syndrome
OT  - Myocardial Infarction
OT  - Psoriasis
OT  - Rheumatoid Arthritis
OT  - Stroke
COIS- Conflict of interest statement: Dr. Lewis reports consulting for Merck and 
      Pfizer, outside of submitted work. Dr. Lewis and Dr. Wu reports having a patent, 
      “Compositions and methods comprising a defined microbiome and methods of use 
      thereof,” Dr. Kelly reports research support from Finch Therapeutics for a 
      clinical trial. Unpaid clinical advisor to OpenBiome
EDAT- 2020/12/12 06:00
MHDA- 2022/03/17 06:00
PMCR- 2023/04/01
CRDT- 2020/12/11 20:09
PHST- 2020/11/04 00:00 [received]
PHST- 2020/12/03 00:00 [accepted]
PHST- 2020/12/12 06:00 [pubmed]
PHST- 2022/03/17 06:00 [medline]
PHST- 2020/12/11 20:09 [entrez]
PHST- 2023/04/01 00:00 [pmc-release]
AID - S1542-3565(20)31642-6 [pii]
AID - 10.1016/j.cgh.2020.12.004 [doi]
PST - ppublish
SO  - Clin Gastroenterol Hepatol. 2022 Apr;20(4):806-816.e6. doi: 
      10.1016/j.cgh.2020.12.004. Epub 2020 Dec 8.

PMID- 33276814
OWN - NLM
STAT- MEDLINE
DCOM- 20210621
LR  - 20210621
IS  - 1478-6362 (Electronic)
IS  - 1478-6354 (Print)
IS  - 1478-6354 (Linking)
VI  - 22
IP  - 1
DP  - 2020 Dec 4
TI  - Derivation and internal validation of a multi-biomarker-based cardiovascular 
      disease risk prediction score for rheumatoid arthritis patients.
PG  - 282
LID - 10.1186/s13075-020-02355-0 [doi]
LID - 282
AB  - BACKGROUND: Rheumatoid arthritis (RA) patients have increased risk for 
      cardiovascular disease (CVD). Accurate CVD risk prediction could improve care for 
      RA patients. Our goal is to develop and validate a biomarker-based model for 
      predicting CVD risk in RA patients. METHODS: Medicare claims data were linked to 
      multi-biomarker disease activity (MBDA) test results to create an RA patient 
      cohort with age ≥ 40 years that was split 2:1 for training and internal 
      validation. Clinical and RA-related variables, MBDA score, and its 12 biomarkers 
      were evaluated as predictors of a composite CVD outcome: myocardial infarction 
      (MI), stroke, or fatal CVD within 3 years. Model building used Cox proportional 
      hazard regression with backward elimination. The final MBDA-based CVD risk score 
      was internally validated and compared to four clinical CVD risk prediction 
      models. RESULTS: 30,751 RA patients (904 CVD events) were analyzed. Covariates in 
      the final MBDA-based CVD risk score were age, diabetes, hypertension, tobacco 
      use, history of CVD (excluding MI/stroke), MBDA score, leptin, MMP-3 and TNF-R1. 
      In internal validation, the MBDA-based CVD risk score was a strong predictor of 
      3-year risk for a CVD event, with hazard ratio (95% CI) of 2.89 (2.46-3.41). The 
      predicted 3-year CVD risk was low for 9.4% of patients, borderline for 10.2%, 
      intermediate for 52.2%, and high for 28.2%. Model fit was good, with mean 
      predicted versus observed 3-year CVD risks of 4.5% versus 4.4%. The MBDA-based 
      CVD risk score significantly improved risk discrimination by the likelihood ratio 
      test, compared to four clinical models. The risk score also improved prediction, 
      reclassifying 42% of patients versus the simplest clinical model (age + sex), 
      with a net reclassification index (NRI) (95% CI) of 0.19 (0.10-0.27); and 28% of 
      patients versus the most comprehensive clinical model (age + sex + diabetes + 
      hypertension + tobacco use + history of CVD + CRP), with an NRI of 0.07 
      (0.001-0.13). C-index was 0.715 versus 0.661 to 0.696 for the four clinical 
      models. CONCLUSION: A prognostic score has been developed to predict 3-year CVD 
      risk for RA patients by using clinical data, three serum biomarkers and the MBDA 
      score. In internal validation, it had good accuracy and outperformed clinical 
      models with and without CRP. The MBDA-based CVD risk prediction score may improve 
      RA patient care by offering a risk stratification tool that incorporates the 
      effect of RA inflammation.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AUID- ORCID: 0000-0002-8907-8976
AD  - University of Alabama at Birmingham, Birmingham, AL, USA. jrcurtis@uabmc.edu.
FAU - Xie, Fenglong
AU  - Xie F
AD  - University of Alabama at Birmingham, Birmingham, AL, USA.
FAU - Crowson, Cynthia S
AU  - Crowson CS
AD  - Mayo Clinic, Rochester, MN, USA.
FAU - Sasso, Eric H
AU  - Sasso EH
AD  - Crescendo Bioscience, South San Francisco, CA, USA.
AD  - Myriad Genetics Laboratories, Salt Lake City, UT, USA.
FAU - Hitraya, Elena
AU  - Hitraya E
AD  - Crescendo Bioscience, South San Francisco, CA, USA.
AD  - Myriad Genetics Laboratories, Salt Lake City, UT, USA.
FAU - Chin, Cheryl L
AU  - Chin CL
AD  - Crescendo Bioscience, South San Francisco, CA, USA.
AD  - Myriad Genetics Laboratories, Salt Lake City, UT, USA.
FAU - Bamford, Richard D
AU  - Bamford RD
AD  - Crescendo Bioscience, South San Francisco, CA, USA.
AD  - Myriad Genetics Laboratories, Salt Lake City, UT, USA.
FAU - Ben-Shachar, Rotem
AU  - Ben-Shachar R
AD  - Myriad Genetics Laboratories, Salt Lake City, UT, USA.
FAU - Gutin, Alexander
AU  - Gutin A
AD  - Myriad Genetics Laboratories, Salt Lake City, UT, USA.
FAU - Flake, Darl D 2nd
AU  - Flake DD 2nd
AD  - Myriad Genetics Laboratories, Salt Lake City, UT, USA.
FAU - Mabey, Brent
AU  - Mabey B
AD  - Myriad Genetics Laboratories, Salt Lake City, UT, USA.
FAU - Lanchbury, Jerry S
AU  - Lanchbury JS
AD  - Myriad Genetics Laboratories, Salt Lake City, UT, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20201204
PL  - England
TA  - Arthritis Res Ther
JT  - Arthritis research & therapy
JID - 101154438
RN  - 0 (Biomarkers)
SB  - IM
MH  - Adult
MH  - Aged
MH  - *Arthritis, Rheumatoid/diagnosis/epidemiology
MH  - Biomarkers
MH  - *Cardiovascular Diseases/diagnosis/epidemiology
MH  - Disease Progression
MH  - Humans
MH  - Medicare
MH  - Severity of Illness Index
MH  - United States
PMC - PMC7718706
OTO - NOTNLM
OT  - Biomarker
OT  - Cardiovascular risk
OT  - MBDA score
OT  - Multi-biomarker
OT  - Myocardial infarction
OT  - Rheumatoid arthritis
OT  - Stroke
COIS- JC received grants and personal fees from the Abbvie, Amgen, BMS, Corrona, Eli 
      Lilly, Jannsen, Myriad Genetics, Inc., Pfizer, Regeneron, Roche, and UCB during 
      the conduct of the study. FX and CSC received research funding from the Myriad 
      Genetics, Inc., during the conduct of the study. ES, EH, CLC, RB, RB-S, AG, DF, 
      BM, and JL are employed by the Myriad Genetics, Inc., and receive salaries and 
      stock options as compensation.
EDAT- 2020/12/06 06:00
MHDA- 2021/06/22 06:00
PMCR- 2020/12/04
CRDT- 2020/12/05 05:20
PHST- 2020/08/13 00:00 [received]
PHST- 2020/10/15 00:00 [accepted]
PHST- 2020/12/05 05:20 [entrez]
PHST- 2020/12/06 06:00 [pubmed]
PHST- 2021/06/22 06:00 [medline]
PHST- 2020/12/04 00:00 [pmc-release]
AID - 10.1186/s13075-020-02355-0 [pii]
AID - 2355 [pii]
AID - 10.1186/s13075-020-02355-0 [doi]
PST - epublish
SO  - Arthritis Res Ther. 2020 Dec 4;22(1):282. doi: 10.1186/s13075-020-02355-0.

PMID- 33248709
OWN - NLM
STAT- MEDLINE
DCOM- 20210309
LR  - 20210310
IS  - 1942-5546 (Electronic)
IS  - 0025-6196 (Linking)
VI  - 96
IP  - 2
DP  - 2021 Feb
TI  - Acute Myocardial Infarction in Autoimmune Rheumatologic Disease: A Nationwide 
      Analysis of Clinical Outcomes and Predictors of Management Strategy.
PG  - 388-399
LID - S0025-6196(20)30829-6 [pii]
LID - 10.1016/j.mayocp.2020.04.044 [doi]
AB  - OBJECTIVES: To examine national-level differences in management strategies and 
      outcomes in patients with autoimmune rheumatic disease (AIRD) with acute 
      myocardial infarction (AMI) from 2004 through 2014. METHODS: All AMI 
      hospitalizations were analyzed from the National Inpatient Sample, stratified 
      according to AIRD diagnosis into 4 groups: no AIRD, rheumatoid arthritis (RA), 
      systemic lupus erythematosus (SLE), and systemic sclerosis (SSC). The 
      associations between AIRD subtypes and (1) receipt of coronary angiography and 
      percutaneous coronary intervention (PCI) and (2) clinical outcomes were examined 
      compared with patients without AIRD. RESULTS: Of 6,747,797 AMI hospitalizations, 
      109,983 patients (1.6%) had an AIRD diagnosis (RA: 1.3%, SLE: 0.3%, and SSC: 
      0.1%). The prevalence of RA rose from 1.0% (2004) to 1.5% (2014), and SLE and SSC 
      remained stable. Patients with SLE were less likely to receive invasive 
      management (odds ratio [OR] [95% CI]: coronary angiography-0.87; 0.84 to 0.91; 
      PCI-0.93; 0.90 to 0.96), whereas no statistically significant differences were 
      found in the RA and SSC groups. Subsequently, the ORs (95% CIs) of mortality 
      (1.15; 1.07 to 1.23) and bleeding (1.24; 1.16 to 1.31) were increased in patients 
      with SLE; SSC was associated with increased ORs (95% CIs) of major adverse 
      cardiovascular and cerebrovascular events (1.52; 1.38 to 1.68) and mortality 
      (1.81; 1.62 to 2.02) but not bleeding or stroke; the RA group was at no increased 
      risk for any complication. CONCLUSION: In a nationwide cohort of AMI 
      hospitalizations we found lower use of invasive management in patients with SLE 
      and worse outcomes after AMI in patients with SLE and SSC compared with those 
      without AIRD.
CI  - Copyright © 2020 Mayo Foundation for Medical Education and Research. Published by 
      Elsevier Inc. All rights reserved.
FAU - Mohamed, Mohamed O
AU  - Mohamed MO
AD  - Keele Cardiovascular Research Group, Centre for Prognosis Research, Institutes of 
      Applied Clinical Science and Primary Care and Health Sciences, Keele University, 
      UK; Department of Cardiology, Royal Stoke University Hospital, Stoke-on-Trent, 
      UK.
FAU - Roddy, Edward
AU  - Roddy E
AD  - School of Primary, Community, and Social Care, Keele University, UK.
FAU - Ya'qoub, Lina
AU  - Ya'qoub L
AD  - Ochsner-Louisiana State University, Shreveport.
FAU - Myint, Phyo K
AU  - Myint PK
AD  - Ageing Clinical and Experimental Research Team, Institute of Applied Health 
      Sciences, University of Aberdeen, UK.
FAU - Al Alasnag, Mirvat
AU  - Al Alasnag M
AD  - Department of Cardiology, King Fahad Armed Forces Hospital, Jeddah, Saudi Arabia.
FAU - Alraies, Chadi
AU  - Alraies C
AD  - Department of Cardiology, Wayne State University, Detroit Medical Center, Detroit 
      Heart Hospital, MI.
FAU - Clarson, Lorna
AU  - Clarson L
AD  - School of Primary, Community, and Social Care, Keele University, UK.
FAU - Helliwell, Toby
AU  - Helliwell T
AD  - School of Primary, Community, and Social Care, Keele University, UK.
FAU - Mallen, Christian
AU  - Mallen C
AD  - School of Primary, Community, and Social Care, Keele University, UK.
FAU - Fischman, David
AU  - Fischman D
AD  - Department of Medicine (Cardiology), Thomas Jefferson University Hospital, 
      Philadelphia, PA.
FAU - Al Shaibi, Khalid
AU  - Al Shaibi K
AD  - Department of Cardiology, King Fahad Armed Forces Hospital, Jeddah, Saudi Arabia.
FAU - Abhishek, Abhishek
AU  - Abhishek A
AD  - Academic Rheumatology, University of Nottingham, UK; Nottingham National 
      Institute for Health Research Biomedical Research Centre, UK.
FAU - Mamas, Mamas A
AU  - Mamas MA
AD  - Keele Cardiovascular Research Group, Centre for Prognosis Research, Institutes of 
      Applied Clinical Science and Primary Care and Health Sciences, Keele University, 
      UK; Department of Cardiology, Royal Stoke University Hospital, Stoke-on-Trent, 
      UK; Department of Medicine (Cardiology), Thomas Jefferson University Hospital, 
      Philadelphia, PA. Electronic address: mamasmamas1@yahoo.co.uk.
LA  - eng
GR  - RP-PG-0617-20005/DH_/Department of Health/United Kingdom
GR  - RP_2014-04-026/DH_/Department of Health/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20201126
PL  - England
TA  - Mayo Clin Proc
JT  - Mayo Clinic proceedings
JID - 0405543
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Cause of Death
MH  - Coronary Angiography
MH  - Coronary Artery Bypass
MH  - Female
MH  - Humans
MH  - Lupus Erythematosus, Systemic/*complications/epidemiology/immunology
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*epidemiology/*therapy
MH  - Percutaneous Coronary Intervention
MH  - Prevalence
MH  - Rheumatic Diseases/*complications/epidemiology/immunology
MH  - Scleroderma, Systemic/*complications/epidemiology/immunology
MH  - United States/epidemiology
EDAT- 2020/11/30 06:00
MHDA- 2021/03/10 06:00
CRDT- 2020/11/29 20:26
PHST- 2020/01/22 00:00 [received]
PHST- 2020/03/11 00:00 [revised]
PHST- 2020/04/14 00:00 [accepted]
PHST- 2020/11/30 06:00 [pubmed]
PHST- 2021/03/10 06:00 [medline]
PHST- 2020/11/29 20:26 [entrez]
AID - S0025-6196(20)30829-6 [pii]
AID - 10.1016/j.mayocp.2020.04.044 [doi]
PST - ppublish
SO  - Mayo Clin Proc. 2021 Feb;96(2):388-399. doi: 10.1016/j.mayocp.2020.04.044. Epub 
      2020 Nov 26.

PMID- 33246339
OWN - NLM
STAT- MEDLINE
DCOM- 20210629
LR  - 20210629
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 60
IP  - 5
DP  - 2021 May 14
TI  - Ten-year risk of cerebrovascular accidents in incident rheumatoid arthritis: a 
      population-based study of trends over time.
PG  - 2267-2276
LID - 10.1093/rheumatology/keaa579 [doi]
AB  - OBJECTIVE: To evaluate secular trends in 10-year risk of incident cerebrovascular 
      accidents (CVA), in incident RA relative to the general population. METHODS: We 
      conducted a retrospective study of a population-based incident cohort with RA 
      onset from 1997 to 2004 in British Columbia, Canada, with matched general 
      population controls (2:1), using administrative health data. RA and general 
      population cohorts were divided according to year of RA onset, defined according 
      to the first RA visit of the case definition. Incident CVA was defined as the 
      first CVA occurring within 10 years from the first RA visit. Secular trend was 
      assessed using delayed-entry Cox models with a two-way interaction term between 
      the year of RA onset and indicator of RA vs general population. Linear, quadratic 
      and spline functions of year of RA onset were compared with assess non-linear 
      effects. The model with the lowest Akaike Information Criterion was selected. 
      RESULTS: Overall, 23 545 RA and 47 090 general population experienced 658 and 
      1220 incident CVAs, respectively. A spline Cox model with a knot at year of onset 
      1999 was selected. A significant decline in risk of CVA was observed in 
      individuals with RA onset after 1999 [0.90 (0.86, 0.95); P = 0.0001]. The change 
      in CVA risk over time differed significantly in RA with onset from 1999 onwards 
      compared with the general population (P-value of interaction term = 0.03), but 
      not before 1999 (P = 0.06). CONCLUSION: Our findings suggest that people with RA 
      onset from 1999 onwards, had a significantly greater decline in 10-year risk of 
      CVA compared with the general population.
CI  - © The Author(s) 2020. Published by Oxford University Press on behalf of the 
      British Society for Rheumatology. All rights reserved. For permissions, please 
      email: journals.permissions@oup.com.
FAU - Yazdani, Kiana
AU  - Yazdani K
AUID- ORCID: 0000-0003-1929-729X
AD  - Arthritis Research Canada, Richmond.
AD  - Department of Medicine, Faculty of Medicine, Experimental Medicine Program, 
      University of British Columbia, Vancouver.
FAU - Xie, Hui
AU  - Xie H
AD  - Arthritis Research Canada, Richmond.
AD  - Faculty of Health Sciences, Simon Fraser University, Vancouver.
FAU - Avina-Zubieta, J Antonio
AU  - Avina-Zubieta JA
AD  - Arthritis Research Canada, Richmond.
AD  - Department of Medicine, Faculty of Medicine, Experimental Medicine Program, 
      University of British Columbia, Vancouver.
AD  - Division of Rheumatology, Department of Medicine, Faculty of Medicine, University 
      of British Columbia, Vancouver, BC.
FAU - Zheng, Yufei
AU  - Zheng Y
AD  - Arthritis Research Canada, Richmond.
FAU - Abrahamowicz, Michal
AU  - Abrahamowicz M
AD  - Arthritis Research Canada, Richmond.
AD  - Department of Epidemiology, Biostatistics and Occupational Health, McGill 
      University, Montreal, QC, Canada.
FAU - Lacaille, Diane
AU  - Lacaille D
AD  - Arthritis Research Canada, Richmond.
AD  - Department of Medicine, Faculty of Medicine, Experimental Medicine Program, 
      University of British Columbia, Vancouver.
AD  - Division of Rheumatology, Department of Medicine, Faculty of Medicine, University 
      of British Columbia, Vancouver, BC.
LA  - eng
GR  - MOP-130480/CIHR/Canada
GR  - THC-135235/CIHR/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - British Columbia/epidemiology
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Ischemic Stroke/*epidemiology
MH  - Male
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Risk
OTO - NOTNLM
OT  - administrative data
OT  - cerebrovascular accidents
OT  - epidemiology
OT  - rheumatoid arthritis
OT  - temporal trends
EDAT- 2020/11/28 06:00
MHDA- 2021/06/30 06:00
CRDT- 2020/11/27 20:15
PHST- 2020/04/28 00:00 [received]
PHST- 2020/07/22 00:00 [revised]
PHST- 2020/11/28 06:00 [pubmed]
PHST- 2021/06/30 06:00 [medline]
PHST- 2020/11/27 20:15 [entrez]
AID - 6007759 [pii]
AID - 10.1093/rheumatology/keaa579 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2021 May 14;60(5):2267-2276. doi: 
      10.1093/rheumatology/keaa579.

PMID- 33227081
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201125
IS  - 0034-6233 (Print)
IS  - 2084-9834 (Electronic)
IS  - 0034-6233 (Linking)
VI  - 58
IP  - 5
DP  - 2020
TI  - The importance of homocysteine in the development of cardiovascular complications 
      in patients with rheumatoid arthritis.
PG  - 282-288
LID - 10.5114/reum.2020.99732 [doi]
AB  - Rheumatoid arthritis (RA) not only leads to disability due to joint changes, but 
      also significantly shortens the life expectancy of patients, mainly due to more 
      frequent occurrence of heart attacks and strokes. Accelerated atherosclerosis in 
      these patients is caused, among other factors, by high homocysteine (HCY) 
      concentration in blood. Numerous studies have shown that treatment with vitamin B 
      significantly reduces the concentration of HCY in blood, but does not reduce the 
      risk of heart diseases. Recent studies have shown, however, that folic acid (FA) 
      administration reduces the risk of stroke by 10-20%. Due to the fact that in 
      patients with RA strokes are more frequent than in the general population and 
      hyperhomocysteinemia (HHCY) is often found, determination of HCY concentration in 
      blood is advisable, and in persons with HHCY it is recommended to use FA in 
      primary and secondary stroke prevention.
CI  - Copyright: © 2020 Narodowy Instytut Geriatrii, Reumatologii i Rehabilitacji w 
      Warszawie.
FAU - Głuszek, Jerzy
AU  - Głuszek J
AD  - The State Higher Vocational School in Kalisz, Poland.
FAU - Wierzowiecka, Małgorzata
AU  - Wierzowiecka M
AD  - Department of Hypertension, Angiology and Internal Medicine, Poznan University of 
      Medical Sciences, Poland.
FAU - Niklas, Karolina
AU  - Niklas K
AD  - Department of Rheumatology, Rehabilitation and Internal Medicine, Poznan 
      University of Medical Sciences, Poland.
FAU - Niklas, Arkadiusz
AU  - Niklas A
AD  - Department of Hypertension, Angiology and Internal Medicine, Poznan University of 
      Medical Sciences, Poland.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20201012
PL  - Poland
TA  - Reumatologia
JT  - Reumatologia
JID - 20130190R
PMC - PMC7667944
OTO - NOTNLM
OT  - folic acid
OT  - homocysteine
OT  - rheumatoid arthritis
OT  - stroke
COIS- The authors declare no conflict of interest.
EDAT- 2020/11/24 06:00
MHDA- 2020/11/24 06:01
PMCR- 2020/01/01
CRDT- 2020/11/23 17:10
PHST- 2020/07/20 00:00 [received]
PHST- 2020/09/16 00:00 [accepted]
PHST- 2020/11/23 17:10 [entrez]
PHST- 2020/11/24 06:00 [pubmed]
PHST- 2020/11/24 06:01 [medline]
PHST- 2020/01/01 00:00 [pmc-release]
AID - 42008 [pii]
AID - 10.5114/reum.2020.99732 [doi]
PST - ppublish
SO  - Reumatologia. 2020;58(5):282-288. doi: 10.5114/reum.2020.99732. Epub 2020 Oct 12.

PMID- 33217802
OWN - NLM
STAT- MEDLINE
DCOM- 20201204
LR  - 20221005
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 99
IP  - 47
DP  - 2020 Nov 20
TI  - Systemic sclerosis and risk of cardiovascular disease: A PRISMA-compliant 
      systemic review and meta-analysis of cohort studies.
PG  - e23009
LID - 10.1097/MD.0000000000023009 [doi]
LID - e23009
AB  - BACKGROUND: Systemic sclerosis (SSc) is an autoimmune disorder leading to 
      extensive fibrosis and microvascular injury. Macrovascular disease is well 
      documented in other autoimmune rheumatic diseases such as systemic lupus 
      erythematosus and rheumatoid arthritis. However, the link is unclear between SSc 
      and macrovascular disease, particularly atherosclerotic cardiovascular disease 
      (CVD). This meta-analysis aimed to investigate the association between SSc and 
      CVD. METHODS: A thorough literature search was conducted in the Cochrane, Embase, 
      Medline, and PubMed to identify all cohort studies comparing the risk of CVD with 
      and without SSc. The pooled hazard ratios (HRs) with 95% confidence intervals 
      (CIs) of cardiovascular end points were calculated. The risk of bias of included 
      studies was assessed by the Newcastle-Ottawa scale. RESULTS: Seven cohort studies 
      with a total of 14,813 study participants were included. In a comparison of SSc 
      patients versus non-SSc controls, the pooled HR for cardiovascular disease was 
      2.36 (95% CI 1.97-2.81); for peripheral vascular disease was 5.27 (95%CI 
      4.27-6.51); for myocardial infarction was 2.36 (95% CI 1.71-3.25); and for stroke 
      was 1.52 (95% CI 1.18-1.96). CONCLUSION: This meta-analysis revealed that SSc was 
      associated with an increased risk of CVD. Clinicians who manage patients with SSc 
      should be aware of the increased cardiovascular burden and undertake preventive 
      measures.
FAU - Cen, Xintao
AU  - Cen X
AUID- ORCID: 0000-0002-5980-3719
AD  - Department of Dermatology, Zhujiang Hospital, Southern Medical University.
FAU - Feng, Sining
AU  - Feng S
AD  - Department of Dermatology, Zhujiang Hospital, Southern Medical University.
FAU - Wei, Shanshan
AU  - Wei S
AD  - Department of Dermatology, Zhujiang Hospital, Southern Medical University.
FAU - Yan, Lu
AU  - Yan L
AD  - Department of Dermatology, Zhujiang Hospital, Southern Medical University.
FAU - Sun, Ledong
AU  - Sun L
AD  - Department of Dermatology, Zhujiang Hospital, Southern Medical University.
AD  - Department of Dermatology, the Fifth Affiliated Hospital of Southern Medical 
      University, Guangzhou, China.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Systematic Review
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
SB  - IM
MH  - Cardiovascular Diseases/*etiology
MH  - Cohort Studies
MH  - Humans
MH  - Risk Factors
MH  - Scleroderma, Systemic/*complications
PMC - PMC7676589
COIS- The authors have no conflicts of interest to disclose.
EDAT- 2020/11/22 06:00
MHDA- 2020/12/15 06:00
PMCR- 2020/11/20
CRDT- 2020/11/21 01:00
PHST- 2020/11/21 01:00 [entrez]
PHST- 2020/11/22 06:00 [pubmed]
PHST- 2020/12/15 06:00 [medline]
PHST- 2020/11/20 00:00 [pmc-release]
AID - 00005792-202011200-00017 [pii]
AID - MD-D-20-05421 [pii]
AID - 10.1097/MD.0000000000023009 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2020 Nov 20;99(47):e23009. doi: 
      10.1097/MD.0000000000023009.

PMID- 33195306
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201117
IS  - 2296-858X (Print)
IS  - 2296-858X (Electronic)
IS  - 2296-858X (Linking)
VI  - 7
DP  - 2020
TI  - Joint Destruction Is Associated With All Types of Cardiovascular Events in French 
      Rheumatoid Patients: A Real-Life Study With Very Long Follow-Up.
PG  - 556086
LID - 10.3389/fmed.2020.556086 [doi]
LID - 556086
AB  - Objective: Rheumatoid arthritis (RA) leads not only to joint destruction but also 
      to systemic manifestations, with an increased incidence of cardiovascular events 
      (CVE). Many studies have shown a link between RA severity and CV risk, but the 
      duration of follow-up remains often insufficient to allow a conclusion. The CVE 
      definition was generally reduced to myocardial infarction and stroke, and few 
      studies were conducted in non-Anglo-Saxon countries with low CV incidence. This 
      study aimed to assess the relationship between joint destruction and the 
      occurrence of different types of CVE in a large cohort of French RA patients with 
      a long-term follow-up. Methods: This historical cohort study included 571 RA 
      patients followed between 1992 and 2012 in Lyon, France. The primary endpoint was 
      the first occurrence of a CVE. Logistic regressions were used to identify factors 
      associated with CVE occurrence. Cox proportional hazard models were performed as 
      a separate analysis to take advantage of the long-term follow-up. Results: During 
      a mean follow-up of 16.1 years, 30.3% of patients experienced a CVE, mostly acute 
      arterial events. Joint destruction was associated with an increased risk of CVE 
      [odds ratio = 3.72; 95% confidence interval (CI), 1.09-15.35; p = 0.047] among 
      non-smoker RA patients. A survival analysis revealed that joint destruction was 
      associated with a shorter time to onset of the first CVE only among non-smokers 
      (hazard ratio = 3.44; 95% CI, 1.07-11.04; p = 0.038). Conclusion: Joint 
      destruction is associated with CVE occurrence in RA patients from a population 
      with a lower incidence of CV disease. This study suggests that RA patients, 
      especially those with destruction, merit the institution of precise guidelines to 
      manage this CV risk, and trials are required to evaluate them.
CI  - Copyright © 2020 Robert, Hot, Mifsud, Ndongo-Thiam and Miossec.
FAU - Robert, Marie
AU  - Robert M
AD  - Department of Clinical Immunology and Rheumatology, Immunogenomics and 
      Inflammation Research Unit EA 4130, University of Lyon 1, Hôpital Edouard 
      Herriot, Lyon, France.
FAU - Hot, Arnaud
AU  - Hot A
AD  - Department of Internal Medicine, Immunogenomics and Inflammation Research Unit EA 
      4130, University of Lyon 1, Hôpital Edouard Herriot, Lyon, France.
FAU - Mifsud, François
AU  - Mifsud F
AD  - Department of Clinical Immunology and Rheumatology, Immunogenomics and 
      Inflammation Research Unit EA 4130, University of Lyon 1, Hôpital Edouard 
      Herriot, Lyon, France.
FAU - Ndongo-Thiam, Ndiémé
AU  - Ndongo-Thiam N
AD  - Department of Clinical Immunology and Rheumatology, Immunogenomics and 
      Inflammation Research Unit EA 4130, University of Lyon 1, Hôpital Edouard 
      Herriot, Lyon, France.
FAU - Miossec, Pierre
AU  - Miossec P
AD  - Department of Clinical Immunology and Rheumatology, Immunogenomics and 
      Inflammation Research Unit EA 4130, University of Lyon 1, Hôpital Edouard 
      Herriot, Lyon, France.
LA  - eng
PT  - Journal Article
DEP - 20201030
PL  - Switzerland
TA  - Front Med (Lausanne)
JT  - Frontiers in medicine
JID - 101648047
PMC - PMC7661545
OTO - NOTNLM
OT  - cardiovascular diseases
OT  - inflammation
OT  - joint destruction
OT  - rheumatoid arthritis
OT  - vessels
EDAT- 2020/11/17 06:00
MHDA- 2020/11/17 06:01
PMCR- 2020/10/30
CRDT- 2020/11/16 08:54
PHST- 2020/04/27 00:00 [received]
PHST- 2020/09/30 00:00 [accepted]
PHST- 2020/11/16 08:54 [entrez]
PHST- 2020/11/17 06:00 [pubmed]
PHST- 2020/11/17 06:01 [medline]
PHST- 2020/10/30 00:00 [pmc-release]
AID - 10.3389/fmed.2020.556086 [doi]
PST - epublish
SO  - Front Med (Lausanne). 2020 Oct 30;7:556086. doi: 10.3389/fmed.2020.556086. 
      eCollection 2020.

PMID- 33144158
OWN - NLM
STAT- MEDLINE
DCOM- 20210208
LR  - 20210208
IS  - 1879-1913 (Electronic)
IS  - 0002-9149 (Linking)
VI  - 140
DP  - 2021 Feb 1
TI  - Outcomes of Percutaneous Coronary Intervention in Patients With Rheumatoid 
      Arthritis.
PG  - 39-46
LID - S0002-9149(20)31181-4 [pii]
LID - 10.1016/j.amjcard.2020.10.048 [doi]
AB  - Rheumatoid arthritis (RA) is the most common inflammatory arthritis and is 
      associated with increased risk of cardiovascular events and mortality. Evidence 
      regarding outcomes following PCI is limited. This study aimed to assess 
      differences in outcomes following percutaneous coronary intervention (PCI) 
      between patients with and without RA. The Melbourne Interventional Group PCI 
      registry (2005 to 2018) was used to identify 756 patients with RA. Outcomes were 
      compared with the remaining cohort (n = 38,579). Patients with RA were older, 
      more often female, with higher rates of hypertension, previous stroke, peripheral 
      vascular disease, obstructive sleep apnea, chronic lung disease, myocardial 
      infarction, and renal impairment, whereas rates of dyslipidemia and current 
      smoking were lower, all p <0.05. Lesions in patients with RA were more frequently 
      complex (ACC/AHA type B2/C), requiring longer stents, with higher rates of no 
      reflow, all p <0.05. Risk of long-term mortality, adjusted for potential 
      confounders, was higher for patients with RA (hazard ratio 1.53, 95% confidence 
      interval 1.30 to 1.80; median follow-up 5.0 years), whereas 30-day outcomes 
      including mortality, major adverse cardiovascular events, bleeding, stroke, 
      myocardial infarction, coronary artery bypass surgery, and target vessel 
      revascularization were similar. In subgroup analysis, patients with RA and lower 
      BMI (P(for interaction) < 0.001) and/or acute coronary syndromes (P(for 
      interaction) = 0.05) had disproportionately higher risk of long-term mortality 
      compared with patients without RA. In conclusion, patients with RA who underwent 
      PCI had more co-morbidities and longer, complex coronary lesions. Risk of 
      short-term adverse outcomes was similar, whereas risk of long-term mortality was 
      higher, especially among patients with acute coronary syndromes and lower body 
      mass index.
CI  - Copyright © 2020. Published by Elsevier Inc.
FAU - Dawson, Luke P
AU  - Dawson LP
AD  - Department of Cardiology, Royal Melbourne Hospital, Melbourne, Victoria, 
      Australia.
FAU - Dinh, Diem
AU  - Dinh D
AD  - Centre of Cardiovascular Research and Education in Therapeutics, Monash 
      University, Melbourne, Victoria, Australia.
FAU - O'Brien, Jessica
AU  - O'Brien J
AD  - Department of Cardiology, The Alfred Hospital, Melbourne, Victoria, Australia.
FAU - Duffy, Stephen J
AU  - Duffy SJ
AD  - Centre of Cardiovascular Research and Education in Therapeutics, Monash 
      University, Melbourne, Victoria, Australia; Department of Cardiology, The Alfred 
      Hospital, Melbourne, Victoria, Australia; Baker Heart and Diabetes Institute, 
      Melbourne, Victoria, Australia.
FAU - Guymer, Emma
AU  - Guymer E
AD  - Department of Rheumatology, Monash Medical Centre, Melbourne, Victoria, 
      Australia; Department of Medicine, Monash University, Melbourne, Victoria, 
      Australia.
FAU - Brennan, Angela
AU  - Brennan A
AD  - Centre of Cardiovascular Research and Education in Therapeutics, Monash 
      University, Melbourne, Victoria, Australia.
FAU - Clark, David
AU  - Clark D
AD  - Department of Cardiology, Austin Health, Melbourne, Victoria, Australia.
FAU - Oqueli, Ernesto
AU  - Oqueli E
AD  - Department of Cardiology, Ballarat Health Services, Ballarat, Victoria, 
      Australia; School of Medicine, Faculty of Health, Deakin University, Geelong, 
      Victoria, Australia.
FAU - Hiew, Chin
AU  - Hiew C
AD  - Department of Cardiology, University Hospital, Geelong, Victoria, Australia.
FAU - Freeman, Melanie
AU  - Freeman M
AD  - Department of Cardiology, Box Hill Hospital, Melbourne, Victoria, Australia.
FAU - Reid, Christopher M
AU  - Reid CM
AD  - Centre of Cardiovascular Research and Education in Therapeutics, Monash 
      University, Melbourne, Victoria, Australia.
FAU - Ajani, Andrew E
AU  - Ajani AE
AD  - Department of Cardiology, Royal Melbourne Hospital, Melbourne, Victoria, 
      Australia; Centre of Cardiovascular Research and Education in Therapeutics, 
      Monash University, Melbourne, Victoria, Australia; Department of Medicine, 
      Melbourne University, Victoria, Australia. Electronic address: 
      andrew.ajani@mh.org.au.
CN  - Melbourne Interventional Group (MIG) Investigators
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20201102
PL  - United States
TA  - Am J Cardiol
JT  - The American journal of cardiology
JID - 0207277
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*complications/mortality
MH  - Coronary Artery Disease/complications/mortality/*surgery
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Percutaneous Coronary Intervention/*methods
MH  - Propensity Score
MH  - Prospective Studies
MH  - *Registries
MH  - Risk Factors
MH  - Survival Rate/trends
MH  - Time Factors
MH  - Treatment Outcome
MH  - Victoria/epidemiology
EDAT- 2020/11/05 06:00
MHDA- 2021/02/09 06:00
CRDT- 2020/11/04 05:35
PHST- 2020/08/03 00:00 [received]
PHST- 2020/10/21 00:00 [revised]
PHST- 2020/10/22 00:00 [accepted]
PHST- 2020/11/05 06:00 [pubmed]
PHST- 2021/02/09 06:00 [medline]
PHST- 2020/11/04 05:35 [entrez]
AID - S0002-9149(20)31181-4 [pii]
AID - 10.1016/j.amjcard.2020.10.048 [doi]
PST - ppublish
SO  - Am J Cardiol. 2021 Feb 1;140:39-46. doi: 10.1016/j.amjcard.2020.10.048. Epub 2020 
      Nov 2.

PMID- 33081544
OWN - NLM
STAT- MEDLINE
DCOM- 20210514
LR  - 20210514
IS  - 1473-2300 (Electronic)
IS  - 0300-0605 (Print)
IS  - 0300-0605 (Linking)
VI  - 48
IP  - 10
DP  - 2020 Oct
TI  - Reduced salivary flow and caries status are correlated with disease activity and 
      severity in patients with diffuse cutaneous systemic sclerosis.
PG  - 300060520941375
LID - 10.1177/0300060520941375 [doi]
LID - 0300060520941375
AB  - OBJECTIVE: To analyze the correlations of saliva production and pH value with 
      disease activity, disease severity, and oral health-related quality of life in 
      patients with diffuse cutaneous systemic sclerosis (dcSSc) without concomitant 
      Sjögren's syndrome (SS) or SS-related antibodies. METHODS: This cross-sectional 
      study included 28 patients with dcSSc and matching healthy controls. Sialometric 
      assessment and caries status were compared between the two groups. Clinical and 
      laboratory parameters were used to evaluate disease severity, in accordance with 
      the Medsger Severity Scale. RESULTS: In patients with dsSSc, reduced saliva 
      production and higher pH value were associated with disease activity and 
      severity; moreover, caries status was correlated with SSc disease 
      characteristics, including disease duration and disease severity. Oral 
      health-related quality of life was negatively correlated with mean salivary flow 
      rate. CONCLUSIONS: These findings contradict the existing notion that reduced 
      saliva production in patients with SSc is linked to SS-related antibodies or 
      caused by underlying SS. In addition, patients with dcSSc exhibit elevated risk 
      of cardiovascular disease and invasive dental treatment has been shown to enhance 
      the rates of stroke and heart attack in the general population; therefore, oral 
      health is particularly important in patients with SSc.
FAU - Parat, Katica
AU  - Parat K
AD  - Department of Oral Medicine and Periodontology, Study of Dental Medicine, School 
      of Medicine, University of Split, Split, Croatia.
FAU - Radić, Mislav
AU  - Radić M
AD  - Division of Rheumatology and Clinical Immunology, Center of Excellence for 
      Systemic Sclerosis in Croatia, University Hospital Split, Split, Croatia.
AD  - University of Split School of Medicine, Split, Croatia.
FAU - Perković, Dijana
AU  - Perković D
AD  - Division of Rheumatology and Clinical Immunology, Center of Excellence for 
      Systemic Sclerosis in Croatia, University Hospital Split, Split, Croatia.
AD  - University of Split School of Medicine, Split, Croatia.
FAU - Lukenda, Dolores Biočina
AU  - Lukenda DB
AD  - Department of Oral Medicine and Periodontology, Study of Dental Medicine, School 
      of Medicine, University of Split, Split, Croatia.
FAU - Kaliterna, Dusanka Martinović
AU  - Kaliterna DM
AD  - Division of Rheumatology and Clinical Immunology, Center of Excellence for 
      Systemic Sclerosis in Croatia, University Hospital Split, Split, Croatia.
AD  - University of Split School of Medicine, Split, Croatia.
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Int Med Res
JT  - The Journal of international medical research
JID - 0346411
SB  - IM
MH  - Cross-Sectional Studies
MH  - Dental Caries Susceptibility
MH  - Humans
MH  - Quality of Life
MH  - Saliva
MH  - *Scleroderma, Diffuse/diagnosis
MH  - *Sjogren's Syndrome/diagnosis
PMC - PMC7588767
OTO - NOTNLM
OT  - Diffuse cutaneous systemic sclerosis
OT  - activity
OT  - caries
OT  - salivary flow
OT  - severity
OT  - tooth status
COIS- The authors declare that there is no conflict of interest.
EDAT- 2020/10/22 06:00
MHDA- 2021/05/15 06:00
PMCR- 2020/10/20
CRDT- 2020/10/21 05:36
PHST- 2020/10/21 05:36 [entrez]
PHST- 2020/10/22 06:00 [pubmed]
PHST- 2021/05/15 06:00 [medline]
PHST- 2020/10/20 00:00 [pmc-release]
AID - 10.1177_0300060520941375 [pii]
AID - 10.1177/0300060520941375 [doi]
PST - ppublish
SO  - J Int Med Res. 2020 Oct;48(10):300060520941375. doi: 10.1177/0300060520941375.

PMID- 33065756
OWN - NLM
STAT- MEDLINE
DCOM- 20210818
LR  - 20210818
IS  - 1399-3038 (Electronic)
IS  - 0905-6157 (Linking)
VI  - 32
IP  - 2
DP  - 2021 Feb
TI  - Associations between pediatric asthma and adult non-communicable diseases.
PG  - 314-321
LID - 10.1111/pai.13395 [doi]
AB  - BACKGROUND: To date, there is no comprehensive study examining how asthma 
      diagnosed in childhood or adolescence is associated with diagnoses of subsequent 
      non-communicable diseases (NCDs) during adulthood. Our study aimed to examine the 
      associations between pediatric asthma and several adult NCDs, with temporality 
      and long interval times between asthma and NCD diagnoses. METHODS: We used RAND 
      Indonesian Family Life Survey Fifth Wave (IFLS5) fielded in 2014-2015, to study 
      whether being diagnosed with pediatric asthma at 0-19 years of age was associated 
      with increased risks of hypertension, diabetes, rheumatoid arthritis, stomach 
      diseases, kidney diseases, and heart diseases or stroke diagnosed in adulthood. 
      We used the weighted Poisson regression adjusting for age, sex, urbanicity, and 
      insurance status to estimate risk ratios. Subgroup analyses were performed by sex 
      and age of asthma and other NCD diagnoses. RESULTS: Pediatric asthma 
      significantly increased risks of hypertension, diabetes, and stomach diseases 
      diagnosed at 20 years of age or above. Males with pediatric asthma diagnosed at 
      0-10 years of age had significantly higher risk of hypertension, while females 
      with pediatric asthma diagnosed at 0-10 years of age had significantly higher 
      risks of diabetes and stomach diseases. Females with pediatric asthma diagnosed 
      at 11-19 years of age had significantly higher risks of diabetes, arthritis, 
      stomach diseases, and kidney diseases. We also found varying associations by age 
      of NCD diagnosis. CONCLUSION: Our results suggest pediatric asthma is associated 
      with increased risks of several adult NCDs, and these associations may vary by 
      sex and age of asthma and other NCD diagnoses.
CI  - © 2020 European Academy of Allergy and Clinical Immunology and John Wiley & Sons 
      Ltd.
FAU - Juber, Nirmin F
AU  - Juber NF
AD  - Institute of Public Health, National Yang-Ming University, Taipei, Taiwan.
FAU - Lee, Chien-Chang
AU  - Lee CC
AD  - Department of Emergency Medicine, National Taiwan University Hospital, Taipei, 
      Taiwan.
FAU - Pan, Wen-Chi
AU  - Pan WC
AD  - Institute of Environmental and Occupational Health Sciences, National Yang-Ming 
      University, Taipei, Taiwan.
FAU - Liu, Jason J
AU  - Liu JJ
AUID- ORCID: 0000-0002-7379-5022
AD  - Institute of Public Health, National Yang-Ming University, Taipei, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20201101
PL  - England
TA  - Pediatr Allergy Immunol
JT  - Pediatric allergy and immunology : official publication of the European Society 
      of Pediatric Allergy and Immunology
JID - 9106718
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - *Asthma/epidemiology
MH  - Child
MH  - *Diabetes Mellitus
MH  - Female
MH  - Humans
MH  - *Hypertension
MH  - Infant, Newborn
MH  - Male
MH  - *Noncommunicable Diseases/epidemiology
MH  - Risk Factors
OTO - NOTNLM
OT  - adolescents
OT  - adult non-communicable diseases
OT  - asthma
OT  - children
OT  - pediatric asthma
OT  - susceptibility
EDAT- 2020/10/17 06:00
MHDA- 2021/08/19 06:00
CRDT- 2020/10/16 20:19
PHST- 2020/09/07 00:00 [received]
PHST- 2020/10/03 00:00 [revised]
PHST- 2020/10/09 00:00 [accepted]
PHST- 2020/10/17 06:00 [pubmed]
PHST- 2021/08/19 06:00 [medline]
PHST- 2020/10/16 20:19 [entrez]
AID - 10.1111/pai.13395 [doi]
PST - ppublish
SO  - Pediatr Allergy Immunol. 2021 Feb;32(2):314-321. doi: 10.1111/pai.13395. Epub 
      2020 Nov 1.

PMID- 33060309
OWN - NLM
STAT- MEDLINE
DCOM- 20211013
LR  - 20211013
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
VI  - 48
IP  - 6
DP  - 2021 Jun
TI  - Benefits of Methotrexate Use on Cardiovascular Disease Risk Among Rheumatoid 
      Arthritis Patients Initiating Biologic Disease-modifying Antirheumatic Drugs.
PG  - 804-812
LID - 10.3899/jrheum.191326 [doi]
AB  - OBJECTIVE: Methotrexate (MTX) has been associated with reduced risk for 
      cardiovascular disease (CVD) events among patients with rheumatoid arthritis (RA) 
      not exposed to biologic disease-modifying antirheumatic drugs (bDMARDs). The 
      effect of concomitant MTX on CVD risk among RA patients initiating bDMARDs 
      remains unknown. METHODS: A retrospective cohort study was conducted to assess 
      the effect of MTX on CVD risk using 2006-2015 Medicare claims data for patients 
      with RA initiating bDMARD. The main exposure was current use of MTX, updated in a 
      time-varying fashion. The primary outcome was a composite of incident myocardial 
      infarction (MI), stroke, and fatal CVD. Secondary outcomes were each event that 
      comprised the primary outcome. Incidence rates (IR) and 95% CI were calculated 
      using Poisson regression. Associations between MTX and risk of CVD were assessed 
      using Cox regression. RESULTS: A total of 88,255 bDMARD initiations and 1861 CVD 
      events were included in this study. Mean age was 64.6 (12.3) years, 84.0% were 
      female, and 68.2% were non-Hispanic White. The crude IRs (95% CI) for CVD were 
      17.9 (16.9-18.8) and 12.1 (11.1-13.2) per 1000 patient-years among MTX unexposed 
      and exposed, respectively. The multivariable adjusted HR (95% CI) for CVD events 
      associated with MTX was 0.76 (0.68-0.85). Multivariable adjusted HRs were 0.78 
      (0.66-0.91), 0.74 (0.62-0.88), 0.77 (0.68-0.86), and 0.82 (0.73-0.93) for MI, 
      stroke, MI or stroke, and a composite CVD outcome, respectively. Results were 
      robust in sensitivity and subgroup analyses. CONCLUSION: Among patients with RA 
      receiving biologics, concomitant MTX use was associated with a 24% lower risk for 
      CVD events.
CI  - Copyright © 2021 by the Journal of Rheumatology.
FAU - Xie, Fenglong
AU  - Xie F
AD  - F. Xie, PhD, H. Yun, PhD, J.R. Curtis, MD, MS, MPH, Division of Clinical 
      Immunology and Rheumatology, and Department of Epidemiology, University of 
      Alabama at Birmingham.
FAU - Chen, Lang
AU  - Chen L
AD  - L. Chen, PhD, Division of Clinical Immunology and Rheumatology, University of 
      Alabama at Birmingham.
FAU - Yun, Huifeng
AU  - Yun H
AD  - F. Xie, PhD, H. Yun, PhD, J.R. Curtis, MD, MS, MPH, Division of Clinical 
      Immunology and Rheumatology, and Department of Epidemiology, University of 
      Alabama at Birmingham.
FAU - Levitan, Emily B
AU  - Levitan EB
AD  - E.B. Levitan, ScD, Department of Epidemiology, University of Alabama at 
      Birmingham, Birmingham, Alabama, USA.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AUID- ORCID: 0000-0002-8907-8976
AD  - F. Xie, PhD, H. Yun, PhD, J.R. Curtis, MD, MS, MPH, Division of Clinical 
      Immunology and Rheumatology, and Department of Epidemiology, University of 
      Alabama at Birmingham; jrcurtis@uabmc.edu.
LA  - eng
PT  - Journal Article
DEP - 20201015
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Aged
MH  - *Antirheumatic Agents/adverse effects
MH  - *Arthritis, Rheumatoid/drug therapy
MH  - *Biological Products/adverse effects
MH  - *Cardiovascular Diseases/drug therapy/epidemiology
MH  - Female
MH  - Humans
MH  - Medicare
MH  - Methotrexate/therapeutic use
MH  - Middle Aged
MH  - Retrospective Studies
MH  - United States/epidemiology
OTO - NOTNLM
OT  - biologics
OT  - fatal cardiovascular disease
OT  - methotrexate
OT  - myocardial infarction
OT  - rheumatoid arthritis
OT  - stroke
EDAT- 2020/10/17 06:00
MHDA- 2021/10/14 06:00
CRDT- 2020/10/16 05:40
PHST- 2020/09/28 00:00 [accepted]
PHST- 2020/10/17 06:00 [pubmed]
PHST- 2021/10/14 06:00 [medline]
PHST- 2020/10/16 05:40 [entrez]
AID - jrheum.191326 [pii]
AID - 10.3899/jrheum.191326 [doi]
PST - ppublish
SO  - J Rheumatol. 2021 Jun;48(6):804-812. doi: 10.3899/jrheum.191326. Epub 2020 Oct 
      15.

PMID- 32984893
OWN - NLM
STAT- MEDLINE
DCOM- 20210629
LR  - 20211215
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 60
IP  - 3
DP  - 2021 Mar 2
TI  - Cardiovascular risk and mortality in rheumatoid arthritis compared with diabetes 
      mellitus and the general population.
PG  - 1400-1409
LID - 10.1093/rheumatology/keaa374 [doi]
AB  - OBJECTIVES: To compare risk of cardiovascular disease and mortality in patients 
      with incident RA, diabetes mellitus (DM) and the general population (GP). 
      METHODS: Patients diagnosed with incident RA were matched 1:5 by age, sex and 
      year of RA diagnosis with the GP. In the same period, patients with incident DM 
      were included. Outcomes were heart failure (HF), myocardial infarction (MI), 
      coronary revascularization, stroke, major adverse cardiovascular events (MACE) 
      and death up to 10 years after diagnosis. RESULTS: We included 15 032 patients 
      with incident RA, 301 246 patients with DM and 75 160 persons from the GP. RA 
      patients had an increased risk of HF [hazard ratio (HR) 1.51, 95% CI: 1.38, 
      1.64], MI (HR 1.58, 95% CI: 1.43, 1.74), percutaneous coronary intervention (PCI; 
      HR 1.44, 95% CI: 1.27, 1.62), coronary artery bypass grafting (CABG; HR 1.30, 95% 
      CI: 1.05, 1.62) and stroke (HR 1.22, 95% CI: 1.12-1.33) compared with the GP. 
      However, the 10-year all-cause mortality was at the same level as observed in the 
      GP. Cardiac death and MACE were increased in RA compared with the GP. When 
      compared with patients with DM, RA patients had a lower adjusted risk of HF (HR 
      0.79, 95% CI: 0.73, 0.85), CABG (HR 0.62, 95% CI: 0.51, 0.76) and stroke (HR 
      0.82, 95% CI: 0.76, 0.89), and similar risk of MI and PCI. DM patients had the 
      highest risk of 10-year mortality, cardiac death and MACE. CONCLUSION: This study 
      demonstrates that RA is associated with an increased risk of HF, MI, stroke and 
      coronary revascularization than found in the GP but without reaching the risk 
      levels observed in DM patients.
CI  - © The Author(s) 2020. Published by Oxford University Press on behalf of the 
      British Society for Rheumatology. All rights reserved. For permissions, please 
      email: journals.permissions@oup.com.
FAU - Løgstrup, Brian B
AU  - Løgstrup BB
AD  - Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
FAU - Ellingsen, Torkell
AU  - Ellingsen T
AD  - Clinic for Rational and Innovative Patient Pathways, Diagnostic Center, Regional 
      Hospital Silkeborg, Silkeborg, Denmark.
AD  - Rheumatology Research Unit, Department of Rheumatology, Odense University 
      Hospital, Odense, Denmark.
FAU - Pedersen, Alma B
AU  - Pedersen AB
AD  - Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.
FAU - Darvalics, Bianka
AU  - Darvalics B
AD  - Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark.
FAU - Olesen, Kevin K W
AU  - Olesen KKW
AD  - Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
FAU - Bøtker, Hans Erik
AU  - Bøtker HE
AD  - Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
FAU - Maeng, Michael
AU  - Maeng M
AD  - Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
SB  - IM
CIN - Rheumatology (Oxford). 2021 Nov 3;60(11):e418. doi: 10.1093/rheumatology/keab650. 
      PMID: 34387301
CIN - Rheumatology (Oxford). 2021 Nov 3;60(11):e419-e420. doi: 
      10.1093/rheumatology/keab652. PMID: 34387306
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications/mortality
MH  - Cardiovascular Diseases/*etiology/mortality
MH  - Case-Control Studies
MH  - Cause of Death
MH  - Denmark/epidemiology
MH  - Diabetes Complications/complications/*mortality
MH  - Female
MH  - *Heart Disease Risk Factors
MH  - Heart Failure/etiology/mortality
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/etiology/mortality
MH  - Percutaneous Coronary Intervention/statistics & numerical data
MH  - Stroke/etiology/mortality
OTO - NOTNLM
OT  - death
OT  - diabetes mellitus
OT  - heart failure
OT  - ischaemic heart disease
OT  - rheumatoid arthritis
OT  - risk
OT  - stroke
EDAT- 2020/09/29 06:00
MHDA- 2021/06/30 06:00
CRDT- 2020/09/28 05:48
PHST- 2020/03/21 00:00 [received]
PHST- 2020/06/01 00:00 [revised]
PHST- 2020/09/29 06:00 [pubmed]
PHST- 2021/06/30 06:00 [medline]
PHST- 2020/09/28 05:48 [entrez]
AID - 5912188 [pii]
AID - 10.1093/rheumatology/keaa374 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2021 Mar 2;60(3):1400-1409. doi: 
      10.1093/rheumatology/keaa374.

PMID- 32978937
OWN - NLM
STAT- MEDLINE
DCOM- 20220208
LR  - 20220208
IS  - 1536-4844 (Electronic)
IS  - 1078-0998 (Linking)
VI  - 27
IP  - 7
DP  - 2021 Jun 15
TI  - Cardiovascular Risk Assessment and Impact of Medications on Cardiovascular 
      Disease in Inflammatory Bowel Disease.
PG  - 1107-1115
LID - 10.1093/ibd/izaa258 [doi]
AB  - There is increased risk of cardiovascular disease in patients with chronic 
      inflammatory disorders such as rheumatoid arthritis, psoriatic arthritis, and 
      systemic lupus erythematosus. Studies have shown association between 
      cardiovascular disease (eg, myocardial infarction, heart failure, stroke) and 
      inflammatory bowel disease. Medications such as infliximab and adalimumab 
      (monoclonal antibodies to tumor necrosis factor α) may help decrease the 
      inflammatory burden and cardiovascular risk; however, there have been reports of 
      hypertriglyceridemia and worsening of moderate to severe heart failure with these 
      medications. Janus kinase inhibitors, such as tofacitinib, have been associated 
      with hyperlipidemia and thromboembolism. We aim to discuss clinical and imaging 
      modalities to assess cardiovascular risk in inflammatory bowel disease patients 
      and review the role of various medications with respect to cardiovascular disease 
      in this population.
CI  - © 2020 Crohn’s & Colitis Foundation. Published by Oxford University Press. All 
      rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
FAU - Sinh, Preetika
AU  - Sinh P
AD  - Division of Gastroenterology and Hepatology, Medical College of Wisconsin, 
      Milwaukee, WI, USA.
FAU - Cross, Raymond
AU  - Cross R
AD  - Division of Gastroenterology and Hepatology, University of Maryland School of 
      Medicine, Baltimore, Maryland, USA.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Inflamm Bowel Dis
JT  - Inflammatory bowel diseases
JID - 9508162
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - B72HH48FLU (Infliximab)
RN  - FYS6T7F842 (Adalimumab)
SB  - IM
MH  - Adalimumab
MH  - Antibodies, Monoclonal, Humanized
MH  - *Cardiovascular Diseases/etiology
MH  - *Heart Disease Risk Factors
MH  - Humans
MH  - *Inflammatory Bowel Diseases/complications/drug therapy
MH  - Infliximab
MH  - Risk Factors
OTO - NOTNLM
OT  - atherosclerosis
OT  - cardiovascular risk
OT  - inflammatory bowel disease
OT  - medications
EDAT- 2020/09/27 06:00
MHDA- 2022/02/09 06:00
CRDT- 2020/09/26 08:32
PHST- 2020/07/03 00:00 [received]
PHST- 2020/09/27 06:00 [pubmed]
PHST- 2022/02/09 06:00 [medline]
PHST- 2020/09/26 08:32 [entrez]
AID - 5911946 [pii]
AID - 10.1093/ibd/izaa258 [doi]
PST - ppublish
SO  - Inflamm Bowel Dis. 2021 Jun 15;27(7):1107-1115. doi: 10.1093/ibd/izaa258.

PMID- 32974020
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230413
IS  - 2050-3121 (Print)
IS  - 2050-3121 (Electronic)
IS  - 2050-3121 (Linking)
VI  - 8
DP  - 2020
TI  - Incident arterial vascular events in a cohort of Puerto Ricans with rheumatoid 
      arthritis.
PG  - 2050312120958844
LID - 10.1177/2050312120958844 [doi]
LID - 2050312120958844
AB  - OBJECTIVE: The increased morbidity and mortality associated with cardiovascular 
      events in patients with rheumatoid arthritis has been linked to traditional and 
      nontraditional factors. However, these factors vary among different ethnicities. 
      Few studies have described these features in Hispanic populations. Thus, we 
      determined the clinical correlates of arterial vascular events in Hispanics from 
      Puerto Rico. METHODS: A cross-sectional study was performed in a cohort of 405 
      Puerto Ricans with rheumatoid arthritis. Demographic parameters, health-related 
      behaviors, clinical manifestations, disease activity (per Disease Activity Score 
      28), functional status (per Health Assessment Questionnaire), comorbidities, and 
      pharmacotherapy were compared in patients with and without incident arterial 
      vascular events. The latter was defined as the occurrence of myocardial 
      infarction, angina pectoris, vascular procedures for coronary artery disease, 
      stroke, or peripheral artery disease. Study groups were analyzed using bivariate 
      and multivariate analyses. RESULTS: Of the total study population, 87.2% were 
      woman. The mean age at study visit was 56.1 ± 13.9 years, and the mean disease 
      duration was 15.0 ± 13.2 years. Arterial vascular events occurred in 43 patients 
      (10.6%). In the multivariate analysis adjusted for age and sex, arterial 
      hypertension, dyslipidemia, metabolic syndrome, extra-articular manifestations, 
      higher Health Assessment Questionnaire score, and number of hospitalizations were 
      associated with arterial cardiovascular events. CONCLUSION: In this cohort of 
      Puerto Ricans with rheumatoid arthritis, traditional and nontraditional factors, 
      particularly extra-articular manifestations and functional disability, were 
      associated with arterial vascular events. Awareness of these associations may 
      help to implement clinical strategies in this group of rheumatoid arthritis 
      patients at risk of arterial vascular events.
CI  - © The Author(s) 2020.
FAU - González-Meléndez, Ariana
AU  - González-Meléndez A
AD  - Division of Rheumatology, Department of Medicine, University of Puerto Rico 
      Medical Sciences Campus, San Juan, Puerto Rico.
FAU - Fred-Jiménez, Ruth M
AU  - Fred-Jiménez RM
AD  - Division of Rheumatology, Department of Medicine, University of Puerto Rico 
      Medical Sciences Campus, San Juan, Puerto Rico.
FAU - Arroyo-Ávila, Mariangelí
AU  - Arroyo-Ávila M
AD  - Division of Rheumatology, Department of Medicine, University of Puerto Rico 
      Medical Sciences Campus, San Juan, Puerto Rico.
FAU - Díaz-Correa, Leyda
AU  - Díaz-Correa L
AD  - Division of Rheumatology, Department of Medicine, University of Puerto Rico 
      Medical Sciences Campus, San Juan, Puerto Rico.
FAU - Pérez-Ríos, Naydi
AU  - Pérez-Ríos N
AD  - Puerto Rico Clinical and Translational Research Center, University of Puerto Rico 
      Medical Sciences Campus, San Juan, Puerto Rico.
FAU - Rodríguez, Noelia
AU  - Rodríguez N
AD  - Division of Rheumatology, Department of Medicine, University of Puerto Rico 
      Medical Sciences Campus, San Juan, Puerto Rico.
FAU - Ríos, Grissel
AU  - Ríos G
AD  - Division of Rheumatology, Department of Medicine, University of Puerto Rico 
      Medical Sciences Campus, San Juan, Puerto Rico.
FAU - Vilá, Luis M
AU  - Vilá LM
AUID- ORCID: 0000-0002-6679-2704
AD  - Division of Rheumatology, Department of Medicine, University of Puerto Rico 
      Medical Sciences Campus, San Juan, Puerto Rico.
LA  - eng
GR  - U54 GM133807/GM/NIGMS NIH HHS/United States
GR  - U54 MD007587/MD/NIMHD NIH HHS/United States
PT  - Journal Article
DEP - 20200915
PL  - England
TA  - SAGE Open Med
JT  - SAGE open medicine
JID - 101624744
PMC - PMC7495931
OTO - NOTNLM
OT  - Hispanics
OT  - Puerto Ricans
OT  - Rheumatoid arthritis
OT  - arterial vascular events
OT  - clinical outcomes
COIS- Declaration of conflicting interests: The author(s) declared no potential 
      conflicts of interest with respect to the research, authorship, and/or 
      publication of this article.
EDAT- 2020/09/26 06:00
MHDA- 2020/09/26 06:01
PMCR- 2020/09/15
CRDT- 2020/09/25 06:03
PHST- 2019/12/19 00:00 [received]
PHST- 2020/08/25 00:00 [accepted]
PHST- 2020/09/25 06:03 [entrez]
PHST- 2020/09/26 06:00 [pubmed]
PHST- 2020/09/26 06:01 [medline]
PHST- 2020/09/15 00:00 [pmc-release]
AID - 10.1177_2050312120958844 [pii]
AID - 10.1177/2050312120958844 [doi]
PST - epublish
SO  - SAGE Open Med. 2020 Sep 15;8:2050312120958844. doi: 10.1177/2050312120958844. 
      eCollection 2020.

PMID- 32950628
OWN - NLM
STAT- MEDLINE
DCOM- 20211011
LR  - 20211011
IS  - 1097-6809 (Electronic)
IS  - 0741-5214 (Linking)
VI  - 73
IP  - 4
DP  - 2021 Apr
TI  - Outcomes of abdominal aortic aneurysm repair among patients with rheumatoid 
      arthritis.
PG  - 1261-1268.e5
LID - S0741-5214(20)32059-0 [pii]
LID - 10.1016/j.jvs.2020.08.134 [doi]
AB  - OBJECTIVE: In the present study, we compared the outcomes of elective abdominal 
      aortic aneurysm (AAA) repair in patients with and without rheumatoid arthritis 
      (RA) stratified by the type of surgery. METHODS: A retrospective population-based 
      cohort study was conducted from 2003 to 2016. Linked administrative health data 
      from Ontario, Canada were used to identify all patients aged ≥65 years who had 
      undergone elective open or endovascular AAA repair during the study period. 
      Patients were identified using validated procedure and billing codes and matching 
      using propensity scores. The primary outcome was survival. The secondary outcomes 
      were major adverse cardiovascular events (MACE)-free survival (defined as freedom 
      from death, myocardial infarction, and stroke), reintervention, and secondary 
      rupture. RESULTS: Of 14,816 patients undergoing elective AAA repair, a diagnosis 
      of RA was present for 309 (2.0%). The propensity-matched cohort included 234 
      pairs of RA and control patients. The matched cohort was followed up for a mean ± 
      standard deviation of 4.93 ± 3.35 years, and the median survival was 6.76 and 
      7.31 years for the RA and control groups, respectively. Cox regression analysis 
      demonstrated no statistically significant differences in the hazards for death, 
      MACE, reintervention, or secondary rupture. Analysis of the differences in 
      outcomes stratified by repair approach also showed no statistically significant 
      differences in the hazards for death, MACE, reintervention, or secondary rupture. 
      CONCLUSIONS: We found no statistically significant differences in survival, MACE, 
      reintervention, or secondary rupture among patients with RA undergoing elective 
      AAA repair compared with controls. Further studies are required to evaluate the 
      impact of comorbidities and antirheumatic medications on the outcomes of elective 
      AAA repair.
CI  - Copyright © 2020 Society for Vascular Surgery. Published by Elsevier Inc. All 
      rights reserved.
FAU - Salata, Konrad
AU  - Salata K
AD  - Division of Vascular Surgery, Li Ka Shing Knowledge Institute, St. Michael's 
      Hospital, University of Toronto, Toronto, Ontario, Canada.
FAU - Almaghlouth, Ibrahim
AU  - Almaghlouth I
AD  - Rheumatology Unit, Department of Medicine, King Saud University, Riyadh, Kingdom 
      of Saudi Arabia; College of Medicine Research Center, King Saud University, 
      Riyadh, Kingdom of Saudi Arabia.
FAU - Hussain, Mohamad A
AU  - Hussain MA
AD  - Division of Vascular Surgery, Li Ka Shing Knowledge Institute, St. Michael's 
      Hospital, University of Toronto, Toronto, Ontario, Canada.
FAU - de Mestral, Charles
AU  - de Mestral C
AD  - Division of Vascular Surgery, Li Ka Shing Knowledge Institute, St. Michael's 
      Hospital, University of Toronto, Toronto, Ontario, Canada.
FAU - Greco, Elisa
AU  - Greco E
AD  - Division of Vascular Surgery, Li Ka Shing Knowledge Institute, St. Michael's 
      Hospital, University of Toronto, Toronto, Ontario, Canada.
FAU - Aljabri, Badr A
AU  - Aljabri BA
AD  - Division of Vascular Surgery, Li Ka Shing Knowledge Institute, St. Michael's 
      Hospital, University of Toronto, Toronto, Ontario, Canada; Department of Surgery, 
      King Saud University, Riyadh, Kingdom of Saudi Arabia.
FAU - Mamdani, Muhammad
AU  - Mamdani M
AD  - Li Ka Shing Centre for Healthcare Analytics Research and Training, Li Ka Shing 
      Knowledge Institute, St. Michael's Hospital, University of Toronto, Toronto, 
      Ontario, Canada; Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, 
      Ontario, Canada.
FAU - Forbes, Thomas L
AU  - Forbes TL
AD  - Division of Vascular Surgery, Peter Munk Cardiac Centre, University Health 
      Network, University of Toronto, Toronto, Ontario, Canada.
FAU - Verma, Subodh
AU  - Verma S
AD  - Division of Cardiac Surgery, Li Ka Shing Knowledge Institute, St. Michael's 
      Hospital, University of Toronto, Toronto, Ontario, Canada.
FAU - Al-Omran, Mohammed
AU  - Al-Omran M
AD  - Division of Vascular Surgery, Li Ka Shing Knowledge Institute, St. Michael's 
      Hospital, University of Toronto, Toronto, Ontario, Canada; Department of Surgery, 
      King Saud University, Riyadh, Kingdom of Saudi Arabia. Electronic address: 
      alomranm@smh.ca.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20200918
PL  - United States
TA  - J Vasc Surg
JT  - Journal of vascular surgery
JID - 8407742
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Aortic Aneurysm, Abdominal/diagnostic imaging/mortality/*surgery
MH  - Arthritis, Rheumatoid/diagnosis/*epidemiology/mortality
MH  - *Blood Vessel Prosthesis Implantation/adverse effects/mortality
MH  - Comorbidity
MH  - Databases, Factual
MH  - Elective Surgical Procedures
MH  - *Endovascular Procedures/adverse effects/mortality
MH  - Female
MH  - Humans
MH  - Male
MH  - Ontario
MH  - Postoperative Complications/mortality/surgery
MH  - Progression-Free Survival
MH  - Retrospective Studies
MH  - Risk Assessment
MH  - Risk Factors
MH  - Time Factors
OTO - NOTNLM
OT  - Abdominal aortic aneurysm
OT  - Observational study
OT  - Propensity score
OT  - Rheumatoid arthritis
EDAT- 2020/09/21 06:00
MHDA- 2021/10/12 06:00
CRDT- 2020/09/20 20:27
PHST- 2020/02/12 00:00 [received]
PHST- 2020/08/15 00:00 [accepted]
PHST- 2020/09/21 06:00 [pubmed]
PHST- 2021/10/12 06:00 [medline]
PHST- 2020/09/20 20:27 [entrez]
AID - S0741-5214(20)32059-0 [pii]
AID - 10.1016/j.jvs.2020.08.134 [doi]
PST - ppublish
SO  - J Vasc Surg. 2021 Apr;73(4):1261-1268.e5. doi: 10.1016/j.jvs.2020.08.134. Epub 
      2020 Sep 18.

PMID- 32896267
OWN - NLM
STAT- MEDLINE
DCOM- 20210525
LR  - 20220622
IS  - 0392-856X (Print)
IS  - 0392-856X (Linking)
VI  - 39
IP  - 3
DP  - 2021 May-Jun
TI  - Cardiovascular events and change in cholesterol levels in patients with 
      rheumatoid arthritis treated with tocilizumab: data from the REGATE Registry.
PG  - 501-507
LID - 10.55563/clinexprheumatol/hfceu3 [doi]
AB  - OBJECTIVES: Rheumatoid arthritis (RA) is responsible for excess mortality mainly 
      due to cardiovascular disease. Studies have found elevated cholesterol levels in 
      RA patients who received tocilizumab (TCZ). We studied the occurrence of major 
      cardiovascular events in RA patients who received TCZ in current practice. We 
      also analysed cholesterol level changes in these patients. METHODS: Data were 
      collected from the French REGATE Registry, a multicentre observational study 
      including patients with RA treated with TCZ. All cardiovascular complications 
      were analysed. Changes in cholesterol levels were studied. Factors associated 
      with major adverse cardiac and cerebrovascular events were analysed by 
      multivariate analysis, estimating odds ratios and 95% confidence intervals. 
      RESULTS: During an exposure time of 5591 patient-years (PYs), 35 cardiovascular 
      events occurred in 33 patients, corresponding to an incidence of 0.63/100 PYs. 
      The incidence of ischaemic stroke and cardiac ischaemia was 0.41 and 0.21/100 
      PYs. Age and personal history of cardiovascular events were identified as risk 
      factors associated with cardiovascular events: OR=1.06 [95% CI 1.02-1.09] and 
      4.10 [1.90-8.83]. Female sex was a protective factor (OR=0.29 [95% CI 
      0.14-0.64]). Glucocorticoids may play a role but was not statistically 
      significant. All cholesterol variables were increased in level after the third 
      month of treatment with TCZ, with a 15.4%, 18.9% and 13.4% increase for total 
      cholesterol, LDL-C and HDL-C, at 3 months. CONCLUSIONS: In current practice, 
      cardiovascular events occurring under TCZ treatment is in the range of what is 
      expected in RA patients despite a global increase in cholesterol levels.
FAU - Lukas, Cédric
AU  - Lukas C
AD  - Department of Rheumatology, CHU Montpellier, Montpellier University, France.
FAU - Redondin, Manon
AU  - Redondin M
AD  - Department of Rheumatology, CHU Montpellier, Montpellier University, France.
FAU - Pane, Isabelle
AU  - Pane I
AD  - Data Manager, Centre d'Épidémiologie Clinique, APHP, France.
FAU - Soubrier, Martin
AU  - Soubrier M
AD  - Department of Rheumatology, CHU Clermont-Ferrand, Clermont-Ferrand University, 
      France.
FAU - Houvenagel, Eric
AU  - Houvenagel E
AD  - Department of Rheumatology, CHU Lille, Lille University, France.
FAU - Sibilia, Jean
AU  - Sibilia J
AD  - Department of Rheumatology, CHU Strasbourg, Strasbourg University, France.
FAU - Combe, Bernard
AU  - Combe B
AD  - Department of Rheumatology, CHU Montpellier, Montpellier University, France.
FAU - Morel, Jacques
AU  - Morel J
AD  - Department of Rheumatology, CHU Montpellier, Montpellier University, France. 
      j-morel@chu-montpellier.fr.
LA  - eng
PT  - Journal Article
PT  - Observational Study
DEP - 20200903
PL  - Italy
TA  - Clin Exp Rheumatol
JT  - Clinical and experimental rheumatology
JID - 8308521
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Antirheumatic Agents)
RN  - 97C5T2UQ7J (Cholesterol)
RN  - I031V2H011 (tocilizumab)
SB  - IM
MH  - Antibodies, Monoclonal, Humanized
MH  - *Antirheumatic Agents/therapeutic use
MH  - *Arthritis, Rheumatoid/diagnosis/drug therapy/epidemiology
MH  - *Brain Ischemia/drug therapy
MH  - Cholesterol/therapeutic use
MH  - Female
MH  - Humans
MH  - Registries
MH  - *Stroke
EDAT- 2020/09/09 06:00
MHDA- 2021/05/26 06:00
CRDT- 2020/09/08 08:45
PHST- 2020/03/11 00:00 [received]
PHST- 2020/05/05 00:00 [accepted]
PHST- 2020/09/09 06:00 [pubmed]
PHST- 2021/05/26 06:00 [medline]
PHST- 2020/09/08 08:45 [entrez]
AID - 15461 [pii]
AID - 10.55563/clinexprheumatol/hfceu3 [doi]
PST - ppublish
SO  - Clin Exp Rheumatol. 2021 May-Jun;39(3):501-507. doi: 
      10.55563/clinexprheumatol/hfceu3. Epub 2020 Sep 3.

PMID- 32878203
OWN - NLM
STAT- MEDLINE
DCOM- 20201204
LR  - 20201214
IS  - 1660-4601 (Electronic)
IS  - 1661-7827 (Print)
IS  - 1660-4601 (Linking)
VI  - 17
IP  - 17
DP  - 2020 Aug 31
TI  - Coexistence of Lack of Clinical Manifestation of Oral Mycosis and Systemic 
      Diseases in Edentulous Patients Using Removable Prosthetic Restorations.
LID - 10.3390/ijerph17176348 [doi]
LID - 6348
AB  - OBJECTIVE: It is believed that oral infections can increase the risk of 
      systematic diseases, such as atherosclerosis and coronary heart disease, stroke, 
      chronic obstructive pulmonary disease, diabetes, cancer, rheumatoid arthritis, 
      etc. It seems that oral invasive pathogens induce a systemic inflammatory 
      response via mediators released by the cardiovascular system and liver, which 
      increases the risk to the patient of these systematic infections, such as 
      hypertension. On the basis of previous studies of the stomatognathic system, 
      investigating the coexistence of systemic diseases and inflammation in the oral 
      cavity, it can be expected that there is a connection between inflammation of the 
      denture-bearing area in patients using acrylic removable dentures and the 
      presence of systemic diseases, and that patients with inflammation in oral mucosa 
      are more likely to have systemic diseases. MATERIAL AND METHOD: A retrospective 
      study was carried out on a group of patients seeking prosthetic treatment at the 
      Prosthetic Department of the University Dental Clinic (UKS) from March 2012 to 
      February 2013. All data were collected using a UKS electronic database with 
      KS-SOMED. The minimum period of use for removable prostheses was five years. 
      RESULTS: According to anamnesis, the most common systemic diseases in our study 
      group were hypertension disease. In total, 58% of patients with hypertension 
      disease had no inflammation in the oral cavity. CONCLUSIONS: The occurrence of 
      systemic diseases in edentulous people using removable prosthetic restorations, 
      and the subsequent use of medications for these diseases, may result in a lack of 
      clinical symptoms of concomitant fungal infection of the oral mucosa.
FAU - Gacon, Izabela
AU  - Gacon I
AD  - Department of Dental Prosthetics, Institute of Dentistry at Jagiellonian 
      University, 31-155 Krakow, Poland.
FAU - Wieczorek, Aneta
AU  - Wieczorek A
AUID- ORCID: 0000-0003-2506-7394
AD  - Department of Dental Prosthetics, Institute of Dentistry at Jagiellonian 
      University, 31-155 Krakow, Poland.
LA  - eng
PT  - Journal Article
DEP - 20200831
PL  - Switzerland
TA  - Int J Environ Res Public Health
JT  - International journal of environmental research and public health
JID - 101238455
SB  - IM
MH  - *Dental Prosthesis
MH  - Humans
MH  - *Inflammation
MH  - *Mouth Diseases/complications/immunology
MH  - Mouth Mucosa
MH  - Mouth, Edentulous
MH  - *Mycoses
MH  - Retrospective Studies
PMC - PMC7503360
OTO - NOTNLM
OT  - candida albicans
OT  - stomatitis
OT  - systemic diseases
COIS- The authors declare no conflict of interest.
EDAT- 2020/09/04 06:00
MHDA- 2020/12/15 06:00
PMCR- 2020/09/01
CRDT- 2020/09/04 06:00
PHST- 2020/06/29 00:00 [received]
PHST- 2020/08/18 00:00 [revised]
PHST- 2020/08/28 00:00 [accepted]
PHST- 2020/09/04 06:00 [entrez]
PHST- 2020/09/04 06:00 [pubmed]
PHST- 2020/12/15 06:00 [medline]
PHST- 2020/09/01 00:00 [pmc-release]
AID - ijerph17176348 [pii]
AID - ijerph-17-06348 [pii]
AID - 10.3390/ijerph17176348 [doi]
PST - epublish
SO  - Int J Environ Res Public Health. 2020 Aug 31;17(17):6348. doi: 
      10.3390/ijerph17176348.

PMID- 32869533
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230428
IS  - 2578-5745 (Electronic)
IS  - 2578-5745 (Linking)
VI  - 2
IP  - 9
DP  - 2020 Sep
TI  - Ethnic Disparities in Atherosclerotic Cardiovascular Disease Incidence and 
      Prevalence Among Rheumatoid Arthritis Patients in the United States: a Systematic 
      Review.
PG  - 525-532
LID - 10.1002/acr2.11170 [doi]
AB  - OBJECTIVE: Rheumatoid arthritis (RA) is associated with increased atherosclerotic 
      cardiovascular disease (ASCVD). General population cohorts have shown African 
      American individuals to have greater and Hispanic Americans to have lower 
      cardiovascular disease prevalence when compared with non-Hispanic white 
      individuals; however, the reasons for these findings are not clear. This 
      systematic review seeks to describe the incidence and prevalence of ASCVD 
      stratified by race/ethnicity within the US RA population. METHODS: MEDLINE, 
      Embase, and Cochrane databases were searched for studies that reported incidence 
      or prevalence of ASCVD (including, but not limited to, fatal and nonfatal stroke, 
      myocardial infarction, and cardiovascular death) in those with RA. Abstracts and 
      full texts were screened separately for inclusion by two reviewers, with a third 
      reviewer to resolve discrepancies. RESULTS: We screened 2625 abstracts and fully 
      reviewed 138 manuscripts. Twenty-one were included that cited at a minimum the 
      percentage of non-Hispanic whites in their population. No publication meeting 
      entry criteria initially stratified ASCVD by race/ethnicity. The average 
      prevalent ASCVD in RA is 46.9% (95% CI: 46.8-47) (range of prevalent ASCVD: 
      30%-47%). The average incident ASCVD is 8.2% (95% CI: 8.14-8.25) (range of 
      incident ASCVD 1%-46%). CONCLUSION: In this systematic review, we found a paucity 
      of data on racially/ethnically diverse RA patients and ASCVD outcomes. Future 
      studies should report the prevalence of ASCVD in various races/ethnicities with 
      RA in the United States. These data would help inform clinicians on how best to 
      manage cardiovascular disease risk in RA.
CI  - © 2020 The Authors. ACR Open Rheumatology published by Wiley Periodicals LLC on 
      behalf of American College of Rheumatology.
FAU - Daniel, Christina M
AU  - Daniel CM
AUID- ORCID: 0000-0003-0315-6185
AD  - University of Texas Southwestern Medical Center, Dallas, Texas.
FAU - Davila, Lesley
AU  - Davila L
AD  - University of Texas Southwestern Medical Center, Dallas, Texas.
FAU - Makris, Una E
AU  - Makris UE
AD  - University of Texas Southwestern Medical Center, Dallas, Texas and Medical 
      Service VA North Texas Health Care System, Dallas, Texas.
FAU - Mayo, Helen
AU  - Mayo H
AD  - Health Sciences Digital Library and Learning Center, UT Southwestern Medical 
      Center, Dallas, Texas.
FAU - Caplan, Liron
AU  - Caplan L
AUID- ORCID: 0000-0002-2799-3036
AD  - Rocky Mountain Regional Veterans Affairs Medical Center, Aurora, Colorado and 
      University of Colorado, Aurora.
FAU - Davis, Lisa
AU  - Davis L
AUID- ORCID: 0000-0002-1801-174X
AD  - University of Colorado, Aurora.
FAU - Solow, E Blair
AU  - Solow EB
AD  - University of Texas Southwestern Medical Center, Dallas, Texas.
LA  - eng
GR  - UL1 TR001105/TR/NCATS NIH HHS/United States
GR  - P30 AG022845/AG/NIA NIH HHS/United States
GR  - IK2 HX001916/HX/HSRD VA/United States
GR  - KL2 TR001103/TR/NCATS NIH HHS/United States
GR  - R24 HS022418/HS/AHRQ HHS/United States
PT  - Journal Article
DEP - 20200901
PL  - United States
TA  - ACR Open Rheumatol
JT  - ACR open rheumatology
JID - 101740025
PMC - PMC7504478
EDAT- 2020/09/02 06:00
MHDA- 2020/09/02 06:01
PMCR- 2020/09/01
CRDT- 2020/09/02 06:00
PHST- 2020/02/27 00:00 [received]
PHST- 2020/07/17 00:00 [accepted]
PHST- 2020/09/02 06:00 [pubmed]
PHST- 2020/09/02 06:01 [medline]
PHST- 2020/09/02 06:00 [entrez]
PHST- 2020/09/01 00:00 [pmc-release]
AID - ACR211170 [pii]
AID - 10.1002/acr2.11170 [doi]
PST - ppublish
SO  - ACR Open Rheumatol. 2020 Sep;2(9):525-532. doi: 10.1002/acr2.11170. Epub 2020 Sep 
      1.

PMID- 32801134
OWN - NLM
STAT- MEDLINE
DCOM- 20210927
LR  - 20210927
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
VI  - 48
IP  - 5
DP  - 2021 May
TI  - The Risk of Cardiovascular Events Associated With Disease-modifying Antirheumatic 
      Drugs in Rheumatoid Arthritis.
PG  - 648-655
LID - 10.3899/jrheum.200265 [doi]
AB  - OBJECTIVE: To examine the comparative effects of biologic disease-modifying 
      antirheumatic drugs (bDMARD) and tofacitinib against conventional synthetic DMARD 
      (csDMARD) on incident cardiovascular disease (CVD) in patients with rheumatoid 
      arthritis (RA). METHODS: RA patients with ≥ 1 year of participation in the 
      FORWARD study, from 1998 through 2017, were assessed for incident composite CVD 
      events (myocardial infarction, stroke, heart failure, and CVD-related death 
      validated from hospital/death records). DMARD were categorized into 7 mutually 
      exclusive groups: (1) csDMARD-referent; (2) tumor necrosis factor-α inhibitor 
      (TNFi); (3) abatacept (ABA); (4) rituximab; (5) tocilizumab; (6) anakinra; and 
      (7) tofacitinib. Glucocorticoids (GC) were assessed using a weighted cumulative 
      exposure model, which combines information about duration, intensity, and timing 
      of exposure into a summary measure by using the weighted sum of past oral doses 
      (prednisolone equivalent). Cox proportional hazard models were used to adjust for 
      confounders. RESULTS: During median (IQR) 4.0 (1.7-8.0) years of follow-up, 1801 
      CVD events were identified in 18,754 RA patients. The adjusted model showed CVD 
      risk reduction with TNFi (HR 0.81, 95% CI 0.71-0.93) and ABA (HR 0.50, 95% CI 
      0.30-0.83) compared to csDMARD. While higher GC exposure as weighted cumulative 
      exposure was associated with increased CVD risk (HR 1.15, 95% CI 1.11-1.19), 
      methotrexate (MTX) use was associated with CVD risk reduction [use vs nonuse HR 
      0.82, 95% CI 0.74-0.90, and high dose (> 15 mg/week) vs low dose (≤ 15 mg/week) 
      HR 0.83, 95% CI 0.70-0.99]. CONCLUSION: ABA and TNFi were associated with 
      decreased risk of CVD compared to csDMARD. Minimizing GC use and optimizing MTX 
      dose may improve cardiovascular outcomes in patients with RA.
CI  - Copyright © 2021 by the Journal of Rheumatology.
FAU - Ozen, Gulsen
AU  - Ozen G
AUID- ORCID: 0000-0002-5423-393X
AD  - G. Ozen, MD, University of Nebraska Medical Center, Omaha, Nebraska.
FAU - Pedro, Sofia
AU  - Pedro S
AD  - S. Pedro, MS, FORWARD, The National Databank for Rheumatic Diseases, Wichita, 
      Kansas.
FAU - Michaud, Kaleb
AU  - Michaud K
AUID- ORCID: 0000-0002-5350-3934
AD  - K. Michaud, PhD, University of Nebraska Medical Center, Omaha, Nebraska, and 
      FORWARD, The National Databank for Rheumatic Diseases, Wichita, Kansas, USA. 
      kmichaud@unmc.edu.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200815
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - *Antirheumatic Agents/adverse effects
MH  - *Arthritis, Rheumatoid/drug therapy
MH  - *Biological Products/therapeutic use
MH  - *Cardiovascular Diseases/chemically induced/drug therapy/epidemiology
MH  - Humans
MH  - Methotrexate/therapeutic use
MH  - Tumor Necrosis Factor-alpha
OTO - NOTNLM
OT  - DMARD
OT  - biologics
OT  - cardiovascular
OT  - cohort study
OT  - rheumatoid arthritis
EDAT- 2020/08/18 06:00
MHDA- 2021/09/28 06:00
CRDT- 2020/08/18 06:00
PHST- 2020/06/08 00:00 [accepted]
PHST- 2020/08/18 06:00 [pubmed]
PHST- 2021/09/28 06:00 [medline]
PHST- 2020/08/18 06:00 [entrez]
AID - jrheum.200265 [pii]
AID - 10.3899/jrheum.200265 [doi]
PST - ppublish
SO  - J Rheumatol. 2021 May;48(5):648-655. doi: 10.3899/jrheum.200265. Epub 2020 Aug 
      15.

PMID- 32703278
OWN - NLM
STAT- MEDLINE
DCOM- 20210514
LR  - 20210514
IS  - 1752-1947 (Electronic)
IS  - 1752-1947 (Linking)
VI  - 14
IP  - 1
DP  - 2020 Jul 24
TI  - Patient with rheumatoid arthritis with deep vein thrombosis presenting as a calf 
      strain: a case report.
PG  - 114
LID - 10.1186/s13256-020-02441-6 [doi]
LID - 114
AB  - BACKGROUND: Patients with rheumatoid arthritis experience various comorbidities, 
      including cardiovascular disease. More data and awareness exist regarding the 
      adverse effects of rheumatoid arthritis affecting the arterial side of the 
      cardiovascular system, such as stroke or myocardial infarction, than regarding 
      adverse venous complications, such as deep vein thrombosis and pulmonary 
      embolism. Rheumatoid arthritis affects more women than men, and the risk of 
      venous thromboembolism in rheumatoid arthritis tends to increase with age; 
      therefore, the presentation in this case report of deep vein thrombosis in a 
      nonsmoking, young, fit man with rheumatoid arthritis is rare. This patient was 
      sent away from a minor injuries unit with a diagnosis of a calf strain. Further 
      assessment at an accident and emergency department later in the day confirmed 
      deep vein thrombosis via ultrasonography. This case report underlines the need 
      for vigilance because deep vein thrombosis is a risk factor in rheumatoid 
      arthritis, even in young, male, and physically fit individuals. CASE 
      PRESENTATION: A nonsmoking 39-year-old Caucasian man with a 2-year history of 
      rheumatoid arthritis presented for assessment at a private physiotherapy clinic 
      with a 4-week history of right-sided posterior calf pain that had developed 
      following exercise at a gym. The patient therefore believed his symptoms were due 
      to a calf strain. Findings at physiotherapy assessment suggested that the actual 
      cause of the patient's symptoms were as a result of deep vein thrombosis. The 
      patient was directed to a local minor injuries unit with a referral letter from 
      the author outlining this diagnosis. Following clinical assessment at the minor 
      injuries unit, the patient was told that there was no likelihood of deep vein 
      thrombosis, and his diagnosis was a calf strain. The patient harbored concerns at 
      this point and decided to seek further medical opinion at a nearby accident and 
      emergency department, where deep vein thrombosis was diagnosed 
      using ultrasonography, and the patient was commenced on anticoagulants. 
      CONCLUSIONS: Venous thromboembolism risk in rheumatoid arthritis is stated as 
      being less recognized as an arterial complication. This is borne out by this 
      patient's clinical journey, wherein his youth, fitness, athletic appearance, and 
      onset of symptoms during exercise were said to suggest a diagnosis of a calf 
      strain at a minor injuries unit. Ultrasonography at a different accident and 
      emergency unit later that day ultimately was used to diagnose deep vein 
      thrombosis.
FAU - Lewis, Trevor
AU  - Lewis T
AUID- ORCID: 0000-0002-4566-9686
AD  - Extended Scope Physiotherapy Practitioner MSc MCSP, Physiotherapy Department, 
      Aintree University Hospital, Liverpool, UK. messagetrevorlewis@gmail.com.
LA  - eng
PT  - Case Reports
PT  - Journal Article
DEP - 20200724
PL  - England
TA  - J Med Case Rep
JT  - Journal of medical case reports
JID - 101293382
RN  - 0 (Anticoagulants)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Anticoagulants/therapeutic use
MH  - *Arthritis, Rheumatoid/complications/drug therapy
MH  - Female
MH  - Humans
MH  - Male
MH  - *Pulmonary Embolism/diagnostic imaging/etiology
MH  - Ultrasonography
MH  - *Venous Thrombosis/diagnostic imaging/etiology
PMC - PMC7379825
OTO - NOTNLM
OT  - Calf strain
OT  - Deep vein thrombosis
OT  - Rheumatoid arthritis
COIS- The author declares that there are no competing interests.
EDAT- 2020/07/25 06:00
MHDA- 2021/05/15 06:00
PMCR- 2020/07/24
CRDT- 2020/07/25 06:00
PHST- 2019/11/25 00:00 [received]
PHST- 2020/06/26 00:00 [accepted]
PHST- 2020/07/25 06:00 [entrez]
PHST- 2020/07/25 06:00 [pubmed]
PHST- 2021/05/15 06:00 [medline]
PHST- 2020/07/24 00:00 [pmc-release]
AID - 10.1186/s13256-020-02441-6 [pii]
AID - 2441 [pii]
AID - 10.1186/s13256-020-02441-6 [doi]
PST - epublish
SO  - J Med Case Rep. 2020 Jul 24;14(1):114. doi: 10.1186/s13256-020-02441-6.

PMID- 32693768
OWN - NLM
STAT- MEDLINE
DCOM- 20201207
LR  - 20201214
IS  - 1875-6212 (Electronic)
IS  - 1570-1611 (Linking)
VI  - 18
IP  - 6
DP  - 2020
TI  - Cardio-Rheumatology: Two Collaborating Disciplines to Deal with the Enhanced 
      Cardiovascular Risk in Autoimmune Rheumatic Diseases.
PG  - 533-537
LID - 10.2174/1570161118666200721145718 [doi]
AB  - In Part 1 of this Thematic Issue entitled "Systemic Autoimmune Rheumatic Diseases 
      and Cardiology", a panel of specialists and experts in cardiology, rheumatology, 
      immunology and related fields discussed the cardiovascular complications of 
      spondyloarthritides, rheumatoid arthritis, Sjogren's syndrome and vasculitides, 
      as well as relevant cardiovascular issues related to non-biologic and biologic 
      disease-modifying anti-rheumatic drugs (DMARDs), and provided their 
      recommendations for prevention and management of these complications. In part 2 
      of this Thematic Issue, experts discuss the enhanced cardiovascular risk 
      conferred by additional autoimmune rheumatic diseases (ARDs), including systemic 
      lupus erythematosus, the antiphospholipid syndrome, psoriasis and psoriatic 
      arthritis and juvenile idiopathic arthritis. These, and the previous articles, 
      place inflammation as the key common link to explain the enhanced risk of 
      cardiovascular complications in patients with ARDs. It follows that treatment 
      should probably target inflammation. From all these contemporary reviews, the 
      conclusion that is derived further supports the notion of the emerging field of 
      Cardio- Rheumatology where physicians and experts from these two disciplines 
      collaborate in risk stratification and optimization of preventive strategies and 
      drug therapies in patients with ARDs.
CI  - Copyright© Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Manolis, Antonis S
AU  - Manolis AS
AD  - Third Department of Cardiology, Athens University School of Medicine, Athens, 
      Greece.
FAU - Tzioufas, Athanasios G
AU  - Tzioufas AG
AD  - Department of Pathophysiology, Athens University School of Medicine, Athens, 
      Greece.
LA  - eng
PT  - Editorial
PT  - Introductory Journal Article
PL  - United Arab Emirates
TA  - Curr Vasc Pharmacol
JT  - Current vascular pharmacology
JID - 101157208
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/therapeutic use
MH  - Antirheumatic Agents/therapeutic use
MH  - *Autoimmune Diseases/diagnosis/drug therapy/epidemiology/immunology
MH  - *Cardiology
MH  - *Cardiovascular Diseases/diagnosis/epidemiology/immunology/prevention & control
MH  - Cooperative Behavior
MH  - Heart Disease Risk Factors
MH  - Humans
MH  - *Inflammation/diagnosis/drug therapy/epidemiology/immunology
MH  - *Interdisciplinary Communication
MH  - *Patient Care Team
MH  - Prognosis
MH  - Protective Factors
MH  - *Rheumatic Diseases/diagnosis/drug therapy/epidemiology/immunology
MH  - *Rheumatology
MH  - Risk Assessment
MH  - Specialization
OTO - NOTNLM
OT  - Autoimmune rheumatic disease
OT  - acute coronary syndromes
OT  - antiphospholipid syndrome
OT  - antirheumatic drugs
OT  - atherosclerosis
OT  - cardiorheumatology
OT  - cardiovascular disease
OT  - cardiovascular imaging
OT  - coronary artery disease
OT  - juvenile idiopathic arthritis
OT  - myocardial infarction
OT  - psoriasis
OT  - psoriatic arthritis
OT  - stroke
OT  - systemic lupus erythematosus
EDAT- 2020/07/23 06:00
MHDA- 2020/12/15 06:00
CRDT- 2020/07/23 06:00
PHST- 2020/07/23 06:00 [pubmed]
PHST- 2020/12/15 06:00 [medline]
PHST- 2020/07/23 06:00 [entrez]
AID - CVP-EPUB-108386 [pii]
AID - 10.2174/1570161118666200721145718 [doi]
PST - ppublish
SO  - Curr Vasc Pharmacol. 2020;18(6):533-537. doi: 10.2174/1570161118666200721145718.

PMID- 32672719
OWN - NLM
STAT- MEDLINE
DCOM- 20211025
LR  - 20240329
IS  - 2474-7661 (Electronic)
IS  - 2474-7661 (Linking)
VI  - 4
IP  - 7
DP  - 2020 Jul
TI  - Chronic Corticosteroid Use as a Risk Factor for Perioperative Complications in 
      Patients Undergoing Total Joint Arthroplasty.
PG  - e2000001
LID - 10.5435/JAAOSGlobal-D-20-00001 [doi]
LID - e20.00001
AB  - BACKGROUND: Osteoarthritis may be caused by or concurrent with diseases such as 
      rheumatoid arthritis or systemic lupus erythematosus, which rely on chronic 
      corticosteroids regimens for treatment. If a total knee or hip arthroplasty is 
      needed, this chronic treatment method has been associated with poorer surgical 
      outcomes. METHODS: A retrospective analysis of data collected by the American 
      College of Surgeons National Surgical Quality Improvement Program was conducted. 
      The Current Procedural Terminology codes were used to identify 403,566 total knee 
      arthroplasty and total hip arthroplasty patients who were then stratified by the 
      use of chronic corticosteroids for univariate analysis. RESULTS: Forteen thousand 
      seven hundred seventy-four of the patients identified were prescribed chronic 
      corticosteroid regimens. A statistically significant difference was observed in 
      perioperative complications for patients prescribed with corticosteroids, 
      including higher rates of surgical site infection (P = 0.0001), occurrence of 
      deep incisional surgical site infection (P < 0.0001), occurrences of organ space 
      surgical site infection (P < 0.0001), wound dehiscence (P < 0.0001), general 
      would infection (P < 0.0001), pneumonia (P < 0.0001), occurrences of unplanned 
      intubation (P = 0.0002), urinary tract infection (P < 0.0001), and readmission (P 
      < 0.0001). No statistically significant difference was observed in the 30-day 
      mortality between the 2 groups (0.63), venous thromboembolic event (0.42), 
      cerebrovascular accident (0.12), myocardial infarction (0.49), cardiac arrest 
      (0.098), deep vein thrombosis (0.17), or sepsis (0.52). CONCLUSION: Many of the 
      notable differences in complications may be directly attributed to the 
      immunosuppressive nature of corticosteroids. With increased knowledge of which 
      perioperative complications to monitor, surgeons can tailor treatment strategies 
      to this population that reduce morbidity and improve outcomes.
FAU - Kittle, Haley
AU  - Kittle H
AD  - From the Department of Orthopaedics, University of Illinois College of Medicine 
      (Ms. Kittle and Dr. Ormseth), and the Department of Orthopaedics, University of 
      Illinois College of Medicine (Dr. Patetta, Dr. Sood, and Dr. Gonzalez), Chicago, 
      IL.
FAU - Ormseth, Andrew
AU  - Ormseth A
FAU - Patetta, Michael J
AU  - Patetta MJ
FAU - Sood, Anshum
AU  - Sood A
FAU - Gonzalez, Mark H
AU  - Gonzalez MH
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Am Acad Orthop Surg Glob Res Rev
JT  - Journal of the American Academy of Orthopaedic Surgeons. Global research & 
      reviews
JID - 101724868
RN  - 0 (Adrenal Cortex Hormones)
MH  - Adrenal Cortex Hormones/adverse effects
MH  - *Arthroplasty, Replacement, Hip/adverse effects
MH  - *Arthroplasty, Replacement, Knee/adverse effects
MH  - Humans
MH  - Retrospective Studies
MH  - Risk Factors
PMC - PMC7366416
COIS- None of the following authors or any immediate family member has received 
      anything of value from or has stock or stock options held in a commercial company 
      or institution related directly or indirectly to the subject of this article: 
      Kittle, Ormseth, Patetta, Sood, and Gonzalez.
EDAT- 2020/07/17 06:00
MHDA- 2021/10/26 06:00
PMCR- 2020/07/01
CRDT- 2020/07/17 06:00
PHST- 2020/07/17 06:00 [entrez]
PHST- 2020/07/17 06:00 [pubmed]
PHST- 2021/10/26 06:00 [medline]
PHST- 2020/07/01 00:00 [pmc-release]
AID - 01979360-202007000-00001 [pii]
AID - JAAOSGlobal-D-20-00001 [pii]
AID - 10.5435/JAAOSGlobal-D-20-00001 [doi]
PST - ppublish
SO  - J Am Acad Orthop Surg Glob Res Rev. 2020 Jul;4(7):e2000001. doi: 
      10.5435/JAAOSGlobal-D-20-00001.

PMID- 32654116
OWN - NLM
STAT- MEDLINE
DCOM- 20211004
LR  - 20211204
IS  - 1365-2362 (Electronic)
IS  - 0014-2972 (Linking)
VI  - 50
IP  - 12
DP  - 2020 Dec
TI  - Cardiovascular risk estimation with 5 different algorithms before and after 5 
      years of bDMARD treatment in rheumatoid arthritis.
PG  - e13343
LID - 10.1111/eci.13343 [doi]
AB  - BACKGROUND: Assessing cardiovascular (CV) risk represents a challenge for 
      clinicians because more variables can impact CV risk. The aim of this study was 
      to evaluate the change of CV risk after 5 years of biological treatment in 
      rheumatoid arthritis (RA) patients and impact of prolonged low disease activity 
      on 5 different CV risk algorithms. MATERIALS AND METHODS: We estimated the CV 
      risk, at baseline and at 5-year follow-up (FU), with the Systematic COronary Risk 
      Evaluation(SCORE) charts, the algorithm 'Progetto Cuore', the QRISK3-2018 score, 
      the Reynold Risk Score(RRS) and the Expanded Risk Score in RA(ERS-RA). Clinical 
      disease activity index(CDAI) was used to define RA activity. Wilcoxon signed-rank 
      test was used to compare CV risk scores. RESULTS: In 110 patients with a 5-year 
      FU on biological disease-modifying anti-rheumatic drug treatment, we observed an 
      increase in the 10-year CV risk estimated by SCORE charts [from mean (SD) 0.9% 
      (1.4) to 1.1% (1.5), P < .001], 'Progetto Cuore' [from mean (SD) 5.5% (7.2) to 
      6.2% (6.8), P < .001], QRISK3-2018 [from mean (SD) 9.3% (10.1) to 11.9% (10.8), 
      P < .001) and RRS [from mean (SD) 5.6% (6.4) to 6.2% (7.5), P < .05], mainly due 
      to age raise. ERS-RA highlighted a significant decrease of estimated CV risk in 
      patients with persistent CDAI ≤ 10[from mean (SD) 9.6% (11.2) to 7.3% (6.4), 
      P < .05], despite age increase and its impact on the CV risk score. CONCLUSIONS: 
      Algorithms commonly used to estimate 10-year CV risk in RA perform differently. 
      Scores that include specific inflammatory RA-related variables seem to decrease 
      with amelioration of disease activity. Further investigations are warranted to 
      explore the predictive value of their changing over time.
CI  - © 2020 Stichting European Society for Clinical Investigation Journal Foundation.
FAU - Cacciapaglia, Fabio
AU  - Cacciapaglia F
AD  - DETO-Department of Emergency and Organ Transplantation-Rheumatology Unit, 
      University of Bari, Bari, Italy.
FAU - Fornaro, Marco
AU  - Fornaro M
AUID- ORCID: 0000-0003-1716-7432
AD  - DETO-Department of Emergency and Organ Transplantation-Rheumatology Unit, 
      University of Bari, Bari, Italy.
FAU - Venerito, Vincenzo
AU  - Venerito V
AUID- ORCID: 0000-0002-2573-5930
AD  - DETO-Department of Emergency and Organ Transplantation-Rheumatology Unit, 
      University of Bari, Bari, Italy.
FAU - Perniola, Simone
AU  - Perniola S
AD  - DETO-Department of Emergency and Organ Transplantation-Rheumatology Unit, 
      University of Bari, Bari, Italy.
AD  - Department of Medicine, University of Verona, Verona, Italy.
FAU - Urso, Livio
AU  - Urso L
AD  - DETO-Department of Emergency and Organ Transplantation-Rheumatology Unit, 
      University of Bari, Bari, Italy.
FAU - Iannone, Florenzo
AU  - Iannone F
AUID- ORCID: 0000-0003-0474-5344
AD  - DETO-Department of Emergency and Organ Transplantation-Rheumatology Unit, 
      University of Bari, Bari, Italy.
LA  - eng
PT  - Journal Article
DEP - 20200731
PL  - England
TA  - Eur J Clin Invest
JT  - European journal of clinical investigation
JID - 0245331
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - 0 (Cholesterol, HDL)
RN  - 0 (Glucocorticoids)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Adult
MH  - Age Factors
MH  - Angina Pectoris/epidemiology
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy/epidemiology
MH  - Atrial Fibrillation/epidemiology
MH  - Biological Products/*therapeutic use
MH  - Blood Pressure
MH  - Body Mass Index
MH  - C-Reactive Protein/metabolism
MH  - Cardiovascular Diseases/*epidemiology/mortality
MH  - Cholesterol/blood
MH  - Cholesterol, HDL/blood
MH  - Diabetes Mellitus/epidemiology
MH  - Ethnicity/statistics & numerical data
MH  - Female
MH  - Follow-Up Studies
MH  - Glucocorticoids/therapeutic use
MH  - Heart Disease Risk Factors
MH  - Humans
MH  - Hyperlipidemias/blood/drug therapy/epidemiology
MH  - Hypertension/drug therapy/epidemiology
MH  - Ischemic Attack, Transient/epidemiology
MH  - Male
MH  - Medical History Taking
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology
MH  - Renal Insufficiency, Chronic/epidemiology
MH  - Sex Factors
MH  - Smoking/epidemiology
MH  - Stroke/epidemiology
OTO - NOTNLM
OT  - algorithms
OT  - cardiovascular risk
OT  - disease activity
OT  - rheumatoid arthritis
EDAT- 2020/07/13 06:00
MHDA- 2021/10/05 06:00
CRDT- 2020/07/13 06:00
PHST- 2020/04/07 00:00 [received]
PHST- 2020/06/18 00:00 [revised]
PHST- 2020/06/23 00:00 [accepted]
PHST- 2020/07/13 06:00 [pubmed]
PHST- 2021/10/05 06:00 [medline]
PHST- 2020/07/13 06:00 [entrez]
AID - 10.1111/eci.13343 [doi]
PST - ppublish
SO  - Eur J Clin Invest. 2020 Dec;50(12):e13343. doi: 10.1111/eci.13343. Epub 2020 Jul 
      31.

PMID- 32632509
OWN - NLM
STAT- MEDLINE
DCOM- 20210311
LR  - 20210311
IS  - 1433-2965 (Electronic)
IS  - 0937-941X (Linking)
VI  - 31
IP  - 12
DP  - 2020 Dec
TI  - Blindness increases the risk for hip fracture and vertebral fracture but not the 
      risk for distal radius fracture: a longitudinal follow-up study using a national 
      sample cohort.
PG  - 2345-2354
LID - 10.1007/s00198-020-05475-0 [doi]
AB  - The risks for hip fracture and vertebral fracture, but not the risk for distal 
      radius fracture, were significantly higher in the blindness group than in the 
      control group with a maximum 12-year follow-up. PURPOSE: To evaluate the 
      influence of visual impairment on the risk for osteoporotic fractures at common 
      sites: hip, thoracic/lumbar vertebra, and distal radius. METHODS: This 
      longitudinal follow-up study used a database of a national sample cohort from 
      2002 to 2013 provided by the Korean National Health Insurance Service. Of a total 
      of 1,125,691 subjects, 3918 patients with visual impairment and age ≥ 50 years 
      were enrolled in a 1:4 ratio; 15,672 control participants were matched for age, 
      sex, income, and region of residence. Stratified Cox proportional-hazards models 
      were used to evaluate the crude and adjusted (for steroid medication, rheumatoid 
      arthritis, depression, osteoporosis, diabetes mellitus, and stroke history) 
      hazard ratios (HRs) for each fracture site. Fracture diagnoses were based on the 
      ICD-10 codes: hip fracture (S720, S721, S722), vertebral fracture (S220, S320), 
      and distal radius fracture (S525). RESULTS: The HRs for hip and vertebral 
      fracture were significantly higher in the blindness group (adjusted HR = 2.46, p 
      < 0.001 for hip fracture; adjusted HR = 1.42, p = 0.020 for thoracic/lumbar 
      vertebral fracture) than in the matched control group. However, the HR for distal 
      radius fracture was not higher in the blindness group. The HRs for all three 
      fracture sites were not significantly higher in the non-blindness visual 
      impairment group after adjustment. CONCLUSION: The risks for hip fracture and 
      vertebral fracture were significantly higher in the blindness group. However, the 
      risk for distal radius fracture was not related to visual impairment including 
      blindness.
FAU - Choi, H G
AU  - Choi HG
AD  - Department of Otorhinolaryngology-Head & Neck Surgery, Hallym University College 
      of Medicine, Anyang, Republic of Korea.
AD  - Hallym Data Science Laboratory, Hallym University College of Medicine, Anyang, 
      Republic of Korea.
FAU - Lee, J K
AU  - Lee JK
AUID- ORCID: 0000-0003-3710-5714
AD  - Department of Orthopaedic Surgery, Konkuk University Medical Center, Research 
      Institute of Medical Science, Konkuk University School of Medicine, Seoul, 
      Republic of Korea.
FAU - Lee, M J
AU  - Lee MJ
AD  - Department of Ophthalmology, Hallym University College of Medicine, Anyang, 
      Republic of Korea.
FAU - Park, B
AU  - Park B
AD  - Department of Otorhinolaryngology-Head & Neck Surgery, Hallym University College 
      of Medicine, Anyang, Republic of Korea.
FAU - Sim, S
AU  - Sim S
AD  - Department of Statistics and Institute of Statistics, Hallym University, 1 
      Hallymdaehak-gil, Chuncheon-si, Gangwon-do, 24252, Republic of Korea. 
      sysim@hallym.ac.kr.
FAU - Lee, S-M
AU  - Lee SM
AUID- ORCID: 0000-0002-9018-8216
AD  - Department of Cornea, External Disease & Refractive Surgery, HanGil Eye Hospital, 
      Catholic Kwandong University College of Medicine, 35 Bupyeong-daero, Bupyeong-gu, 
      Incheon, 21388, Republic of Korea. lsm10003@gmail.com.
LA  - eng
GR  - NRF-2015R1D1A1A01060860/National Research Foundation of Korea (KR)/
GR  - NRF-2017R1D1A1B03031577/National Research Foundation of Korea (KR)/
PT  - Journal Article
DEP - 20200706
PL  - England
TA  - Osteoporos Int
JT  - Osteoporosis international : a journal established as result of cooperation 
      between the European Foundation for Osteoporosis and the National Osteoporosis 
      Foundation of the USA
JID - 9100105
SB  - IM
MH  - Blindness
MH  - Follow-Up Studies
MH  - *Hip Fractures/epidemiology/etiology
MH  - Humans
MH  - *Osteoporotic Fractures/epidemiology/etiology
MH  - *Radius Fractures/epidemiology
MH  - Risk Factors
MH  - *Spinal Fractures/epidemiology/etiology
OTO - NOTNLM
OT  - Epidemiology
OT  - Forearm fracture
OT  - Hip fracture
OT  - Osteoporosis
OT  - Vertebral fracture
OT  - Visual impairment
EDAT- 2020/07/08 06:00
MHDA- 2021/03/12 06:00
CRDT- 2020/07/08 06:00
PHST- 2019/11/25 00:00 [received]
PHST- 2020/05/21 00:00 [accepted]
PHST- 2020/07/08 06:00 [pubmed]
PHST- 2021/03/12 06:00 [medline]
PHST- 2020/07/08 06:00 [entrez]
AID - 10.1007/s00198-020-05475-0 [pii]
AID - 10.1007/s00198-020-05475-0 [doi]
PST - ppublish
SO  - Osteoporos Int. 2020 Dec;31(12):2345-2354. doi: 10.1007/s00198-020-05475-0. Epub 
      2020 Jul 6.

PMID- 32615604
OWN - NLM
STAT- MEDLINE
DCOM- 20210201
LR  - 20210201
IS  - 1439-4413 (Electronic)
IS  - 0012-0472 (Linking)
VI  - 145
IP  - 13
DP  - 2020 Jul
TI  - [Inflammatory Muscle Pain: Polymyalgia Rheumatica with or without Large Vessel 
      Vasculitis].
PG  - 895-902
LID - 10.1055/a-1074-7685 [doi]
AB  - Polymyalgia rheumatica (PMR) is characterized by rapidly evolving shoulder and 
      pelvic girdle pain with fatigue, weight loss, night sweats and elevated CRP and 
      ESR. Giant cell arteritis (GCA) can occur in PMR and vice versa. Headache and 
      scalp tenderness are typical for GCA. GCA may be complicated by visual loss or by 
      strokes.Imaging, particularly ultrasound, is helpful for distinguishing PMR from 
      similar conditions such as shoulder osteoarthritis, rheumatoid arthritis and 
      chondrocalcinosis. Subdeltoid bursitis, biceps tenosynovitis and hip joint 
      effusions are common in PMR. The diagnosis of GCA needs to be either confirmed by 
      imaging or by histology. Ultrasound is the imaging method of choice provided that 
      expertise and adequate equipment are available. Inflamed arteries exhibit a 
      concentric wall thickening. Patients with extracranial GCA are younger, more 
      often female. Vasculitis commonly involves the aorta, subclavian arteries, 
      axillary arteries and other arteries. The diagnosis of extracranial GCA may be 
      confirmed by ultrasound, CT, MRI or PET.Prednisolone with a starting dose of 
      15-25 mg/d for PMR and of 40-60 mg/d for GCA results in rapid improvement of 
      symptoms. Fast-track clinics provide clinical and ultrasound examinations by 
      experts within 24 hours. Their introduction led to a decrease of visual loss in 
      GCA. The prednisolone dose can be discontinued within 1 year in about 50 % of GCA 
      patients. Additional treatment with tocilizumab allows to reduce flares and 
      decrease glucocorticoid doses. Tocilizumab is particularly useful in patients 
      with relapses and with increased risk of glucocorticoid side effects.
CI  - © Georg Thieme Verlag KG Stuttgart · New York.
FAU - Schmidt, Wolfgang A
AU  - Schmidt WA
LA  - ger
PT  - Case Reports
PT  - Journal Article
PT  - Review
TT  - Polymyalgia rheumatica mit und ohne Großgefäßvaskulitis.
DEP - 20200702
PL  - Germany
TA  - Dtsch Med Wochenschr
JT  - Deutsche medizinische Wochenschrift (1946)
JID - 0006723
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 9PHQ9Y1OLM (Prednisolone)
RN  - I031V2H011 (tocilizumab)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Aged
MH  - Antibodies, Monoclonal, Humanized/therapeutic use
MH  - Blindness/diagnosis
MH  - Diagnosis, Differential
MH  - Fatigue/etiology
MH  - Female
MH  - Giant Cell Arteritis/diagnosis
MH  - Humans
MH  - Methotrexate/therapeutic use
MH  - Polymyalgia Rheumatica/*diagnosis
MH  - Prednisolone/therapeutic use
MH  - Stroke/etiology
MH  - Ultrasonography
MH  - Vasculitis/*diagnosis
COIS- Honorare für Vorträge: Chugai, Medac, Novartis, Roche, SanofiHororare für 
      Beratertätigkeit: Chugai, Novartis, Roche, SanofiPrinicple Investigator von 
      Studien: Novartis, SanofiArbeitgeber: Immanuel Krankenhaus Berlin, Rheumaklinik 
      Berlin-Buch, Leitender OberarztMitgliedschaften:EULAR: Coopted Member of Standing 
      Committee on Musculoskeletal ImagingAmerican College of Rheumatology 
      (ACR)Deutsche Gesellschaft für Rheumatologie (DGRh)Deutsche Gesellschaft für 
      Ultraschall in der Medizin (DEGUM): Stufe 3 BewegungsorganeBerufsverband 
      Deutscher Internisten (BDI)Deutsche Rheumaliga
EDAT- 2020/07/03 06:00
MHDA- 2021/02/02 06:00
CRDT- 2020/07/03 06:00
PHST- 2020/07/03 06:00 [entrez]
PHST- 2020/07/03 06:00 [pubmed]
PHST- 2021/02/02 06:00 [medline]
AID - 10.1055/a-1074-7685 [doi]
PST - ppublish
SO  - Dtsch Med Wochenschr. 2020 Jul;145(13):895-902. doi: 10.1055/a-1074-7685. Epub 
      2020 Jul 2.

PMID- 32610637
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201020
IS  - 2227-9032 (Print)
IS  - 2227-9032 (Electronic)
IS  - 2227-9032 (Linking)
VI  - 8
IP  - 3
DP  - 2020 Jun 29
TI  - Obesity and Morbidity Risk in the U.S. Veteran.
LID - 10.3390/healthcare8030191 [doi]
LID - 191
AB  - The obesity epidemic in the United States has been well documented and serves as 
      the basis for a number of health interventions across the nation. However, those 
      who have served in the U.S. military (Veteran population) suffer from obesity in 
      higher numbers and have an overall disproportionate poorer health status when 
      compared to the health of the older non-Veteran population in the U.S. which may 
      further compound their overall health risk. This study examined both the 
      commonalities and the differences in obesity rates and the associated 
      co-morbidities among the U.S. Veteran population, utilizing data from the 2018 
      Behavioral Risk Factor Surveillance System (BRFSS). These data are considered by 
      the Centers for Disease Control and Prevention (CDC) to be the nation's best 
      source for health-related survey data, and the 2018 version includes 437,467 
      observations. Study findings show not only a significantly higher risk of obesity 
      in the U.S. Veteran population, but also a significantly higher level (higher 
      odds ratio) of the associated co-morbidities when compared to non-Veterans, 
      including coronary heart disease (CHD) or angina (odds ratio (OR) = 2.63); stroke 
      (OR = 1.86); skin cancer (OR = 2.18); other cancers (OR = 1.73); chronic 
      obstructive pulmonary disease (COPD) (OR = 1.52), emphysema, or chronic 
      bronchitis; arthritis (OR = 1.52), rheumatoid arthritis, gout, lupus, or 
      fibromyalgia; depressive disorders (OR = 0.84), and diabetes (OR = 1.61) at the 
      0.95 confidence interval level.
FAU - Betancourt, Jose A
AU  - Betancourt JA
AD  - School of Health Administration, Texas State University, San Marcos, TX 78666, 
      USA.
FAU - Stigler Granados, Paula
AU  - Stigler Granados P
AD  - School of Health Administration, Texas State University, San Marcos, TX 78666, 
      USA.
FAU - Pacheco, Gerardo J
AU  - Pacheco GJ
AD  - School of Health Administration, Texas State University, San Marcos, TX 78666, 
      USA.
FAU - Shanmugam, Ramalingam
AU  - Shanmugam R
AD  - School of Health Administration, Texas State University, San Marcos, TX 78666, 
      USA.
FAU - Kruse, C Scott
AU  - Kruse CS
AD  - School of Health Administration, Texas State University, San Marcos, TX 78666, 
      USA.
FAU - Fulton, Lawrence V
AU  - Fulton LV
AD  - School of Health Administration, Texas State University, San Marcos, TX 78666, 
      USA.
LA  - eng
PT  - Journal Article
DEP - 20200629
PL  - Switzerland
TA  - Healthcare (Basel)
JT  - Healthcare (Basel, Switzerland)
JID - 101666525
PMC - PMC7551346
OTO - NOTNLM
OT  - U.S. veteran health
OT  - comorbidities
OT  - diabetes
OT  - obesity
OT  - overweight
OT  - risk-factors
COIS- All authors declare they have no conflicts of interest.
EDAT- 2020/07/03 06:00
MHDA- 2020/07/03 06:01
PMCR- 2020/06/29
CRDT- 2020/07/03 06:00
PHST- 2020/05/27 00:00 [received]
PHST- 2020/06/16 00:00 [revised]
PHST- 2020/06/25 00:00 [accepted]
PHST- 2020/07/03 06:00 [entrez]
PHST- 2020/07/03 06:00 [pubmed]
PHST- 2020/07/03 06:01 [medline]
PHST- 2020/06/29 00:00 [pmc-release]
AID - healthcare8030191 [pii]
AID - healthcare-08-00191 [pii]
AID - 10.3390/healthcare8030191 [doi]
PST - epublish
SO  - Healthcare (Basel). 2020 Jun 29;8(3):191. doi: 10.3390/healthcare8030191.

PMID- 32603700
OWN - NLM
STAT- MEDLINE
DCOM- 20210519
LR  - 20210519
IS  - 1916-7075 (Electronic)
IS  - 0828-282X (Linking)
VI  - 36
IP  - 11
DP  - 2020 Nov
TI  - Biologic Agents Reduce Cardiovascular Events in Rheumatoid Arthritis Not 
      Responsive to Tumour Necrosis Factor Inhibitors: A National Cohort Study.
PG  - 1739-1746
LID - S0828-282X(20)30035-0 [pii]
LID - 10.1016/j.cjca.2020.01.003 [doi]
AB  - BACKGROUND: Tumour necrosis factor inhibitors (TNFis) improve joints outcomes and 
      reduce cardiovascular (CV) risk in patients with rheumatoid arthritis (RA). 
      However, 20%-45% of RA patients are TNFi poor responders and have a significantly 
      higher risk of CV events. In these TNFi nonresponders, the use of second-line 
      biologic agents to improve synovial outcomes is supported by clinical trials and 
      real-world experience. However, it remains unknown what kind of immune-mediated 
      agent has the best CV prevention effect in this high-risk population. METHODS: A 
      nationwide RA cohort obtained from Taiwan's National Health Insurance claims 
      database was constructed. RA patients first treated with TNFis who then received 
      either rituximab, tocilizumab, or abatacept were enrolled and followed for 2 
      years. RESULTS: A total of 89,973 RA patients were screened and 1,584 patients 
      ultimately included. The incidences of major adverse cardiac events (MACE) at 2 
      years in the rituximab, tocilizumab, and abatacept groups were 7.17%, 2.75% and 
      2.38%, respectively. Multivariate adjusted Cox analysis showed that tocilizumab 
      had significantly lower risk than rituximab in myocardial infarction (hazard 
      ratio [HR] 0.12, 95% confidence interval [CI] 0.02-0.56; P = 0.008), and MACE (HR 
      0.41, 95% CI 0.23-0.72; P = 0.002). In addition, abatacept also had significant 
      lower adjusted risk than rituximab in stroke (HR 0.18, 95% CI 0.05-0.64; P = 
      0.008), heart failure (HR 0.20, 95% CI 0.05-0.83; P = 0.027), and MACE (HR 0.25, 
      95% CI 0.11-0.55; P < 0.001) in multivariate analysis. CONCLUSIONS: 
      TNFi-nonresponder patients with RA who received second-line tocilizumab or 
      abatacept had more benefit on CV events prevention compared with those who 
      received rituximab.
CI  - Copyright © 2020 Canadian Cardiovascular Society. Published by Elsevier Inc. All 
      rights reserved.
FAU - Hsieh, Ming-Jer
AU  - Hsieh MJ
AD  - Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial 
      Hospital, Linkou Medical Center, Taoyuan, Taiwan; College of Medicine, Chang Gung 
      University, Taoyuan, Taiwan.
FAU - Lee, Cheng-Hung
AU  - Lee CH
AD  - Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial 
      Hospital, Linkou Medical Center, Taoyuan, Taiwan; College of Medicine, Chang Gung 
      University, Taoyuan, Taiwan.
FAU - Tsai, Ming-Lung
AU  - Tsai ML
AD  - Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial 
      Hospital, Linkou Medical Center, Taoyuan, Taiwan; College of Medicine, Chang Gung 
      University, Taoyuan, Taiwan.
FAU - Kao, Chang-Fu
AU  - Kao CF
AD  - College of Medicine, Chang Gung University, Taoyuan, Taiwan; Division of 
      Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, 
      Chang Gung University College of Medicine, Taoyuan, Taiwan.
FAU - Lan, Wen-Ching
AU  - Lan WC
AD  - Center for Big Data Analytics and Statistics, Chang Gung Memorial Hospital, 
      Linkou Medical Center, Taoyuan, Taiwan.
FAU - Huang, Yu-Tung
AU  - Huang YT
AD  - Center for Big Data Analytics and Statistics, Chang Gung Memorial Hospital, 
      Linkou Medical Center, Taoyuan, Taiwan.
FAU - Tseng, Wen-Yi
AU  - Tseng WY
AD  - College of Medicine, Chang Gung University, Taoyuan, Taiwan; Division of 
      Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, 
      Keelung Branch, Taiwan.
FAU - Wen, Ming-Shien
AU  - Wen MS
AD  - Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial 
      Hospital, Linkou Medical Center, Taoyuan, Taiwan; College of Medicine, Chang Gung 
      University, Taoyuan, Taiwan.
FAU - Chang, Shang-Hung
AU  - Chang SH
AD  - Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial 
      Hospital, Linkou Medical Center, Taoyuan, Taiwan; Center for Big Data Analytics 
      and Statistics, Chang Gung Memorial Hospital, Linkou Medical Center, Taoyuan, 
      Taiwan; Graduate Institute of Nursing, Chang Gung University of Science and 
      Technology, Taoyuan, Taiwan. Electronic address: afen.chang@gmail.com.
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20200115
PL  - England
TA  - Can J Cardiol
JT  - The Canadian journal of cardiology
JID - 8510280
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Factors)
SB  - IM
CIN - Can J Cardiol. 2020 Nov;36(11):1700-1702. doi: 10.1016/j.cjca.2020.03.023. PMID: 
      32619444
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/complications/*drug therapy
MH  - Biological Factors/*therapeutic use
MH  - Cardiovascular Diseases/epidemiology/etiology/*prevention & control
MH  - Databases, Factual
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - *Population Surveillance
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Taiwan/epidemiology
EDAT- 2020/07/01 06:00
MHDA- 2021/05/20 06:00
CRDT- 2020/07/01 06:00
PHST- 2019/07/24 00:00 [received]
PHST- 2020/01/02 00:00 [revised]
PHST- 2020/01/02 00:00 [accepted]
PHST- 2020/07/01 06:00 [pubmed]
PHST- 2021/05/20 06:00 [medline]
PHST- 2020/07/01 06:00 [entrez]
AID - S0828-282X(20)30035-0 [pii]
AID - 10.1016/j.cjca.2020.01.003 [doi]
PST - ppublish
SO  - Can J Cardiol. 2020 Nov;36(11):1739-1746. doi: 10.1016/j.cjca.2020.01.003. Epub 
      2020 Jan 15.

PMID- 32596727
OWN - NLM
STAT- MEDLINE
DCOM- 20210416
LR  - 20210416
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 60
IP  - 1
DP  - 2021 Jan 5
TI  - Comparable or higher prevalence of comorbidities in antiphospholipid syndrome vs 
      rheumatoid arthritis: a multicenter, case-control study.
PG  - 170-178
LID - 10.1093/rheumatology/keaa321 [doi]
AB  - OBJECTIVES: Evidence on comorbidity prevalence in antiphospholipid syndrome (APS) 
      and its difference from high comorbidity burden rheumatic diseases is limited. 
      Herein, we compare multiple comorbidities between APS and RA. METHODS: A total of 
      326 patients from the Greek APS registry [237 women, mean age 48.7 (13.4) years, 
      161 primary APS (PAPS), 165 SLE-APS] were age/sex matched (1:2 ratio) with 652 
      patients from a Greek multicentre RA cohort of 3115 patients. Prevalence of 
      cardiovascular (CV) risk factors, stroke, coronary artery disease (CAD), 
      osteoporosis, diabetes mellitus (DM), chronic obstructive pulmonary disease 
      (COPD), depression and neoplasms were compared between APS and RA patients using 
      multivariate regression analysis. RESULTS: Ηyperlipidemia and obesity 
      (ΒΜΙ ≥ 30 kg/m2) were comparable while hypertension, smoking, stroke and CAD were 
      more prevalent in APS compared with RA patients. Osteoporosis and depression were 
      more frequent in APS, while DM, COPD and neoplasms did not differ between the two 
      groups. Comparison of APS subgroups to 1:2 matched RA patients revealed that 
      smoking and stroke were more prevalent in both PAPS and SLE-APS vs RA. 
      Hypertension, CAD and osteoporosis were more frequent only in SLE-APS vs RA, 
      whereas DM was less prevalent in PAPS vs RA. Hyperlipidaemia was independently 
      associated with CV events (combined stroke and CAD) in PAPS and SLE-APS, while CS 
      duration was associated with osteoporosis in SLE-APS. CONCLUSION: Comorbidity 
      burden in APS (PAPS and SLE-APS) is comparable or higher than that in RA, 
      entailing a high level of diligence for CV risk prevention, awareness for 
      depression and CS exposure minimization.
CI  - © The Author(s) 2020. Published by Oxford University Press on behalf of the 
      British Society for Rheumatology. All rights reserved. For permissions, please 
      email: journals.permissions@oup.com.
FAU - Panopoulos, Stylianos
AU  - Panopoulos S
AD  - Joint Rheumatology Program, Medical School, National and Kapodistrian University 
      of Athens, Athens.
FAU - Thomas, Konstantinos
AU  - Thomas K
AD  - Joint Rheumatology Program, Medical School, National and Kapodistrian University 
      of Athens, Athens.
FAU - Georgiopoulos, Georgios
AU  - Georgiopoulos G
AD  - Joint Rheumatology Program, Medical School, National and Kapodistrian University 
      of Athens, Athens.
FAU - Boumpas, Dimitrios
AU  - Boumpas D
AD  - Joint Rheumatology Program, Medical School, National and Kapodistrian University 
      of Athens, Athens.
FAU - Katsiari, Christina
AU  - Katsiari C
AD  - Medical School, University of Thessaly, Larissa.
FAU - Bertsias, George
AU  - Bertsias G
AD  - Medical School, University of Crete, Heraklion.
FAU - Drosos, Alexandros A
AU  - Drosos AA
AD  - Medical School, University of Ioannina, Ioannina.
FAU - Boki, Kyriaki
AU  - Boki K
AD  - Sismanogleio General Hospital, Athens.
FAU - Dimitroulas, Theodoros
AU  - Dimitroulas T
AD  - Medical School, Aristotle University of Thessaloniki, Thessaloniki.
FAU - Garyfallos, Alexandros
AU  - Garyfallos A
AD  - Medical School, Aristotle University of Thessaloniki, Thessaloniki.
FAU - Papagoras, Charalampos
AU  - Papagoras C
AD  - Medical School, University of Thrace, Alexandroupoli.
FAU - Katsimbri, Pelagia
AU  - Katsimbri P
AD  - Joint Rheumatology Program, Medical School, National and Kapodistrian University 
      of Athens, Athens.
FAU - Tziortziotis, Apostolos
AU  - Tziortziotis A
AD  - Medical School, University of Thessaly, Larissa.
FAU - Adamichou, Christina
AU  - Adamichou C
AD  - Medical School, University of Crete, Heraklion.
FAU - Kaltsonoudis, Evripidis
AU  - Kaltsonoudis E
AD  - Medical School, University of Ioannina, Ioannina.
FAU - Argyriou, Evangelia
AU  - Argyriou E
AD  - Sismanogleio General Hospital, Athens.
FAU - Vosvotekas, Georgios
AU  - Vosvotekas G
AD  - Private practice, Thessaloniki, Greece.
FAU - Sfikakis, Petros P
AU  - Sfikakis PP
AD  - Joint Rheumatology Program, Medical School, National and Kapodistrian University 
      of Athens, Athens.
FAU - Vassilopoulos, Dimitrios
AU  - Vassilopoulos D
AD  - Joint Rheumatology Program, Medical School, National and Kapodistrian University 
      of Athens, Athens.
FAU - Tektonidou, Maria G
AU  - Tektonidou MG
AD  - Joint Rheumatology Program, Medical School, National and Kapodistrian University 
      of Athens, Athens.
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
SB  - IM
MH  - Antiphospholipid Syndrome/*epidemiology
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Case-Control Studies
MH  - Comorbidity
MH  - Coronary Artery Disease/epidemiology
MH  - Depression/epidemiology
MH  - Diabetes Mellitus/epidemiology
MH  - Female
MH  - Greece/epidemiology
MH  - *Heart Disease Risk Factors
MH  - Humans
MH  - Hyperlipidemias/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Neoplasms/epidemiology
MH  - Obesity/epidemiology
MH  - Osteoporosis/epidemiology
MH  - Prevalence
MH  - Pulmonary Disease, Chronic Obstructive/epidemiology
MH  - Regression Analysis
MH  - Risk Factors
MH  - Smoking/epidemiology
MH  - Stroke/epidemiology
OTO - NOTNLM
OT  - antiphospholipid syndrome
OT  - cardiovascular disease burden
OT  - comorbidities
OT  - depression
OT  - osteoporosis
OT  - rheumatoid arthritis
EDAT- 2020/07/01 06:00
MHDA- 2021/04/17 06:00
CRDT- 2020/06/30 06:00
PHST- 2020/02/29 00:00 [received]
PHST- 2020/05/07 00:00 [revised]
PHST- 2020/07/01 06:00 [pubmed]
PHST- 2021/04/17 06:00 [medline]
PHST- 2020/06/30 06:00 [entrez]
AID - 5864536 [pii]
AID - 10.1093/rheumatology/keaa321 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2021 Jan 5;60(1):170-178. doi: 
      10.1093/rheumatology/keaa321.

PMID- 32572804
OWN - NLM
STAT- MEDLINE
DCOM- 20210514
LR  - 20211214
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Print)
IS  - 0770-3198 (Linking)
VI  - 40
IP  - 1
DP  - 2021 Jan
TI  - Similar risk of cardiovascular events in idiopathic inflammatory myopathy and 
      rheumatoid arthritis in the first 5 years after diagnosis.
PG  - 231-238
LID - 10.1007/s10067-020-05237-7 [doi]
AB  - OBJECTIVES: To estimate the incidence of cardiovascular (CV) events in idiopathic 
      inflammatory myopathy (IIM) compared to patients with rheumatoid arthritis (RA) 
      and the general population. To explore the contribution of traditional CV risk 
      factors to any difference observed. METHODS: A retrospective matched 
      population-based cohort study was conducted using UK Clinical Practice Research 
      Datalink (CPRD) from 1987 to 2013. The incidence of CV events was calculated for 
      each cohort over time and compared using Cox proportional hazards models. 
      Multivariable analyses were used to adjust for traditional CV risk factors. 
      RESULTS: A total of 603 patients with IIM 4047 RA and 4061 healthy controls were 
      included. The rate of CV events in IIM was significantly greater than healthy 
      controls [hazard ratio (HR) 1.47 (95% confidence interval (CI) 1.18-1.83)] and 
      remained significant after adjustment for CV risk factors [HR 1.38 (95% CI 
      1.11-1.72)]. Risk was similar between IIM and RA [HR 1.01 (95% CI 0.78-1.31)]. 
      The rate of myocardial infarction [HR 1.61 (95% CI 1.27-2.04)] but not stroke [HR 
      0.92 (95% CI 0.59-1.44)] was significantly greater in IIM compared to healthy 
      controls. After the first 5 years, the rate of CV events for RA remained 
      significantly greater compared to the control group, but appeared to return to 
      that of the healthy controls in the IIM group. CONCLUSION: IIM is associated with 
      an increased risk of CV events in the first 5 years after diagnosis similar to 
      that of RA. Beyond 5 years, the risk appears to return to that of the general 
      population in IIM but not RA. Key Points • The excess risk of cardiovascular 
      events in IIM is similar to that found in RA. • The excess risk of cardiovascular 
      events is greatest in the first 5 years after diagnosis.
FAU - Párraga Prieto, Cristina
AU  - Párraga Prieto C
AUID- ORCID: 0000-0003-4377-4535
AD  - Centre for Rheumatic Diseases, King's College London, London, UK. 
      cristina_parraga_prieto@outlook.es.
FAU - Ibrahim, Fowzia
AU  - Ibrahim F
AD  - Centre for Rheumatic Diseases, King's College London, London, UK.
FAU - Campbell, Richard
AU  - Campbell R
AD  - Centre for Rheumatic Diseases, King's College London, London, UK.
FAU - Chinoy, Hector
AU  - Chinoy H
AD  - Rheumatology Department, Salford Royal NHS Foundation Trust, Manchester Academic 
      Health Science Centre, Salford, UK.
AD  - NIHR Manchester Biomedical Research Centre, Manchester Academic Health Science 
      Centre, Manchester University NHS Foundation Trust, The University of Manchester, 
      Manchester, UK.
FAU - Galloway, James
AU  - Galloway J
AD  - Centre for Rheumatic Diseases, King's College London, London, UK.
FAU - Gordon, Patrick
AU  - Gordon P
AD  - Centre for Rheumatic Diseases, King's College London, London, UK.
LA  - eng
GR  - MR/N003322/1/MRC_/Medical Research Council/United Kingdom
GR  - ISAC 13_1377R/CPRD Independent Scientific Advisory Committee/
PT  - Journal Article
DEP - 20200622
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
SB  - IM
MH  - *Arthritis, Rheumatoid/complications/epidemiology
MH  - *Cardiovascular Diseases/epidemiology
MH  - Cohort Studies
MH  - Humans
MH  - *Myositis/complications/epidemiology
MH  - Retrospective Studies
MH  - Risk Factors
PMC - PMC7782367
OTO - NOTNLM
OT  - Atherosclerosis
OT  - Cardiovascular event
OT  - Dermatomyositis
OT  - Idiopathic inflammatory myopathy
OT  - Polymyositis
EDAT- 2020/06/24 06:00
MHDA- 2021/05/15 06:00
PMCR- 2020/06/22
CRDT- 2020/06/24 06:00
PHST- 2020/03/06 00:00 [received]
PHST- 2020/06/10 00:00 [accepted]
PHST- 2020/06/06 00:00 [revised]
PHST- 2020/06/24 06:00 [pubmed]
PHST- 2021/05/15 06:00 [medline]
PHST- 2020/06/24 06:00 [entrez]
PHST- 2020/06/22 00:00 [pmc-release]
AID - 10.1007/s10067-020-05237-7 [pii]
AID - 5237 [pii]
AID - 10.1007/s10067-020-05237-7 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2021 Jan;40(1):231-238. doi: 10.1007/s10067-020-05237-7. Epub 
      2020 Jun 22.

PMID- 32562092
OWN - NLM
STAT- MEDLINE
DCOM- 20211101
LR  - 20211101
IS  - 1534-6307 (Electronic)
IS  - 1523-3774 (Linking)
VI  - 22
IP  - 8
DP  - 2020 Jun 19
TI  - Is There a Brain/Heart Interaction in Rheumatoid Arthritis and Seronegative 
      Spondyloartropathies? A Combined Brain/Heart Magnetic Resonance Imaging Reveals 
      the Answer.
PG  - 39
LID - 10.1007/s11926-020-00922-7 [doi]
AB  - PURPOSE OF REVIEW: To present the interaction between brain/heart and emphasize 
      the role of combined brain/heart magnetic resonance imaging (MRI) in patients 
      with rheumatoid arthritis (RA) and other seronegative spondyloarthropathies 
      (SNA). RECENT FINDINGS: Both traditional cardiovascular disease (CVD) risk 
      factors and intrinsic RA/SNA features contribute to the increased CVD-related 
      morbidity/mortality. CVD in RA usually occurs a decade earlier than age- and 
      sex-matched controls, and RA patients are twice more likely to develop myocardial 
      infarction irrespective of age, history of prior CVD, and traditional CVD risk 
      factors. RA also increases risk of non-ischemic heart failure (HF), valvular 
      disease, and myo-pericarditis. CVD in SNA affects more commonly patients with 
      long-standing disease. Ascending aortitis, aortic/mitral insufficiency, 
      conduction defects, and diastolic dysfunction are the commonest findings in 
      ankylosing spondylitis (AS). CVD is also the leading cause of death in psoriatic 
      arthritis (PsA), due to myopericarditis, diastolic dysfunction, and valvular 
      disease. Brain damage, due to either ischemic or hemorrhagic stroke and silent 
      vascular damage, such as white matter hyperenhancement (WMH), is increased in 
      both RA/SNA and may lead to cognitive dysfunction, depression, and brain atrophy. 
      Magnetic resonance imaging (MRI) is ideal for serial brain/heart evaluation of 
      patients with systemic diseases. RA/SNA patients are at high risk for brain/heart 
      damage at early age, irrespectively of classic risk factors. Until more data will 
      be obtained, a combined brain/heart MRI evaluation can be proposed in RA/SNA with 
      new onset of arrhythmia and/or HF, cognitive dysfunction and/or depression.
FAU - Markousis-Mavrogenis, George
AU  - Markousis-Mavrogenis G
AD  - Onassis Cardiac Surgery Center, 50 Esperou Street, 175-61 P.Faliro, Athens, 
      Greece.
FAU - Koutsogeorgopoulou, Loukia
AU  - Koutsogeorgopoulou L
AD  - Department of Pathophysiology, Laikon Hospital, Athens, Greece.
FAU - Dimitroulas, Theodoros
AU  - Dimitroulas T
AD  - Fourth Department of Internal Medicine, School of Medicine, Hippokration 
      Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece.
FAU - Katsifis, Gikas
AU  - Katsifis G
AD  - Naval Hospital, Athens, Greece.
FAU - Vartela, Vasiliki
AU  - Vartela V
AD  - Onassis Cardiac Surgery Center, 50 Esperou Street, 175-61 P.Faliro, Athens, 
      Greece.
FAU - Mitsikostas, Dimos
AU  - Mitsikostas D
AD  - Aretaiion Hospital, Athens, Greece.
AD  - Kapodistrian University of Athens, Athens, Greece.
FAU - Kolovou, Genovefa
AU  - Kolovou G
AD  - Onassis Cardiac Surgery Center, 50 Esperou Street, 175-61 P.Faliro, Athens, 
      Greece.
FAU - Voulgari, Paraskevi
AU  - Voulgari P
AD  - Rheumatology Clinic, University of Ioannina, Ioannina, Greece.
FAU - Sfikakis, Petros P
AU  - Sfikakis PP
AD  - Kapodistrian University of Athens, Athens, Greece.
AD  - Joint Rheumatology, Laikon Hospital, Athens, Greece.
FAU - Kitas, George D
AU  - Kitas GD
AD  - Arthritis Research UK Epidemiology Unit, Manchester University, Manchester, UK.
FAU - Mavrogeni, Sophie I
AU  - Mavrogeni SI
AUID- ORCID: 0000-0003-1089-7766
AD  - Onassis Cardiac Surgery Center, 50 Esperou Street, 175-61 P.Faliro, Athens, 
      Greece. soma13@otenet.gr.
AD  - Kapodistrian University of Athens, Athens, Greece. soma13@otenet.gr.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20200619
PL  - United States
TA  - Curr Rheumatol Rep
JT  - Current rheumatology reports
JID - 100888970
SB  - IM
MH  - Arthritis, Psoriatic
MH  - *Arthritis, Rheumatoid/complications/diagnostic imaging
MH  - *Brain/diagnostic imaging
MH  - *Cardiovascular Diseases/diagnostic imaging/etiology
MH  - *Heart/diagnostic imaging
MH  - Humans
MH  - Magnetic Resonance Imaging
MH  - Risk Factors
OTO - NOTNLM
OT  - Arrhythmia
OT  - Brain lesions
OT  - Brain magnetic resonance imaging
OT  - Cardiovascular disease
OT  - Cardiovascular magnetic resonance imaging
OT  - Cognitive dysfunction
OT  - Depression
OT  - Heart failure
OT  - Neuro-psychiatric symptoms
OT  - Rheumatoid arthritis
OT  - Seronegative arthropathies
EDAT- 2020/06/21 06:00
MHDA- 2021/11/03 06:00
CRDT- 2020/06/21 06:00
PHST- 2020/06/21 06:00 [entrez]
PHST- 2020/06/21 06:00 [pubmed]
PHST- 2021/11/03 06:00 [medline]
AID - 10.1007/s11926-020-00922-7 [pii]
AID - 10.1007/s11926-020-00922-7 [doi]
PST - epublish
SO  - Curr Rheumatol Rep. 2020 Jun 19;22(8):39. doi: 10.1007/s11926-020-00922-7.

PMID- 32498083
OWN - NLM
STAT- MEDLINE
DCOM- 20210929
LR  - 20210929
IS  - 1941-7225 (Electronic)
IS  - 0895-7061 (Print)
IS  - 0895-7061 (Linking)
VI  - 33
IP  - 10
DP  - 2020 Oct 21
TI  - TNFα and Reactive Oxygen Signaling in Vascular Smooth Muscle Cells in 
      Hypertension and Atherosclerosis.
PG  - 902-913
LID - 10.1093/ajh/hpaa089 [doi]
AB  - Hypertension and atherosclerosis, the predecessors of stroke and myocardial 
      infarction, are chronic vascular inflammatory reactions. Tumor necrosis factor 
      alpha (TNFα), the "master" proinflammatory cytokine, contributes to both the 
      initiation and maintenance of vascular inflammation. TNFα induces reactive oxygen 
      species (ROS) production which drives the redox reactions that constitute "ROS 
      signaling." However, these ROS may also cause oxidative stress which contributes 
      to vascular dysfunction. Mice lacking TNFα or its receptors are protected against 
      both acute and chronic cardiovascular injury. Humans suffering from TNFα-driven 
      inflammatory conditions such as rheumatoid arthritis and psoriasis are at 
      increased cardiovascular risk. When treated with highly specific biologic agents 
      that target TNFα signaling (Etanercept, etc.) they display marked reductions in 
      that risk. The ability of TNFα to induce endothelial dysfunction, often the first 
      step in a progression toward serious vasculopathy, is well recognized and has 
      been reviewed elsewhere. However, TNFα also has profound effects on vascular 
      smooth muscle cells (VSMCs) including a fundamental change from a contractile to 
      a secretory phenotype. This "phenotypic switching" promotes proliferation and 
      production of extracellular matrix proteins which are associated with medial 
      hypertrophy. Additionally, it promotes lipid storage and enhanced motility, 
      changes that support the contribution of VSMCs to neointima and atherosclerotic 
      plaque formation. This review focuses on the role of TNFα in driving the 
      inflammatory changes in VSMC biology that contribute to cardiovascular disease. 
      Special attention is given to the mechanisms by which TNFα promotes ROS 
      production at specific subcellular locations, and the contribution of these ROS 
      to TNFα signaling.
CI  - © American Journal of Hypertension, Ltd 2020. All rights reserved. For 
      Permissions, please email: journals.permissions@oup.com.
FAU - Lamb, Fred S
AU  - Lamb FS
AD  - Division of Pediatric Critical Care, Department of Pediatrics, Vanderbilt 
      University Medical Center, Nashville, Tennessee, USA.
FAU - Choi, Hyehun
AU  - Choi H
AD  - Division of Pediatric Critical Care, Department of Pediatrics, Vanderbilt 
      University Medical Center, Nashville, Tennessee, USA.
FAU - Miller, Michael R
AU  - Miller MR
AD  - Division of Pediatric Critical Care, Department of Pediatrics, Vanderbilt 
      University Medical Center, Nashville, Tennessee, USA.
FAU - Stark, Ryan J
AU  - Stark RJ
AD  - Division of Pediatric Critical Care, Department of Pediatrics, Vanderbilt 
      University Medical Center, Nashville, Tennessee, USA.
LA  - eng
GR  - K08 GM117367/GM/NIGMS NIH HHS/United States
GR  - R01 HL128386/HL/NHLBI NIH HHS/United States
GR  - T32 HL144446/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - United States
TA  - Am J Hypertens
JT  - American journal of hypertension
JID - 8803676
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Atherosclerosis/*metabolism
MH  - Humans
MH  - Hypertension/*metabolism
MH  - Muscle, Smooth, Vascular/cytology
MH  - Myocytes, Smooth Muscle/*metabolism
MH  - Reactive Oxygen Species/*metabolism
MH  - Signal Transduction
MH  - Tumor Necrosis Factor-alpha/*metabolism
PMC - PMC7577645
OTO - NOTNLM
OT  - LRRC8A
OT  - Nox1
OT  - TNFα
OT  - atherosclerosis
OT  - blood pressure
OT  - hypertension
OT  - reactive oxygen signaling
OT  - vascular smooth muscle
EDAT- 2020/06/05 06:00
MHDA- 2021/09/30 06:00
PMCR- 2021/06/05
CRDT- 2020/06/05 06:00
PHST- 2020/05/10 00:00 [received]
PHST- 2020/05/28 00:00 [revised]
PHST- 2020/05/29 00:00 [accepted]
PHST- 2020/06/05 06:00 [pubmed]
PHST- 2021/09/30 06:00 [medline]
PHST- 2020/06/05 06:00 [entrez]
PHST- 2021/06/05 00:00 [pmc-release]
AID - 5851521 [pii]
AID - hpaa089 [pii]
AID - 10.1093/ajh/hpaa089 [doi]
PST - ppublish
SO  - Am J Hypertens. 2020 Oct 21;33(10):902-913. doi: 10.1093/ajh/hpaa089.

PMID- 32494054
OWN - NLM
STAT- MEDLINE
DCOM- 20201105
LR  - 20210324
IS  - 1759-4804 (Electronic)
IS  - 1759-4790 (Linking)
VI  - 16
IP  - 7
DP  - 2020 Jul
TI  - Atherosclerotic cardiovascular disease prevention in rheumatoid arthritis.
PG  - 361-379
LID - 10.1038/s41584-020-0428-y [doi]
AB  - Patients with rheumatoid arthritis (RA) are at high risk of developing 
      cardiovascular disease (CVD). Inflammation has a pivotal role in the pathogenesis 
      of CVD. RA is an inflammatory joint disease and, compared with the general 
      population, patients with RA have approximately double the risk of 
      atherosclerotic CVD, stroke, heart failure and atrial fibrillation. Although this 
      high risk of CVD has been known for decades, patients with RA receive poorer 
      primary and secondary CVD preventive care than other high-risk patients, and an 
      unmet need exists for improved CVD preventive measures for patients with RA. This 
      Review summarizes the evidence for atherosclerotic CVD in patients with RA and 
      provides a contemporary analysis of what is known and what needs to be further 
      clarified about recommendations for CVD prevention in patients with RA compared 
      with the general population. The management of traditional CVD risk factors, 
      including blood pressure, lipids, diabetes mellitus and lifestyle-related risk 
      factors, as well as the effects of inflammation and the use of antirheumatic 
      medication on CVD risk and risk management in patients with RA are discussed. The 
      main aim is to provide a roadmap of atherosclerotic CVD risk management and 
      prevention for patients with RA.
FAU - Semb, Anne Grete
AU  - Semb AG
AD  - Preventive Cardio-Rheuma Clinic, Department of Rheumatology, Diakonhjemmet 
      Hospital, Oslo, Norway. a-semb@diakonsyk.no.
FAU - Ikdahl, Eirik
AU  - Ikdahl E
AD  - Preventive Cardio-Rheuma Clinic, Department of Rheumatology, Diakonhjemmet 
      Hospital, Oslo, Norway.
FAU - Wibetoe, Grunde
AU  - Wibetoe G
AD  - Preventive Cardio-Rheuma Clinic, Department of Rheumatology, Diakonhjemmet 
      Hospital, Oslo, Norway.
FAU - Crowson, Cynthia
AU  - Crowson C
AUID- ORCID: 0000-0001-5847-7475
AD  - Division of Biomedical Statistics and Informatics, Department of Health Sciences 
      Research, Mayo Clinic, Rochester, MN, USA.
AD  - Division of Rheumatology, Department of Medicine, Mayo Clinic, Rochester, MN, 
      USA.
FAU - Rollefstad, Silvia
AU  - Rollefstad S
AD  - Preventive Cardio-Rheuma Clinic, Department of Rheumatology, Diakonhjemmet 
      Hospital, Oslo, Norway.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20200603
PL  - United States
TA  - Nat Rev Rheumatol
JT  - Nature reviews. Rheumatology
JID - 101500080
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antirheumatic Agents/*adverse effects
MH  - Arthritis, Rheumatoid/*complications/drug therapy
MH  - Atherosclerosis/*physiopathology
MH  - Atrial Fibrillation/epidemiology
MH  - Cardiovascular Diseases/*prevention & control
MH  - Carotid Arteries/diagnostic imaging
MH  - Case-Control Studies
MH  - Drug Interactions
MH  - Female
MH  - Heart Failure/epidemiology
MH  - Humans
MH  - Inflammation/pathology
MH  - Life Style
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - Stroke/epidemiology
MH  - Ultrasonography/methods
EDAT- 2020/06/05 06:00
MHDA- 2020/11/06 06:00
CRDT- 2020/06/05 06:00
PHST- 2020/04/27 00:00 [accepted]
PHST- 2020/06/05 06:00 [pubmed]
PHST- 2020/11/06 06:00 [medline]
PHST- 2020/06/05 06:00 [entrez]
AID - 10.1038/s41584-020-0428-y [pii]
AID - 10.1038/s41584-020-0428-y [doi]
PST - ppublish
SO  - Nat Rev Rheumatol. 2020 Jul;16(7):361-379. doi: 10.1038/s41584-020-0428-y. Epub 
      2020 Jun 3.

PMID- 32487898
OWN - NLM
STAT- MEDLINE
DCOM- 20210303
LR  - 20210303
IS  - 1538-6899 (Electronic)
IS  - 1080-2371 (Linking)
VI  - 26
IP  - 3
DP  - 2020 Jun
TI  - Rheumatologic Disorders and the Nervous System.
PG  - 591-610
LID - 10.1212/CON.0000000000000856 [doi]
AB  - PURPOSE: This article describes the neurologic manifestations of systemic 
      autoimmune diseases. RECENT FINDINGS: Systemic autoimmune diseases can be 
      associated with a wide spectrum of neurologic comorbidities involving the central 
      and peripheral nervous systems. Systemic lupus erythematosus (SLE) can be 
      associated with a number of manifestations predominantly affecting the central 
      nervous system (CNS), whereas peripheral neuropathy is less common. Sjögren 
      syndrome can be associated with peripheral neuropathy in 10% of cases and CNS 
      disease in 2% to 5% of cases. The risk of stroke is increased in SLE, rheumatoid 
      arthritis, temporal arteritis, psoriatic arthritis, and ankylosing spondylitis. 
      Systemic vasculitides present most commonly with mononeuritis multiplex but can 
      also affect the CNS. Cognitive dysfunction is a common symptom among patients 
      with systemic autoimmune diseases, most commonly seen in patients with SLE or 
      Sjögren syndrome. SUMMARY: Neurologic manifestations of systemic autoimmune 
      disease are important to recognize, as they may often be the presenting 
      manifestation leading to diagnosis of the systemic disease or may be associated 
      with increased morbidity, other complications, or mortality. Timely diagnosis and 
      institution of appropriate treatment, often requiring multidisciplinary care, is 
      essential to minimize morbidity and decrease the risk of permanent neurologic 
      deficits.
FAU - Pavlakis, Pantelis P
AU  - Pavlakis PP
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Continuum (Minneap Minn)
JT  - Continuum (Minneapolis, Minn.)
JID - 9509333
SB  - IM
MH  - *Autoimmune Diseases/complications/diagnosis/therapy
MH  - *Central Nervous System Diseases/diagnosis/etiology/therapy
MH  - Humans
MH  - *Peripheral Nervous System Diseases/diagnosis/etiology/therapy
MH  - *Rheumatic Diseases/complications/diagnosis/therapy
EDAT- 2020/06/04 06:00
MHDA- 2021/03/04 06:00
CRDT- 2020/06/04 06:00
PHST- 2020/06/04 06:00 [entrez]
PHST- 2020/06/04 06:00 [pubmed]
PHST- 2021/03/04 06:00 [medline]
AID - 00132979-202006000-00006 [pii]
AID - 10.1212/CON.0000000000000856 [doi]
PST - ppublish
SO  - Continuum (Minneap Minn). 2020 Jun;26(3):591-610. doi: 
      10.1212/CON.0000000000000856.

PMID- 32475073
OWN - NLM
STAT- MEDLINE
DCOM- 20210106
LR  - 20210106
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Linking)
VI  - 72
IP  - 10
DP  - 2020 Oct
TI  - Anti-Citrullinated Protein Antibody Specificities, Rheumatoid Factor Isotypes, 
      and Incident Cardiovascular Events in Patients With Rheumatoid Arthritis.
PG  - 1658-1667
LID - 10.1002/art.41381 [doi]
AB  - OBJECTIVE: To investigate the relationship between anti-citrullinated protein 
      antibodies (ACPAs), specific ACPA subspecificities, rheumatoid factor (RF) 
      isotypes, and incident cardiovascular (CV) events in patients with rheumatoid 
      arthritis (RA). METHODS: Serum samples from Swedish patients with new-onset RA 
      (diagnosed within 1 year of symptom onset between 1996 and 2009) were centrally 
      typed for anti-cyclic citrullinated peptide 2 (anti-CCP2) antibodies, 20 ACPA 
      subspecificities, and RF isotypes. Patients were followed up longitudinally in 
      nationwide registers to monitor the occurrence of acute coronary syndrome (ACS), 
      stroke, CV-related death, and major adverse CV events (MACE). The association 
      between each serologic marker and CV outcome, and the impact of adjustment for 
      the Disease Activity Score in 28 joints (DAS28), smoking status, and income at 
      baseline, were assessed using Cox proportional hazards models. In addition, 
      associations of serologic markers with all-cause mortality were explored. 
      RESULTS: In total, 2,814 patients with RA were included in the study. The median 
      follow-up was 13 years, during which the CV end points of ACS, stroke, or 
      CV-related death were reported to occur in 375 patients. Occurrence and/or levels 
      of anti-CCP2 were associated with risk of incident ACS (hazard ratio [HR] 1.46, 
      95% confidence interval [95% CI] 1.03-2.06), stroke (HR 1.47, 95% CI 1.03-2.10), 
      CV-related death (P = 0.024 for association with anti-CCP2 levels), and MACE (HR 
      1.34, 95% CI 1.06-1.70). Similarly, an association with the number of ACPA 
      subspecificities was observed; however, this could not be attributed to any 
      individual or group of ACPA subspecificities. Presence of IgM-RF was associated 
      with all CV end points except ACS, and IgA-RF was exclusively associated with 
      CV-related death. Adjustment for smoking status, income, and DAS28 scores 
      decreased most of the HRs, whereas IgA-RF remained associated with CV-related 
      death (HR 1.61, 95% CI 1.05-2.48). All of the assessed serologic makers were 
      associated with all-cause mortality. CONCLUSION: RF isotypes and ACPAs are 
      associated with future CV events in patients with RA. ACPA levels and number of 
      subspecificities seem more important than the occurrence of particular 
      subspecificities, and these associations were not explained by a history of ever 
      smoking.
CI  - © 2020 The Authors. Arthritis & Rheumatology published by Wiley Periodicals LLC 
      on behalf of American College of Rheumatology.
FAU - Westerlind, Helga
AU  - Westerlind H
AUID- ORCID: 0000-0003-3380-5342
AD  - Karolinska Institutet, Stockholm, Sweden.
FAU - Rönnelid, Johan
AU  - Rönnelid J
AUID- ORCID: 0000-0003-1186-3226
AD  - Uppsala University, Uppsala, Sweden.
FAU - Hansson, Monika
AU  - Hansson M
AD  - Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
FAU - Alfredsson, Lars
AU  - Alfredsson L
AD  - Karolinska Institutet, Stockholm, Sweden.
FAU - Mathsson-Alm, Linda
AU  - Mathsson-Alm L
AD  - Uppsala University and Thermo Fisher Scientific, Uppsala, Sweden.
FAU - Serre, Guy
AU  - Serre G
AD  - Laboratory of Epithelial Differentiation and Rheumatoid Autoimmunity, U1056 
      INSERM, Toulouse University, Toulouse, France.
FAU - Cornillet, Martin
AU  - Cornillet M
AD  - Laboratory of Epithelial Differentiation and Rheumatoid Autoimmunity, U1056 
      INSERM, Toulouse University, Toulouse, France.
FAU - Holmdahl, Rikard
AU  - Holmdahl R
AD  - Karolinska Institutet, Stockholm, Sweden.
FAU - Jakobsson, Per-Johan
AU  - Jakobsson PJ
AD  - Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
FAU - Skriner, Karl
AU  - Skriner K
AD  - Charité University Hospital, Berlin, Germany.
FAU - Klareskog, Lars
AU  - Klareskog L
AD  - Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
FAU - Saevarsdottir, Saedis
AU  - Saevarsdottir S
AD  - Karolinska Institutet, Stockholm, Sweden, and University of Iceland School of 
      Health Sciences and Faculty of Medicine, Reykjavik, Iceland.
FAU - Askling, Johan
AU  - Askling J
AUID- ORCID: 0000-0003-0433-0616
AD  - Karolinska Institutet, Stockholm, Sweden.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200907
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Anti-Citrullinated Protein Antibodies)
RN  - 0 (Immunoglobulin Isotypes)
RN  - 9009-79-4 (Rheumatoid Factor)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Anti-Citrullinated Protein Antibodies/blood
MH  - Antibody Specificity
MH  - Arthritis, Rheumatoid/blood/complications/*immunology
MH  - Cardiovascular Diseases/*enzymology/etiology
MH  - Case-Control Studies
MH  - Female
MH  - Humans
MH  - Immunoglobulin Isotypes/*blood
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Rheumatoid Factor/*immunology
MH  - Sweden
EDAT- 2020/06/01 06:00
MHDA- 2021/01/07 06:00
CRDT- 2020/06/01 06:00
PHST- 2019/11/01 00:00 [received]
PHST- 2020/05/21 00:00 [accepted]
PHST- 2020/06/01 06:00 [pubmed]
PHST- 2021/01/07 06:00 [medline]
PHST- 2020/06/01 06:00 [entrez]
AID - 10.1002/art.41381 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2020 Oct;72(10):1658-1667. doi: 10.1002/art.41381. Epub 2020 
      Sep 7.

PMID- 32471895
OWN - NLM
STAT- MEDLINE
DCOM- 20200930
LR  - 20230201
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 79
IP  - 9
DP  - 2020 Sep
TI  - Impact of rheumatoid arthritis on major cardiovascular events in patients with 
      and without coronary artery disease.
PG  - 1182-1188
LID - 10.1136/annrheumdis-2020-217154 [doi]
AB  - INTRODUCTION: Rheumatoid arthritis (RA) is a risk factor for cardiovascular 
      disease. The clinical consequences of coincident RA and coronary artery disease 
      (CAD) are unknown. OBJECTIVE: We aimed to estimate the impact of RA on the risk 
      of adverse cardiovascular events in patients with and without CAD. METHODS: A 
      population-based cohort of patients registered in the Western Denmark Heart 
      Registry, who underwent coronary angiography (CAG) between 2003 and 2016, was 
      stratified according to the presence of RA and CAD. Endpoints were myocardial 
      infarction (MI), major adverse cardiovascular events (MACE; MI, ischaemic stroke 
      and cardiac death) and all-cause mortality. RESULTS: A total of 125 331 patients 
      were included (RA: n=1732). Median follow-up was 5.2 years. Using patients with 
      neither RA nor CAD as reference (cumulative MI incidence 2.7%), the 10-year risk 
      of MI was increased for patients with RA alone (3.8%; adjusted incidence rate 
      ratio (IRR(adj)) 1.63, 95% CI 1.04 to 2.54), for patients with CAD alone (9.9%; 
      IRR(adj) 3.35, 95% CI 3.10 to 3.62), and highest for patients with both RA and 
      CAD (12.2%; IRR(adj) 4.53, 95% CI 3.66 to 5.59). Similar associations were 
      observed for MACE an all-cause mortality. CONCLUSIONS: In patients undergoing 
      CAG, RA is significantly associated with the 10-year risk of MI, MACE and 
      all-cause mortality regardless of the presence of CAD. However, patients with RA 
      and CAD carry the largest risk, while the additive risk of RA in patients without 
      CAD is minor. Among patients with RA, risk stratification by presence or absence 
      of documented CAD may allow for screening and personalised treatment strategies.
CI  - © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and 
      permissions. Published by BMJ.
FAU - Løgstrup, Brian Bridal
AU  - Løgstrup BB
AUID- ORCID: 0000-0002-4218-0033
AD  - Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark 
      bbl@dadlnet.dk.
FAU - Olesen, Kevin Kris Warnakula
AU  - Olesen KKW
AUID- ORCID: 0000-0002-0560-3615
AD  - Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
FAU - Masic, Dzenan
AU  - Masic D
AD  - Department of Rheumatology, Silkeborg Regional Hospital, Silkeborg, Denmark.
FAU - Gyldenkerne, Christine
AU  - Gyldenkerne C
AD  - Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
FAU - Thrane, Pernille Gro
AU  - Thrane PG
AD  - Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
FAU - Ellingsen, Torkell
AU  - Ellingsen T
AUID- ORCID: 0000-0003-0426-4962
AD  - Department of Rheumatology, Odense University Hospital, Odense, Denmark.
FAU - Bøtker, Hans Erik
AU  - Bøtker HE
AD  - Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
FAU - Maeng, Michael
AU  - Maeng M
AD  - Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
LA  - eng
PT  - Evaluation Study
PT  - Journal Article
DEP - 20200529
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
CIN - Ann Rheum Dis. 2023 Jan;82(1):e12. doi: 10.1136/annrheumdis-2020-219231. PMID: 
      33139308
CIN - Ann Rheum Dis. 2023 Jan;82(1):e11. doi: 10.1136/annrheumdis-2020-219201. PMID: 
      33139310
MH  - Aged
MH  - Arthritis, Rheumatoid/complications/*mortality
MH  - Cardiovascular Diseases/etiology/*mortality
MH  - Cohort Studies
MH  - Coronary Artery Disease/complications/*mortality
MH  - Denmark/epidemiology
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/etiology/*mortality
MH  - Registries
MH  - Risk Assessment
MH  - Risk Factors
MH  - Stroke/etiology/*mortality
OTO - NOTNLM
OT  - atherosclerosis
OT  - cardiovascular disease
OT  - epidemiology
OT  - outcomes research
OT  - rheumatoid arthritis
COIS- Competing interests: None declared.
EDAT- 2020/05/31 06:00
MHDA- 2020/10/02 06:00
CRDT- 2020/05/31 06:00
PHST- 2020/02/14 00:00 [received]
PHST- 2020/04/15 00:00 [revised]
PHST- 2020/05/15 00:00 [accepted]
PHST- 2020/05/31 06:00 [pubmed]
PHST- 2020/10/02 06:00 [medline]
PHST- 2020/05/31 06:00 [entrez]
AID - annrheumdis-2020-217154 [pii]
AID - 10.1136/annrheumdis-2020-217154 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2020 Sep;79(9):1182-1188. doi: 10.1136/annrheumdis-2020-217154. 
      Epub 2020 May 29.

PMID- 32463807
OWN - NLM
STAT- MEDLINE
DCOM- 20200529
LR  - 20200611
IS  - 1545-861X (Electronic)
IS  - 0149-2195 (Print)
IS  - 0149-2195 (Linking)
VI  - 69
IP  - 21
DP  - 2020 May 29
TI  - Prevalence of and Changes in Tooth Loss Among Adults Aged ≥50 Years with Selected 
      Chronic Conditions - United States, 1999-2004 and 2011-2016.
PG  - 641-646
LID - 10.15585/mmwr.mm6921a1 [doi]
AB  - Extensive tooth loss can lead to poor diet resulting in weight loss or obesity 
      (1). It can also detract from physical appearance and impede speech, factors that 
      can restrict social contact, inhibit intimacy, and lower self-esteem (1). Chronic 
      medical conditions and oral conditions share common risk factors (2). Persons 
      with chronic conditions are more likely to have untreated dental disease, which 
      can result in tooth loss. Three measures of tooth loss during 1999-2004 and 
      2011-2016 were estimated by comparing data from the National Health and Nutrition 
      Examination Survey (NHANES) for each period among adults aged ≥50 years with 
      selected chronic conditions.* The three measures were 1) edentulism (having no 
      teeth); 2) severe tooth loss (having eight or fewer teeth) (3); and 3) lacking 
      functional dentition (having <20 teeth out of 28, which is considered a full set 
      for the purpose of NHANES assessments) (4). During 2011-2016, prevalences of 
      edentulism and severe tooth loss were ≥50% higher among adults with fair or poor 
      general health, rheumatoid arthritis, asthma, diabetes, emphysema, heart disease, 
      liver condition, or stroke than among those with those adults without the chronic 
      condition. Lack of functional dentition was also more prevalent among adults with 
      chronic conditions than among persons without these conditions. Tooth loss is 
      preventable with self-care and routine dental visits (1). To encourage these 
      behaviors, public health professionals can educate the public about the 
      association between having a chronic condition and tooth loss, and primary care 
      providers can educate their patients about the importance of healthy behaviors 
      and screen and refer them for needed dental care.
FAU - Parker, Marcia L
AU  - Parker ML
FAU - Thornton-Evans, Gina
AU  - Thornton-Evans G
FAU - Wei, Liang
AU  - Wei L
FAU - Griffin, Susan O
AU  - Griffin SO
LA  - eng
PT  - Journal Article
DEP - 20200529
PL  - United States
TA  - MMWR Morb Mortal Wkly Rep
JT  - MMWR. Morbidity and mortality weekly report
JID - 7802429
SB  - IM
MH  - Aged
MH  - Chronic Disease/*epidemiology
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Nutrition Surveys
MH  - Prevalence
MH  - Tooth Loss/*epidemiology
MH  - United States/epidemiology
PMC - PMC7269607
COIS- All authors have completed and submitted the International Committee of Medical 
      Journal Editors form for disclosure of potential conflicts of interest. No 
      potential conflicts of interest were disclosed.
EDAT- 2020/05/29 06:00
MHDA- 2020/05/30 06:00
PMCR- 2020/05/29
CRDT- 2020/05/29 06:00
PHST- 2020/05/29 06:00 [entrez]
PHST- 2020/05/29 06:00 [pubmed]
PHST- 2020/05/30 06:00 [medline]
PHST- 2020/05/29 00:00 [pmc-release]
AID - mm6921a1 [pii]
AID - 10.15585/mmwr.mm6921a1 [doi]
PST - epublish
SO  - MMWR Morb Mortal Wkly Rep. 2020 May 29;69(21):641-646. doi: 
      10.15585/mmwr.mm6921a1.

PMID- 32410564
OWN - NLM
STAT- MEDLINE
DCOM- 20201207
LR  - 20201214
IS  - 1875-6212 (Electronic)
IS  - 1570-1611 (Linking)
VI  - 18
IP  - 5
DP  - 2020
TI  - Cardio-Rheumatology: Cardiovascular Complications in Systemic Autoimmune 
      Rheumatic Diseases / Is Inflammation the Common Link and Target?
PG  - 425-430
LID - 10.2174/1570161118666200514222236 [doi]
AB  - In the current Thematic Issue of Current Vascular Pharmacology (CVP), entitled 
      "Systemic Autoimmune Rheumatic Diseases and Cardiology", presented in two parts, 
      Part 1 and Part 2, review articles are included from specialists in cardiology, 
      rheumatology, immunology and related fields. These reviews discuss the 
      cardiovascular complications of the main systemic Autoimmune Rheumatic Diseases 
      (ARDs). For example, the underlying pathogenetic mechanisms, the role of 
      cardiovascular imaging and recommendations for prevention and management. These 
      articles place inflammation as the key process, linking cardiovascular 
      complications with ARDs. From all these reviews, the conclusion is the need for 
      collaboration between the disciplines of Rheumatology and Cardiology to establish 
      the emerging field of Cardio- Rheumatology. This will aid to fine-tune risk 
      stratification and optimize preventive strategies and pharmacological therapies 
      for patients with ARDs.
CI  - Copyright© Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Manolis, Antonis S
AU  - Manolis AS
AD  - Third Department of Cardiology, Athens University, School of Medicine, Athens, 
      Greece.
FAU - Tzioufas, Athanasios G
AU  - Tzioufas AG
AD  - Department of Pathopyhysiology, Athens University, School of Medicine, Athens, 
      Greece.
LA  - eng
PT  - Editorial
PT  - Introductory Journal Article
PL  - United Arab Emirates
TA  - Curr Vasc Pharmacol
JT  - Current vascular pharmacology
JID - 101157208
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/therapeutic use
MH  - Antirheumatic Agents/therapeutic use
MH  - Autoimmune Diseases/*complications/drug therapy/immunology/mortality
MH  - Cardiovascular Diseases/*etiology/immunology/mortality/prevention & control
MH  - Heart Disease Risk Factors
MH  - Humans
MH  - Inflammation/*complications/drug therapy/immunology/mortality
MH  - Protective Factors
MH  - Rheumatic Diseases/*complications/drug therapy/immunology/mortality
OTO - NOTNLM
OT  - Autoimmune rheumatic disease
OT  - Sjogren’s disease
OT  - acute coronary syndromes
OT  - antirheumatic drugs
OT  - atherosclerosis
OT  - cardiorheumatology
OT  - cardiovascular disease
OT  - cardiovascular imaging
OT  - coronary artery disease
OT  - myocardial infarction
OT  - psoriasis
OT  - psoriatic arthritis
OT  - rheumatoid arthritis
OT  - spondyloarthropathies
OT  - stroke
OT  - systemic lupus erythematosus
OT  - systemic sclerosis
OT  - vasculitis
EDAT- 2020/05/16 06:00
MHDA- 2020/12/15 06:00
CRDT- 2020/05/16 06:00
PHST- 2020/02/16 00:00 [received]
PHST- 2020/05/05 00:00 [revised]
PHST- 2020/05/05 00:00 [accepted]
PHST- 2020/05/16 06:00 [pubmed]
PHST- 2020/12/15 06:00 [medline]
PHST- 2020/05/16 06:00 [entrez]
AID - CVP-EPUB-106636 [pii]
AID - 10.2174/1570161118666200514222236 [doi]
PST - ppublish
SO  - Curr Vasc Pharmacol. 2020;18(5):425-430. doi: 10.2174/1570161118666200514222236.

PMID- 32320330
OWN - NLM
STAT- MEDLINE
DCOM- 20200915
LR  - 20220316
IS  - 1931-843X (Electronic)
IS  - 1540-9996 (Print)
IS  - 1540-9996 (Linking)
VI  - 29
IP  - 4
DP  - 2020 Apr
TI  - Sex Differences in Autoimmune Multimorbidity in Type 1 Diabetes Mellitus and the 
      Risk of Cardiovascular and Renal Disease: A Longitudinal Study in the United 
      States, 2001-2017.
PG  - 511-519
LID - 10.1089/jwh.2019.7935 [doi]
AB  - Background: Autoimmune diseases are usually more prevalent in women. The risks of 
      cardiovascular and renal disease in those with multiple autoimmune diseases have 
      not been fully described. Materials and Methods: Using a national database from a 
      large health insurer in the United States (years 2001-2017) containing ∼75 
      million members, we calculated age- and sex-specific co-prevalence of 12 
      autoimmune disorders for individuals with type 1 diabetes. We then evaluated 
      whether concomitant autoimmune diseases were associated with renal failure, 
      ischemic stroke, and myocardial infarction. Results: Of the 179,248 people 
      diagnosed with type 1 diabetes, 1 in 4 had a concomitant autoimmune disease 
      (27.03%; 95% confidence interval [CI] = 26.83%-27.24%), with hypothyroidism, 
      rheumatoid arthritis, and celiac disease being the most common. The prevalence of 
      autoimmune disease was 1.9 times greater in female than male patients 
      (p < 0.001). In female patients with type 1 diabetes, one in three had another 
      autoimmune disease (35.62%; 95% CI = 35.30%-35.94%) compared with one in five 
      male patients (19.17%; 95% CI = 18.92%-19.42%). The risk of renal failure, 
      ischemic stroke, and myocardial infarction increased with a greater number of 
      concomitant autoimmune diseases (p < 0.001, test for trend for both female and 
      male patients). Patients with type 1 diabetes who had multiple sclerosis or 
      myasthenia gravis experienced an approximate threefold increase in risk of 
      ischemic stroke (odds ratio [OR] = 3.57, OR = 3.22, respectively). Patients with 
      type 1 diabetes and Addison's disease had a threefold increased risk of renal 
      failure. Conclusions: Patients with type 1 diabetes, particularly women, 
      frequently have coexisting autoimmune diseases that are associated with higher 
      rates of renal failure, ischemic stroke, and myocardial infarction. Additional 
      study is warranted, as are preventive efforts in this high-risk population.
FAU - Rogers, Mary A M
AU  - Rogers MAM
AD  - Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan.
AD  - The Institute for Healthcare Policy and Innovation, University of Michigan, Ann 
      Arbor, Michigan.
FAU - Wei, Melissa Y
AU  - Wei MY
AD  - Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan.
AD  - The Institute for Healthcare Policy and Innovation, University of Michigan, Ann 
      Arbor, Michigan.
FAU - Kim, Catherine
AU  - Kim C
AD  - Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan.
AD  - The Institute for Healthcare Policy and Innovation, University of Michigan, Ann 
      Arbor, Michigan.
FAU - Lee, Joyce M
AU  - Lee JM
AD  - The Institute for Healthcare Policy and Innovation, University of Michigan, Ann 
      Arbor, Michigan.
AD  - Pediatric Endocrinology, Child Health Evaluation and Research Unit (CHEAR), 
      University of Michigan, Ann Arbor, Michigan.
LA  - eng
GR  - P30 DK092926/DK/NIDDK NIH HHS/United States
GR  - UL1 TR002240/TR/NCATS NIH HHS/United States
GR  - K23 AG056638/AG/NIA NIH HHS/United States
GR  - UL1 TR000433/TR/NCATS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Womens Health (Larchmt)
JT  - Journal of women's health (2002)
JID - 101159262
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Autoimmune Diseases/*epidemiology
MH  - Child
MH  - Child, Preschool
MH  - Diabetes Mellitus, Type 1/*epidemiology
MH  - Female
MH  - Humans
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Multimorbidity
MH  - Myocardial Infarction/*epidemiology
MH  - Prevalence
MH  - Renal Insufficiency/*epidemiology
MH  - Risk Factors
MH  - Sex Characteristics
MH  - Stroke/*epidemiology
MH  - United States
MH  - Young Adult
PMC - PMC7194310
OTO - NOTNLM
OT  - autoimmunity
OT  - multimorbidity
OT  - sex
OT  - type 1 diabetes
COIS- No competing financial interests exist.
EDAT- 2020/04/23 06:00
MHDA- 2020/09/17 06:00
PMCR- 2021/04/01
CRDT- 2020/04/23 06:00
PHST- 2020/04/23 06:00 [entrez]
PHST- 2020/04/23 06:00 [pubmed]
PHST- 2020/09/17 06:00 [medline]
PHST- 2021/04/01 00:00 [pmc-release]
AID - 10.1089/jwh.2019.7935 [pii]
AID - 10.1089/jwh.2019.7935 [doi]
PST - ppublish
SO  - J Womens Health (Larchmt). 2020 Apr;29(4):511-519. doi: 10.1089/jwh.2019.7935.

PMID- 32319221
OWN - NLM
STAT- MEDLINE
DCOM- 20210111
LR  - 20210111
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Linking)
VI  - 72
IP  - 9
DP  - 2020 Sep
TI  - Biologics May Prevent Cardiovascular Events in Rheumatoid Arthritis by Inhibiting 
      Coronary Plaque Formation and Stabilizing High-Risk Lesions.
PG  - 1467-1475
LID - 10.1002/art.41293 [doi]
AB  - OBJECTIVE: To evaluate whether biologic disease-modifying antirheumatic drugs 
      (DMARDs) decrease cardiovascular disease (CVD) risk in rheumatoid arthritis (RA) 
      and whether biologic DMARDs might have a beneficial effect on coronary plaque 
      formation or progression. METHODS: In this single-center observational cohort 
      study, 150 patients underwent computed tomographic angiography for evaluation of 
      coronary atherosclerosis (total, noncalcified, mixed/calcified, and 
      low-attenuation plaque); 101 had repeat assessments within a mean ± SD of 6.9 ± 
      0.3 years to evaluate plaque progression. All CVD events were prospectively 
      recorded, including cardiac death, myocardial infarction, unstable angina, 
      revascularization, stroke, claudication, and hospitalization for heart failure. 
      The Framingham-D'Agostino score was used to assess cardiovascular risk. The 
      segment stenosis score was used to measure plaque burden. Odds ratios (ORs) with 
      95% confidence intervals (95% CIs) were calculated. RESULTS: After adjustment for 
      the segment stenosis score, the Framingham-D'Agostino score, and time-varying 
      Disease Activity Score in 28 joints using the C-reactive protein level using 
      marginal structural models, current biologic DMARD use was associated with lower 
      long-term CVD risk (OR 0.15 [95% CI 0.04-0.60]). Noncalcified and low-attenuation 
      plaque presence moderated the effect of biologic DMARDs on CVD risk; 
      specifically, biologic DMARD use was associated with lower CVD risk in patients 
      with noncalcified or low-attenuation plaque at baseline (OR 0.21 [95% CI 
      0.04-0.99] and OR 0.08 [95% CI 0.01-0.70], respectively), but not in those 
      without noncalcified or low-attenuation plaque. Per-segment plaque progression 
      analyses showed that biologic DMARD exposure was associated with transition of 
      noncalcified to mixed/calcified plaque (OR 4.00 [95% CI 1.05-15.32]). Biologic 
      DMARD exposure predicted a lower likelihood of new plaque forming in segments 
      without plaque among patients without mixed/calcified plaque in other coronary 
      segments (OR 0.40 [95% CI 0.17-0.93]), but not among those with calcification. 
      Biologic DMARD treatment also predicted low-attenuation plaque loss (P = 0.042). 
      CONCLUSION: Our findings indicate that in RA, biologic DMARD use is associated 
      with reduced CVD risk, protective calcification of noncalcified lesions, and 
      lower likelihood of new plaque formation in patients with early atherosclerosis.
CI  - © 2020, American College of Rheumatology.
FAU - Karpouzas, George A
AU  - Karpouzas GA
AUID- ORCID: 0000-0003-1065-1563
AD  - Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, 
      Torrance, California.
FAU - Ormseth, Sarah R
AU  - Ormseth SR
AD  - Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, 
      Torrance, California.
FAU - Hernandez, Elizabeth
AU  - Hernandez E
AD  - Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, 
      Torrance, California.
FAU - Budoff, Matthew J
AU  - Budoff MJ
AD  - Harbor-UCLA Medical Center and Lundquist Institute for Biomedical Innovation, 
      Torrance, California.
LA  - eng
PT  - Journal Article
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20200807
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
SB  - IM
MH  - Adult
MH  - Angina, Unstable/epidemiology
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy/epidemiology
MH  - Biological Products/*therapeutic use
MH  - Cardiovascular Diseases/diagnostic imaging/*epidemiology/mortality
MH  - Computed Tomography Angiography
MH  - Coronary Angiography
MH  - Coronary Artery Disease/diagnostic imaging/*epidemiology
MH  - Female
MH  - Heart Disease Risk Factors
MH  - Heart Failure/epidemiology
MH  - Hospitalization/statistics & numerical data
MH  - Humans
MH  - Intermittent Claudication/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Multidetector Computed Tomography
MH  - Myocardial Infarction/epidemiology
MH  - Myocardial Revascularization/statistics & numerical data
MH  - Plaque, Atherosclerotic/diagnostic imaging/*epidemiology
MH  - Stroke/epidemiology
MH  - Vascular Calcification/diagnostic imaging/epidemiology
EDAT- 2020/04/23 06:00
MHDA- 2021/01/12 06:00
CRDT- 2020/04/23 06:00
PHST- 2019/09/28 00:00 [received]
PHST- 2020/04/16 00:00 [accepted]
PHST- 2020/04/23 06:00 [pubmed]
PHST- 2021/01/12 06:00 [medline]
PHST- 2020/04/23 06:00 [entrez]
AID - 10.1002/art.41293 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2020 Sep;72(9):1467-1475. doi: 10.1002/art.41293. Epub 2020 
      Aug 7.

PMID- 32248767
OWN - NLM
STAT- MEDLINE
DCOM- 20211025
LR  - 20220531
IS  - 1747-4949 (Electronic)
IS  - 1747-4930 (Linking)
VI  - 15
IP  - 8
DP  - 2020 Oct
TI  - Incidence and risk factors for stroke following percutaneous coronary 
      intervention.
PG  - 909-922
LID - 10.1177/1747493020912607 [doi]
AB  - BACKGROUND: Stroke rates and risk factors may change as percutaneous coronary 
      intervention practice evolves and no data are available comparing stroke 
      incidence after percutaneous coronary intervention to the general population. 
      AIMS: This study aimed to identify the incidence and risk factors for inpatient 
      and subsequent stroke following percutaneous coronary intervention with 
      comparison to age-matched controls. METHODS: Data were prospectively collected 
      from 22,618 patients undergoing percutaneous coronary intervention in the 
      Melbourne Interventional Group registry (2005-2015). The cohort was compared to 
      the North-East Melbourne Stroke Incidence Study population-based cohort 
      (1997-1999) and predefined variables assessed for association with inpatient or 
      outpatient stroke. RESULTS: Inpatient stroke occurred in 0.33% (65.3% ischemic, 
      28.0% haemorrhagic, and 6.7% cause unknown), while outpatient stroke occurred in 
      0.55%. Inpatient and outpatient stroke were associated with higher rates of 
      in-hospital major adverse cardiovascular outcomes (p < 0.0001) and mortality 
      (p < 0.0001), as well as 12-month mortality (p < 0.0001). Factors independently 
      associated with inpatient stroke were renal impairment, ST-elevation myocardial 
      infarction, previous stroke, left ventricular ejection fraction 30-45%, and 
      female sex, while those associated with outpatient stroke were previous stroke, 
      chronic lung disease, previous myocardial infarction, rheumatoid arthritis, 
      female sex, and older age. Compared to the age-standardized population-based 
      cohort, stroke rates in the 12 months following discharge were higher for 
      percutaneous coronary intervention patients <65 years old, but lower for 
      percutaneous coronary intervention patients ≥65 years old. CONCLUSIONS: Risk of 
      inpatient stroke following percutaneous coronary intervention appears to be 
      largely associated with clinical status at presentation, while outpatient stroke 
      relates more to age and chronic disease. Compared to the general population, 
      outpatient stroke rates following percutaneous coronary intervention are higher 
      for younger, but not older, patients.
FAU - Dawson, Luke P
AU  - Dawson LP
AUID- ORCID: 0000-0003-3789-5808
AD  - Department of Cardiovascular Medicine, The Alfred Hospital, Melbourne, Australia.
AD  - Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia.
FAU - Cole, Justin A
AU  - Cole JA
AD  - Department of Cardiovascular Medicine, The Alfred Hospital, Melbourne, Australia.
AD  - Baker IDI Heart and Diabetes Institute, Melbourne, Australia.
FAU - Lancefield, Terase F
AU  - Lancefield TF
AD  - Department of Cardiology, Austin Health, Melbourne, Australia.
FAU - Ajani, Andrew E
AU  - Ajani AE
AD  - Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia.
FAU - Andrianopoulos, Nick
AU  - Andrianopoulos N
AD  - Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, 
      Australia.
FAU - Thrift, Amanda G
AU  - Thrift AG
AUID- ORCID: 0000-0001-8533-4170
AD  - Stroke and Ageing Research, Department of Medicine, School of Clinical Sciences 
      at Monash Health, Monash University, Melbourne, Australia.
FAU - Clark, David J
AU  - Clark DJ
AD  - Department of Cardiology, Austin Health, Melbourne, Australia.
FAU - Brennan, Angela L
AU  - Brennan AL
AD  - Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, 
      Australia.
FAU - Freeman, Melanie
AU  - Freeman M
AD  - Department of Cardiology, Box Hill Hospital, Melbourne, Australia.
FAU - O'Brien, Jessica
AU  - O'Brien J
AD  - Department of Cardiovascular Medicine, The Alfred Hospital, Melbourne, Australia.
FAU - Sebastian, Martin
AU  - Sebastian M
AD  - Department of Cardiology, University Hospital Geelong, Geelong, Australia.
FAU - Chan, William
AU  - Chan W
AD  - Department of Cardiovascular Medicine, The Alfred Hospital, Melbourne, Australia.
AD  - Baker IDI Heart and Diabetes Institute, Melbourne, Australia.
FAU - Shaw, James A
AU  - Shaw JA
AD  - Department of Cardiovascular Medicine, The Alfred Hospital, Melbourne, Australia.
FAU - Dinh, Diem
AU  - Dinh D
AD  - Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, 
      Australia.
FAU - Reid, Christopher M
AU  - Reid CM
AD  - Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, 
      Australia.
AD  - School of Public Health, Curtin University, Perth, Australia.
FAU - Duffy, Stephen J
AU  - Duffy SJ
AD  - Department of Cardiovascular Medicine, The Alfred Hospital, Melbourne, Australia.
AD  - Baker IDI Heart and Diabetes Institute, Melbourne, Australia.
AD  - Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, 
      Australia.
CN  - Melbourne Interventional Group (MIG) Investigators, CCRE Therapeutics, Monash 
      University, Melbourne Victoria, Australia
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200404
PL  - United States
TA  - Int J Stroke
JT  - International journal of stroke : official journal of the International Stroke 
      Society
JID - 101274068
SB  - IM
MH  - Aged
MH  - Child, Preschool
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - *Percutaneous Coronary Intervention/adverse effects
MH  - Risk Factors
MH  - *Stroke/epidemiology
MH  - Stroke Volume
MH  - Time Factors
MH  - Ventricular Function, Left
OTO - NOTNLM
OT  - Stroke
OT  - clinical outcomes
OT  - percutaneous coronary intervention
OT  - risk factors
EDAT- 2020/04/07 06:00
MHDA- 2021/10/26 06:00
CRDT- 2020/04/07 06:00
PHST- 2020/04/07 06:00 [pubmed]
PHST- 2021/10/26 06:00 [medline]
PHST- 2020/04/07 06:00 [entrez]
AID - 10.1177/1747493020912607 [doi]
PST - ppublish
SO  - Int J Stroke. 2020 Oct;15(8):909-922. doi: 10.1177/1747493020912607. Epub 2020 
      Apr 4.

PMID- 32242478
OWN - NLM
STAT- MEDLINE
DCOM- 20210308
LR  - 20210308
IS  - 2047-9980 (Electronic)
IS  - 2047-9980 (Linking)
VI  - 9
IP  - 7
DP  - 2020 Apr 7
TI  - Characterization, Pathogenesis, and Clinical Implications of Inflammation-Related 
      Atrial Myopathy as an Important Cause of Atrial Fibrillation.
PG  - e015343
LID - 10.1161/JAHA.119.015343 [doi]
LID - e015343
AB  - Historically, atrial fibrillation has been observed in clinical settings of 
      prolonged hemodynamic stress, eg, hypertension and valvular heart disease. 
      However, recently, the most prominent precedents to atrial fibrillation are 
      metabolic diseases that are associated with adipose tissue inflammation (ie, 
      obesity and diabetes mellitus) and systemic inflammatory disorders (ie, 
      rheumatoid arthritis and psoriasis). These patients typically have little 
      evidence of left ventricular hypertrophy or dilatation; instead, imaging reveals 
      abnormalities of the structure or function of the atria, particularly the left 
      atrium, indicative of an atrial myopathy. The left atrium is enlarged, fibrotic 
      and noncompliant, potentially because the predisposing disorder leads to an 
      expansion of epicardial adipose tissue, which transmits proinflammatory mediators 
      to the underlying left atrium. The development of an atrial myopathy not only 
      leads to atrial fibrillation, but also contributes to pulmonary venous 
      hypertension and systemic thromboembolism. These mechanisms explain why disorders 
      of systemic or adipose tissue inflammation are accompanied an increased risk of 
      atrial fibrillation, abnormalities of left atrium geometry and an enhanced risk 
      of stroke. The risk of stroke exceeds that predicted by conventional 
      cardiovascular risk factors or thromboembolism risk scores used to guide the use 
      of anticoagulation, but it is strongly linked to clinical evidence and biomarkers 
      of systemic inflammation.
FAU - Packer, Milton
AU  - Packer M
AD  - Baylor Heart and Vascular Institute Baylor University Medical Center Dallas TX.
AD  - Imperial College London United Kingdom.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20200403
PL  - England
TA  - J Am Heart Assoc
JT  - Journal of the American Heart Association
JID - 101580524
RN  - 0 (Inflammation Mediators)
SB  - IM
MH  - Adipose Tissue/metabolism
MH  - Animals
MH  - Atrial Fibrillation/*etiology/metabolism/physiopathology
MH  - *Atrial Function, Left
MH  - *Atrial Remodeling
MH  - Fibrosis
MH  - Heart Atria/metabolism/*physiopathology
MH  - Humans
MH  - Inflammation/*complications/metabolism/physiopathology
MH  - Inflammation Mediators/metabolism
MH  - Prognosis
MH  - Risk Assessment
MH  - Risk Factors
PMC - PMC7428644
OTO - NOTNLM
OT  - atrial fibrillation
OT  - atrial myopathy
OT  - stroke
EDAT- 2020/04/04 06:00
MHDA- 2021/03/09 06:00
PMCR- 2020/04/07
CRDT- 2020/04/04 06:00
PHST- 2020/04/04 06:00 [entrez]
PHST- 2020/04/04 06:00 [pubmed]
PHST- 2021/03/09 06:00 [medline]
PHST- 2020/04/07 00:00 [pmc-release]
AID - JAH34924 [pii]
AID - 10.1161/JAHA.119.015343 [doi]
PST - ppublish
SO  - J Am Heart Assoc. 2020 Apr 7;9(7):e015343. doi: 10.1161/JAHA.119.015343. Epub 
      2020 Apr 3.

PMID- 32209618
OWN - NLM
STAT- MEDLINE
DCOM- 20210628
LR  - 20210628
IS  - 1468-201X (Electronic)
IS  - 1355-6037 (Print)
IS  - 1355-6037 (Linking)
VI  - 106
IP  - 20
DP  - 2020 Oct
TI  - Cardiovascular risk factors and outcomes in early rheumatoid arthritis: a 
      population-based study.
PG  - 1566-1572
LID - 10.1136/heartjnl-2019-316193 [doi]
AB  - OBJECTIVE: To assess the burden of cardiovascular disease (CVD) at and prior to 
      diagnosis in people with early rheumatoid arthritis (RA) and subsequent CVD in 
      these patients. METHODS: A retrospective case-control study using a large English 
      primary care database. People with RA (n=6591) diagnosed between 2004 and 2016 
      (inclusive) were identified using a validated algorithm, matched 1:1 by age and 
      gender to those without RA (n=6591) and followed for a median of 5.4 years. We 
      assessed differences in CVD at, before and after diagnosis, and the impact of 
      traditional and RA-related risk factors (C reactive protein, RA-related 
      autoantibodies and medication use) on incident CVD (a composite of myocardial 
      infarction (MI), stroke or heart failure). RESULTS: RA cases and their matched 
      controls were both of mean age 58.7 (SD 15.5) at cohort entry, and 67.5% were 
      female. Some CVD risk factors were more common at RA diagnosis including smoking 
      and diabetes; however, total and low-density lipoprotein cholesterol were lower 
      in patients with RA. CVD was more common in RA at cohort entry; stroke (3.9% vs 
      2.7%, p<0.001), heart failure (1.6% vs 1.0%, p=0.001), and non-significantly MI 
      (3.1% vs 2.8%, p=0.092). Excess CVD developed in the 5 years preceding diagnosis. 
      After adjustment for traditional and RA-related risk factors, RA was associated 
      with greater risk of post-diagnosis CVD (HR 1.33, 95% CI 1.07 to 1.65, p=0.010). 
      CONCLUSIONS: An excess of stroke and heart failure occurs before diagnosis of RA. 
      There is excess risk for further cardiovascular events after diagnosis, which is 
      not explained by differences in traditional CVD or RA-related risk factors at 
      diagnosis.
CI  - © Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No 
      commercial re-use. See rights and permissions. Published by BMJ.
FAU - Nikiphorou, Elena
AU  - Nikiphorou E
AD  - Centre for Rheumatic Diseases, King's College London, London, UK.
AD  - Department of Rheumatology, King's College Hospital, London, UK.
FAU - de Lusignan, Simon
AU  - de Lusignan S
AUID- ORCID: 0000-0002-8553-2641
AD  - Department of Clinical and Experimental Medicine, University of Surrey, 
      Guildford, Surrey, UK.
AD  - Royal College of General Practitioners (RCGP) Research and Surveillance Centre 
      (RSC), Royal College of General Practitioners, London, UK.
FAU - Mallen, Christian D
AU  - Mallen CD
AD  - Primary Care Centre Versus Arthritis, School of Primary, Community and Social 
      Care, Keele University, Keele, Staffordshire, UK.
FAU - Khavandi, Kaivan
AU  - Khavandi K
AD  - Pfizer Medical Affairs, Inflammation & Immunology, International Developed 
      Markets, Pfizer Innovative Health, Pfizer Ltd, Tadworth, UK.
FAU - Bedarida, Gabriella
AU  - Bedarida G
AD  - Pfizer Medical Affairs, Inflammation & Immunology, International Developed 
      Markets, Pfizer Innovative Health, Pfizer Ltd, Tadworth, UK.
FAU - Buckley, Christopher D
AU  - Buckley CD
AD  - Rheumatology Research Group, Institute of Inflammation and Ageing and Research 
      into Inflammatory Arthritis Centre Versus Arthritis, University of Birmingham, 
      College of Medical and Dental Sciences, Birmingham, UK.
AD  - University of Oxford, Kennedy Institute of Rheumatology, London, UK.
FAU - Galloway, James
AU  - Galloway J
AD  - Centre for Rheumatic Diseases, King's College London, London, UK.
FAU - Raza, Karim
AU  - Raza K
AD  - Rheumatology Research Group, Institute of Inflammation and Ageing and Research 
      into Inflammatory Arthritis Centre Versus Arthritis, University of Birmingham, 
      College of Medical and Dental Sciences, Birmingham, UK K.Raza@bham.ac.uk.
AD  - Department of Rheumatology, Sandwell and West Birmingham Hospitals NHS Trust, 
      Birmingham, UK.
LA  - eng
GR  - NIHR-RP-2014-04-026/DH_/Department of Health/United Kingdom
PT  - Journal Article
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20200324
PL  - England
TA  - Heart
JT  - Heart (British Cardiac Society)
JID - 9602087
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/diagnosis/*epidemiology
MH  - Cardiovascular Diseases/diagnosis/*epidemiology
MH  - Databases, Factual
MH  - England/epidemiology
MH  - Female
MH  - Heart Disease Risk Factors
MH  - Heart Failure/epidemiology
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology
MH  - Prevalence
MH  - Prognosis
MH  - Retrospective Studies
MH  - Risk Assessment
MH  - Stroke/epidemiology
MH  - Time Factors
PMC - PMC7525791
OTO - NOTNLM
OT  - electronic medical records
OT  - epidemiology
OT  - statistics and study design
COIS- Competing interests: EN has received speaker honoraria and has participated in 
      advisory boards for Pfizer, Sanofi, 110 Gilead, Celltrion, AbbVie and Lilly. SdL 
      declares no conflicts of interest. CDM declares no conflicts of interest. KK is 
      an employee of Pfizer. GB is an employee of Pfizer. CDB declares no conflicts of 
      interest. JG has received honoraria and/or sponsorships for conferences from 
      AbbVie, Celgene, Janssen, Pfizer and UCB. KR has received research funding from 
      AbbVie and Pfizer and honoraria/consultancy fees from AbbVie, Sanofi, Lilly, 
      Bristol-Myers Squibb, UCB, Pfizer, Janssen and Roche Chugai.
EDAT- 2020/03/27 06:00
MHDA- 2021/06/29 06:00
PMCR- 2020/09/30
CRDT- 2020/03/27 06:00
PHST- 2019/10/30 00:00 [received]
PHST- 2020/02/16 00:00 [revised]
PHST- 2020/02/19 00:00 [accepted]
PHST- 2020/03/27 06:00 [pubmed]
PHST- 2021/06/29 06:00 [medline]
PHST- 2020/03/27 06:00 [entrez]
PHST- 2020/09/30 00:00 [pmc-release]
AID - heartjnl-2019-316193 [pii]
AID - 10.1136/heartjnl-2019-316193 [doi]
PST - ppublish
SO  - Heart. 2020 Oct;106(20):1566-1572. doi: 10.1136/heartjnl-2019-316193. Epub 2020 
      Mar 24.

PMID- 32194408
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 11
DP  - 2020
TI  - Adjunctive Chinese Herbal Products Therapy Reduces the Risk of Ischemic Stroke 
      Among Patients With Rheumatoid Arthritis.
PG  - 169
LID - 10.3389/fphar.2020.00169 [doi]
LID - 169
AB  - We performed a retrospective cohort study to investigate the association between 
      the risk of ischemic stroke (IS) and the use of Chinese herbal products (CHP) in 
      combination with western medicine (WM) among patients with rheumatoid arthritis 
      (RA). The data were sourced from the registry for beneficiaries, inpatient and 
      ambulatory care claims, and Registry for Catastrophic Illness from the National 
      Health Insurance Research Database (NHIRD) in Taiwan between 1997 and 2011. 
      Patients, who were newly diagnosed with RA between 1997 and 2010, were classified 
      as the CHP group or non-CHP group depending on the presence of absence the 
      adjunctive use of CHP following a diagnosis of RA. A total of 4,148 RA patients 
      were in both the CHP and non-CHP groups after 1:1 matching. Patients in the CHP 
      group had a significantly lower risk of IS compared to patients in the non-CHP 
      group (adjusted hazard ratio [aHR], 0.67; 95% confidence interval [CI], 
      0.52-0.86). In the CHP group, patients who used CHP for more than 30 days had a 
      lower risk of IS than their counterparts (aHR: 0.61, 95% CI: 0.40-0.91). 
      Gui-Zhi-Shao-Yao-Zhi-Mu-Tang, Shu-Jin-Huo-Xie-Tang, and Du-Huo-Ji-Sheng-Tang 
      might be associated with a lower risk of IS. Finally, the use of CHP in 
      combination with WM was associated with a decreased risk of IS in patients with 
      RA, especially among those who had used CHP for more than 30 days. A further 
      randomized control trial is required to clarify the casual relationship between 
      these results.
CI  - Copyright © 2020 Shen, Chiang and Hsiung.
FAU - Shen, Hsuan-Shu
AU  - Shen HS
AD  - Department of Chinese Medicine, Hualien Tzu Chi Hospital, Buddhist Tzu Chi 
      Medical Foundation, Hualien, Taiwan.
AD  - School of Post-Baccalaureate Chinese Medicine, Tzu Chi University, Hualien, 
      Taiwan.
FAU - Chiang, Jen-Huai
AU  - Chiang JH
AD  - Management Office for Health Data, China Medical University Hospital, Taichung, 
      Taiwan.
AD  - College of Medicine, China Medical University, Taichung, Taiwan.
FAU - Hsiung, Nai-Huan
AU  - Hsiung NH
AD  - Department of Nursing, Asia University, Taichung, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20200304
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC7064546
OTO - NOTNLM
OT  - Chinese herbal products
OT  - National Health Insurance Research Database
OT  - ischemic stroke
OT  - rheumatoid arthritis
OT  - traditional Chinese medicine
EDAT- 2020/03/21 06:00
MHDA- 2020/03/21 06:01
PMCR- 2020/03/04
CRDT- 2020/03/21 06:00
PHST- 2019/03/23 00:00 [received]
PHST- 2020/02/07 00:00 [accepted]
PHST- 2020/03/21 06:00 [entrez]
PHST- 2020/03/21 06:00 [pubmed]
PHST- 2020/03/21 06:01 [medline]
PHST- 2020/03/04 00:00 [pmc-release]
AID - 10.3389/fphar.2020.00169 [doi]
PST - epublish
SO  - Front Pharmacol. 2020 Mar 4;11:169. doi: 10.3389/fphar.2020.00169. eCollection 
      2020.

PMID- 32059458
OWN - NLM
STAT- MEDLINE
DCOM- 20201116
LR  - 20201116
IS  - 1648-9144 (Electronic)
IS  - 1010-660X (Print)
IS  - 1010-660X (Linking)
VI  - 56
IP  - 2
DP  - 2020 Feb 12
TI  - Predicting the Risk of Ischemic Stroke among Patients with Rheumatoid Arthritis 
      Using a Simplified RA-CHADSV Score Based on the CHA(2)DS(2)-VASc Score.
LID - 10.3390/medicina56020073 [doi]
LID - 73
AB  - BACKGROUND AND OBJECTIVES: The aim of this retrospective cohort study was to 
      develop a new score (RA-CHADSV) (rheumatoid arthritis - congestive heart failure, 
      hypertension, age ≥75 years, diabetes mellitus, stroke/transient ischemic 
      attack/thromboembolism, and vascular disease), modified from the CHA(2)DS(2)-VASc 
      score (congestive heart failure, hypertension, age ≥75 years (doubled), diabetes 
      mellitus, stroke/transient ischemic attack (doubled), vascular disease, age 65-74 
      years, and female), in predicting the risk of ischemic stroke in rheumatoid 
      arthritis (RA) patients without atrial fibrillation (AF). MATERIALS AND METHODS: 
      Using the Taiwan's National Health Insurance Research Database, 592 patients with 
      RA diagnosed between 2000 and 2002 were identified and followed until first 
      occurrence of ischemic stroke or the last available date in the database. 
      Incidence rate ratios (IRR) of ischemic stroke for the CHA(2)DS(2)-VASc score 
      were calculated using Poisson regression models. A new prediction score RA-CHADSV 
      was developed using multiple logistic regression analysis with bootstrap 
      validation. RESULTS: The area under the receiver operating characteristic curve 
      of the newly developed RA-CHADSV score and the CHA(2)DS(2)-VASc score were 0.73 
      (95% confidence interval (CI) 0.64-0.82) and 0.70 (95% CI 0.61-0.79), 
      respectively. The RA-CHADSV score was significantly associated with a higher 
      ischemic stroke incidence in the patients who scored ≥1 (adjusted IRR 7.39, p < 
      0.001). CONCLUSIONS: A simplified RA-CHADSV score, with comparable efficiency as 
      the CHA(2)DS(2)-VASc score, but easier to use clinically was developed for 
      predicting the risk of ischemic stroke among non-AF RA patients.
FAU - Hsu, Chia-Wen
AU  - Hsu CW
AD  - Department of Medical Research, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical 
      Foundation, Dalin, Chiayi 62247, Taiwan.
AD  - School of Nursing, College of Medicine, Chang Gung University, Taoyuan City 
      33302, Taiwan.
FAU - Ng, Khai-Jing
AU  - Ng KJ
AD  - Division of Allergy, Immunology and Rheumatology, Dalin Tzu Chi Hospital, 
      Buddhist Tzu Chi Medical Foundation, Dalin, Chiayi 62247, Taiwan.
FAU - Lu, Ming-Chi
AU  - Lu MC
AD  - Division of Allergy, Immunology and Rheumatology, Dalin Tzu Chi Hospital, 
      Buddhist Tzu Chi Medical Foundation, Dalin, Chiayi 62247, Taiwan.
AD  - School of Medicine, Tzu Chi University, Hualien City, Hualien 97004, Taiwan.
FAU - Koo, Malcolm
AU  - Koo M
AD  - Graduate Institute of Long-term Care, Tzu Chi University of Science and 
      Technology, Hualien City, Hualien 97005, Taiwan.
AD  - Dalla Lana School of Public Health, University of Toronto, Toronto, M5T 3M7 ON, 
      Canada.
LA  - eng
PT  - Journal Article
DEP - 20200212
PL  - Switzerland
TA  - Medicina (Kaunas)
JT  - Medicina (Kaunas, Lithuania)
JID - 9425208
RN  - 0 (Biomarkers)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*blood/epidemiology/physiopathology
MH  - Biomarkers/*analysis/blood
MH  - Brain Ischemia/blood/epidemiology/physiopathology
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Risk Assessment/*methods/standards/statistics & numerical data
MH  - Severity of Illness Index
MH  - Stroke/*blood/epidemiology/physiopathology
MH  - Taiwan/epidemiology
PMC - PMC7073594
OTO - NOTNLM
OT  - atrial fibrillation
OT  - brain ischemia
OT  - rheumatoid arthritis
OT  - risk assessment
OT  - stroke
COIS- The authors declare there are no conflicts of interest.
EDAT- 2020/02/16 06:00
MHDA- 2020/11/18 06:00
PMCR- 2020/02/12
CRDT- 2020/02/16 06:00
PHST- 2020/01/02 00:00 [received]
PHST- 2020/02/04 00:00 [revised]
PHST- 2020/02/06 00:00 [accepted]
PHST- 2020/02/16 06:00 [entrez]
PHST- 2020/02/16 06:00 [pubmed]
PHST- 2020/11/18 06:00 [medline]
PHST- 2020/02/12 00:00 [pmc-release]
AID - medicina56020073 [pii]
AID - medicina-56-00073 [pii]
AID - 10.3390/medicina56020073 [doi]
PST - epublish
SO  - Medicina (Kaunas). 2020 Feb 12;56(2):73. doi: 10.3390/medicina56020073.

PMID- 32057655
OWN - NLM
STAT- MEDLINE
DCOM- 20200914
LR  - 20200914
IS  - 1532-8511 (Electronic)
IS  - 1052-3057 (Linking)
VI  - 29
IP  - 5
DP  - 2020 May
TI  - An Embolic Stroke in a Patient With PROC p.Lys193del.
PG  - 104597
LID - S1052-3057(19)30701-3 [pii]
LID - 10.1016/j.jstrokecerebrovasdis.2019.104597 [doi]
AB  - We report a 58-year-old woman who suddenly developed brain infarction with 
      weakness of the left lower extremity and left perioral dysesthesia during 
      postoperative tamoxifen therapy for breast cancer and prednisolone therapy for 
      rheumatoid arthritis. Diffusion-weighted images detected multiple areas of 
      hyperintensity in the posterior circulation system of the brain. Despite 
      extensive examinations, we could not identify any embolic sources except 
      hypoplasia of the right vertebral artery. We found decreased activity of protein 
      C against its antigen level (activity: 59% versus antigen: 122%) with enhanced 
      activity of coagulation factor VIII (178%) and von Willebrand factor (285%). DNA 
      sequencing identified trinucleotide deletion of the PROC gene leading to 1 amino 
      acid deletion at Lys-193 (p.Lys193del). We speculate that the PROC gene 
      polymorphism may have participated in tamoxifen- and prednisolone- associated 
      hypercoagulable state, leading to development of an embolic stroke in this 
      patient.
CI  - Copyright © 2019 Elsevier Inc. All rights reserved.
FAU - Ueki, Kana
AU  - Ueki K
AD  - Department of Medicine and Clinical Science, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, Japan. Electronic address: 
      kana1028@intmed2.med.kyushu-u.ac.jp.
FAU - Nakamura, Kuniyuki
AU  - Nakamura K
AD  - Department of Medicine and Clinical Science, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, Japan.
FAU - Wakisaka, Yoshinobu
AU  - Wakisaka Y
AD  - Department of Medicine and Clinical Science, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, Japan.
FAU - Wada, Shinichi
AU  - Wada S
AD  - Department of Medicine and Clinical Science, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, Japan.
FAU - Yoshikawa, Yoji
AU  - Yoshikawa Y
AD  - Department of Medicine and Clinical Science, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, Japan.
FAU - Matsumoto, Shinya
AU  - Matsumoto S
AD  - Clinical Chemistry and Laboratory Medicine, Kyushu University Hospital, Fukuoka, 
      Japan.
FAU - Hotta, Taeko
AU  - Hotta T
AD  - Clinical Chemistry and Laboratory Medicine, Kyushu University Hospital, Fukuoka, 
      Japan.
FAU - Kang, Dongchong
AU  - Kang D
AD  - Clinical Chemistry and Laboratory Medicine, Kyushu University Hospital, Fukuoka, 
      Japan; Department of Clinical Chemistry and Laboratory Medicine, Graduate School 
      of Medical Sciences, Kyushu University, Fukuoka, Japan.
FAU - Kitazono, Takanari
AU  - Kitazono T
AD  - Department of Medicine and Clinical Science, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, Japan.
FAU - Ago, Tetsuro
AU  - Ago T
AD  - Department of Medicine and Clinical Science, Graduate School of Medical Sciences, 
      Kyushu University, Fukuoka, Japan.
LA  - eng
PT  - Case Reports
DEP - 20200211
PL  - United States
TA  - J Stroke Cerebrovasc Dis
JT  - Journal of stroke and cerebrovascular diseases : the official journal of National 
      Stroke Association
JID - 9111633
RN  - 0 (Anticoagulants)
RN  - 0 (Antineoplastic Agents, Hormonal)
RN  - 0 (Glucocorticoids)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Protein C)
RN  - 094ZI81Y45 (Tamoxifen)
RN  - X4W7ZR7023 (Methylprednisolone)
SB  - IM
MH  - Anticoagulants/therapeutic use
MH  - Antineoplastic Agents, Hormonal/adverse effects
MH  - Blood Coagulation/drug effects/*genetics
MH  - Female
MH  - Genetic Predisposition to Disease
MH  - Glucocorticoids/adverse effects
MH  - Humans
MH  - Intracranial Embolism/blood/diagnostic imaging/drug therapy/*etiology
MH  - Methylprednisolone/adverse effects
MH  - Middle Aged
MH  - Neuroprotective Agents/therapeutic use
MH  - Phenotype
MH  - Protein C/*genetics
MH  - Protein C Deficiency/blood/complications/diagnosis/*genetics
MH  - Recurrence
MH  - Risk Factors
MH  - *Sequence Deletion
MH  - Stroke/blood/diagnostic imaging/drug therapy/*etiology
MH  - Tamoxifen/adverse effects
MH  - Treatment Outcome
OTO - NOTNLM
OT  - Embolic stroke
OT  - hypercoagulable state
OT  - hypoplastic vertebral artery
OT  - protein C p.Lys193del
OT  - tamoxifen
EDAT- 2020/02/15 06:00
MHDA- 2020/09/15 06:00
CRDT- 2020/02/15 06:00
PHST- 2019/10/03 00:00 [received]
PHST- 2019/11/19 00:00 [revised]
PHST- 2019/12/09 00:00 [accepted]
PHST- 2020/02/15 06:00 [pubmed]
PHST- 2020/09/15 06:00 [medline]
PHST- 2020/02/15 06:00 [entrez]
AID - S1052-3057(19)30701-3 [pii]
AID - 10.1016/j.jstrokecerebrovasdis.2019.104597 [doi]
PST - ppublish
SO  - J Stroke Cerebrovasc Dis. 2020 May;29(5):104597. doi: 
      10.1016/j.jstrokecerebrovasdis.2019.104597. Epub 2020 Feb 11.

PMID- 31990337
OWN - NLM
STAT- MEDLINE
DCOM- 20210125
LR  - 20210125
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 59
IP  - 9
DP  - 2020 Sep 1
TI  - Percutaneous coronary intervention outcomes in patients with rheumatoid 
      arthritis, systemic lupus erythematosus and systemic sclerosis.
PG  - 2512-2522
LID - 10.1093/rheumatology/kez639 [doi]
AB  - OBJECTIVE: Patients with autoimmune rheumatic disease (AIRD) are at an increased 
      risk of coronary artery disease. The present study sought to examine the 
      prevalence and outcomes of AIRD patients undergoing percutaneous coronary 
      intervention (PCI) from a national perspective. METHODS: All PCI-related 
      hospitalizations recorded in the US National Inpatient Sample (2004-2014) were 
      included, stratified into four groups: no AIRD, RA, SLE and SSc. We examined the 
      prevalence of AIRD subtypes and assessed their association with in-hospital 
      adverse events using multivariable logistic regression [odds ratios (OR) (95% 
      CI)]. RESULTS: Patients with AIRD represented 1.4% (n = 90 469) of PCI 
      hospitalizations. The prevalence of RA increased from 0.8% in 2004 to 1.4% in 
      2014, but other AIRD subtypes remained stable. In multivariable analysis, the 
      adjusted odds ratio (aOR) of in-hospital complications [aOR any complication 1.13 
      (95% CI 1.01, 1.26), all-cause mortality 1.32 (1.03, 1.71), bleeding 1.50 (1.30, 
      1.74), stroke 1.36 (1.14, 1.62)] were significantly higher in patients with SSc 
      compared with those without AIRD. There was no difference in complications 
      between the SLE and RA groups and those without AIRD, except higher odds of 
      bleeding in SLE patients [aOR 1.19 (95% CI 1.09, 1.29)] and reduced odds of 
      all-cause mortality in RA patients [aOR 0.79 (95% CI 0.70, 0.88)]. CONCLUSION: In 
      a nationwide cohort of US hospitalizations, we demonstrate increased rates of all 
      adverse clinical outcomes following PCI in people with SSc and increased bleeding 
      in SLE. Management of such patients should involve a multiteam approach with 
      rheumatologists.
CI  - © The Author(s) 2020. Published by Oxford University Press on behalf of the 
      British Society for Rheumatology. All rights reserved. For permissions, please 
      email: journals.permissions@oup.com.
FAU - Martinez, Sara C
AU  - Martinez SC
AD  - Division of Cardiology, Providence St. Peter Hospital, Olympia, WA, USA.
FAU - Mohamed, Mohamed
AU  - Mohamed M
AD  - Keele Cardiovascular Research Group, Centre for Prognosis Research, Keele 
      University, UK.
AD  - Royal Stoke University Hospital, Stoke-on-Trent, UK.
FAU - Potts, Jessica
AU  - Potts J
AD  - Keele Cardiovascular Research Group, Centre for Prognosis Research, Keele 
      University, UK.
FAU - Abhishek, Abhishek
AU  - Abhishek A
AD  - Academic Rheumatology, University of Nottingham, Nottingham, UK.
FAU - Roddy, Edward
AU  - Roddy E
AD  - School of Primary, Community and Social Care, Keele University, UK.
AD  - Haywood Academic Rheumatology Centre, Midland Partnership NHS Foundation Trust, 
      Haywood Hospital, Burslem, UK.
FAU - Savage, Michael
AU  - Savage M
AD  - Department of Medicine (Cardiology), Thomas Jefferson University Hospital, 
      Philadelphia, PA, USA.
FAU - Bharadwaj, Aditya
AU  - Bharadwaj A
AD  - Cardiology, Loma Linda University, Loma Linda, CA, USA.
FAU - Kwok, Chun Shing
AU  - Kwok CS
AD  - Keele Cardiovascular Research Group, Centre for Prognosis Research, Keele 
      University, UK.
AD  - Royal Stoke University Hospital, Stoke-on-Trent, UK.
FAU - Bagur, Rodrigo
AU  - Bagur R
AD  - Keele Cardiovascular Research Group, Centre for Prognosis Research, Keele 
      University, UK.
FAU - Mamas, Mamas A
AU  - Mamas MA
AD  - Keele Cardiovascular Research Group, Centre for Prognosis Research, Keele 
      University, UK.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
SB  - IM
EIN - Rheumatology (Oxford). 2020 Sep 1;59(9):2655. doi: 10.1093/rheumatology/keaa101. 
      PMID: 32097490
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Blood Loss, Surgical/*statistics & numerical data
MH  - Cause of Death
MH  - *Coronary Artery Disease/epidemiology/surgery
MH  - Female
MH  - Hospitalization/statistics & numerical data
MH  - Humans
MH  - Lupus Erythematosus, Systemic/*epidemiology
MH  - Male
MH  - Middle Aged
MH  - Outcome and Process Assessment, Health Care/statistics & numerical data
MH  - *Percutaneous Coronary Intervention/adverse effects/methods/mortality
MH  - Prevalence
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Scleroderma, Systemic/*epidemiology
MH  - *Stroke/diagnosis/etiology
MH  - United States/epidemiology
OTO - NOTNLM
OT  - outcomes
OT  - percutaneous coronary intervention
OT  - rheumatoid arthritis
OT  - systemic lupus erythematosus
OT  - systemic sclerosis
EDAT- 2020/01/29 06:00
MHDA- 2021/01/26 06:00
CRDT- 2020/01/29 06:00
PHST- 2019/09/27 00:00 [received]
PHST- 2019/11/28 00:00 [revised]
PHST- 2020/01/29 06:00 [pubmed]
PHST- 2021/01/26 06:00 [medline]
PHST- 2020/01/29 06:00 [entrez]
AID - 5716645 [pii]
AID - 10.1093/rheumatology/kez639 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2020 Sep 1;59(9):2512-2522. doi: 
      10.1093/rheumatology/kez639.

PMID- 31982165
OWN - NLM
STAT- MEDLINE
DCOM- 20210514
LR  - 20210514
IS  - 1874-1754 (Electronic)
IS  - 0167-5273 (Linking)
VI  - 304
DP  - 2020 Apr 1
TI  - Outcomes of percutaneous coronary intervention (PCI) among patients with 
      connective tissue disease: Propensity match analysis.
PG  - 29-34
LID - S0167-5273(19)35002-8 [pii]
LID - 10.1016/j.ijcard.2019.12.055 [doi]
AB  - BACKGROUND: Inflammation is the hallmark of coronary artery disease (CAD) and 
      CTD. There are reports of increased prevalence of CAD among patients with CTD 
      such as Rheumatoid Arthritis. However, there is a paucity of data regarding the 
      outcomes of PCI among patients with CTD. METHODS: Using the National Inpatient 
      Database, patients that underwent PCI between 2007 and 2015 were identified using 
      ICD-9-CM codes. Propensity match analysis with 1: 3 matching of patients with and 
      without CTD was performed. Outcomes were acute kidney injury (AKI), access site 
      complication (ASC), ventricular fibrillation (VF), cardiogenic shock (CS), 
      Stroke, In-hospital mortality and hospital length of stay (LOS) compared between 
      both groups. RESULT: We identified 17,422 patients with CTD and matched with 52, 
      266 patients without CTD. Patients were predominantly female (63.1%) and white 
      (77.2%), with a mean age of 63 ± 12.1 years. AKI (8.3% vs. 6.6%, p < 0.001), ASC 
      (3.2% vs. 2.7%, p = 0.01) and hospital stay (4.2 ± 4.8 vs. 3.8 ± 5.2, p < 0.001) 
      were higher among patients with CTD. There was no statistically significant 
      difference in rates of VF, CS, stroke, and In-hospital mortality among the two 
      groups. However, in subgroup analysis, rates of VF were lower among patients with 
      Systemic Lupus Erythematosus (SLE) (1.5% vs. 2.2%, p = 0.006). CONCLUSIONS: 
      Patients with CTD undergoing PCI have a higher rate of AKI, Access site 
      complications, and prolonged hospital stay.
CI  - Published by Elsevier B.V.
FAU - Alliu, Samson
AU  - Alliu S
AD  - Heart and Vascular Institute, Maimonides Medical Center, Brooklyn, NY, USA. 
      Electronic address: salliu@maimonidesmed.org.
FAU - Ugwu, Justin
AU  - Ugwu J
AD  - Department of Cardiology, University of Texas Medical Center, Galveston, TX, USA.
FAU - Babalola, Omotooke
AU  - Babalola O
AD  - Department of Internal Medicine, St. Elizabeth Hospital, Youngstown, OH, USA.
FAU - Obiagwu, Chukwudi
AU  - Obiagwu C
AD  - Heart and Vascular Institute, Maimonides Medical Center, Brooklyn, NY, USA.
FAU - Moskovits, Norbert
AU  - Moskovits N
AD  - Heart and Vascular Institute, Maimonides Medical Center, Brooklyn, NY, USA.
FAU - Ayzenberg, Sergey
AU  - Ayzenberg S
AD  - Heart and Vascular Institute, Maimonides Medical Center, Brooklyn, NY, USA.
FAU - Hollander, Gerald
AU  - Hollander G
AD  - Heart and Vascular Institute, Maimonides Medical Center, Brooklyn, NY, USA.
FAU - Frankel, Robert
AU  - Frankel R
AD  - Heart and Vascular Institute, Maimonides Medical Center, Brooklyn, NY, USA.
FAU - Shani, Jacob
AU  - Shani J
AD  - Heart and Vascular Institute, Maimonides Medical Center, Brooklyn, NY, USA.
LA  - eng
PT  - Journal Article
DEP - 20200109
PL  - Netherlands
TA  - Int J Cardiol
JT  - International journal of cardiology
JID - 8200291
SB  - IM
MH  - *Acute Kidney Injury
MH  - Aged
MH  - *Connective Tissue Diseases
MH  - *Coronary Artery Disease/epidemiology/surgery
MH  - Female
MH  - Humans
MH  - Middle Aged
MH  - *Percutaneous Coronary Intervention/adverse effects
MH  - Risk Factors
MH  - Shock, Cardiogenic
MH  - Treatment Outcome
OTO - NOTNLM
OT  - Access site complication (ASC)
OT  - Acute kidney injury (AKI)
OT  - Connective tissue disease (CTD)
OT  - Percutaneous coronary intervention (PCI)
COIS- Declaration of competing interest The authors report no relationships that could 
      be construed as a conflict of interest.
EDAT- 2020/01/27 06:00
MHDA- 2021/05/15 06:00
CRDT- 2020/01/27 06:00
PHST- 2019/10/09 00:00 [received]
PHST- 2019/11/04 00:00 [revised]
PHST- 2019/12/27 00:00 [accepted]
PHST- 2020/01/27 06:00 [pubmed]
PHST- 2021/05/15 06:00 [medline]
PHST- 2020/01/27 06:00 [entrez]
AID - S0167-5273(19)35002-8 [pii]
AID - 10.1016/j.ijcard.2019.12.055 [doi]
PST - ppublish
SO  - Int J Cardiol. 2020 Apr 1;304:29-34. doi: 10.1016/j.ijcard.2019.12.055. Epub 2020 
      Jan 9.

PMID- 31973602
OWN - NLM
STAT- MEDLINE
DCOM- 20201221
LR  - 20201221
IS  - 2047-9980 (Electronic)
IS  - 2047-9980 (Linking)
VI  - 9
IP  - 3
DP  - 2020 Feb 4
TI  - Potential Role of Atrial Myopathy in the Pathogenesis of Stroke in Rheumatoid 
      Arthritis and Psoriasis: A Conceptual Framework and Implications for Prophylaxis.
PG  - e014764
LID - 10.1161/JAHA.119.014764 [doi]
LID - e014764
FAU - Packer, Milton
AU  - Packer M
AD  - Baylor Heart and Vascular Institute Baylor University Medical Center Dallas TX.
AD  - Imperial College London United Kingdom.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20200124
PL  - England
TA  - J Am Heart Assoc
JT  - Journal of the American Heart Association
JID - 101580524
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Anti-Inflammatory Agents/therapeutic use
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/*complications/diagnosis/drug therapy/physiopathology
MH  - *Atrial Function, Left/drug effects
MH  - *Atrial Remodeling/drug effects
MH  - Heart Disease Risk Factors
MH  - Heart Diseases/diagnosis/*etiology/physiopathology/prevention & control
MH  - Humans
MH  - Prognosis
MH  - Psoriasis/diagnosis/drug therapy/*etiology/physiopathology
MH  - Risk Assessment
MH  - Stroke/diagnosis/*etiology/physiopathology/prevention & control
PMC - PMC7033881
OTO - NOTNLM
OT  - atrial strain
OT  - psoriasis
OT  - rheumatoid arthritis
OT  - stroke
EDAT- 2020/01/25 06:00
MHDA- 2020/12/22 06:00
PMCR- 2020/02/04
CRDT- 2020/01/25 06:00
PHST- 2020/01/25 06:00 [entrez]
PHST- 2020/01/25 06:00 [pubmed]
PHST- 2020/12/22 06:00 [medline]
PHST- 2020/02/04 00:00 [pmc-release]
AID - JAH34692 [pii]
AID - 10.1161/JAHA.119.014764 [doi]
PST - ppublish
SO  - J Am Heart Assoc. 2020 Feb 4;9(3):e014764. doi: 10.1161/JAHA.119.014764. Epub 
      2020 Jan 24.

PMID- 31958282
OWN - NLM
STAT- MEDLINE
DCOM- 20210419
LR  - 20231113
IS  - 2056-5933 (Electronic)
IS  - 2056-5933 (Linking)
VI  - 6
IP  - 1
DP  - 2020 Jan
TI  - ​Risk of major adverse cardiovascular events among patients with rheumatoid 
      arthritis after initial CT-based diagnosis and treatment.
LID - 10.1136/rmdopen-2019-001113 [doi]
LID - e001113
AB  - OBJECTIVE: Rheumatoid arthritis (RA) is a known risk factor for developing 
      coronary artery disease (CAD). The influence of RA on the prognosis after initial 
      CAD diagnosis and treatment is however largely unknown. We examined the risk of 
      major cardiovascular events among RA and non-RA patients with chest pain referred 
      to cardiac CT. METHODS: This was a follow-up study, using data from the Western 
      Denmark Heart Registry, containing data on CT angiography examinations (Cardiac 
      CT). Information on RA diagnosis and covariates were identified through 
      nationwide administrative registers. The primary outcome was a combined outcome 
      including, myocardial infarction, ischaemic or unspecified stroke, coronary 
      artery bypass grafting, percutaneous coronary intervention, and all-cause 
      mortality. Median time until events or censoring was 3.5 years (min/max: 0.0: 
      9.2). Cox proportional hazard models were used to examine the association between 
      RA/non-RA patients and outcomes. RESULTS: Among 42 257 patients, referred between 
      2008 and 2016, we identified 358 (0.8%) with RA. An increased risk was seen in RA 
      compared with non-RA (adjusted HR 1.35, 95% CI 0.93 to 1.96). Among patients who 
      had received flare treatment more than once prior to cardiac CT the adjusted HR 
      1.80 (95% CI 1.08 to 3.00), and among patients with seropositive RA the adjusted 
      HR 1.42 (95% CI 0.93 to 2.16). CONCLUSION: In patients referred to cardiac CT due 
      to chest pain, we found a trend of an association between RA and the combined 
      primary outcome, supporting that RA per se, but in particular seropositive and 
      active RA, may increase the risk of CAD even after initial CAD diagnosis and 
      treatment.
CI  - © Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No 
      commercial re-use. See rights and permissions. Published by BMJ.
FAU - de Thurah, Annette
AU  - de Thurah A
AUID- ORCID: 0000-0003-0103-4328
AD  - Department of Rheumatology, Aarhus University Hospital Skejby, Aarhus N, Denmark 
      annethur@rm.dk.
AD  - Department of Clinical Medicine, Aarhus University, Aarhus N, Denmark.
FAU - Andersen, Ina Trolle
AU  - Andersen IT
AD  - Department of Clinical Epidemiology, Aarhus University Hospital Skejby, Aarhus N, 
      Denmark.
FAU - Tinggaard, Andreas Bugge
AU  - Tinggaard AB
AD  - Department of Cardiology, Hospital Unit West, Herning, Denmark.
FAU - Riis, Anders Hammerich
AU  - Riis AH
AD  - Department of Clinical Epidemiology, Aarhus University Hospital Skejby, Aarhus N, 
      Denmark.
FAU - Therkildsen, Josephine
AU  - Therkildsen J
AD  - Department of Cardiology, Hospital Unit West, Herning, Denmark.
FAU - Bøtker, Hans Erik
AU  - Bøtker HE
AD  - Department of Clinical Medicine, Aarhus University, Aarhus N, Denmark.
AD  - Department of Cardiology, Aarhus University Hospital Skejby, Aarhus N, Denmark.
FAU - Bøttcher, Morthen
AU  - Bøttcher M
AD  - Department of Cardiology, Hospital Unit West, Herning, Denmark.
FAU - Hauge, Ellen-Margrethe
AU  - Hauge EM
AD  - Department of Rheumatology, Aarhus University Hospital Skejby, Aarhus N, Denmark.
AD  - Department of Clinical Medicine, Aarhus University, Aarhus N, Denmark.
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - RMD Open
JT  - RMD open
JID - 101662038
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/complications/*mortality
MH  - Cardiovascular Diseases/etiology/*mortality
MH  - Coronary Artery Disease/complications/*mortality
MH  - Denmark/epidemiology
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Myocardial Infarction/etiology/*mortality
MH  - Prognosis
MH  - Proportional Hazards Models
MH  - Registries
MH  - Risk Factors
MH  - Tomography, X-Ray Computed
PMC - PMC6999677
OTO - NOTNLM
OT  - cardiovascular disease
OT  - epidemiology
OT  - rheumatoid arthritis
COIS- Competing interests: None declared.
EDAT- 2020/01/21 06:00
MHDA- 2021/04/20 06:00
PMCR- 2020/01/15
CRDT- 2020/01/21 06:00
PHST- 2019/09/29 00:00 [received]
PHST- 2019/12/12 00:00 [revised]
PHST- 2019/12/15 00:00 [accepted]
PHST- 2020/01/21 06:00 [entrez]
PHST- 2020/01/21 06:00 [pubmed]
PHST- 2021/04/20 06:00 [medline]
PHST- 2020/01/15 00:00 [pmc-release]
AID - rmdopen-2019-001113 [pii]
AID - 10.1136/rmdopen-2019-001113 [doi]
PST - ppublish
SO  - RMD Open. 2020 Jan;6(1):e001113. doi: 10.1136/rmdopen-2019-001113.

PMID- 31929568
OWN - NLM
STAT- MEDLINE
DCOM- 20200410
LR  - 20240724
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 15
IP  - 1
DP  - 2020
TI  - The impact of rehabilitation frequency on the risk of stroke in patients with 
      rheumatoid arthritis.
PG  - e0227514
LID - 10.1371/journal.pone.0227514 [doi]
LID - e0227514
AB  - BACKGROUND: Patients with rheumatoid arthritis are at higher risk of developing 
      stroke due to augmented systemic inflammation. While regular exercise has been 
      shown to reduce inflammation in human subjects, the purpose of our study is to 
      determine whether increased frequency of rehabilitation is protective against 
      stroke or not. METHODS: A total of 16,224 rheumatoid arthritis patients with a 
      catastrophic illness certificate were identified in our database from 2000 to 
      2006, and 663 of them developed stroke before the end of 2013. After 
      statistically matching for age, sex, and the time interval between the diagnosis 
      of rheumatoid arthritis and stroke, 642 patients without stroke were identified 
      as the control group. Analyses with Student's t test and Chi-square test were 
      done to compare the clinical characteristics of patients with and without stroke, 
      and logistic regression analysis was then performed to evaluate the odds ratio of 
      stroke. RESULTS: Higher odds ratio of stroke was revealed in patients with 
      hypertension, diabetes mellitus, and moderate degree of rheumatoid arthritis 
      disease severity. Furthermore, more than 40 rehabilitation sessions per year 
      reduced the risk of developing stroke in patients with moderate disease severity. 
      CONCLUSIONS: Physical activities brought by more rehabilitation sessions are 
      beneficial and should be encouraged in patients with rheumatoid arthritis, 
      particularly for those with higher disease activity but not taking biologic 
      agents.
FAU - Cheng, Yuan-Yang
AU  - Cheng YY
AD  - Department of Physical Medicine and Rehabilitation, Taichung Veterans General 
      Hospital, Taichung, Taiwan.
AD  - School of Medicine, National Yang-Ming University, Taipei, Taiwan.
FAU - Chang, Shin-Tsu
AU  - Chang ST
AD  - Department of Physical Medicine and Rehabilitation, Taichung Veterans General 
      Hospital, Taichung, Taiwan.
AD  - Department of Physical Medicine and Rehabilitation, Tri-Service General Hospital, 
      Taipei, Taiwan.
AD  - School of Medicine, National Defense Medical Center, Taipei, Taiwan.
AD  - School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
FAU - Kao, Chung-Lan
AU  - Kao CL
AD  - School of Medicine, National Yang-Ming University, Taipei, Taiwan.
AD  - Department of Physical Medicine and Rehabilitation, Taipei Veterans General 
      Hospital, Taipei, Taiwan.
FAU - Chen, Yi-Huei
AU  - Chen YH
AD  - Department of Medical Research, Taichung Veterans General Hospital, Taichung, 
      Taiwan.
FAU - Lin, Ching-Heng
AU  - Lin CH
AUID- ORCID: 0000-0002-2450-6108
AD  - Department of Medical Research, Taichung Veterans General Hospital, Taichung, 
      Taiwan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200113
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/complications/pathology/*rehabilitation
MH  - Case-Control Studies
MH  - Databases, Factual
MH  - Diabetes Complications
MH  - Diabetes Mellitus/pathology
MH  - Exercise
MH  - Female
MH  - Humans
MH  - Hypertension/complications
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Odds Ratio
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Stroke/complications/*diagnosis
PMC - PMC6957159
COIS- The authors have declared that no competing interests exist.
EDAT- 2020/01/14 06:00
MHDA- 2020/04/11 06:00
PMCR- 2020/01/13
CRDT- 2020/01/14 06:00
PHST- 2019/08/08 00:00 [received]
PHST- 2019/12/19 00:00 [accepted]
PHST- 2020/01/14 06:00 [entrez]
PHST- 2020/01/14 06:00 [pubmed]
PHST- 2020/04/11 06:00 [medline]
PHST- 2020/01/13 00:00 [pmc-release]
AID - PONE-D-19-22440 [pii]
AID - 10.1371/journal.pone.0227514 [doi]
PST - epublish
SO  - PLoS One. 2020 Jan 13;15(1):e0227514. doi: 10.1371/journal.pone.0227514. 
      eCollection 2020.

PMID- 31854508
OWN - NLM
STAT- MEDLINE
DCOM- 20201119
LR  - 20201119
IS  - 1756-185X (Electronic)
IS  - 1756-1841 (Linking)
VI  - 23
IP  - 1
DP  - 2020 Jan
TI  - Usefulness of CHA(2) DS(2) -VASc score to predict mortality and hospitalization 
      in patients with inflammatory arthritis.
PG  - 106-115
LID - 10.1111/1756-185X.13751 [doi]
AB  - BACKGROUND: Inflammatory arthritis including rheumatoid arthritis (RA), 
      ankylosing spondylitis (AS) and psoriatic arthritis (PsA) are disorders at 
      increased risk of morbidity and mortality for which a validated prognostic tool 
      for facilitating clinical management is needed. CHA(2) DS(2) -VASc (congestive 
      heart failure/hypertension/age diabetes/stroke/vascular disease/age/sex category) 
      score was initially conceived and used to estimate thromboembolic risk in 
      non-valvular atrial fibrillation, and then successfully applied in community 
      populations with sinus rhythm. We tested CHA(2) DS(2) -VASc-score as a 
      prognosticator of adverse outcomes in patients in sinus rhythm with RA/AS/PsA. 
      METHODS: Between March 2014 and March 2015, 414 patients (214 RA, 75 AS, 125 PsA) 
      in sinus rhythm without cardiac disease were consecutively analyzed and 
      prospectively followed-up. Primary and co-primary end-points were a composite of 
      all-cause death/all-cause hospitalization and CV death/CV hospitalization, 
      respectively. RESULTS: Patients were divided into LOWscore and HIGHscore groups 
      if CHA(2) DS(2) -VASc was = 0/1 point or greater than 1 point, respectively. The 
      HIGHscore group comprised 190 patients who were older with higher prevalence of 
      CV risk factors and arthritis disease activity than 224 LOWscore patients. During 
      a follow up of 36 months, the event rate for primary and co-primary end-point was 
      37% and 12% in the HIGHscore vs 22% and 4% in LOWscore group (P = .001 and .002 
      respectively). At multivariate Cox regression analysis CHA(2) DS(2) -VASc-score 
      was related to primary end-point (hazards ratio [HR] 1.30 [1.07-1.59], P = .009) 
      and co-primary end-point (HR 1.35 [1.01-1.79], P = .04) independently of 
      traditional CV risk factors analyzed individually and indexes of inflammation or 
      disease duration. CONCLUSION: CHA(2) DS(2) -VASc-score accurately identifies in 
      the mid-term patients in sinus rhythm with RA/AS/PsA at different risks for CV 
      and non-CV mortality and hospitalization.
CI  - © 2019 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons 
      Australia, Ltd.
FAU - Cioffi, Giovanni
AU  - Cioffi G
AUID- ORCID: 0000-0002-2805-9982
AD  - Rheumatology Section, Department of Medicine, University of Verona, Verona, 
      Italy.
FAU - Viapiana, Ombretta
AU  - Viapiana O
AD  - Rheumatology Section, Department of Medicine, University of Verona, Verona, 
      Italy.
FAU - Orsolini, Giovanni
AU  - Orsolini G
AD  - Rheumatology Section, Department of Medicine, University of Verona, Verona, 
      Italy.
FAU - Idolazzi, Luca
AU  - Idolazzi L
AD  - Rheumatology Section, Department of Medicine, University of Verona, Verona, 
      Italy.
FAU - Fracassi, Elena
AU  - Fracassi E
AD  - Rheumatology Section, Department of Medicine, University of Verona, Verona, 
      Italy.
FAU - Ognibeni, Federica
AU  - Ognibeni F
AD  - Rheumatology Section, Department of Medicine, University of Verona, Verona, 
      Italy.
FAU - Dalbeni, Andrea
AU  - Dalbeni A
AD  - Department of Medicine, General Medicine and Hypertension Unit, University of 
      Verona and Azienda Ospedaliera Universitaria Integrata of Verona, Verona, Italy.
FAU - Gatti, Davide
AU  - Gatti D
AD  - Rheumatology Section, Department of Medicine, University of Verona, Verona, 
      Italy.
FAU - Carletto, Antonio
AU  - Carletto A
AD  - Rheumatology Section, Department of Medicine, University of Verona, Verona, 
      Italy.
FAU - Fassio, Angelo
AU  - Fassio A
AD  - Rheumatology Section, Department of Medicine, University of Verona, Verona, 
      Italy.
FAU - Rossini, Maurizio
AU  - Rossini M
AD  - Rheumatology Section, Department of Medicine, University of Verona, Verona, 
      Italy.
FAU - Giollo, Alessandro
AU  - Giollo A
AD  - Rheumatology Section, Department of Medicine, University of Verona, Verona, 
      Italy.
LA  - eng
PT  - Journal Article
DEP - 20191219
PL  - England
TA  - Int J Rheum Dis
JT  - International journal of rheumatic diseases
JID - 101474930
SB  - IM
MH  - Aged
MH  - Arthritis/*epidemiology/therapy
MH  - Cardiovascular Diseases/*epidemiology
MH  - Comorbidity
MH  - Female
MH  - Hospitalization/*statistics & numerical data
MH  - Humans
MH  - Italy/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Morbidity/trends
MH  - Prognosis
MH  - Prospective Studies
MH  - Survival Rate/trends
OTO - NOTNLM
OT  - CHA2DS2-VASc score
OT  - ankylosing spondylitis
OT  - cardiovascular risk factors
OT  - clinical outcomes
OT  - psoriatic arthritis
OT  - rheumatoid arthritis
EDAT- 2019/12/20 06:00
MHDA- 2020/11/20 06:00
CRDT- 2019/12/20 06:00
PHST- 2019/09/02 00:00 [received]
PHST- 2019/10/22 00:00 [revised]
PHST- 2019/10/26 00:00 [accepted]
PHST- 2019/12/20 06:00 [pubmed]
PHST- 2020/11/20 06:00 [medline]
PHST- 2019/12/20 06:00 [entrez]
AID - 10.1111/1756-185X.13751 [doi]
PST - ppublish
SO  - Int J Rheum Dis. 2020 Jan;23(1):106-115. doi: 10.1111/1756-185X.13751. Epub 2019 
      Dec 19.

PMID- 31837960
OWN - NLM
STAT- MEDLINE
DCOM- 20210224
LR  - 20240803
IS  - 1873-2615 (Electronic)
IS  - 1050-1738 (Print)
IS  - 1050-1738 (Linking)
VI  - 30
IP  - 8
DP  - 2020 Nov
TI  - Chronic inflammation, cardiometabolic diseases and effects of treatment: 
      Psoriasis as a human model.
PG  - 472-478
LID - S1050-1738(19)30151-3 [pii]
LID - 10.1016/j.tcm.2019.11.001 [doi]
AB  - Chronic inflammation in humans is associated with accelerated development of 
      cardiometabolic diseases such as myocardial infarction, stroke, and diabetes. 
      Strong evidence from animal models and human interventional trials including 
      CANTOS (The Canakinumab Anti-inflammatory Thrombosis Outcome Study) suggests that 
      targeting residual systemic inflammation in humans may impart a benefit in 
      reducing cardiometabolic diseases. Diseases associated with heightened 
      immune-activation and systemic inflammation including psoriasis, rheumatoid 
      arthritis, systemic lupus erythematosus, and human immunodeficiency virus 
      infection are associated with upwards of two to seven-fold risk of future adverse 
      cardiac events even when adjusted for traditional risk factors. Over the past 
      decade, psoriasis has been utilized as a human model to study 
      inflammatory-induced cardiometabolic dysfunction and to better understand 
      residual risk due to inflammation. The high prevalence and early onset of 
      cardiovascular disease in psoriasis enhances the likelihood of discovering novel 
      pathways in vascular disease progression when followed over time. Furthermore, 
      the United States Food and Drug Administration approved treatments for psoriasis 
      include cytokine inhibitors (anti-tumor necrosis factor, anti-interleukin 17, 
      anti-interleukin 12/23) which while treating the skin disease provide a unique 
      opportunity to characterize how treating the inflammatory pathways may impact 
      atherosclerosis. Herein, we provide a review of chronic inflammation, 
      cardiometabolic disease associations, and treatment effects with a focus on 
      psoriasis as a human model of study.
CI  - Published by Elsevier Inc.
FAU - Aksentijevich, Milena
AU  - Aksentijevich M
AD  - National Heart, Lung, Blood Institute, National Institutes of Health, 10 Center 
      Drive, Clinical Research Center, Room 5-5140 Bethesda, MD 20892, USA.
FAU - Lateef, Sundus S
AU  - Lateef SS
AD  - National Heart, Lung, Blood Institute, National Institutes of Health, 10 Center 
      Drive, Clinical Research Center, Room 5-5140 Bethesda, MD 20892, USA.
FAU - Anzenberg, Paula
AU  - Anzenberg P
AD  - National Heart, Lung, Blood Institute, National Institutes of Health, 10 Center 
      Drive, Clinical Research Center, Room 5-5140 Bethesda, MD 20892, USA.
FAU - Dey, Amit K
AU  - Dey AK
AD  - National Heart, Lung, Blood Institute, National Institutes of Health, 10 Center 
      Drive, Clinical Research Center, Room 5-5140 Bethesda, MD 20892, USA.
FAU - Mehta, Nehal N
AU  - Mehta NN
AD  - National Heart, Lung, Blood Institute, National Institutes of Health, 10 Center 
      Drive, Clinical Research Center, Room 5-5140 Bethesda, MD 20892, USA. Electronic 
      address: nehal.mehta@nih.gov.
LA  - eng
GR  - ZIA HL006193-05/ImNIH/Intramural NIH HHS/United States
GR  - ZIA HL006235-01/ImNIH/Intramural NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20191120
PL  - United States
TA  - Trends Cardiovasc Med
JT  - Trends in cardiovascular medicine
JID - 9108337
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
SB  - IM
CIN - Trends Cardiovasc Med. 2020 Nov;30(8):479-480. doi: 10.1016/j.tcm.2019.11.008. 
      PMID: 31810858
MH  - Animals
MH  - Anti-Inflammatory Agents/*therapeutic use
MH  - Cardiometabolic Risk Factors
MH  - Cardiovascular Diseases/epidemiology/immunology/metabolism/*prevention & control
MH  - Chronic Disease
MH  - Cytokines/*antagonists & inhibitors/metabolism
MH  - Humans
MH  - Inflammation/*drug therapy/epidemiology/immunology/metabolism
MH  - Inflammation Mediators/*antagonists & inhibitors/metabolism
MH  - Metabolic Syndrome/epidemiology/immunology/metabolism/*prevention & control
MH  - Prognosis
MH  - Psoriasis/*drug therapy/epidemiology/immunology/metabolism
MH  - Risk Assessment
MH  - Signal Transduction
PMC - PMC7428846
MID - NIHMS1545534
OTO - NOTNLM
OT  - Adipose dysfunction
OT  - Cardiometabolic disease
OT  - Immune activation
OT  - Inflammation
OT  - Lipoprotein dysfunction
OT  - Psoriasis
COIS- Declarations Competing interests: 1. NNM is a full-time US government employee 
      and has served as a consultant for Amgen, Eli Lilly, and Leo Pharma receiving 
      grants/other payments; as a principal investigator and/or investigator for 
      AbbVie, Celgene, Janssen Pharmaceuticals, Inc, and Novartis receiving grants 
      and/or research funding and as a principal investigator for the National 
      Institute of Health receiving grants and/or research funding. 2. SSL is funded by 
      the NIH Medical Research Scholars Program, a public-private partnership supported 
      jointly by the NIH and contributions to the Foundation for the NIH from the Doris 
      Duke Charitable Foundation, the American Association for Dental Research, the 
      Colgate-Palmolive Company, and other private donors. 3. All other authors have no 
      conflict of interest.
EDAT- 2019/12/16 06:00
MHDA- 2021/02/25 06:00
PMCR- 2021/11/01
CRDT- 2019/12/16 06:00
PHST- 2019/08/13 00:00 [received]
PHST- 2019/10/22 00:00 [revised]
PHST- 2019/11/02 00:00 [accepted]
PHST- 2019/12/16 06:00 [pubmed]
PHST- 2021/02/25 06:00 [medline]
PHST- 2019/12/16 06:00 [entrez]
PHST- 2021/11/01 00:00 [pmc-release]
AID - S1050-1738(19)30151-3 [pii]
AID - 10.1016/j.tcm.2019.11.001 [doi]
PST - ppublish
SO  - Trends Cardiovasc Med. 2020 Nov;30(8):472-478. doi: 10.1016/j.tcm.2019.11.001. 
      Epub 2019 Nov 20.

PMID- 31631437
OWN - NLM
STAT- MEDLINE
DCOM- 20200921
LR  - 20200921
IS  - 1365-2796 (Electronic)
IS  - 0954-6820 (Linking)
VI  - 287
IP  - 2
DP  - 2020 Feb
TI  - Response to Letter to the Editor by Bartoloni et al: 'Interplay of anti-SSA/SSB 
      status and hypertension in determining cardiovascular risk in primary Sjögren's 
      syndrome'.
PG  - 216-217
LID - 10.1111/joim.12996 [doi]
FAU - Mofors, J
AU  - Mofors J
AD  - Division of Rheumatology, Department of Medicine, Karolinska Institutet, 
      Karolinska University Hospital, Stockholm, Sweden.
FAU - Wahren-Herlenius, M
AU  - Wahren-Herlenius M
AUID- ORCID: 0000-0002-0915-7245
AD  - Division of Rheumatology, Department of Medicine, Karolinska Institutet, 
      Karolinska University Hospital, Stockholm, Sweden.
FAU - Nordmark, G
AU  - Nordmark G
AUID- ORCID: 0000-0002-3829-7431
AD  - Department of Medical Sciences, Rheumatology and Science for Life Laboratory, 
      Uppsala University, Uppsala, Sweden.
LA  - eng
PT  - Comment
PT  - Letter
DEP - 20191105
PL  - England
TA  - J Intern Med
JT  - Journal of internal medicine
JID - 8904841
RN  - 0 (Biomarkers)
SB  - IM
CON - J Intern Med. 2019 Oct;286(4):458-468. doi: 10.1111/joim.12941. PMID: 31127862
CON - J Intern Med. 2020 Feb;287(2):214-215. doi: 10.1111/joim.12988. PMID: 31631415
MH  - Biomarkers
MH  - *Cardiovascular Diseases
MH  - Cerebral Infarction
MH  - Humans
MH  - *Hypertension
MH  - Risk Factors
MH  - *Sjogren's Syndrome
MH  - *Venous Thromboembolism
EDAT- 2019/10/22 06:00
MHDA- 2020/09/22 06:00
CRDT- 2019/10/22 06:00
PHST- 2019/10/22 06:00 [pubmed]
PHST- 2020/09/22 06:00 [medline]
PHST- 2019/10/22 06:00 [entrez]
AID - 10.1111/joim.12996 [doi]
PST - ppublish
SO  - J Intern Med. 2020 Feb;287(2):216-217. doi: 10.1111/joim.12996. Epub 2019 Nov 5.

PMID- 31631415
OWN - NLM
STAT- MEDLINE
DCOM- 20200921
LR  - 20200921
IS  - 1365-2796 (Electronic)
IS  - 0954-6820 (Linking)
VI  - 287
IP  - 2
DP  - 2020 Feb
TI  - Interplay of anti-SSA/SSB status and hypertension in determining cardiovascular 
      risk in primary Sjögren's syndrome.
PG  - 214-215
LID - 10.1111/joim.12988 [doi]
FAU - Bartoloni, E
AU  - Bartoloni E
AUID- ORCID: 0000-0003-4776-2136
AD  - From the, Rheumatology Unit, Department of Medicine, University of Perugia, 
      Perugia, Italy.
FAU - Baldini, C
AU  - Baldini C
AD  - Rheumatology Unit, Department of Clinical and Experimental Medicine, University 
      of Pisa, Pisa, Italy.
FAU - De Vita, S
AU  - De Vita S
AD  - Rheumatology Clinic, Department of Medical Area, Udine University Hospital, 
      University of Udine, Udine, Italy.
FAU - Priori, R
AU  - Priori R
AD  - Rheumatology Unit, Sapienza University, Rome, Italy.
FAU - Giacomelli, R
AU  - Giacomelli R
AD  - Division of Rheumatology, Department of Biotechnological and Applied Clinical 
      Sciences, University of L'Aquila, L'Aquila, Italy.
FAU - Bini, V
AU  - Bini V
AD  - Internal Medicine, Endocrinal and Metabolic Science, University of Perugia, 
      Perugia, Italy.
FAU - Gerli, R
AU  - Gerli R
AUID- ORCID: 0000-0002-4684-575X
AD  - From the, Rheumatology Unit, Department of Medicine, University of Perugia, 
      Perugia, Italy.
LA  - eng
PT  - Comment
PT  - Letter
DEP - 20191031
PL  - England
TA  - J Intern Med
JT  - Journal of internal medicine
JID - 8904841
RN  - 0 (Biomarkers)
SB  - IM
CON - J Intern Med. 2019 Oct;286(4):458-468. doi: 10.1111/joim.12941. PMID: 31127862
CIN - J Intern Med. 2020 Feb;287(2):216-217. doi: 10.1111/joim.12996. PMID: 31631437
MH  - Biomarkers
MH  - *Cardiovascular Diseases
MH  - Cerebral Infarction
MH  - Humans
MH  - *Hypertension
MH  - Risk Factors
MH  - *Sjogren's Syndrome
MH  - *Venous Thromboembolism
EDAT- 2019/10/22 06:00
MHDA- 2020/09/22 06:00
CRDT- 2019/10/22 06:00
PHST- 2019/10/22 06:00 [pubmed]
PHST- 2020/09/22 06:00 [medline]
PHST- 2019/10/22 06:00 [entrez]
AID - 10.1111/joim.12988 [doi]
PST - ppublish
SO  - J Intern Med. 2020 Feb;287(2):214-215. doi: 10.1111/joim.12988. Epub 2019 Oct 31.

PMID- 31614442
OWN - NLM
STAT- MEDLINE
DCOM- 20200226
LR  - 20200226
IS  - 1660-4601 (Electronic)
IS  - 1661-7827 (Print)
IS  - 1660-4601 (Linking)
VI  - 16
IP  - 20
DP  - 2019 Oct 11
TI  - Incidence of Cellulitis Following Acupuncture Treatments in Taiwan.
LID - 10.3390/ijerph16203831 [doi]
LID - 3831
AB  - Background: Cellulitis is a complication of acupuncture, but the risk factors and 
      annualized incidence remain unclear. Objective: This study analyzed the incidence 
      and risk factors of cellulitis related to acupuncture in a cohort of one million 
      participants derived from Taiwan's Longitudinal Health Insurance Database. 
      Methods: We tracked this cohort between 1997 and 2012 and recorded all outpatient 
      medical information including diagnosis and treatment. Patients were categorized 
      according to age, gender, comorbidities, residential area, and number of 
      acupuncture treatments. We compared the incidence and risk of cellulitis between 
      different demographics and comorbidities by logistic regression analysis and 
      adjusted odds ratio (aOR) with a 95% confidence interval (95% CI). Results: We 
      included 407,802 patients and 6,207,378 acupuncture treatments. The incidence of 
      cellulitis after acupuncture was 64.4 per 100,000 courses of acupuncture 
      treatment. The most common sites of cellulitis after acupuncture were the legs, 
      feet, and face. Comorbidity was associated with post-acupuncture cellulitis; a 
      multivariate logistic regression analysis showed that chronic kidney disease 
      (aOR, 1.71; 95% CI, 1.55-1.88), rheumatoid arthritis (aOR, 1.86; 95% CI, 
      1.21-3.60), liver cirrhosis (aOR, 1.23; 95% CI, 1.15-1.32), diabetes mellitus 
      (aOR, 1.69; 95% CI, 1.57-1.82), stroke (aOR, 1.44; 95% CI, 1.31-1.58), varicose 
      veins (aOR, 2.38; 95% CI, 2.17-2.84), or heart failure (aOR, 1.81; 95% CI, 
      1.65-1.98) significantly increased cellulitis. Repeated exposure to acupuncture 
      treatment was associated with an increased risk of cellulitis. Conclusions: A 
      variety of chronic diseases may increase the risk of cellulitis after 
      acupuncture. Physicians asked about past medical history before acupuncture might 
      help to reduce cellulitis.
FAU - Lin, Shun-Ku
AU  - Lin SK
AUID- ORCID: 0000-0003-0067-2280
AD  - Department of Chinese Medicine, Taipei City Hospital, Renai Branch, Taipei 106, 
      Taiwan. gigilaskl@gmail.com.
AD  - Institute of Public Health, National Yang-Ming University, Taipei 112, Taiwan. 
      gigilaskl@gmail.com.
FAU - Liu, Jui-Ming
AU  - Liu JM
AUID- ORCID: 0000-0003-3868-085X
AD  - Division of Urology, Department of Surgery, Taoyuan General Hospital, Ministry of 
      Health and Welfare, Taoyuan 330, Taiwan. mento1218@gmail.com.
AD  - Department of Medicine, National Yang-Ming University, Taipei 112, Taiwan. 
      mento1218@gmail.com.
AD  - Graduate Institute of Life Sciences, National Defense Medical Center, Taipei 114, 
      Taiwan. mento1218@gmail.com.
FAU - Wang, Pin-Hsuan
AU  - Wang PH
AD  - Department of Chinese Medicine, Taipei City Hospital, Renai Branch, Taipei 106, 
      Taiwan. u102022004@cmu.edu.tw.
AD  - Department of Chinese Medicine, China Medical University, Taichung 404, Taiwan. 
      u102022004@cmu.edu.tw.
FAU - Hung, Sheng-Ping
AU  - Hung SP
AD  - Department of Chinese Medicine, Taipei City Hospital, Renai Branch, Taipei 106, 
      Taiwan. haopinhe707@gmail.com.
FAU - Hsu, Ren-Jun
AU  - Hsu RJ
AD  - Graduate Institute of Life Sciences, National Defense Medical Center, Taipei 114, 
      Taiwan. hsurnai@gmail.com.
AD  - Cancer Medicine Center of Buddhist Hualien Tzu Chi Hospital, Tzu Chi University, 
      Hualien 970, Taiwan. hsurnai@gmail.com.
AD  - Department of Pathology and Graduate Institute of Pathology and Parasitology, 
      Tri-Service General Hospital, National Defense Medical Center, Taipei 114, 
      Taiwan. hsurnai@gmail.com.
FAU - Chuang, Heng-Chang
AU  - Chuang HC
AD  - Division of Urology, Department of Surgery, Taoyuan General Hospital, Ministry of 
      Health and Welfare, Taoyuan 330, Taiwan. chuang20110617@yahoo.com.tw.
FAU - Lin, Po-Hung
AU  - Lin PH
AUID- ORCID: 0000-0001-8245-4302
AD  - Division of Urology, Department of Surgery, Chang Gung Memorial Hospital at 
      Linkou, Taoyuan 333, Taiwan. m7587@cgmh.org.tw.
AD  - Graduate Institute of Clinical Medical Science, College of Medicine, Chang Gung 
      University, Taoyuan 333, Taiwan. m7587@cgmh.org.tw.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20191011
PL  - Switzerland
TA  - Int J Environ Res Public Health
JT  - International journal of environmental research and public health
JID - 101238455
SB  - IM
MH  - Acupuncture Therapy/*adverse effects
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Cellulitis/epidemiology/*etiology
MH  - Cohort Studies
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Odds Ratio
MH  - Risk Factors
MH  - Taiwan/epidemiology
MH  - Young Adult
PMC - PMC6843534
OTO - NOTNLM
OT  - acupuncture
OT  - cellulitis
OT  - heart failure
OT  - liver cirrhosis
OT  - risk factors
OT  - varicose veins
COIS- The authors declare no conflict of interest.
EDAT- 2019/10/17 06:00
MHDA- 2020/02/27 06:00
PMCR- 2019/10/01
CRDT- 2019/10/17 06:00
PHST- 2019/08/19 00:00 [received]
PHST- 2019/10/04 00:00 [revised]
PHST- 2019/10/07 00:00 [accepted]
PHST- 2019/10/17 06:00 [entrez]
PHST- 2019/10/17 06:00 [pubmed]
PHST- 2020/02/27 06:00 [medline]
PHST- 2019/10/01 00:00 [pmc-release]
AID - ijerph16203831 [pii]
AID - ijerph-16-03831 [pii]
AID - 10.3390/ijerph16203831 [doi]
PST - epublish
SO  - Int J Environ Res Public Health. 2019 Oct 11;16(20):3831. doi: 
      10.3390/ijerph16203831.

PMID- 31600392
OWN - NLM
STAT- MEDLINE
DCOM- 20200824
LR  - 20210206
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Print)
IS  - 1462-0324 (Linking)
VI  - 59
IP  - 6
DP  - 2020 Jun 1
TI  - Outcomes of acute cardiovascular events in rheumatoid arthritis and systemic 
      lupus erythematosus: a population-based study.
PG  - 1355-1363
LID - 10.1093/rheumatology/kez456 [doi]
AB  - OBJECTIVES: Patients with RA and SLE have an excess cardiovascular risk. We aimed 
      to evaluate outcomes of acute cardiovascular events in these patients. METHODS: 
      Using a nationwide database of Taiwan, we identified adult patients who 
      experienced first-time acute myocardial infarction (n = 191 008), intracranial 
      haemorrhage (n = 169 923) and ischaemic stroke (n = 486 890) over a 13-year 
      period. Odds ratios (ORs) of in-hospital mortality and hazard ratios (HRs) of 
      overall mortality and adverse outcomes during long-term follow-up in relation to 
      RA and SLE were estimated with adjustment for potential confounders. RESULTS: In 
      each cohort, 748, 410 and 1419 patients had established RA; 256, 292 and 622 
      patients had SLE. Among acute myocardial infarction patients, RA and SLE were 
      associated with in-hospital mortality (RA: OR 1.61, 95% CI 1.33, 1.95; SLE: OR 
      2.31, 95% CI 1.62, 3.28) and overall mortality. Additionally, RA (HR 1.28, 95% CI 
      1.18, 1.38) and SLE (HR 1.46, 95% CI 1.27, 1.69) increased the risk of major 
      adverse cardiac events. After intracranial haemorrhage, patients with RA and SLE 
      had higher risks of in-hospital mortality (RA: OR 1.61, 95% CI 1.26, 2.06; SLE: 
      OR 3.00, 95% CI 2.33, 3.86) and overall mortality. After ischaemic stroke, RA and 
      SLE increased in-hospital mortality (RA: OR 1.45, 95% CI 1.15, 1.83; SLE: OR 
      2.18, 95% CI 1.57, 3.02), overall mortality and recurrent cerebrovascular events 
      (RA: HR 1.10, 95% CI 1.002, 1.21; SLE: HR 1.31, 95% CI 1.14, 1.51), among which 
      ischaemic stroke (HR 1.39, 95% CI 1.19, 1.62) was more likely to recur in SLE 
      patients. CONCLUSION: Both RA and SLE are consistently associated with adverse 
      outcomes following acute cardiovascular events, highlighting the necessity of 
      integrated care for affected patients.
CI  - © The Author(s) 2019. Published by Oxford University Press on behalf of the 
      British Society for Rheumatology. All rights reserved. For permissions, please 
      email: journals.permissions@oup.com.
FAU - Lai, Chao-Han
AU  - Lai CH
AD  - Department of Surgery, National Cheng Kung University Hospital, College of 
      Medicine, National Cheng Kung University, Tainan, Taiwan.
AD  - Center for Quantitative Sciences, Vanderbilt University Medical Center, 
      Nashville, TN.
AD  - Department of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, 
      USA.
FAU - Hsieh, Cheng-Yang
AU  - Hsieh CY
AD  - Department of Neurology, Tainan Sin Lau Hospital, Tainan, Taiwan.
FAU - Barnado, April
AU  - Barnado A
AD  - Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
FAU - Huang, Li-Ching
AU  - Huang LC
AD  - Center for Quantitative Sciences, Vanderbilt University Medical Center, 
      Nashville, TN.
AD  - Department of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, 
      USA.
FAU - Chen, Sheau-Chiann
AU  - Chen SC
AD  - Center for Quantitative Sciences, Vanderbilt University Medical Center, 
      Nashville, TN.
AD  - Department of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, 
      USA.
FAU - Tsai, Liang-Miin
AU  - Tsai LM
AD  - Department of Internal Medicine, National Cheng Kung University Hospital, College 
      of Medicine, National Cheng Kung University, Tainan.
FAU - Shyr, Yu
AU  - Shyr Y
AD  - Center for Quantitative Sciences, Vanderbilt University Medical Center, 
      Nashville, TN.
AD  - Department of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, 
      USA.
FAU - Li, Chung-Yi
AU  - Li CY
AD  - Department of Public Health, College of Medicine, National Cheng Kung University, 
      Tainan.
AD  - Department of Public Health, College of Public Health, China Medical University, 
      Taichung, Taiwan.
LA  - eng
GR  - K08 AR072757/AR/NIAMS NIH HHS/United States
PT  - Evaluation Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
SB  - IM
MH  - Acute Disease
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications
MH  - Brain Ischemia/etiology/*mortality
MH  - Cohort Studies
MH  - Female
MH  - Hospital Mortality
MH  - Humans
MH  - Lupus Erythematosus, Systemic/*complications
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/etiology/*mortality
MH  - Odds Ratio
MH  - Proportional Hazards Models
MH  - Risk Factors
MH  - Stroke/etiology/*mortality
MH  - Taiwan
PMC - PMC7849999
OTO - NOTNLM
OT  - RA
OT  - SLE
OT  - acute myocardial infarction
OT  - intracranial haemorrhage
OT  - ischaemic stroke
EDAT- 2019/10/11 06:00
MHDA- 2020/08/25 06:00
PMCR- 2020/10/10
CRDT- 2019/10/11 06:00
PHST- 2019/04/07 00:00 [received]
PHST- 2019/09/04 00:00 [revised]
PHST- 2019/10/11 06:00 [pubmed]
PHST- 2020/08/25 06:00 [medline]
PHST- 2019/10/11 06:00 [entrez]
PHST- 2020/10/10 00:00 [pmc-release]
AID - 5585443 [pii]
AID - kez456 [pii]
AID - 10.1093/rheumatology/kez456 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2020 Jun 1;59(6):1355-1363. doi: 
      10.1093/rheumatology/kez456.

PMID- 31600032
OWN - NLM
STAT- MEDLINE
DCOM- 20201228
LR  - 20201228
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Linking)
VI  - 72
IP  - 12
DP  - 2020 Dec
TI  - Coronary Artery Disease in Adults With a History of Juvenile Arthritis.
PG  - 1790-1793
LID - 10.1002/acr.24087 [doi]
AB  - OBJECTIVE: To define the risk of coronary artery disease (CAD) in adults with a 
      history of juvenile arthritis (JA). METHODS: We used the National Health and 
      Nutrition Examination 2007-2014 surveys. Two comparison groups were identified: a 
      random sample of patients without arthritis, and respondents with reported having 
      rheumatoid arthritis (RA). CAD was defined as a "yes" response to the survey 
      question, "Have you ever been told you had congestive heart failure, coronary 
      heart disease, angina/angina pectoris, heart attack, or stroke?" Potential 
      confounders for CAD included age, sex, race, smoking status, and any component of 
      metabolic syndrome. RESULTS: A total of 232 respondents reported having JA. We 
      randomly selected 1,028 without arthritis and 1,105 who reported having RA. In 
      simple logistic regression, the JA group had a 3-fold increased odds of CAD 
      compared to those without arthritis (odds ratio [OR] 3.2 [95% confidence interval 
      (95% CI) 2.1-4.8], P < 0.0001). Controlling for confounders, the odds of CAD in 
      JA continued to be increased (OR 4.2 [95% CI 4.7-10.5], P = 0.002). When 
      comparing the JA and RA groups, in simple logistic regression, the JA group had a 
      lower odds of CAD (OR 0.7 [95% CI 0.5-0.9], P = 0.03). Controlling for 
      confounders, there was no significant difference in the odds of CAD between 
      groups (OR 0.8 [95% CI 0.5-1.3], P = 0.4). CONCLUSION: Adults with a history of 
      JA have a higher risk of CAD compared to adults without arthritis. Providers 
      should be aware of the increased risk of CAD in adults with JA and aggressively 
      screen these patients for modifiable risk factors.
CI  - © 2020, American College of Rheumatology.
FAU - Sule, Sangeeta
AU  - Sule S
AUID- ORCID: 0000-0002-5876-376X
AD  - Children's National Health System, Washington, DC.
FAU - Fontaine, Kevin
AU  - Fontaine K
AD  - University of Alabama at Birmingham.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Observational Study
DEP - 20201106
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Juvenile/diagnosis/*epidemiology
MH  - Coronary Artery Disease/diagnosis/*epidemiology
MH  - Female
MH  - Heart Disease Risk Factors
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Nutrition Surveys
MH  - Risk Assessment
MH  - United States/epidemiology
EDAT- 2019/10/11 06:00
MHDA- 2020/12/29 06:00
CRDT- 2019/10/11 06:00
PHST- 2018/12/06 00:00 [received]
PHST- 2019/10/01 00:00 [accepted]
PHST- 2019/10/11 06:00 [pubmed]
PHST- 2020/12/29 06:00 [medline]
PHST- 2019/10/11 06:00 [entrez]
AID - 10.1002/acr.24087 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2020 Dec;72(12):1790-1793. doi: 10.1002/acr.24087. 
      Epub 2020 Nov 6.

PMID- 31552141
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231014
IS  - 2056-7944 (Electronic)
IS  - 2056-7944 (Linking)
VI  - 4
DP  - 2019
TI  - A Mendelian randomization study of IL6 signaling in cardiovascular diseases, 
      immune-related disorders and longevity.
PG  - 23
LID - 10.1038/s41525-019-0097-4 [doi]
LID - 23
AB  - Growing evidence suggests that inflammation is a significant contributor to 
      different cardiovascular diseases (CVDs). Mendelian randomization (MR) was 
      performed to assess the causal inference between plasma soluble IL6 receptor 
      (sIL6R), a negative regulator of IL6 signaling, and different cardiovascular and 
      immune-related disorders. Cis-MR with multiple instrumental variables showed an 
      inverse association of sIL6R with rheumatoid arthritis, atrial fibrillation, 
      stroke, coronary artery disease, and abdominal aortic aneurysm. However, 
      genetically-determined sIL6R level was positively associated with atopic 
      dermatitis and asthma. Also, sIL6R level was associated with longevity, as 
      evaluated by parental age at death, a heritable trait. Gene-based association 
      analysis with S-PrediXcan by using tissues from GTExV7 showed that IL6R tissue 
      expression-disease pair associations were consistent with the directional effect 
      of IL6 signaling identified in MR. Genetically-determined reduced IL6 signaling 
      lowers the risk of multiple CVDs and is associated with increased longevity, but 
      at the expense of higher atopic risk.
FAU - Rosa, Mickael
AU  - Rosa M
AD  - 1Laboratory of Cardiovascular Pathobiology, Quebec Heart and Lung 
      Institute/Research Center, Department of Surgery, Laval University, Quebec, 
      Canada. ISNI: 0000 0004 1936 8390. GRID: grid.23856.3a
FAU - Chignon, Arnaud
AU  - Chignon A
AD  - 1Laboratory of Cardiovascular Pathobiology, Quebec Heart and Lung 
      Institute/Research Center, Department of Surgery, Laval University, Quebec, 
      Canada. ISNI: 0000 0004 1936 8390. GRID: grid.23856.3a
FAU - Li, Zhonglin
AU  - Li Z
AD  - 1Laboratory of Cardiovascular Pathobiology, Quebec Heart and Lung 
      Institute/Research Center, Department of Surgery, Laval University, Quebec, 
      Canada. ISNI: 0000 0004 1936 8390. GRID: grid.23856.3a
FAU - Boulanger, Marie-Chloé
AU  - Boulanger MC
AD  - 1Laboratory of Cardiovascular Pathobiology, Quebec Heart and Lung 
      Institute/Research Center, Department of Surgery, Laval University, Quebec, 
      Canada. ISNI: 0000 0004 1936 8390. GRID: grid.23856.3a
FAU - Arsenault, Benoit J
AU  - Arsenault BJ
AD  - 2Department of Medicine, Laval University, Quebec, Canada. ISNI: 0000 0004 1936 
      8390. GRID: grid.23856.3a
FAU - Bossé, Yohan
AU  - Bossé Y
AUID- ORCID: 0000-0002-3067-3711
AD  - 3Department of Molecular Medicine, Laval University, Quebec, Canada. ISNI: 0000 
      0004 1936 8390. GRID: grid.23856.3a
FAU - Thériault, Sébastien
AU  - Thériault S
AD  - 4Department of Molecular Biology, Medical Biochemistry and Pathology, Laval 
      University, Quebec, Canada. ISNI: 0000 0004 1936 8390. GRID: grid.23856.3a
FAU - Mathieu, Patrick
AU  - Mathieu P
AD  - 1Laboratory of Cardiovascular Pathobiology, Quebec Heart and Lung 
      Institute/Research Center, Department of Surgery, Laval University, Quebec, 
      Canada. ISNI: 0000 0004 1936 8390. GRID: grid.23856.3a
LA  - eng
PT  - Journal Article
DEP - 20190920
PL  - England
TA  - NPJ Genom Med
JT  - NPJ genomic medicine
JID - 101685193
PMC - PMC6754413
OTO - NOTNLM
OT  - Cardiovascular diseases
OT  - Genetics research
COIS- Competing interestsP.M. is a consultant for Casebia Therapeutics. The rest of the 
      authors declare no competing interests.
EDAT- 2019/09/26 06:00
MHDA- 2019/09/26 06:01
PMCR- 2019/09/20
CRDT- 2019/09/26 06:00
PHST- 2019/04/17 00:00 [received]
PHST- 2019/08/29 00:00 [accepted]
PHST- 2019/09/26 06:00 [entrez]
PHST- 2019/09/26 06:00 [pubmed]
PHST- 2019/09/26 06:01 [medline]
PHST- 2019/09/20 00:00 [pmc-release]
AID - 97 [pii]
AID - 10.1038/s41525-019-0097-4 [doi]
PST - epublish
SO  - NPJ Genom Med. 2019 Sep 20;4:23. doi: 10.1038/s41525-019-0097-4. eCollection 
      2019.

PMID- 31469238
OWN - NLM
STAT- MEDLINE
DCOM- 20200317
LR  - 20200317
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Linking)
VI  - 72
IP  - 1
DP  - 2020 Jan
TI  - Cardiovascular Safety of Tocilizumab Versus Etanercept in Rheumatoid Arthritis: A 
      Randomized Controlled Trial.
PG  - 31-40
LID - 10.1002/art.41095 [doi]
AB  - OBJECTIVE: To assess the risk of major adverse cardiovascular events (MACE) in 
      patients with rheumatoid arthritis (RA) treated with tocilizumab compared to 
      those treated with the tumor necrosis factor inhibitor etanercept. METHODS: This 
      randomized, open-label, parallel-group trial enrolled patients with active 
      seropositive RA (n = 3,080) who had an inadequate response to conventional 
      synthetic disease-modifying antirheumatic drugs and who had at least 1 
      cardiovascular (CV) risk factor. Patients were randomly assigned 1:1 to receive 
      open-label tocilizumab at 8 mg/kg/month or etanercept at 50 mg/week. All patients 
      were followed up for a mean of 3.2 years. The primary end point was comparison of 
      time to first occurrence of MACE. The trial was powered to exclude a relative 
      hazard ratio for MACE of 1.8 or higher in the tocilizumab group compared to the 
      etanercept group. RESULTS: By week 4 of treatment, the serum low-density 
      lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride 
      levels were a median 11.1%, 5.7%, and 13.6% higher, respectively, in patients 
      receiving tocilizumab compared to those receiving etanercept (each P < 0.001). 
      During follow-up, 83 MACE occurred in the tocilizumab group compared to 78 MACE 
      in the etanercept group. The estimated hazard ratio for occurrence of MACE in the 
      tocilizumab group relative to the etanercept group was 1.05 (95% confidence 
      interval 0.77-1.43). Results were similar in sensitivity analyses and in the 
      on-treatment population analysis. Adverse events occurred more frequently in the 
      tocilizumab group, including serious infection and gastrointestinal perforation. 
      CONCLUSION: The results of this trial, which provide insights into the CV safety 
      of tocilizumab as compared to etanercept, ruled out a risk for occurrence of MACE 
      of 1.43 or higher in patients treated with tocilizumab. This result should be 
      interpreted in the context of the clinical efficacy and non-CV safety of 
      tocilizumab.
CI  - © 2019, American College of Rheumatology.
FAU - Giles, Jon T
AU  - Giles JT
AUID- ORCID: 0000-0002-8792-0402
AD  - Columbia University College of Physicians & Surgeons, New York, New York.
FAU - Sattar, Naveed
AU  - Sattar N
AD  - University of Glasgow, Glasgow, UK.
FAU - Gabriel, Sherine
AU  - Gabriel S
AD  - Rutgers Robert Wood Johnson Medical School, New Brunswick, New Jersey.
FAU - Ridker, Paul M
AU  - Ridker PM
AD  - Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
FAU - Gay, Steffen
AU  - Gay S
AD  - University Hospital Zurich, Zurich, Switzerland.
FAU - Warne, Charles
AU  - Warne C
AD  - Roche Products Ltd., Welwyn Garden City, UK.
FAU - Musselman, David
AU  - Musselman D
AD  - Genentech, Inc., South San Francisco, California.
FAU - Brockwell, Laura
AU  - Brockwell L
AD  - Roche Products Ltd., Welwyn Garden City, UK.
FAU - Shittu, Emma
AU  - Shittu E
AD  - Roche Products Ltd., Welwyn Garden City, UK.
FAU - Klearman, Micki
AU  - Klearman M
AD  - Genentech, Inc., South San Francisco, California.
FAU - Fleming, Thomas R
AU  - Fleming TR
AD  - University of Washington, Seattle.
LA  - eng
SI  - ClinicalTrials.gov/NCT01331837
PT  - Comparative Study
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor Inhibitors)
RN  - I031V2H011 (tocilizumab)
RN  - OP401G7OJC (Etanercept)
SB  - IM
CIN - Arthritis Rheumatol. 2020 Jan;72(1):4-6. doi: 10.1002/art.41092. PMID: 31469243
MH  - Aged
MH  - Antibodies, Monoclonal, Humanized/*therapeutic use
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Cardiovascular Diseases/*mortality
MH  - Etanercept/*therapeutic use
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*epidemiology
MH  - Proportional Hazards Models
MH  - Risk Factors
MH  - Stroke/*epidemiology
MH  - Tumor Necrosis Factor Inhibitors/*therapeutic use
EDAT- 2019/08/31 06:00
MHDA- 2020/03/18 06:00
CRDT- 2019/08/31 06:00
PHST- 2019/02/16 00:00 [received]
PHST- 2019/08/27 00:00 [accepted]
PHST- 2019/08/31 06:00 [pubmed]
PHST- 2020/03/18 06:00 [medline]
PHST- 2019/08/31 06:00 [entrez]
AID - 10.1002/art.41095 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2020 Jan;72(1):31-40. doi: 10.1002/art.41095.

PMID- 31464678
OWN - NLM
STAT- MEDLINE
DCOM- 20191007
LR  - 20191210
IS  - 0392-856X (Print)
IS  - 0392-856X (Linking)
VI  - 37 Suppl 118
IP  - 3
DP  - 2019 May-Jun
TI  - Application of artificial neural network analysis in the evaluation of 
      cardiovascular risk in primary Sjögren's syndrome: a novel pathogenetic scenario?
PG  - 133-139
AB  - OBJECTIVES: The aim of the present study was to verify whether artificial neural 
      networks (ANNs) might help to elucidate the mechanisms underlying the increased 
      prevalence of cardiovascular events (CV) in primary Sjögren's syndrome (pSS). 
      METHODS: 408 pSS patients (395 F: 13 M), with a mean age of 61 (±14) years and 
      mean disease duration of 8.8 (±7.8) years were retrospectively included. CV risk 
      factors and events were analysed and correlated with the other pSS clinical and 
      serological manifestations by using both a traditional statistical approach (i.e. 
      Agglomerative Hierarchical Clustering (AHC)) and Auto-CM, a data mining tool 
      based on ANNs. RESULTS: Five percent of pSS patients experienced one or more CV 
      events, including heart failure (8/408), transient ischaemic attack (6/408), 
      stroke (4/408), angina (4/408), myocardial infarction (3/408) and peripheral 
      obliterative arteriopathy (2/408). The AHC provided a dendrogram with at least 
      three clusters that did not allow us to infer specific differential associations 
      among variables (i.e. CV comorbidity and pSS manifestations). On the other hand, 
      Auto-CM identified two different patterns of distributions in CV risk factors, 
      pSS-related features, and CV events. The first pattern, centered on 
      "non-ischaemic CV events/generic condition of HF", was characterised by the 
      presence of traditional CV risk factors and by a closer link with pSS glandular 
      features rather than to pSS extra-glandular manifestations. The second pattern 
      included "ischaemic neurological, cardiac events and peripheral obliterative 
      arteriopathy" and appeared to be strictly associated with extra-glandular disease 
      activity and longer disease duration. CONCLUSIONS: This study represents the 
      first application of ANNs to the analysis of factors contributing to CV events in 
      pSS. When compared to AHC, ANNs had the advantage of better stratifying CV risk 
      in pSS, opening new avenues for planning specific interventions to prevent 
      long-term CV complications in pSS patients.
FAU - Bartoloni, Elena
AU  - Bartoloni E
AD  - Rheumatology Unit, Department of Medicine, University of Perugia, Italy. 
      elena.bartolonibocci@unipg.it.
FAU - Baldini, Chiara
AU  - Baldini C
AD  - Rheumatology Unit, Department of Clinical and Experimental Medicine, University 
      of Pisa, Italy.
FAU - Ferro, Francesco
AU  - Ferro F
AD  - Rheumatology Unit, Department of Clinical and Experimental Medicine, University 
      of Pisa, Italy.
FAU - Alunno, Alessia
AU  - Alunno A
AD  - Rheumatology Unit, Department of Medicine, University of Perugia, Italy.
FAU - Carubbi, Francesco
AU  - Carubbi F
AD  - Rheumatology Unit, University of L'Aquila, Italy.
FAU - Cafaro, Giacomo
AU  - Cafaro G
AD  - Rheumatology Unit, Department of Medicine, University of Perugia, Italy.
FAU - Bombardieri, Stefano
AU  - Bombardieri S
AD  - Rheumatology Unit, Department of Clinical and Experimental Medicine, University 
      of Pisa, Italy.
FAU - Gerli, Roberto
AU  - Gerli R
AD  - Rheumatology Unit, Department of Medicine, University of Perugia, Italy.
FAU - Grossi, Enzo
AU  - Grossi E
AD  - Villa Santa Maria Foundation, Tavernerio, Italy.
LA  - eng
PT  - Journal Article
DEP - 20190828
PL  - Italy
TA  - Clin Exp Rheumatol
JT  - Clinical and experimental rheumatology
JID - 8308521
SB  - IM
MH  - Aged
MH  - *Cardiovascular Diseases/epidemiology/etiology
MH  - Comorbidity
MH  - Diagnosis, Computer-Assisted/methods
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Neural Networks, Computer
MH  - Retrospective Studies
MH  - Risk Assessment
MH  - Risk Factors
MH  - *Sjogren's Syndrome/complications/epidemiology
EDAT- 2019/08/30 06:00
MHDA- 2019/10/08 06:00
CRDT- 2019/08/30 06:00
PHST- 2019/07/02 00:00 [received]
PHST- 2019/07/22 00:00 [accepted]
PHST- 2019/08/30 06:00 [entrez]
PHST- 2019/08/30 06:00 [pubmed]
PHST- 2019/10/08 06:00 [medline]
AID - 14489 [pii]
PST - ppublish
SO  - Clin Exp Rheumatol. 2019 May-Jun;37 Suppl 118(3):133-139. Epub 2019 Aug 28.

PMID- 31433302
OWN - NLM
STAT- MEDLINE
DCOM- 20210319
LR  - 20210319
IS  - 1600-0641 (Electronic)
IS  - 0168-8278 (Linking)
VI  - 71
IP  - 6
DP  - 2019 Dec
TI  - Sustained virological response from interferon-based hepatitis C regimens is 
      associated with reduced risk of extrahepatic manifestations.
PG  - 1116-1125
LID - S0168-8278(19)30462-3 [pii]
LID - 10.1016/j.jhep.2019.07.021 [doi]
AB  - BACKGROUND & AIMS: HCV infection is associated with several extrahepatic 
      manifestations (EHMs). We evaluated the impact of sustained virological response 
      (SVR) on the risk of 7 EHMs that contribute to the burden of extrahepatic 
      disease: type 2 diabetes mellitus, chronic kidney disease or end-stage renal 
      disease, stroke, ischemic heart disease, major adverse cardiac events, mood and 
      anxiety disorders, and rheumatoid arthritis. METHODS: A longitudinal cohort study 
      was conducted using data from the British Columbia Hepatitis Testers Cohort, 
      which included ~1.3 million individuals screened for HCV. We identified all 
      HCV-infected individuals who were treated with interferon-based therapies between 
      1999 and 2014. SVR was defined as a negative HCV RNA test ≥24 weeks 
      post-treatment or after end-of-treatment, if unavailable. We computed adjusted 
      subdistribution hazard ratios (asHR) for the effect of SVR on each EHM using 
      competing risk proportional hazard models. Subgroup analyses by birth cohort, 
      sex, injection drug exposure and genotype were also performed. RESULTS: Overall, 
      10,264 HCV-infected individuals were treated with interferon, of whom 6,023 (59%) 
      achieved SVR. Compared to those that failed treatment, EHM risk was significantly 
      reduced among patients with SVR for type 2 diabetes mellitus (asHR 0.65; 95%CI 
      0.55-0.77), chronic kidney disease or end-stage renal disease (asHR 0.53; 95% CI 
      0.43-0.65), ischemic or hemorrhagic stroke (asHR 0.73; 95%CI 0.49-1.09), and mood 
      and anxiety disorders (asHR 0.82; 95%CI 0.71-0.95), but not for ischemic heart 
      disease (asHR 1.23; 95%CI 1.03-1.47), major adverse cardiac events (asHR 0.93; 
      95%CI 0.79-1.11) or rheumatoid arthritis (asHR 1.09; 95% CI 0.73-1.64). 
      CONCLUSIONS: SVR was associated with a reduction in the risk of several EHMs. 
      Increased uptake of antiviral therapy may reduce the growing burden of EHMs in 
      this population. LAY SUMMARY: We estimated the rates of chronic comorbidities 
      other than liver disease between those who were cured and those who failed 
      treatment for hepatitis C virus (HCV) infection. Our findings showed that the 
      rates of these non-liver diseases were largely reduced for those who were cured 
      with interferon-based treatments. Early HCV treatments could provide many 
      benefits in the prevention of various HCV complications beyond liver disease.
CI  - Copyright © 2019 European Association for the Study of the Liver. Published by 
      Elsevier B.V. All rights reserved.
FAU - Rossi, Carmine
AU  - Rossi C
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      Department of Pathology and Laboratory Medicine, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Jeong, Dahn
AU  - Jeong D
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      School of Population and Public Health, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Wong, Stanley
AU  - Wong S
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada.
FAU - McKee, Geoffrey
AU  - McKee G
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      School of Population and Public Health, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Butt, Zahid Ahmad
AU  - Butt ZA
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      School of Population and Public Health, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Buxton, Jane
AU  - Buxton J
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      School of Population and Public Health, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Wong, Jason
AU  - Wong J
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      School of Population and Public Health, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Darvishian, Maryam
AU  - Darvishian M
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      School of Population and Public Health, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Bartlett, Sofia
AU  - Bartlett S
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      Department of Pathology and Laboratory Medicine, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Samji, Hasina
AU  - Samji H
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada.
FAU - Yu, Amanda
AU  - Yu A
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada.
FAU - Binka, Mawuena
AU  - Binka M
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      Department of Pathology and Laboratory Medicine, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Alvarez, Maria
AU  - Alvarez M
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada.
FAU - Adu, Prince Asumadu
AU  - Adu PA
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      School of Population and Public Health, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Tyndall, Mark
AU  - Tyndall M
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      School of Population and Public Health, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Krajden, Mel
AU  - Krajden M
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      Department of Pathology and Laboratory Medicine, University of British Columbia, 
      Vancouver, British Columbia, Canada.
FAU - Janjua, Naveed Zafar
AU  - Janjua NZ
AD  - British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada; 
      School of Population and Public Health, University of British Columbia, 
      Vancouver, British Columbia, Canada. Electronic address: naveed.janjua@bccdc.ca.
CN  - BC Hepatitis Testers Cohort Team
LA  - eng
GR  - CIHR/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190806
PL  - Netherlands
TA  - J Hepatol
JT  - Journal of hepatology
JID - 8503886
RN  - 0 (Antiviral Agents)
RN  - 9008-11-1 (Interferons)
SB  - IM
MH  - Antiviral Agents/therapeutic use
MH  - *Anxiety Disorders/epidemiology/prevention & control
MH  - British Columbia/epidemiology
MH  - Cohort Studies
MH  - *Diabetes Mellitus, Type 2/epidemiology/prevention & control
MH  - Female
MH  - Health Status Indicators
MH  - *Hepacivirus/drug effects/isolation & purification
MH  - *Hepatitis C, Chronic/drug therapy/epidemiology/physiopathology/psychology
MH  - Humans
MH  - Incidence
MH  - Interferons/*therapeutic use
MH  - Male
MH  - Middle Aged
MH  - *Mood Disorders/epidemiology/prevention & control
MH  - *Renal Insufficiency, Chronic/epidemiology/prevention & control
MH  - Risk Reduction Behavior
MH  - *Stroke/epidemiology/prevention & control
OTO - NOTNLM
OT  - Antiviral therapy
OT  - Canada
OT  - Comorbidity
OT  - Epidemiology
OT  - Extrahepatic
OT  - Hepatitis C virus
OT  - Sustained virologic response
EDAT- 2019/08/23 06:00
MHDA- 2021/03/20 06:00
CRDT- 2019/08/22 06:00
PHST- 2018/12/14 00:00 [received]
PHST- 2019/06/26 00:00 [revised]
PHST- 2019/07/22 00:00 [accepted]
PHST- 2019/08/23 06:00 [pubmed]
PHST- 2021/03/20 06:00 [medline]
PHST- 2019/08/22 06:00 [entrez]
AID - S0168-8278(19)30462-3 [pii]
AID - 10.1016/j.jhep.2019.07.021 [doi]
PST - ppublish
SO  - J Hepatol. 2019 Dec;71(6):1116-1125. doi: 10.1016/j.jhep.2019.07.021. Epub 2019 
      Aug 6.

PMID- 31414971
OWN - NLM
STAT- MEDLINE
DCOM- 20200608
LR  - 20200615
IS  - 1557-8100 (Electronic)
IS  - 1536-2310 (Linking)
VI  - 23
IP  - 12
DP  - 2019 Dec
TI  - Systematic Review: Immunoglobulin G N-Glycans as Next-Generation Diagnostic 
      Biomarkers for Common Chronic Diseases.
PG  - 607-614
LID - 10.1089/omi.2019.0032 [doi]
AB  - Glycomics is a new subspecialty in omics systems sciences that offers significant 
      promise for next-generation biomarkers on disease susceptibility, drug target 
      discovery, and precision medicine. In this context, alternative immunoglobulin G 
      (IgG) N-glycosylation has been reportedly implicated in several common chronic 
      diseases, although systematic assessment is currently lacking in the literature. 
      We conducted a systematic review of observational studies on IgG N-glycan 
      variability and susceptibility to common chronic diseases. Observational studies 
      reporting an association between diseases (such as colorectal cancer, 
      dyslipidemia, ischemic stroke, rheumatoid arthritis, and systemic lupus 
      erythematosus) and IgG N-glycans quantified by ultraperformance liquid 
      chromatography were included. The glycans were categorized into 24 initial IgG 
      glycan peaks (GPs). Notably, aging positively correlated with GP1, GP2, GP4-7, 
      GP10, GP11, GP19, and GP24, while negatively correlated with GP8, GP12-15, GP17, 
      GP18, GP20, GP21, and GP23 (p < 0.05). The absolute value of significant 
      correlation coefficients of age and IgG glycans ranged from 0.043 to 0.645. We 
      found that the high levels of GP1-4, GP6, GP7, and GP24 and low levels of GP9, 
      GP13-15, GP18, and GP23 could potentially increase the risk of disease. In 
      conclusion, the present systematic review suggests that the field of glycomics, 
      and GP1-4, GP6, GP7, GP9, GP13-15, GP18, GP23, and GP24 in particular, holds 
      promise for further candidate biomarker research on susceptibility to common 
      chronic diseases.
FAU - Liu, Di
AU  - Liu D
AD  - Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital 
      Medical University, Beijing, China.
FAU - Li, Qihuan
AU  - Li Q
AD  - Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital 
      Medical University, Beijing, China.
FAU - Zhang, Xiaoyu
AU  - Zhang X
AD  - Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital 
      Medical University, Beijing, China.
FAU - Wang, Hao
AU  - Wang H
AD  - Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital 
      Medical University, Beijing, China.
AD  - School of Medical and Health Sciences, Edith Cowan University, Perth, Australia.
FAU - Cao, Weijie
AU  - Cao W
AD  - Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital 
      Medical University, Beijing, China.
FAU - Li, Dong
AU  - Li D
AD  - School of Public Health, Shandong First Medical University & Shandong Academy of 
      Medical Sciences, Taian, China.
FAU - Xing, Weijia
AU  - Xing W
AD  - School of Public Health, Shandong First Medical University & Shandong Academy of 
      Medical Sciences, Taian, China.
FAU - Song, Manshu
AU  - Song M
AD  - Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital 
      Medical University, Beijing, China.
FAU - Wang, Wei
AU  - Wang W
AD  - Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital 
      Medical University, Beijing, China.
AD  - School of Medical and Health Sciences, Edith Cowan University, Perth, Australia.
AD  - School of Public Health, Shandong First Medical University & Shandong Academy of 
      Medical Sciences, Taian, China.
FAU - Meng, Qun
AU  - Meng Q
AD  - Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital 
      Medical University, Beijing, China.
FAU - Wang, Youxin
AU  - Wang Y
AD  - Beijing Key Laboratory of Clinical Epidemiology, School of Public Health, Capital 
      Medical University, Beijing, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Systematic Review
DEP - 20190816
PL  - United States
TA  - OMICS
JT  - Omics : a journal of integrative biology
JID - 101131135
RN  - 0 (Biomarkers)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Polysaccharides)
RN  - 0 (glycosylated IgG)
SB  - IM
MH  - Animals
MH  - Biomarkers/metabolism
MH  - Chronic Disease
MH  - Glycomics/*methods
MH  - Glycosylation
MH  - Humans
MH  - Immunoglobulin G/*metabolism
MH  - Observational Studies as Topic
MH  - Polysaccharides/metabolism
OTO - NOTNLM
OT  - chronic disease biomarkers
OT  - diagnostic innovation
OT  - glycomics
OT  - immunoglobulin G N-glycans
OT  - next-generation biomarkers
OT  - systematic review
EDAT- 2019/08/16 06:00
MHDA- 2020/06/09 06:00
CRDT- 2019/08/16 06:00
PHST- 2019/08/16 06:00 [pubmed]
PHST- 2020/06/09 06:00 [medline]
PHST- 2019/08/16 06:00 [entrez]
AID - 10.1089/omi.2019.0032 [doi]
PST - ppublish
SO  - OMICS. 2019 Dec;23(12):607-614. doi: 10.1089/omi.2019.0032. Epub 2019 Aug 16.

PMID- 31385441
OWN - NLM
STAT- MEDLINE
DCOM- 20200205
LR  - 20200205
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Print)
IS  - 2326-5191 (Linking)
VI  - 71
IP  - 9
DP  - 2019 Sep
TI  - Risk Factors for Major Adverse Cardiovascular Events in Phase III and Long-Term 
      Extension Studies of Tofacitinib in Patients With Rheumatoid Arthritis.
PG  - 1450-1459
LID - 10.1002/art.40911 [doi]
AB  - OBJECTIVE: Tofacitinib is an oral JAK inhibitor for the treatment of rheumatoid 
      arthritis (RA). This study was undertaken to evaluate the risk of major adverse 
      cardiovascular events (MACE) in patients with RA receiving tofacitinib. METHODS: 
      Data were pooled from patients with moderately to severely active RA receiving ≥1 
      tofacitinib dose in 6 phase III and 2 long-term extension studies over 7 years. 
      MACE (myocardial infarction, stroke, cardiovascular death) were independently 
      adjudicated. Cox regression models were used to evaluate associations between 
      baseline variables and time to first MACE. Following 24 weeks of tofacitinib, 
      changes in variables and time to future MACE were evaluated after adjusment for 
      age, baseline values, and time-varying tofacitinib dose. Hazard ratios and 95% 
      confidence intervals were calculated. RESULTS: Fifty-two MACE occurred in 
      4,076 patients over 12,873 patient-years of exposure (incidence rate 0.4 patients 
      with events per 100 patient-years). In univariable analyses of baseline 
      variables, traditional cardiovascular risk factors and glucocorticoid and statin 
      use were associated with MACE risk; disease activity and inflammation measures 
      were not. In subsequent multivariable analyses, baseline age, hypertension, and 
      the total cholesterol to high-density lipoprotein (HDL) cholesterol ratio 
      remained significantly associated with risk of MACE. After 24 weeks of treatment, 
      an increase in HDL cholesterol and a decrease in the total to HDL cholesterol 
      were associated with decreased MACE risk; changes in total cholesterol, 
      low-density lipoprotein (LDL) cholesterol, and disease activity measures were 
      not. Increased erythrocyte sedimentation rates trended with increased future MACE 
      risk. CONCLUSION: In this post hoc analysis, after 24 weeks of tofacitinib 
      treatment, increased HDL cholesterol, but not increased LDL cholesterol or total 
      cholesterol, appeared to be associated with lower future MACE risk. Further data 
      are needed to test the cardiovascular safety of tofacitinib.
CI  - © 2019, Pfizer Inc. Arthritis & Rheumatology published by Wiley Periodicals, Inc. 
      on behalf of American College of Rheumatology.
FAU - Charles-Schoeman, Christina
AU  - Charles-Schoeman C
AD  - University of California, Los Angeles.
FAU - DeMasi, Ryan
AU  - DeMasi R
AD  - Pfizer Inc, Collegeville, Pennsylvania.
FAU - Valdez, Hernan
AU  - Valdez H
AD  - Pfizer Inc, New York, New York.
FAU - Soma, Koshika
AU  - Soma K
AD  - Pfizer Inc, Groton, Connecticut.
FAU - Hwang, Lie-Ju
AU  - Hwang LJ
AD  - Pfizer Inc, New York, New York.
FAU - Boy, Mary G
AU  - Boy MG
AD  - Pfizer Inc, Groton, Connecticut.
FAU - Biswas, Pinaki
AU  - Biswas P
AD  - Pfizer Inc, New York, New York.
FAU - McInnes, Iain B
AU  - McInnes IB
AD  - University of Glasgow, Glasgow, UK.
LA  - eng
GR  - Pfizer Inc/International
GR  - R01 HL123064/HL/NHLBI NIH HHS/United States
PT  - Evaluation Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20190806
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Cholesterol, HDL)
RN  - 0 (Cholesterol, LDL)
RN  - 0 (Piperidines)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Pyrimidines)
RN  - 0 (Pyrroles)
RN  - 87LA6FU830 (tofacitinib)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/blood/*complications/*drug therapy
MH  - Blood Sedimentation
MH  - Cardiovascular Diseases/epidemiology/*etiology
MH  - Cholesterol/blood
MH  - Cholesterol, HDL/blood
MH  - Cholesterol, LDL/blood
MH  - Clinical Trials, Phase III as Topic
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology/etiology
MH  - Piperidines/*therapeutic use
MH  - Proportional Hazards Models
MH  - Protein Kinase Inhibitors/*therapeutic use
MH  - Pyrimidines/*therapeutic use
MH  - Pyrroles/*therapeutic use
MH  - Risk Factors
MH  - Stroke/epidemiology/etiology
MH  - Treatment Outcome
PMC - PMC6754249
MID - NIHMS1044055
EDAT- 2019/08/07 06:00
MHDA- 2020/02/06 06:00
PMCR- 2019/10/01
CRDT- 2019/08/07 06:00
PHST- 2018/03/15 00:00 [received]
PHST- 2019/04/11 00:00 [accepted]
PHST- 2019/08/07 06:00 [pubmed]
PHST- 2020/02/06 06:00 [medline]
PHST- 2019/08/07 06:00 [entrez]
PHST- 2019/10/01 00:00 [pmc-release]
AID - ART40911 [pii]
AID - 10.1002/art.40911 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2019 Sep;71(9):1450-1459. doi: 10.1002/art.40911. Epub 2019 
      Aug 6.

PMID- 31369575
OWN - NLM
STAT- MEDLINE
DCOM- 20200304
LR  - 20231013
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 14
IP  - 8
DP  - 2019
TI  - Cardiovascular safety of tocilizumab: A systematic review and network 
      meta-analysis.
PG  - e0220178
LID - 10.1371/journal.pone.0220178 [doi]
LID - e0220178
AB  - OBJECTIVES: Our objective was to compare the cardiovascular safety of tocilizumab 
      and other biological disease-modifying antirheumatic drugs (bDMARD) in rheumatoid 
      arthritis using a network meta-analysis (NMA). METHODS: A systematic literature 
      search through May 2018 identified randomized controlled trials (RCT) or 
      observational studies (cohort only) reporting cardiovascular outcomes of 
      tocilizumab (TCZ) and/or abatacept (ABA) and/or rituximab (RTX) and/or tumor 
      necrosis factor inhibitors (TNFi) in rheumatoid arthritis patients. The composite 
      primary outcome was the rate of major adverse cardiovascular outcomes (MACE, 
      myocardial infarction (MI), peripheral artery disease (PAD) and cardiac heart 
      failure (CHF)). RESULTS: 19 studies were included in the NMA, including 11 RCTs 
      and 8 cohort studies. We found less events with RTX (5.41 [1.70;17.26]. We found 
      no difference between TCZ and other treatments. Concerning MI, we found no 
      difference between TCZ and csDMARD (4.23 [0.22;80.64]), no difference between TCZ 
      and TNFi (2.00 [0.18;21.84]). There was no difference between TCZ and csDMARD 
      (1.51[0.02;103.50] and between TCZ and TNFi (1.00 [0.06;15.85]) for stroke event. 
      With cohorts and RCT NMA, we found no difference between TCZ and other treatments 
      for MACE (0.66 [0.42;1.03] with ABA, 1.04 [0.60;1.81] with RTX, 0.78[0.53;1.16] 
      and 0.91 [0.54;1.51] with csDMARD), but the risk of myocardial infarction was 
      lower with TCZ compared to ABA (0.67 [0.47;0.97]). We lacked data to compare TCZ 
      and other bDMARD for stoke and MI. Not enough data was available to perform a NMA 
      for CHF and PAD. CONCLUSIONS: Despite an increase in cholesterol levels, TCZ has 
      safe cardiovascular outcomes compared to other bDMARD.
FAU - Castagné, Benjamin
AU  - Castagné B
AUID- ORCID: 0000-0002-4588-8651
AD  - Rheumatology Department, Gabriel-Montpied University Hospital, Clermont-Ferrand, 
      France.
AD  - HESPER EA 7425, University of Lyon, Claude Bernard University Lyon 1, Lyon, 
      France.
FAU - Viprey, Marie
AU  - Viprey M
AD  - HESPER EA 7425, University of Lyon, Claude Bernard University Lyon 1, Lyon, 
      France.
AD  - Public Health Centre, Hospices Civils de Lyon, Lyon, France.
FAU - Martin, Julie
AU  - Martin J
AD  - HESPER EA 7425, University of Lyon, Claude Bernard University Lyon 1, Lyon, 
      France.
AD  - Public Health Centre, Hospices Civils de Lyon, Lyon, France.
FAU - Schott, Anne-Marie
AU  - Schott AM
AD  - HESPER EA 7425, University of Lyon, Claude Bernard University Lyon 1, Lyon, 
      France.
AD  - Public Health Centre, Hospices Civils de Lyon, Lyon, France.
FAU - Cucherat, Michel
AU  - Cucherat M
AD  - University Lyon, UMR 5558, Laboratory of Biometry and Evolutionary Biology, CNRS, 
      Villeurbanne, France.
AD  - Department of Pharmacology and Toxicology, Hospices Civils de Lyon, Lyon, France.
FAU - Soubrier, Martin
AU  - Soubrier M
AD  - Rheumatology Department, Gabriel-Montpied University Hospital, Clermont-Ferrand, 
      France.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Systematic Review
DEP - 20190801
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Antirheumatic Agents)
RN  - I031V2H011 (tocilizumab)
SB  - IM
MH  - Antibodies, Monoclonal, Humanized/*therapeutic use
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Cardiovascular Diseases/*prevention & control
MH  - Humans
MH  - Network Meta-Analysis
MH  - Patient Safety
MH  - Prognosis
PMC - PMC6675055
COIS- The authors have declared that no competing interests exist.
EDAT- 2019/08/02 06:00
MHDA- 2020/03/05 06:00
PMCR- 2019/08/01
CRDT- 2019/08/02 06:00
PHST- 2018/12/19 00:00 [received]
PHST- 2019/07/10 00:00 [accepted]
PHST- 2019/08/02 06:00 [entrez]
PHST- 2019/08/02 06:00 [pubmed]
PHST- 2020/03/05 06:00 [medline]
PHST- 2019/08/01 00:00 [pmc-release]
AID - PONE-D-18-34263 [pii]
AID - 10.1371/journal.pone.0220178 [doi]
PST - epublish
SO  - PLoS One. 2019 Aug 1;14(8):e0220178. doi: 10.1371/journal.pone.0220178. 
      eCollection 2019.

PMID- 31331548
OWN - NLM
STAT- MEDLINE
DCOM- 20200109
LR  - 20200109
IS  - 1873-6963 (Electronic)
IS  - 0965-2299 (Linking)
VI  - 45
DP  - 2019 Aug
TI  - Use of Chinese herbal medicines by rheumatoid arthritis patients was associated 
      with lower risk of stroke: A retrospective cohort study.
PG  - 124-129
LID - S0965-2299(19)30233-X [pii]
LID - 10.1016/j.ctim.2019.05.029 [doi]
AB  - BACKGROUND AND PURPOSE: Rheumatoid arthritis (RA) patients have increased risk of 
      developing stroke. The use Chinese herbal medicines (CHMs) is increasing, but 
      whether they can reduce the risk of developing stroke remains unclear. We 
      conducted a longitudinal cohort study to compare the effect of CHMs use on the 
      subsequent stroke risk in RA individuals. MATERIALS AND METHODS: Using claims 
      data from the National Health Insurance of Taiwan, we identified 7925 
      newly-diagnosed RA patients with no history of previous stroke who were 20 years 
      of age or older between 1998 and 2010. From this sample, we enrolled 3134 CHMs 
      users and 3134 non-CHMs users, randomly selected using propensity scores matching 
      from the remaining cases. They were followed until the end of 2012 to record 
      stroke incidence. A Cox proportional hazards regression model was used to compute 
      the hazard ratio of stroke with regard to CHMs use. RESULTS: During the 
      follow-up, 299 CHMs users and 395 non-CHMs users developed stroke, representing 
      incidence rates of 10.94 and 16.69, respectively, per 1000 person-years. CHMs use 
      was associated with 38% (adjusted HR: 0.62; 95% confidence interval: 0.54-0.73) 
      lower subsequent risk of stroke. The most prominent effect was observed in those 
      receiving CHMs for over two years. The following seven commonly-prescribed CHMs 
      were found to lessen the stroke risk: Dan-Shen, Tian-Hua-Feng, Fu-Zi, 
      Shao-Yao-Gan-Cao-Tang, Jia-Wei-Xiao-Yao-San, Ge-Gen-Tang, and 
      Gui-Zhi-Shao-Yao-Zhi-Mu-Tang. CONCLUSION: The CHMs use was associated with lower 
      risk of stroke for RA patients, suggesting that it could be integrated into 
      conventional therapy to prevent subsequent stroke incident.
CI  - Copyright © 2019 Elsevier Ltd. All rights reserved.
FAU - Lai, Ning-Sheng
AU  - Lai NS
AD  - Division of Allergy, Immunology and Rheumatology, Dalin Tzuchi Hospital, The 
      Buddhist Tzuchi Medical Foundation, 2 Minsheng Road, Dalin Township, Chiayi 
      62247, Taiwan; School of Medicine, Tzu Chi University, 701 Jhongyang Road Section 
      3, Hualien 97004, Taiwan.
FAU - Livneh, Hanoch
AU  - Livneh H
AD  - Rehabilitation Counseling Program, Portland State University, Portland, OR 
      97207-0751, USA.
FAU - Fan, Yu-Hsuan
AU  - Fan YH
AD  - Department of Rehabilitation, Dalin Tzuchi Hospital, The Buddhist Tzuchi Medical 
      Foundation, 2 Minsheng Road, Dalin Township, Chiayi 62247, Taiwan.
FAU - Lu, Ming-Chi
AU  - Lu MC
AD  - Division of Allergy, Immunology and Rheumatology, Dalin Tzuchi Hospital, The 
      Buddhist Tzuchi Medical Foundation, 2 Minsheng Road, Dalin Township, Chiayi 
      62247, Taiwan; School of Medicine, Tzu Chi University, 701 Jhongyang Road Section 
      3, Hualien 97004, Taiwan.
FAU - Liao, Hou-Hsun
AU  - Liao HH
AD  - Department of Chinese Medicine, Dalin Tzuchi Hospital, The Buddhist Tzuchi 
      Medical Foundation, 2 Minsheng Road, Dalin Township, Chiayi 62247, Taiwan; 
      Graduate Institute of Chinese Medicine, School of Chinese Medicine, College of 
      Chinese Medicine, China Medical University, Taichung, Taiwan. Electronic address: 
      a202098@cmu.edu.tw.
FAU - Tsai, Tzung-Yi
AU  - Tsai TY
AD  - Department of Environmental and Occupational Health, College of Medicine, 
      National Cheng Kung University, 138 Sheng-Li Road, Tainan 70428, Taiwan; 
      Department of Medical Research, Dalin Tzuchi Hospital, The Buddhist Tzuchi 
      Medical Foundation, 2 Minsheng Road, Dalin Township, Chiayi 62247, Taiwan; 
      Department of Nursing, Tzu Chi University of Science and Technology, 880 
      Chien-Kuo Road Section 2, Hualien 62247, Taiwan. Electronic address: 
      dm732024@tzuchi.com.tw.
LA  - eng
PT  - Journal Article
DEP - 20190601
PL  - Scotland
TA  - Complement Ther Med
JT  - Complementary therapies in medicine
JID - 9308777
RN  - 0 (Drugs, Chinese Herbal)
SB  - IM
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Drugs, Chinese Herbal/*therapeutic use
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Longitudinal Studies
MH  - Male
MH  - Medicine, Chinese Traditional/methods
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Risk
MH  - Stroke/*prevention & control
MH  - Taiwan
OTO - NOTNLM
OT  - Chinese herbal medicines
OT  - Rheumatoid arthritis
OT  - Risk
OT  - Stroke
EDAT- 2019/07/25 06:00
MHDA- 2020/01/10 06:00
CRDT- 2019/07/24 06:00
PHST- 2019/02/18 00:00 [received]
PHST- 2019/04/12 00:00 [revised]
PHST- 2019/05/31 00:00 [accepted]
PHST- 2019/07/24 06:00 [entrez]
PHST- 2019/07/25 06:00 [pubmed]
PHST- 2020/01/10 06:00 [medline]
AID - S0965-2299(19)30233-X [pii]
AID - 10.1016/j.ctim.2019.05.029 [doi]
PST - ppublish
SO  - Complement Ther Med. 2019 Aug;45:124-129. doi: 10.1016/j.ctim.2019.05.029. Epub 
      2019 Jun 1.

PMID- 31327319
OWN - NLM
STAT- MEDLINE
DCOM- 20200114
LR  - 20200309
IS  - 1741-7015 (Electronic)
IS  - 1741-7015 (Linking)
VI  - 17
IP  - 1
DP  - 2019 Jul 22
TI  - Low serum IGF1 is associated with hypertension and predicts early cardiovascular 
      events in women with rheumatoid arthritis.
PG  - 141
LID - 10.1186/s12916-019-1374-x [doi]
LID - 141
AB  - OBJECTIVES: Since low insulin-like growth factor (IGF) 1 is often linked to 
      inflammation, we analyze whether serum levels of IGF1 are associated with 
      cardiovascular disease (CVD) in rheumatoid arthritis (RA) in a longitudinal 
      observational study. METHODS: A CVD risk was estimated (eCVR) in 184 female RA 
      patients (mean age 52 years) and in 132 female patients after ischemic stroke 
      (mean age 56 years) with no rheumatic disease, using the Framingham algorithm. 
      The median level of IGF1 divided the cohorts in IGF1(high) and IGF1(low) groups. 
      A 5-year prospective follow-up for new CVD events was completed in all RA 
      patients. The Mantel-Cox analysis and event-free survival curves were prepared. 
      Unsupervised clustering of proteins within the IGF1 signaling pathway was 
      employed to identify their association with eCVR. RESULTS: Low IGF1 resulted in a 
      higher eCVR in RA patients (7.2% and 3.3%, p = 0.0063) and in stroke (9.3% and 
      7.1%, p = 0.033). RA had higher rate for new CVD events at prospective follow-up 
      (OR 4.96, p = 0.028). Hypertension was the major risk factor associated with low 
      IGF1 in RA and stroke. In hypertension, IGF1 was no longer responsible for 
      intracellular activation and lost its correlation to IRS1/2 adaptor proteins. The 
      clustering analysis confirmed that combination of low IGF1 and IRS1/2 with high 
      IL6, insulin, and glucose predisposed to high eCVR and emphasized the functional 
      role of serum IGF1. CONCLUSIONS: Low serum IGF1 precedes and predicts development 
      of early CVD events in female RA patients. Hypertension and aberrant IGF1 
      receptor signaling are highlighted as the important contributors to IGF1-related 
      CVD events.
FAU - Erlandsson, Malin C
AU  - Erlandsson MC
AUID- ORCID: 0000-0003-1100-7577
AD  - Department of Rheumatology and Inflammation Research, Institute of Medicine, the 
      Sahlgrenska Academy at University of Gothenburg, Guldhedsgatan 10A, SE-41345, 
      Gothenburg, Sweden. malin.erlandsson@rheuma.gu.se.
AD  - Rheumatology Clinic, the Sahlgrenska University Hospital, Gothenburg, Region of 
      West Götaland, Sweden. malin.erlandsson@rheuma.gu.se.
FAU - Lyngfelt, Lovisa
AU  - Lyngfelt L
AUID- ORCID: 0000-0003-4251-431X
AD  - Department of Rheumatology and Inflammation Research, Institute of Medicine, the 
      Sahlgrenska Academy at University of Gothenburg, Guldhedsgatan 10A, SE-41345, 
      Gothenburg, Sweden.
FAU - Åberg, N David
AU  - Åberg ND
AUID- ORCID: 0000-0002-1474-5666
AD  - Department of Internal Medicine, Institute of Medicine, the Sahlgrenska Academy 
      at University of Gothenburg, Gothenburg, Sweden.
FAU - Wasén, Caroline
AU  - Wasén C
AUID- ORCID: 0000-0002-8585-8190
AD  - Department of Rheumatology and Inflammation Research, Institute of Medicine, the 
      Sahlgrenska Academy at University of Gothenburg, Guldhedsgatan 10A, SE-41345, 
      Gothenburg, Sweden.
FAU - Espino, Rachelle A
AU  - Espino RA
AUID- ORCID: 0000-0002-5880-7769
AD  - Department of Rheumatology and Inflammation Research, Institute of Medicine, the 
      Sahlgrenska Academy at University of Gothenburg, Guldhedsgatan 10A, SE-41345, 
      Gothenburg, Sweden.
AD  - Keele University, Keele, UK.
FAU - Silfverswärd, Sofia Töyrä
AU  - Silfverswärd ST
AUID- ORCID: 0000-0002-6641-2759
AD  - Department of Rheumatology and Inflammation Research, Institute of Medicine, the 
      Sahlgrenska Academy at University of Gothenburg, Guldhedsgatan 10A, SE-41345, 
      Gothenburg, Sweden.
FAU - Nadali, Mitra
AU  - Nadali M
AUID- ORCID: 0000-0003-0436-8155
AD  - Department of Rheumatology and Inflammation Research, Institute of Medicine, the 
      Sahlgrenska Academy at University of Gothenburg, Guldhedsgatan 10A, SE-41345, 
      Gothenburg, Sweden.
AD  - Rheumatology Clinic, the Sahlgrenska University Hospital, Gothenburg, Region of 
      West Götaland, Sweden.
FAU - Jood, Katharina
AU  - Jood K
AUID- ORCID: 0000-0001-8746-1771
AD  - Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, 
      the Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
AD  - Department of Neurology, the Sahlgrenska University Hospital, Gothenburg, Sweden.
FAU - Andersson, Karin M E
AU  - Andersson KME
AUID- ORCID: 0000-0002-9475-3040
AD  - Department of Rheumatology and Inflammation Research, Institute of Medicine, the 
      Sahlgrenska Academy at University of Gothenburg, Guldhedsgatan 10A, SE-41345, 
      Gothenburg, Sweden.
FAU - Pullerits, Rille
AU  - Pullerits R
AUID- ORCID: 0000-0002-5383-9817
AD  - Department of Rheumatology and Inflammation Research, Institute of Medicine, the 
      Sahlgrenska Academy at University of Gothenburg, Guldhedsgatan 10A, SE-41345, 
      Gothenburg, Sweden.
AD  - Rheumatology Clinic, the Sahlgrenska University Hospital, Gothenburg, Region of 
      West Götaland, Sweden.
AD  - Department of Clinical Immunology and Transfusion Medicine, the Sahlgrenska 
      University Hospital, Gothenburg, Sweden.
FAU - Bokarewa, Maria I
AU  - Bokarewa MI
AUID- ORCID: 0000-0001-9424-5145
AD  - Department of Rheumatology and Inflammation Research, Institute of Medicine, the 
      Sahlgrenska Academy at University of Gothenburg, Guldhedsgatan 10A, SE-41345, 
      Gothenburg, Sweden. maria.bokarewa@rheuma.gu.se.
AD  - Rheumatology Clinic, the Sahlgrenska University Hospital, Gothenburg, Region of 
      West Götaland, Sweden. maria.bokarewa@rheuma.gu.se.
LA  - eng
PT  - Journal Article
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20190722
PL  - England
TA  - BMC Med
JT  - BMC medicine
JID - 101190723
RN  - 0 (IGF1 protein, human)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*blood/*complications/diagnosis
MH  - Cardiovascular Diseases/blood/complications/*diagnosis
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Hypertension/*blood/*complications/diagnosis
MH  - Insulin-Like Growth Factor I/analysis/*metabolism
MH  - Longitudinal Studies
MH  - Middle Aged
MH  - Predictive Value of Tests
MH  - Prognosis
MH  - Risk Factors
MH  - Stroke/blood/complications/diagnosis
PMC - PMC6643304
OTO - NOTNLM
OT  - Hypertension
OT  - IGF1
OT  - Inflammation
OT  - Ischemic stroke
OT  - Rheumatoid arthritis
COIS- The authors declare that they have no competing interests.
EDAT- 2019/07/23 06:00
MHDA- 2020/01/15 06:00
PMCR- 2019/07/22
CRDT- 2019/07/23 06:00
PHST- 2019/04/17 00:00 [received]
PHST- 2019/06/25 00:00 [accepted]
PHST- 2019/07/23 06:00 [entrez]
PHST- 2019/07/23 06:00 [pubmed]
PHST- 2020/01/15 06:00 [medline]
PHST- 2019/07/22 00:00 [pmc-release]
AID - 10.1186/s12916-019-1374-x [pii]
AID - 1374 [pii]
AID - 10.1186/s12916-019-1374-x [doi]
PST - epublish
SO  - BMC Med. 2019 Jul 22;17(1):141. doi: 10.1186/s12916-019-1374-x.

PMID- 31323333
OWN - NLM
STAT- MEDLINE
DCOM- 20200623
LR  - 20200623
IS  - 1778-7254 (Electronic)
IS  - 1297-319X (Linking)
VI  - 86
IP  - 6
DP  - 2019 Nov
TI  - Cardiovascular profile in osteoarthritis: a meta-analysis of cardiovascular 
      events and risk factors.
PG  - 679-684
LID - S1297-319X(19)30105-8 [pii]
LID - 10.1016/j.jbspin.2019.06.013 [doi]
AB  - INTRODUCTION: Higher cardiovascular risk found in rheumatoid arthritis or 
      psoriatic arthritis is largely due to systemic inflammation. In osteoarthritis 
      (OA), occurrence of systemic inflammation has already been sometimes reported, 
      but the possible association between OA and increased cardiovascular risk remains 
      unclear. In this meta-analysis, we aimed to assess the incidences of myocardial 
      infarction (MI) and stroke, and the cardiovascular risk factors in OA patients. 
      METHODS: We searched PubMed, EMBase, and the Cochrane Library to find references 
      of interest up to June 2018. MI and stroke incidence were calculated using 
      meta-proportion analysis. Differences in cardiovascular risk factors between OA 
      patients and controls were expressed as standardized mean differences using the 
      inverse of variance method. RESULTS: The reviewed studies reported 227 MIs in 
      3550 OA patients (incidence, 7.5%; 95% CI: 3.0-13.8%) and 616 MIs among 12,444 
      control subjects (incidence, 6.0%; 95% CI: 2.8-10.3%). Meta-analysis of the three 
      longitudinal studies revealed a significantly increased MI risk among OA patients 
      (RR=1.22; 95% CI: 1.02-1.45). We also found a significantly increased stroke risk 
      in OA patients (RR=1.43; 95% CI: 1.38-1.48). Concerning cardiovascular risk 
      factors, OA patients exhibited a pro-atherogenic lipid and glycemic profile 
      including high levels of fasting glucose, total cholesterol, and LDL cholesterol 
      and a high body mass index. Concerning atherosclerosis markers, OA patients 
      exhibited a higher risk of metabolic syndrome, and increased pulse wave velocity. 
      CONCLUSION: Our meta-analysis results revealed higher cardiovascular risk in OA 
      patients. This highlights the importance of cardiovascular risk factor management 
      in OA.
CI  - Copyright © 2019 Société française de rhumatologie. Published by Elsevier Masson 
      SAS. All rights reserved.
FAU - Mathieu, Sylvain
AU  - Mathieu S
AD  - Rheumatology department, Gabriel Montpied Teaching Hospital, CHU Gabriel 
      Montpied, 58, rue Montalembert, 63000 Clermont-Ferrand, France. Electronic 
      address: smathieu@chu-clermontferrand.fr.
FAU - Couderc, Marion
AU  - Couderc M
AD  - Rheumatology department, Gabriel Montpied Teaching Hospital, CHU Gabriel 
      Montpied, 58, rue Montalembert, 63000 Clermont-Ferrand, France.
FAU - Tournadre, Anne
AU  - Tournadre A
AD  - Rheumatology department, Gabriel Montpied Teaching Hospital, CHU Gabriel 
      Montpied, 58, rue Montalembert, 63000 Clermont-Ferrand, France.
FAU - Soubrier, Martin
AU  - Soubrier M
AD  - Rheumatology department, Gabriel Montpied Teaching Hospital, CHU Gabriel 
      Montpied, 58, rue Montalembert, 63000 Clermont-Ferrand, France.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
DEP - 20190716
PL  - France
TA  - Joint Bone Spine
JT  - Joint bone spine
JID - 100938016
SB  - IM
MH  - Cardiovascular Diseases/*diagnosis/*epidemiology
MH  - Case-Control Studies
MH  - Comorbidity
MH  - Female
MH  - France
MH  - Humans
MH  - Longitudinal Studies
MH  - Male
MH  - Myocardial Infarction/diagnosis/epidemiology
MH  - Osteoarthritis/*diagnosis/*epidemiology
MH  - Prevalence
MH  - Prognosis
MH  - Risk Assessment
MH  - Stroke/diagnosis/epidemiology
MH  - Survival Analysis
OTO - NOTNLM
OT  - Cardiovascular
OT  - Meta-analysis
OT  - Osteoarthritis
EDAT- 2019/07/20 06:00
MHDA- 2020/06/24 06:00
CRDT- 2019/07/20 06:00
PHST- 2019/02/07 00:00 [received]
PHST- 2019/06/24 00:00 [accepted]
PHST- 2019/07/20 06:00 [pubmed]
PHST- 2020/06/24 06:00 [medline]
PHST- 2019/07/20 06:00 [entrez]
AID - S1297-319X(19)30105-8 [pii]
AID - 10.1016/j.jbspin.2019.06.013 [doi]
PST - ppublish
SO  - Joint Bone Spine. 2019 Nov;86(6):679-684. doi: 10.1016/j.jbspin.2019.06.013. Epub 
      2019 Jul 16.

PMID- 31308681
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220409
IS  - 1176-6336 (Print)
IS  - 1178-203X (Electronic)
IS  - 1176-6336 (Linking)
VI  - 15
DP  - 2019
TI  - Urinary orosomucoid: a new marker of cardiovascular risk in psoriatic patients?
PG  - 831-837
LID - 10.2147/TCRM.S197633 [doi]
AB  - PURPOSE: Psoriasis is one of the most common lifelong lasting dermatologic 
      diseases. According to the latest studies, psoriatic patients have a higher risk 
      of developing cardiovascular diseases. Psoriasis is considered as a systemic 
      inflammatory disease. Several oxidative stress markers have been shown to be 
      elevated in psoriasis. However, a panel of biomarkers has not been used yet. This 
      study was aimed at exploring the connection between a panel of biomarkers 
      (C-reactive protein, asymmetric dimethylarginine, uric acid, total antioxidant 
      capacity, malondialdehyde, and orosomucoid [ORM]) and cardiovascular risk in 
      psoriatic patients. PATIENTS AND METHODS: The inclusion criterion was the onset 
      of psoriasis with skin lesions. Exclusion criteria were impaired renal function 
      (eGFR<60 mL/min/1.73 m(2)), acute inflammations (urinary, respiratory, skin 
      inflammation, etc), autoimmune disorders (rheumatoid arthritis, systemic lupus 
      erythematosus, or inflammatory bowel disease), and any kind of biological 
      antipsoriatic treatment. Patients with a medical history of myocardial 
      infarction, coronary heart disease, stroke, transient ischemic attack, and 
      carotid artery stenosis were also excluded. Biomarkers were measured by routine 
      procedures, ELISA and HPLC. QRISK®2-2017 was used to assess 10-year risk of 
      cardiovascular disease development. Psoriasis severity was measured by the 
      Psoriasis Area and Severity Index. RESULTS: One hundred and fourteen psoriatic 
      patients were enrolled. Only urinary orosomucoid and urinary orosomucoid/urinary 
      creatinine (u-ORM/u-CREAT) ratio showed significant correlation with QRISK score 
      (u-ORM, r=0.245; u-ORM/u-CREAT, r=0.309). When comparing mild psoriatic patients 
      to moderate psoriatic patients, significant differences could only be found in 
      u-ORM and u-ORM/u-CREAT ratio. CONCLUSION: There seems to be a connection between 
      urinary ORM and cardiovascular risk. U-ORM and u-ORM/u-CREAT ratio could be used 
      as an indicator of low-grade inflammation in mild and moderate psoriasis. 
      However, it is the 10-year follow-up of cardiovascular events that will determine 
      the usefulness of this biomarker panel.
FAU - Németh, Balázs
AU  - Németh B
AD  - Dermatology Unit, Zsigmondy Vilmos SPA Hospital, Harkány, Hungary.
AD  - Department of Public Health Medicine, Medical School, University of Pécs, Pécs, 
      Hungary.
FAU - Péter, Iván
AU  - Péter I
AD  - Dermatology Unit, Zsigmondy Vilmos SPA Hospital, Harkány, Hungary.
FAU - Boncz, Imre
AU  - Boncz I
AD  - Dermatology Unit, Zsigmondy Vilmos SPA Hospital, Harkány, Hungary.
FAU - Jagicza, Anna
AU  - Jagicza A
AD  - Dermatology Unit, Zsigmondy Vilmos SPA Hospital, Harkány, Hungary.
FAU - Kiss, István
AU  - Kiss I
AD  - Department of Public Health Medicine, Medical School, University of Pécs, Pécs, 
      Hungary.
FAU - Csergő, Ágnes
AU  - Csergő Á
AD  - Department of Public Health Medicine, Medical School, University of Pécs, Pécs, 
      Hungary.
FAU - Kőszegi, Tamás
AU  - Kőszegi T
AD  - Department of Laboratory Medicine, Medical School, University of Pécs, Pécs, 
      Hungary.
AD  - János Szentágothai Research Centre, University of Pécs, Pécs, Hungary.
FAU - Kustán, Péter
AU  - Kustán P
AD  - Department of Laboratory Medicine, Medical School, University of Pécs, Pécs, 
      Hungary.
AD  - János Szentágothai Research Centre, University of Pécs, Pécs, Hungary.
FAU - Horváth, Iván G
AU  - Horváth IG
AD  - Heart Institute, Medical School, University of Pécs, Pécs, Hungary.
FAU - Ajtay, Zénó
AU  - Ajtay Z
AD  - Dermatology Unit, Zsigmondy Vilmos SPA Hospital, Harkány, Hungary.
AD  - Heart Institute, Medical School, University of Pécs, Pécs, Hungary.
LA  - eng
PT  - Journal Article
DEP - 20190705
PL  - New Zealand
TA  - Ther Clin Risk Manag
JT  - Therapeutics and clinical risk management
JID - 101253281
PMC - PMC6616299
OTO - NOTNLM
OT  - C-reactive protein
OT  - biomarker
OT  - cardiovascular risk
OT  - orosomucoid
OT  - oxidative stress
OT  - psoriasis
COIS- The authors report no conflicts of interest in this work.
EDAT- 2019/07/17 06:00
MHDA- 2019/07/17 06:01
PMCR- 2019/07/05
CRDT- 2019/07/17 06:00
PHST- 2018/12/10 00:00 [received]
PHST- 2019/04/25 00:00 [accepted]
PHST- 2019/07/17 06:00 [entrez]
PHST- 2019/07/17 06:00 [pubmed]
PHST- 2019/07/17 06:01 [medline]
PHST- 2019/07/05 00:00 [pmc-release]
AID - 197633 [pii]
AID - 10.2147/TCRM.S197633 [doi]
PST - epublish
SO  - Ther Clin Risk Manag. 2019 Jul 5;15:831-837. doi: 10.2147/TCRM.S197633. 
      eCollection 2019.

PMID- 31307110
OWN - NLM
STAT- MEDLINE
DCOM- 20201029
LR  - 20201029
IS  - 1360-0443 (Electronic)
IS  - 0965-2140 (Linking)
VI  - 114
IP  - 11
DP  - 2019 Nov
TI  - Association between opioid use disorder and fractures: a population-based study.
PG  - 2008-2015
LID - 10.1111/add.14732 [doi]
AB  - AIMS: To test whether fractures and osteoporosis are more prevalent among 
      patients with opioid use disorder (OUD) than patients without OUD in Taiwan. 
      DESIGN: We conducted a retrospective cohort study using data from the National 
      Health Insurance Research Database (NHIRD) in Taiwan. SETTING: Taiwan. 
      PARTICIPANTS: The number of adult patients with OUD and without OUD was 3695 and 
      14 780, respectively. We established both cohorts from 1 January 1998 to 
      31 December 2011 to observe the incidence of fracture. The occurrence of fracture 
      was followed-up until the end of 2011. MEASUREMENTS: The primary measure was 
      incidence of fracture. The relative risk of fracture was estimated using the Cox 
      proportional hazard model after adjusting for age, sex, index year and 
      comorbidities. Comorbidities included diabetes mellitus, hyperlipidemia, stroke, 
      chronic obstructive pulmonary disease, heart failure, alcohol-related illness, 
      osteoporosis, end-stage renal disease, obesity and rheumatoid arthritis, using 
      the International Classification of Diseases, 9th revision, clinical 
      modification. FINDINGS: Patients with OUD were 4.13 times more likely to suffer 
      fractures than patients without OUD [incidence rate (IR) per 1000 
      person-years = 23.0 versus 5.47, adjusted hazard ratio (HR) = 3.74, 95% 
      confidence interval (CI) = 3.27-4.29]. Compared with the control group, the risk 
      of fracture was higher among the patients with OUD. Risk of fracture was higher 
      in male elderly patients with diabetes mellitus, alcohol-related illness or 
      osteoporosis. The cumulative incidences of fracture over 14 years of patients 
      with OUD and without OUD differed significantly. CONCLUSIONS: Taiwanese patients 
      with opioid use disorder appear to have a higher adjusted hazard ratio for 
      fracture than Taiwanese patients without opioid use disorder.
CI  - © 2019 Society for the Study of Addiction.
FAU - Hsu, Wen-Yu
AU  - Hsu WY
AUID- ORCID: 0000-0002-0008-8642
AD  - Graduate Institute of Clinical Medical Science, China Medical University, 
      Taichung, Taiwan.
AD  - Department of Psychiatry, Changhua Christian Hospital, Changhua, Taiwan.
AD  - School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
FAU - Lin, Cheng-Li
AU  - Lin CL
AD  - Management Office for Health Data, China Medical University Hospital, Taichung, 
      Taiwan.
AD  - College of Medicine, China Medical University, Taichung, Taiwan.
FAU - Kao, Chia-Hung
AU  - Kao CH
AUID- ORCID: 0000-0002-6368-3676
AD  - Graduate Institute of Biomedical Sciences, College of Medicine, China Medical 
      University, Taichung, Taiwan.
AD  - Department of Nuclear Medicine and PET Center, China Medical University Hospital, 
      Taichung, Taiwan.
AD  - Department of Bioinformatics and Medical Engineering, Asia University, Taichung, 
      Taiwan.
LA  - eng
GR  - Katsuzo and Kiyo Aoshima Memorial Funds, Japan/International
GR  - Tseng-Lien Lin Foundation, Taichung, Taiwan/International
GR  - MOST 107-2321-B-039-004-/MOST Clinical Trial Consortium for Stroke/International
GR  - BM10701010021/Academia Sinica Stroke Biosignature Project/International
GR  - CMU107-ASIA-19/China Medical University Hospital/International
GR  - MOHW108-TDU-B-212-133004/Ministry of Health and Welfare, Taiwan/International
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190806
PL  - England
TA  - Addiction
JT  - Addiction (Abingdon, England)
JID - 9304118
SB  - IM
MH  - Adult
MH  - Aged
MH  - Alcohol-Related Disorders/epidemiology
MH  - Coronary Artery Disease/epidemiology
MH  - Diabetes Mellitus/epidemiology
MH  - Female
MH  - Fractures, Bone/*epidemiology
MH  - Heart Failure/epidemiology
MH  - Humans
MH  - Hyperlipidemias/epidemiology
MH  - Hypertension/epidemiology
MH  - Incidence
MH  - Kidney Failure, Chronic/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Opioid-Related Disorders/*epidemiology
MH  - Osteoporosis/*epidemiology
MH  - Proportional Hazards Models
MH  - Pulmonary Disease, Chronic Obstructive/epidemiology
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Sex Factors
MH  - Stroke/epidemiology
MH  - Taiwan/epidemiology
MH  - Young Adult
OTO - NOTNLM
OT  - Bone
OT  - National Health Insurance Research Database
OT  - Opioid Use Disorder
OT  - fracture
OT  - retrospective cohort study
OT  - risk
EDAT- 2019/07/16 06:00
MHDA- 2020/10/30 06:00
CRDT- 2019/07/16 06:00
PHST- 2019/01/03 00:00 [received]
PHST- 2019/03/22 00:00 [revised]
PHST- 2019/07/01 00:00 [accepted]
PHST- 2019/07/16 06:00 [pubmed]
PHST- 2020/10/30 06:00 [medline]
PHST- 2019/07/16 06:00 [entrez]
AID - 10.1111/add.14732 [doi]
PST - ppublish
SO  - Addiction. 2019 Nov;114(11):2008-2015. doi: 10.1111/add.14732. Epub 2019 Aug 6.

PMID- 31286290
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210226
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 38
IP  - 5
DP  - 2019 May
TI  - Correction to: Risk of adverse outcomes in patients with rheumatoid arthritis 
      hospitalized for stroke-a cross-sectional study.
PG  - 1533
LID - 10.1007/s10067-019-04531-3 [doi]
AB  - The authors of the published version of this article incorrectly presented the 
      affiliation of Li-Chin Sung. The revised affiliation is now presented correctly 
      in this article.
FAU - Kang, Jiunn-Horng
AU  - Kang JH
AD  - Department of Physical Medicine and Rehabilitation, Taipei Medical University 
      Hospital, Taipei, Taiwan.
AD  - Department of Physical Medicine and Rehabilitation, School of Medicine, College 
      of Medicine, Taipei Medical University, Taipei, Taiwan.
FAU - Xirasagar, Sudha
AU  - Xirasagar S
AD  - Department of Health Services Policy and Management, Arnold School of Public 
      Health, University of South Carolina, Columbia, SC, USA.
FAU - Lin, Herng-Ching
AU  - Lin HC
AUID- ORCID: 0000-0003-4661-959X
AD  - School of Health Care Administration, Taipei Medical University, 250 Wu-Hsing St, 
      Taipei, 110, Taiwan. henry11111@tmu.edu.tw.
AD  - Sleep Research Center, Taipei Medical University Hospital, Taipei, Taiwan. 
      henry11111@tmu.edu.tw.
FAU - Kao, Pai-Feng
AU  - Kao PF
AD  - Division of Cardiology, Department of Internal Medicine, School of Medicine, 
      College of Medicine, Taipei Medical University, Taipei, Taiwan.
AD  - Division of Cardiology, Department of Internal Medicine, Shuang Ho Hospital, 
      Taipei Medical University Taipei, Taipei, Taiwan.
FAU - Sung, Li-Chin
AU  - Sung LC
AD  - Division of Cardiology, Department of Internal Medicine, School of Medicine, 
      College of Medicine, Taipei Medical University, Taipei, Taiwan.
AD  - Division of Cardiology, Department of Internal Medicine, Shuang Ho Hospital, 
      Taipei Medical University Taipei, Taipei, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Published Erratum
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
EFR - Clin Rheumatol. 2018 Nov;37(11):2917-2926. doi: 10.1007/s10067-018-4287-8. PMID: 
      30209695
EDAT- 2019/07/10 06:00
MHDA- 2019/07/10 06:01
CRDT- 2019/07/10 06:00
PHST- 2019/07/10 06:00 [entrez]
PHST- 2019/07/10 06:00 [pubmed]
PHST- 2019/07/10 06:01 [medline]
AID - 10.1007/s10067-019-04531-3 [pii]
AID - 10.1007/s10067-019-04531-3 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2019 May;38(5):1533. doi: 10.1007/s10067-019-04531-3.

PMID- 31277159
OWN - NLM
STAT- MEDLINE
DCOM- 20190711
LR  - 20221005
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 98
IP  - 27
DP  - 2019 Jul
TI  - Do rheumatoid arthritis patients have more major complications and length of stay 
      after lower extremities fracture surgery?: A nationwide data with propensity 
      score matching.
PG  - e16286
LID - 10.1097/MD.0000000000016286 [doi]
LID - e16286
AB  - Patients with rheumatoid arthritis (RA) have a high risk of cardiovascular 
      diseases and fractures. This retrospective cohort study explored whether patients 
      with RA face higher complication risks or longer hospital stays than other 
      patients when they had a lower limb fracture that required the surgery. Patients 
      aged >45 years who received lower limb fracture surgeries between 2005 and 2012 
      were selected from the National Health Insurance Research Database, and 10 
      related variables including sex and age were used in propensity score matching to 
      pair RA patients with non-RA patients in a 1:4 ratio. The final study sample 
      comprised 1109 patients with RA and 4436 non-RA patients. The results indicated 
      that 5.57% of the study sample had postoperative complications, accounting for 
      5.05% of patients with RA and 5.70% of the control group. After conditional 
      logistic regression analysis was performed, the risk of major complications has 
      no significant differences between patients with RA and the control group (odds 
      ratio [OR] = 0.87; 95% confidence interval [CI]: 0.61-1.24; P > .05). However, 
      the comorbidity severity score exerted a significant effect on complications; 
      patients with scores ≥3 were 2.78 times more likely to experience complications 
      (OR = 2.78; 95% CI 1.52-5.07). When considering different types of complications, 
      patients with RA were less likely to be exposed to the risk of stroke 
      (OR = 0.48). After controlling all related factors, no significant differences 
      were observed in the complication risks or deaths between the 2 groups (P > .05). 
      Regarding hospitalization length, the average stay for all patients was 8.12 
      days; after controlling related factors, the hospitalization length for patients 
      with RA was 0.97 times that of the control group, which was nonsignificant 
      (P > .05). These results may provide some information to healthcare professionals 
      when providing treatments.
FAU - Hsu, Huan
AU  - Hsu H
AD  - Department of Anesthesia, Taichung Veterans General Hospital.
AD  - Department of Health Services Administration, China Medical University.
FAU - Kung, Pei-Tseng
AU  - Kung PT
AD  - Department of Health Administration, Asia University.
AD  - Department of Medical Research, China Medical University Hospital, China Medical 
      University, Taichung.
FAU - Ku, Ming-Chou
AU  - Ku MC
AD  - Department of Orthopedics, Show Chwan Memorial Hospital Show Chwan Memorial 
      Hospital, Changhua.
FAU - Lan, Joung-Liang
AU  - Lan JL
AD  - Department of Medicine, Division of Immunology and Rheumatology, China Medical 
      University Hospital, China Medical University, Taichung, Taiwan.
FAU - Chou, Wen-Yu
AU  - Chou WY
AD  - Department of Health Services Administration, China Medical University.
FAU - Tsai, Wen-Chen
AU  - Tsai WC
AD  - Department of Health Services Administration, China Medical University.
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*complications
MH  - Databases, Factual
MH  - Female
MH  - Fracture Fixation, Internal/*adverse effects
MH  - Fractures, Bone/complications/*surgery
MH  - Humans
MH  - Length of Stay/*trends
MH  - Lower Extremity/*injuries
MH  - Male
MH  - Middle Aged
MH  - Postoperative Complications/*diagnosis/epidemiology
MH  - *Propensity Score
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Taiwan/epidemiology
PMC - PMC6635232
COIS- The authors report no conflicts of interest.
EDAT- 2019/07/07 06:00
MHDA- 2019/07/12 06:00
PMCR- 2019/07/05
CRDT- 2019/07/07 06:00
PHST- 2019/07/07 06:00 [entrez]
PHST- 2019/07/07 06:00 [pubmed]
PHST- 2019/07/12 06:00 [medline]
PHST- 2019/07/05 00:00 [pmc-release]
AID - 00005792-201907050-00074 [pii]
AID - MD-D-18-04737 [pii]
AID - 10.1097/MD.0000000000016286 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2019 Jul;98(27):e16286. doi: 10.1097/MD.0000000000016286.

PMID- 31272806
OWN - NLM
STAT- MEDLINE
DCOM- 20210204
LR  - 20210204
IS  - 1532-866X (Electronic)
IS  - 0049-0172 (Linking)
VI  - 50
IP  - 1
DP  - 2020 Feb
TI  - Risk of medical complications following total hip or knee arthroplasty in 
      patients with rheumatoid arthritis: A register-based cohort study from Denmark.
PG  - 30-35
LID - S0049-0172(19)30281-1 [pii]
LID - 10.1016/j.semarthrit.2019.06.007 [doi]
AB  - OBJECTIVE: To investigate the risk of medical complications following total hip 
      and knee arthroplasty (THA/TKA) among rheumatoid arthritis (RA) compared with 
      osteoarthritis (OA) patients; and, to assess the risk of complications among 
      biologics-treated RA patients. METHODS: In a nationwide register-based study, 
      patients with RA and OA with THA/TKA surgery between 2000 and 2015 were 
      identified and followed up to 90 days after surgery for venous thromboembolism 
      (VTE), myocardial infarction and stroke, and non-surgical infections, 
      respectively. Information on treatment with biologics was obtained in the DANBIO 
      rheumatology register to compare risks of complications with non-biologics 
      treated. RESULTS: A total of 2899 and 112,571 patients with RA and OA had 
      THA/TKA. RA was associated with a hazard ratio (HR) of 1.29 (1.03 to 1.61) for 
      infection following THA/TKA, but a HR of 0.60 (0.26 to 0.98) for VTE following 
      TKA. Biologics treated patients had a HR of 1.35 (0.65 to 2.80) for infection and 
      4.82 (1.67 to 13.90) for VTE compared with non-biologics treated RA patients. RA 
      patients had no increased risk of post-surgical myocardial infarction and stroke 
      (HR 1.16, 0.76 to 1.78) compared with OA, but a higher incidence proportion was 
      observed in biologics treated compared with non-biologics treated (1.0% vs 0.6%); 
      however, the number of events were too small to estimate a HR. CONCLUSION: In 
      this study, RA was a risk factor for infection after THA/TKA, and RA patients 
      treated with biologics had a slightly increased risk compared with non-biologics 
      treated RA patients. Compared with OA, RA patients had a lower risk of VTE 
      following THA/TKA, but our finding of increased incidences of VTE in 
      biologics-treated patients warrants further studies.
CI  - Copyright © 2019 Elsevier Inc. All rights reserved.
FAU - Cordtz, René
AU  - Cordtz R
AD  - Center for Rheumatology and Spine Diseases, Rigshospitalet - Gentofte, 
      Kildegaardsvej 28, Entrance 5, 3rd floor, 2900-DK Hellerup, Copenhagen, Denmark; 
      The Parker Institute, Bispebjerg and Frederiksberg Hospital, Denmark. Electronic 
      address: rene.lindholm.cordtz.03@regionh.dk.
FAU - Odgaard, Anders
AU  - Odgaard A
AD  - Department of Orthopaedic Surgery, Copenhagen University Hospital 
      Herlev-Gentofte, Gentofte, Denmark; Department of Clinical Medicine, Faculty of 
      Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
FAU - Kristensen, Lars E
AU  - Kristensen LE
AD  - The Parker Institute, Bispebjerg and Frederiksberg Hospital, Denmark.
FAU - Overgaard, Søren
AU  - Overgaard S
AD  - Department of Orthopaedic Surgery and Traumatology, Odense University Hospital, 
      Denmark; Department of Clinical Research, University of Southern Denmark, Odense, 
      Denmark.
FAU - Dreyer, Lene
AU  - Dreyer L
AD  - Department of Rheumatology, Aalborg University Hospital, Denmark; Department of 
      Clinical Medicine, University of Aalborg, Denmark; The DANBIO Registry, Denmark.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190613
PL  - United States
TA  - Semin Arthritis Rheum
JT  - Seminars in arthritis and rheumatism
JID - 1306053
RN  - 0 (Biological Products)
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/drug therapy/*surgery
MH  - Arthroplasty, Replacement, Hip/*adverse effects
MH  - Arthroplasty, Replacement, Knee/*adverse effects
MH  - Biological Products/therapeutic use
MH  - Denmark
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Infections/*epidemiology/etiology
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*epidemiology/etiology
MH  - Postoperative Complications/epidemiology/etiology
MH  - Registries
MH  - Risk
MH  - Venous Thromboembolism/*epidemiology/etiology
OTO - NOTNLM
OT  - Biological DMARD
OT  - Cardiovascular disease
OT  - Infection
OT  - Orthopaedic surgery
OT  - Rheumatoid arthritis
COIS- Conflict of interest RC, AO, and SO have no competing interests. LEK has received 
      fees for speaking and/or consultancy from Pfizer, AbbVie, Amgen, UCB, Celgene, 
      BMS, Biogen, Sanofi, MSD, Novartis, Eli Lilly, Janssen Pharmaceuticals. LD has 
      received speaking fees from MSD, Eli Lilly and UCB outside the present work.
EDAT- 2019/07/06 06:00
MHDA- 2021/02/05 06:00
CRDT- 2019/07/06 06:00
PHST- 2019/05/01 00:00 [received]
PHST- 2019/06/03 00:00 [revised]
PHST- 2019/06/10 00:00 [accepted]
PHST- 2019/07/06 06:00 [pubmed]
PHST- 2021/02/05 06:00 [medline]
PHST- 2019/07/06 06:00 [entrez]
AID - S0049-0172(19)30281-1 [pii]
AID - 10.1016/j.semarthrit.2019.06.007 [doi]
PST - ppublish
SO  - Semin Arthritis Rheum. 2020 Feb;50(1):30-35. doi: 
      10.1016/j.semarthrit.2019.06.007. Epub 2019 Jun 13.

PMID- 31240863
OWN - NLM
STAT- MEDLINE
DCOM- 20200129
LR  - 20200129
IS  - 1756-185X (Electronic)
IS  - 1756-1841 (Linking)
VI  - 22
IP  - 8
DP  - 2019 Aug
TI  - Potential benefits of biologics on stroke and mortality in patients with 
      rheumatoid arthritis: A nationwide population-based cohort study in Taiwan.
PG  - 1544-1552
LID - 10.1111/1756-185X.13611 [doi]
AB  - AIM: To examine the changes in the risks of death and cardiovascular diseases 
      (CVD) in rheumatoid arthritis (RA) patients treated with conventional synthetic 
      or biologic disease-modifying antirheumatic drugs (csDMARD or bDMARD) during 
      1997-2013. METHODS: Two cohorts of RA patients and their matched controls were 
      identified from the National Health Insurance Research database. There were 1569 
      patients in the csDMARD cohort who received cyclosporine ≥50 mg/d with 
      concomitant usage of ≥2 csDMARDs during 1997-2003. There were 1530 patients in 
      the bDMARD cohort if patients had ≥1 claim for bDMARD during 2003-2011. Adjusted 
      hazard ratios (aHRs) for the risk of death, myocardial infarction, and stroke, 
      were assessed using the Kaplan-Meier survival curves and the Cox proportional 
      hazards models. RESULTS: Compared with matched cohorts, the incidence of death 
      was higher with csDMARD with a more than 6-fold increase (csDMARD vs controls: 
      33% vs 5%); while it only increased with a much smaller magnitude with bDMARD 
      (bDMARD vs controls: 15% vs 11%). In addition, an increase in the reduction of 
      incidence rate of stroke with bDMARD (bDMARD vs controls: 2% vs 5%) than that 
      with csDMARD (csDMARD vs controls: 3% vs 4%) was found. Results from multivariate 
      analysis showed that RA patients receiving bDMARD had a significantly lower 
      increase in the risk of deaths (aHR 1.05; 95% CI 0.84-1.33) compared with those 
      receiving csDMARD (aHR 8.75; 95% CI 7.43-10.31). In addition, bDMARD was 
      associated with a higher reduction in the risk of stroke compared with csDMARD 
      (bDMARD: aHR 0.37; 95% CI 0.22-0.62; csDMARD: aHR 0.73; 95% CI 0.51-1.05). 
      CONCLUSION: Biologics used in RA patients have been shown to have a beneficial 
      impact on improving clinical outcomes, including decreased risks of death and 
      stroke. The economic burden from costs of biologics may be alleviated by 
      improving outcomes.
CI  - © 2019 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons 
      Australia, Ltd.
FAU - Tang, Chao-Hsiun
AU  - Tang CH
AD  - School of Health Care Administration, Taipei Medical University, Taipei, Taiwan.
FAU - Yu, Fun
AU  - Yu F
AUID- ORCID: 0000-0002-9635-027X
AD  - Pfizer Ltd., New Taipei City, Taiwan.
FAU - Huang, Ching-Ya
AU  - Huang CY
AD  - Formosa Biomedical Technology Corporation, Taipei, Taiwan.
FAU - Chen, Der-Yuan
AU  - Chen DY
AUID- ORCID: 0000-0001-7736-2235
AD  - Rheumatology and Immunology Center, China Medical University Hospital, Taichung, 
      Taiwan.
AD  - College of Medicine, China Medical University, Taichung, Taiwan.
AD  - Translation Medicine Laboratory, Rheumatology and Immunology Center, China 
      Medical University, Taichung, Taiwan.
LA  - eng
GR  - Pfizer Limited Taiwan/
GR  - Formosa Biomedical Technology Corp/
PT  - Comparative Study
PT  - Journal Article
DEP - 20190625
PL  - England
TA  - Int J Rheum Dis
JT  - International journal of rheumatic diseases
JID - 101474930
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
SB  - IM
MH  - Adult
MH  - Antirheumatic Agents/adverse effects/*therapeutic use
MH  - Arthritis, Rheumatoid/diagnosis/*drug therapy/mortality
MH  - Biological Products/adverse effects/*therapeutic use
MH  - Cause of Death
MH  - Cross-Sectional Studies
MH  - Databases, Factual
MH  - Female
MH  - Humans
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Protective Factors
MH  - Retrospective Studies
MH  - Risk Assessment
MH  - Risk Factors
MH  - Stroke/diagnosis/mortality/*prevention & control
MH  - Taiwan/epidemiology
MH  - Time Factors
MH  - Treatment Outcome
OTO - NOTNLM
OT  - biological therapies
OT  - clinical outcomes
OT  - disease-modifying antirheumatic drugs
OT  - rheumatoid arthritis
OT  - stroke
EDAT- 2019/06/27 06:00
MHDA- 2020/01/30 06:00
CRDT- 2019/06/27 06:00
PHST- 2018/08/02 00:00 [received]
PHST- 2019/03/08 00:00 [revised]
PHST- 2019/05/05 00:00 [accepted]
PHST- 2019/06/27 06:00 [pubmed]
PHST- 2020/01/30 06:00 [medline]
PHST- 2019/06/27 06:00 [entrez]
AID - 10.1111/1756-185X.13611 [doi]
PST - ppublish
SO  - Int J Rheum Dis. 2019 Aug;22(8):1544-1552. doi: 10.1111/1756-185X.13611. Epub 
      2019 Jun 25.

PMID- 31208307
OWN - NLM
STAT- MEDLINE
DCOM- 20200212
LR  - 20200212
IS  - 1873-4286 (Electronic)
IS  - 1381-6128 (Linking)
VI  - 25
IP  - 9
DP  - 2019
TI  - Accelerated Atherosclerosis in Rheumatoid Arthritis: Mechanisms and Treatment.
PG  - 969-986
LID - 10.2174/1381612825666190430113212 [doi]
AB  - BACKGROUND: Rheumatoid arthritis (RA) is a chronic systemic autoimmune 
      inflammatory disorder that increases the risk of developing cardiovascular 
      disease. There is accumulating evidence that the RA disease state accelerates the 
      formation of atherosclerotic plaques. Treatments for RA improve joint 
      symptomatology and may reduce inflammation, but consideration of their effects on 
      the cardiovascular system is generally low priority. OBJECTIVE: Since 
      cardiovascular disease is the leading cause of mortality in RA patients, the 
      impact of RA therapies on atherosclerosis is an area in need of attention and the 
      focus of this review. RESULTS: The drugs used to treat RA may be analgesics, 
      conventional disease-modifying anti-rheumatic drugs, and/or biologics, including 
      antibodies against the cytokine tumor necrosis factor-α. Pain relievers such as 
      nonselective non-steroidal anti-inflammatory drugs and cyclooxygenase inhibitors 
      may adversely affect lipid metabolism and cyclooxygenase inhibitors have been 
      associated with increased adverse cardiovascular events, such as myocardial 
      infarction and stroke. Methotrexate, the anchor disease-modifying anti-rheumatic 
      drug in RA treatment has multiple atheroprotective advantages and is often 
      combined with other therapies. Biologic inhibitors of tumor necrosis factor-α may 
      be beneficial in preventing cardiovascular disease because tumor necrosis 
      factor-α promotes the initiation and progression of atherosclerosis. However, 
      some studies show a worsening of the lipid profile in RA with blockade of this 
      cytokine, leading to higher total cholesterol and triglycerides. CONCLUSION: 
      Greater understanding of the pharmacologic activity of RA treatments on the 
      atherosclerotic process may lead to improved care, addressing both damages to the 
      joints and heart.
CI  - Copyright© Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Reiss, Allison B
AU  - Reiss AB
AD  - Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 
      Mineola Boulevard, Suite 4-004, Mineola, NY 11501, United States.
FAU - Silverman, Andrew
AU  - Silverman A
AD  - Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 
      Mineola Boulevard, Suite 4-004, Mineola, NY 11501, United States.
FAU - Khalfan, Muhammed
AU  - Khalfan M
AD  - Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 
      Mineola Boulevard, Suite 4-004, Mineola, NY 11501, United States.
FAU - Vernice, Nicholas A
AU  - Vernice NA
AD  - Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 
      Mineola Boulevard, Suite 4-004, Mineola, NY 11501, United States.
FAU - Kasselman, Lora J
AU  - Kasselman LJ
AD  - Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 
      Mineola Boulevard, Suite 4-004, Mineola, NY 11501, United States.
FAU - Carsons, Steven E
AU  - Carsons SE
AD  - Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 
      Mineola Boulevard, Suite 4-004, Mineola, NY 11501, United States.
FAU - De Leon, Joshua
AU  - De Leon J
AD  - Winthrop Research Institute, Department of Medicine, NYU Winthrop Hospital, 101 
      Mineola Boulevard, Suite 4-004, Mineola, NY 11501, United States.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United Arab Emirates
TA  - Curr Pharm Des
JT  - Current pharmaceutical design
JID - 9602487
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Antirheumatic Agents/*pharmacology
MH  - Arthritis, Rheumatoid/*complications/*drug therapy
MH  - Atherosclerosis/*complications/prevention & control
MH  - Humans
MH  - Methotrexate/pharmacology
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
OTO - NOTNLM
OT  - DMARD
OT  - Rheumatoid arthritis
OT  - atherosclerosis
OT  - biologics
OT  - inflammation
OT  - methotrexate
OT  - tumor necrosis factor.
EDAT- 2019/06/19 06:00
MHDA- 2020/02/13 06:00
CRDT- 2019/06/19 06:00
PHST- 2019/01/26 00:00 [received]
PHST- 2019/04/14 00:00 [accepted]
PHST- 2019/06/19 06:00 [pubmed]
PHST- 2020/02/13 06:00 [medline]
PHST- 2019/06/19 06:00 [entrez]
AID - CPD-EPUB-98302 [pii]
AID - 10.2174/1381612825666190430113212 [doi]
PST - ppublish
SO  - Curr Pharm Des. 2019;25(9):969-986. doi: 10.2174/1381612825666190430113212.

PMID- 31196449
OWN - NLM
STAT- MEDLINE
DCOM- 20200410
LR  - 20210109
IS  - 1558-3597 (Electronic)
IS  - 0735-1097 (Linking)
VI  - 73
IP  - 23
DP  - 2019 Jun 18
TI  - Genetic Risk Score for Coronary Disease Identifies Predispositions to 
      Cardiovascular and Noncardiovascular Diseases.
PG  - 2932-2942
LID - S0735-1097(19)34902-2 [pii]
LID - 10.1016/j.jacc.2019.03.512 [doi]
AB  - BACKGROUND: The taxonomy of cardiovascular (CV) diseases is divided into a broad 
      spectrum of clinical entities. Many such diseases coincide in specific patient 
      groups and suggest shared predisposition. OBJECTIVES: This study focused on 
      coronary artery disease (CAD) and investigated the genetic relationship to CV and 
      non-CV diseases with reported CAD comorbidity. METHODS: This study examined 
      425,196 UK Biobank participants to determine a genetic risk score (GRS) based on 
      300 CAD associated variants (CAD-GRS). This score was associated with 22 traits, 
      including risk factors, diseases secondary to CAD, as well as comorbid and non-CV 
      conditions. Sensitivity analyses were performed in individuals free from CAD or 
      stable angina diagnosis. RESULTS: Hypercholesterolemia (odds ratio [OR]: 1.27; 
      95% CI: 1.26 to 1.29) and hypertension (OR: 1.11; 95% CI: 1.10 to 1.12) were 
      strongly associated with the CAD-GRS, which indicated that the score contained 
      variants predisposing to these conditions. However, the CAD-GRS was also 
      significant in patients with CAD who were free of CAD risk factors (OR: 1.37; 
      95% CI: 1.30 to 1.44). The study observed significant associations between the 
      CAD-GRS and peripheral arterial disease (OR: 1.28; 95% CI: 1.23 to 1.32), 
      abdominal aortic aneurysms (OR: 1.28; 95% CI: 1.20 to 1.37), and stroke (OR: 
      1.08; 95% CI: 1.05 to 1.10), which remained significant in sensitivity analyses 
      that suggested shared genetic predisposition. The score was also associated with 
      heart failure (OR: 1.25; 95% CI: 1.22 to 1.29), atrial fibrillation (OR: 1.08; 
      95% CI: 1.05 to 1.10), and premature death (OR: 1.04; 95% CI: 1.02 to 1.06). 
      These associations were abolished in sensitivity analyses that indicated that 
      they were secondary to prevalent CAD. Finally, an inverse association was 
      observed between the score and migraine headaches (OR: 0.94; 95% CI: 0.93 to 
      0.96). CONCLUSIONS: A wide spectrum of CV conditions, including premature death, 
      might develop consecutively or in parallel with CAD for the same genetic roots. 
      In conditions like heart failure, the study found evidence that the CAD-GRS could 
      be used to stratify patients with no or limited genetic overlap with CAD risk. 
      Increased genetic predisposition to CAD was inversely associated with migraine 
      headaches.
CI  - Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier 
      Inc. All rights reserved.
FAU - Ntalla, Ioanna
AU  - Ntalla I
AD  - Clinical Pharmacology, William Harvey Research Institute, Barts and the London 
      Medical School, Queen Mary University of London, London, United Kingdom; Centre 
      for Genomic Health, Queen Mary University of London, London, United Kingdom.
FAU - Kanoni, Stavroula
AU  - Kanoni S
AD  - Clinical Pharmacology, William Harvey Research Institute, Barts and the London 
      Medical School, Queen Mary University of London, London, United Kingdom; Centre 
      for Genomic Health, Queen Mary University of London, London, United Kingdom.
FAU - Zeng, Lingyao
AU  - Zeng L
AD  - Deutsches Herzzentrum München, Klinik für Herz und Kreislauferkrankungen, 
      Technische Universität München, Munich, Germany.
FAU - Giannakopoulou, Olga
AU  - Giannakopoulou O
AD  - Clinical Pharmacology, William Harvey Research Institute, Barts and the London 
      Medical School, Queen Mary University of London, London, United Kingdom; Centre 
      for Genomic Health, Queen Mary University of London, London, United Kingdom.
FAU - Danesh, John
AU  - Danesh J
AD  - MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary 
      Care, University of Cambridge, Cambridge, United Kingdom; NIHR Blood and 
      Transplant Research Unit in Donor Health and Genomics, Department of Public 
      Health and Primary Care, University of Cambridge, Cambridge, United Kingdom; 
      Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, 
      Cambridge, United Kingdom.
FAU - Watkins, Hugh
AU  - Watkins H
AD  - Division of Cardiovascular Medicine, Radcliffe Department of Medicine, University 
      of Oxford, Oxford, United Kingdom; Wellcome Trust Centre for Human Genetics, 
      University of Oxford, Oxford, United Kingdom.
FAU - Samani, Nilesh J
AU  - Samani NJ
AD  - Department of Cardiovascular Sciences, University of Leicester, Leicester, United 
      Kingdom; National Institute for Health Research Leicester Cardiovascular 
      Biomedical Research Centre, Leicester, United Kingdom.
FAU - Deloukas, Panos
AU  - Deloukas P
AD  - Clinical Pharmacology, William Harvey Research Institute, Barts and the London 
      Medical School, Queen Mary University of London, London, United Kingdom; Centre 
      for Genomic Health, Queen Mary University of London, London, United Kingdom; 
      Princess Al-Jawhara Al-Brahim Centre of Excellence in Research of Hereditary 
      Disorders (PACER-HD), King Abdulaziz University, Jeddah, Saudi Arabia. Electronic 
      address: p.deloukas@qmul.ac.uk.
FAU - Schunkert, Heribert
AU  - Schunkert H
AD  - Deutsches Herzzentrum München, Klinik für Herz und Kreislauferkrankungen, 
      Technische Universität München, Munich, Germany; Deutsches Zentrum für Herz und 
      Kreislauferkrankungen (DZHK), Partner Site Munich Heart Alliance, Munich, 
      Germany.
CN  - UK Biobank CardioMetabolic Consortium CHD Working Group
LA  - eng
GR  - RG/14/5/30893/BHF_/British Heart Foundation/United Kingdom
GR  - FS/14/66/3129/BHF_/British Heart Foundation/United Kingdom
GR  - IS-BRC-1215-20022/DH_/Department of Health/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Am Coll Cardiol
JT  - Journal of the American College of Cardiology
JID - 8301365
SB  - IM
CIN - J Am Coll Cardiol. 2019 Jun 18;73(23):2943-2945. doi: 10.1016/j.jacc.2019.05.002. 
      PMID: 31196450
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/diagnosis/epidemiology/genetics
MH  - Biological Specimen Banks/trends
MH  - Cohort Studies
MH  - Coronary Artery Disease/diagnosis/*epidemiology/*genetics
MH  - Female
MH  - Genetic Predisposition to Disease/*epidemiology/*genetics
MH  - Humans
MH  - Hypercholesterolemia/diagnosis/epidemiology/genetics
MH  - Hypertension/diagnosis/epidemiology/genetics
MH  - Kidney Diseases/diagnosis/epidemiology/genetics
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Prospective Studies
MH  - Risk Assessment/methods
MH  - Risk Factors
MH  - United Kingdom/epidemiology
OTO - NOTNLM
OT  - UK Biobank
OT  - cardiovascular diseases
OT  - coronary artery disease
OT  - genetic risk score
OT  - heart failure
OT  - migraine
EDAT- 2019/06/15 06:00
MHDA- 2020/04/11 06:00
CRDT- 2019/06/15 06:00
PHST- 2018/11/08 00:00 [received]
PHST- 2019/03/08 00:00 [revised]
PHST- 2019/03/19 00:00 [accepted]
PHST- 2019/06/15 06:00 [entrez]
PHST- 2019/06/15 06:00 [pubmed]
PHST- 2020/04/11 06:00 [medline]
AID - S0735-1097(19)34902-2 [pii]
AID - 10.1016/j.jacc.2019.03.512 [doi]
PST - ppublish
SO  - J Am Coll Cardiol. 2019 Jun 18;73(23):2932-2942. doi: 10.1016/j.jacc.2019.03.512.

PMID- 31174819
OWN - NLM
STAT- MEDLINE
DCOM- 20191010
LR  - 20191010
IS  - 1532-1770 (Electronic)
IS  - 1521-6942 (Linking)
VI  - 32
IP  - 4
DP  - 2018 Aug
TI  - Central nervous system involvement in rheumatoid arthritis patients and the 
      potential implications of using biological agents.
PG  - 500-510
LID - S1521-6942(19)30025-7 [pii]
LID - 10.1016/j.berh.2019.02.003 [doi]
AB  - Central nervous system (CNS) involvement is quite unusual in patients with 
      rheumatoid arthritis (RA), although cerebral vasculitis, rheumatoid nodules and 
      meningitis have all been reported, and patients with RA may also have CNS 
      comorbidities such as stroke and neuro-degenerative and demyelinating syndromes. 
      It has been found that biological drugs, especially anti-tumour necrosis 
      factor-alpha (anti-TNF-α) drugs, slightly increase the risk of developing 
      demyelinating diseases, and they are consequently discouraged in patients with 
      multiple sclerosis and related disorders. Furthermore, the risk of opportunistic 
      CNS infections is increased in immunosuppressed patients. To review the current 
      literature concerning CNS involvement in patients with RA (including RA-related 
      forms and comorbidities) and the incidence of new-onset CNS diseases in patients 
      with RA undergoing biological treatment (anti-TNF or non-anti-TNF drugs), the 
      Medline database was searched using the key words 'rheumatoid arthritis', 
      'central nervous system', 'anti-TNF', 'abatacept', 'tocilizumab', 'rituximab' and 
      'anakinra'. Abstracts not in English were excluded. We selected 76 articles 
      published between 1989 and 2017, which were divided into four groups on the basis 
      of whether CNS involvement was RA-related or not and according to the type of 
      biological agent used (TNF inhibitors or other agents). The RA-related diseases 
      included aseptic meningitis, vasculitis and cerebral rheumatoid nodules, which 
      benefit from immunosuppressive treatments. CNS comorbidities included stroke, 
      seizures, dementia and neuropsychiatric disorders, which have been frequently 
      described in biological agent-naïve patients with RA, and other rarely reported 
      neurological diseases, such as extra-pyramidal syndromes and demyelinating 
      disorders. CNS comorbidities are relatively frequent among patients with RA and 
      may be related to systemic inflammation or concomitant medications. The use of 
      anti-TNF drugs is associated with the risk of developing demyelinating diseases, 
      and CNS infections have been described in patients treated with anti-TNF and 
      non-anti-TNF agents. Non-anti-TNF drugs may be preferred in the case of 
      demyelinating diseases, cerebral vasculitis or neurolupus. Patients with RA may 
      suffer from CNS involvement as a manifestation of RA or as a comorbidity. The 
      treatment of such medical conditions should be guided on the basis of their 
      etiopathogenesis: steroids and immunosuppressants are useful in the case of 
      RA-related CNS diseases but are often detrimental in other situations. Similarly, 
      the choice of biological agents in patients with RA with CNS complications should 
      be guided by a correct diagnosis in order to prevent further complications.
CI  - Copyright © 2019 Elsevier Ltd. All rights reserved.
FAU - Atzeni, Fabiola
AU  - Atzeni F
AD  - Rheumatology Unit, University of Messina, Via Consolare Valeria 1, 98100, 
      Messina, Italy. Electronic address: atzenifabiola@hotmail.com.
FAU - Talotta, Rossella
AU  - Talotta R
AD  - Post-graduate School of Pharmacology and Clinical Toxicology, University of 
      Milan, Piazza Ospedale Maggiore 3, 20152, Milano, Italy. Electronic address: 
      rossella.talotta@unimi.it.
FAU - Masala, Ignazio Francesco
AU  - Masala IF
AD  - Orthopedic and Trauma Unit, Santissima Trinità Hospital, Via Is Mirrionis 92, 
      09121, Cagliari, Italy. Electronic address: ifm.franc@hotmail.it.
FAU - Gerardi, Maria Chiara
AU  - Gerardi MC
AD  - Rheumatology Unit, Spedali Civili di Brescia, Piazzale Spedali Civili 1, 25123, 
      Brescia, Italy. Electronic address: mariachiara.geradi@asst-fbf-sacco.it.
FAU - Casale, Roberto
AU  - Casale R
AD  - Habilita Hospitals & Research Rehabilitation Unit, Bergamo, Zingonia, Italy. 
      Electronic address: robertocasale@habilita.it.
FAU - Sarzi-Puttini, Piercarlo
AU  - Sarzi-Puttini P
AD  - Department of Rheumatology, University Hospital ASST-Fatebenefratelli-Sacco, Via 
      GB Grassi 74, 20157, Milano, Italy. Electronic address: 
      sarzi.piercarlo@asst-fbf-sacco.it.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20190227
PL  - Netherlands
TA  - Best Pract Res Clin Rheumatol
JT  - Best practice & research. Clinical rheumatology
JID - 101121149
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Factors)
SB  - IM
MH  - Antirheumatic Agents/pharmacology/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy/*etiology/pathology
MH  - Biological Factors/pharmacology/*therapeutic use
MH  - Central Nervous System/*pathology
MH  - Humans
OTO - NOTNLM
OT  - Abatacept
OT  - Anakinra
OT  - Anti-TNF drugs
OT  - Central nervous system diseases
OT  - Rheumatoid arthritis
OT  - Rituximab
OT  - Tocilizumab
EDAT- 2019/06/09 06:00
MHDA- 2019/10/11 06:00
CRDT- 2019/06/09 06:00
PHST- 2019/06/09 06:00 [entrez]
PHST- 2019/06/09 06:00 [pubmed]
PHST- 2019/10/11 06:00 [medline]
AID - S1521-6942(19)30025-7 [pii]
AID - 10.1016/j.berh.2019.02.003 [doi]
PST - ppublish
SO  - Best Pract Res Clin Rheumatol. 2018 Aug;32(4):500-510. doi: 
      10.1016/j.berh.2019.02.003. Epub 2019 Feb 27.

PMID- 31148950
OWN - NLM
STAT- MEDLINE
DCOM- 20191216
LR  - 20220409
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 2019
DP  - 2019
TI  - Mean Platelet Volume (MPV): New Perspectives for an Old Marker in the Course and 
      Prognosis of Inflammatory Conditions.
PG  - 9213074
LID - 10.1155/2019/9213074 [doi]
LID - 9213074
AB  - Platelet size has been demonstrated to reflect platelet activity and seems to be 
      a useful predictive and prognostic biomarker of cardiovascular events. It is 
      associated with a variety of prothrombotic and proinflammatory diseases. The aim 
      is a review of literature reports concerning changes in the mean platelet volume 
      (MPV) and its possible role as a biomarker in inflammatory processes and 
      neoplastic diseases. PubMed database was searched for sources using the following 
      keywords: platelet activation, platelet count, mean platelet volume and: 
      inflammation, cancer/tumor, cardiovascular diseases, myocardial infarction, 
      diabetes, lupus disease, rheumatoid arthritis, tuberculosis, ulcerative colitis, 
      renal disease, pulmonary disease, influencing factors, age, gender, genetic 
      factors, oral contraceptives, smoking, lifestyle, methods, standardization, and 
      hematological analyzer. Preference was given to the sources which were published 
      within the past 20 years. Increased MPV was observed in cardiovascular diseases, 
      cerebral stroke, respiratory diseases, chronic renal failure, intestine diseases, 
      rheumatoid diseases, diabetes, and various cancers. Decreased MPV was noted in 
      tuberculosis during disease exacerbation, ulcerative colitis, SLE in adult, and 
      different neoplastic diseases. The study of MPV can provide important information 
      on the course and prognosis in many inflammatory conditions. Therefore, from the 
      clinical point of view, it would be interesting to establish an MPV cut-off value 
      indicating the intensity of inflammatory process, presence of the disease, 
      increased risk of disease development, increased risk of thrombotic 
      complications, increased risk of death, and patient's response on applied 
      treatment. Nevertheless, this aspect of MPV evaluation allowing its use in 
      clinical practice is limited and requires further studies.
FAU - Korniluk, Aleksandra
AU  - Korniluk A
AD  - Department of Clinical Laboratory Diagnostics, Medical University of Bialystok, 
      ul. Waszyngtona 15A, 15-276 Białystok, Poland.
FAU - Koper-Lenkiewicz, Olga Martyna
AU  - Koper-Lenkiewicz OM
AUID- ORCID: 0000-0001-5199-2773
AD  - Department of Clinical Laboratory Diagnostics, Medical University of Bialystok, 
      ul. Waszyngtona 15A, 15-276 Białystok, Poland.
FAU - Kamińska, Joanna
AU  - Kamińska J
AD  - Department of Clinical Laboratory Diagnostics, Medical University of Bialystok, 
      ul. Waszyngtona 15A, 15-276 Białystok, Poland.
FAU - Kemona, Halina
AU  - Kemona H
AD  - Department of Clinical Laboratory Diagnostics, Medical University of Bialystok, 
      ul. Waszyngtona 15A, 15-276 Białystok, Poland.
FAU - Dymicka-Piekarska, Violetta
AU  - Dymicka-Piekarska V
AUID- ORCID: 0000-0003-4170-0997
AD  - Department of Clinical Laboratory Diagnostics, Medical University of Bialystok, 
      ul. Waszyngtona 15A, 15-276 Białystok, Poland.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20190417
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
RN  - 0 (Biomarkers)
SB  - IM
MH  - Biomarkers/*metabolism
MH  - Blood Platelets/physiology
MH  - Diabetes Mellitus/metabolism
MH  - Female
MH  - Humans
MH  - Inflammation/*metabolism
MH  - Male
MH  - Mean Platelet Volume
MH  - Myocardial Infarction/metabolism
MH  - Platelet Activation/physiology
MH  - Platelet Count
PMC - PMC6501263
EDAT- 2019/06/01 06:00
MHDA- 2019/12/18 06:00
PMCR- 2019/04/17
CRDT- 2019/06/01 06:00
PHST- 2018/11/14 00:00 [received]
PHST- 2019/02/26 00:00 [revised]
PHST- 2019/02/28 00:00 [accepted]
PHST- 2019/06/01 06:00 [entrez]
PHST- 2019/06/01 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
PHST- 2019/04/17 00:00 [pmc-release]
AID - 10.1155/2019/9213074 [doi]
PST - epublish
SO  - Mediators Inflamm. 2019 Apr 17;2019:9213074. doi: 10.1155/2019/9213074. 
      eCollection 2019.

PMID- 31127862
OWN - NLM
STAT- MEDLINE
DCOM- 20200525
LR  - 20210109
IS  - 1365-2796 (Electronic)
IS  - 0954-6820 (Print)
IS  - 0954-6820 (Linking)
VI  - 286
IP  - 4
DP  - 2019 Oct
TI  - Concomitant Ro/SSA and La/SSB antibodies are biomarkers for the risk of venous 
      thromboembolism and cerebral infarction in primary Sjögren's syndrome.
PG  - 458-468
LID - 10.1111/joim.12941 [doi]
AB  - BACKGROUND: To assess the risk of incident cardiovascular disease in patients 
      with primary Sjögren's syndrome, overall and stratified by Ro/SSA and La/SSB 
      autoantibody status. METHODS: A cohort of patients with primary Sjögren's 
      syndrome in Sweden (n = 960) and matched controls from the general population 
      (n = 9035) were included, and data extracted from the National Patient Register 
      to identify events of myocardial infarction, cerebral infarction and venous 
      thromboembolism. Hazard ratios were estimated using cox proportional hazard 
      regressions. RESULTS: During a median follow-up of 9.5 years, the overall hazard 
      ratio (HR) was 1.6 (95% CI 1.2-2.1) for myocardial infarction, 1.2 (95% CI 
      0.9-1.7) for cerebral infarction and 2.1 (95% CI 1.6-2.9) for venous 
      thromboembolism. Patients positive for both Ro/SSA and La/SSB autoantibodies had 
      a substantially higher risk of cerebral infarction (HR 1.7, 95% CI 1.0-2.9) and 
      venous thromboembolism (HR 3.1, 95% CI 1.9-4.8) than the general population. 
      These risks were not significantly increased in Ro/SSA- and La/SSB-negative 
      patients. Among autoantibody-positive patients, the highest HR of cerebral 
      infarction was seen after ≥10 years disease duration (HR 2.8, 95% CI 1.4-5.4), 
      while the HR for venous thromboembolism was highest 0-5 years after disease 
      diagnosis (HR 4.7, 95% CI 2.3-9.3) and remained high throughout disease duration. 
      CONCLUSIONS: Primary Sjögren's syndrome is associated with a markedly increased 
      risk of cardiovascular disease and the presence of Ro/SSA and La/SSB 
      autoantibodies identify the subgroup of patients carrying the highest risk. These 
      findings suggest that monitoring and prevention of cardiovascular disease in this 
      patient group should be considered.
CI  - © 2019 The Authors. Journal of Internal Medicine published by John Wiley & Sons 
      Ltd on behalf of Association for Publication of The Journal of Internal Medicine.
FAU - Mofors, J
AU  - Mofors J
AD  - From the, Division of Rheumatology, Department of Medicine, Karolinska 
      Institutet, Karolinska University Hospital, Stockholm, Sweden.
FAU - Holmqvist, M
AU  - Holmqvist M
AD  - Division of Clinical Epidemiology, Department of Medicine, Karolinska Institutet, 
      Stockholm, Sweden.
FAU - Westermark, L
AU  - Westermark L
AD  - Department of Medical Sciences, Rheumatology and Science for Life Laboratory, 
      Uppsala University, Uppsala, Sweden.
FAU - Björk, A
AU  - Björk A
AD  - From the, Division of Rheumatology, Department of Medicine, Karolinska 
      Institutet, Karolinska University Hospital, Stockholm, Sweden.
FAU - Kvarnström, M
AU  - Kvarnström M
AD  - From the, Division of Rheumatology, Department of Medicine, Karolinska 
      Institutet, Karolinska University Hospital, Stockholm, Sweden.
FAU - Forsblad-d'Elia, H
AU  - Forsblad-d'Elia H
AD  - Department of Public Health and Clinical Medicine, Rheumatology, Umeå University, 
      Umeå, Sweden.
FAU - Magnusson Bucher, S
AU  - Magnusson Bucher S
AD  - Department of Rheumatology, Faculty of Medicine and Health, Örebro University, 
      Örebro, Sweden.
FAU - Eriksson, P
AU  - Eriksson P
AD  - Division of Rheumatology, Department of Clinical Experimental Medicine, Linköping 
      University, Linköping, Sweden.
FAU - Theander, E
AU  - Theander E
AD  - Department of Clinical Sciences, Malmö, Rheumatology, Lund University, Malmö, 
      Sweden.
FAU - Mandl, T
AU  - Mandl T
AD  - Department of Clinical Sciences, Malmö, Rheumatology, Lund University, Malmö, 
      Sweden.
FAU - Wahren-Herlenius, M
AU  - Wahren-Herlenius M
AUID- ORCID: 0000-0002-0915-7245
AD  - From the, Division of Rheumatology, Department of Medicine, Karolinska 
      Institutet, Karolinska University Hospital, Stockholm, Sweden.
FAU - Nordmark, G
AU  - Nordmark G
AUID- ORCID: 0000-0002-3829-7431
AD  - Department of Medical Sciences, Rheumatology and Science for Life Laboratory, 
      Uppsala University, Uppsala, Sweden.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190617
PL  - England
TA  - J Intern Med
JT  - Journal of internal medicine
JID - 8904841
RN  - 0 (Antibodies, Antinuclear)
RN  - 0 (Biomarkers)
RN  - 0 (SS-A antibodies)
RN  - 0 (SS-B antibodies)
SB  - IM
CIN - J Intern Med. 2020 Feb;287(2):214-215. doi: 10.1111/joim.12988. PMID: 31631415
CIN - J Intern Med. 2020 Feb;287(2):216-217. doi: 10.1111/joim.12996. PMID: 31631437
MH  - Antibodies, Antinuclear/*blood
MH  - Biomarkers/blood
MH  - Case-Control Studies
MH  - Cerebral Infarction/*etiology/immunology
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*etiology/immunology
MH  - Risk Factors
MH  - Sjogren's Syndrome/*complications/immunology
MH  - Sweden
MH  - Venous Thromboembolism/*etiology/immunology
PMC - PMC6851863
OTO - NOTNLM
OT  - La/SSB
OT  - Primary Sjögren's syndrome
OT  - Ro/SSA
OT  - autoantibodies
OT  - cardiovascular disease
COIS- The authors declare no competing interests.
EDAT- 2019/05/28 06:00
MHDA- 2020/05/26 06:00
PMCR- 2019/11/13
CRDT- 2019/05/26 06:00
PHST- 2019/05/28 06:00 [pubmed]
PHST- 2020/05/26 06:00 [medline]
PHST- 2019/05/26 06:00 [entrez]
PHST- 2019/11/13 00:00 [pmc-release]
AID - JOIM12941 [pii]
AID - 10.1111/joim.12941 [doi]
PST - ppublish
SO  - J Intern Med. 2019 Oct;286(4):458-468. doi: 10.1111/joim.12941. Epub 2019 Jun 17.

PMID- 31081876
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220422
IS  - 2168-6157 (Electronic)
IS  - 2168-6149 (Print)
IS  - 2168-6149 (Linking)
VI  - 76
IP  - 8
DP  - 2019 Aug 1
TI  - Derivation and External Validation of a Scoring System for Predicting Fracture 
      Risk After Ischemic Stroke in a Canadian Cohort.
PG  - 925-931
LID - 10.1001/jamaneurol.2019.1114 [doi]
AB  - IMPORTANCE: The risk for low-trauma fracture is increased by more than 30% after 
      ischemic stroke, but existing fracture risk scores do not account for history of 
      stroke as a high-risk condition. OBJECTIVE: To derive a risk score to predict the 
      probability of fracture within 1 year after ischemic stroke and validate it in a 
      separate cohort. DESIGN, SETTING, AND PARTICIPANTS: Prognostic study of a cohort 
      from the Ontario Stroke Registry, a population-based sample of adults in Ontario, 
      Canada, who were hospitalized with ischemic stroke from July 1, 2003, to March 
      31, 2012, with 1 year of follow-up. A population-based validation cohort 
      consisted of a sample of 13 698 consecutive stroke admissions captured across 5 
      years: April 2002 to March 2003, April 2004 to March 2005, April 2008 to March 
      2009, April 2010 to March 2011, and April 2012 to March 2013. EXPOSURES: 
      Predictor variables were selected based on biological plausibility and 
      association with fracture risk. Age, sex, and modified Rankin score were 
      abstracted from the medical records part of the Ontario Stroke Audit, and other 
      characteristics were abstracted from administrative health data. MAIN OUTCOMES 
      AND MEASURES: Incidence of low-trauma fracture within 1 year of discharge, based 
      on administrative health data. RESULTS: The Fracture Risk after Ischemic Stroke 
      (FRAC-Stroke) Score was derived in 20 435 patients hospitalized for ischemic 
      stroke (mean [SD] age, 71.6 [14.0] years; 9564 [46.8%] women) from the Ontario 
      Stroke Registry discharged from July 1, 2003, to March 31, 2012, using Fine-Gray 
      competing risk regression. Low-trauma fracture occurred within 1 year of 
      discharge in 741 of the 20 435 patients (3.6%) in the derivation cohort. Age, 
      discharge modified Rankin score (mRS), and history of rheumatoid arthritis, 
      osteoporosis, falls, and previous fracture were associated with the cumulative 
      incidence of low trauma fracture in the derivation cohort. Model discrimination 
      in the validation cohort (n = 13 698) was good (C statistic, 0.70). Discharge mRS 
      was an important discriminator of risk (relative integrated discrimination 
      improvement, 8.7%), with highest risk in patients with mRS 3 and 4 but lowest in 
      bedbound patients (mRS 5). From the lowest to the highest FRAC-Stroke quintile, 
      the cumulative incidence of 1-year low-trauma fracture increased from 1.3% to 
      9.0% in the validation cohort. Predicted and observed rates of fracture were 
      similar in the external validation cohort. Analysis was conducted from July 2016 
      to January 2019. CONCLUSIONS AND RELEVANCE: The FRAC-Stroke score allows the 
      clinician to identify ischemic stroke survivors at higher risk of low-trauma 
      fracture within 1 year of hospital discharge. This information might be used to 
      select patients for interventions to prevent fractures.
FAU - Smith, Eric E
AU  - Smith EE
AD  - Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada.
FAU - Fang, Jiming
AU  - Fang J
AD  - ICES, Toronto, Canada.
FAU - Alibhai, Shabbir M
AU  - Alibhai SM
AD  - Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
AD  - Institute of Health Policy, Management and Evaluation, University of Toronto, 
      Toronto, Ontario, Canada.
AD  - Division of General Internal Medicine, University Health Network, Toronto, 
      Ontario, Canada.
AD  - Toronto General Research Institute, University Health Network, Toronto, Ontario, 
      Canada.
AD  - Osteoporosis Program and Centre for Excellence in Skeletal Health Assessment, 
      University Health Network, Toronto, Ontario, Canada.
FAU - Cram, Peter
AU  - Cram P
AD  - ICES, Toronto, Canada.
AD  - Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
AD  - Institute of Health Policy, Management and Evaluation, University of Toronto, 
      Toronto, Ontario, Canada.
AD  - Division of General Internal Medicine, University Health Network, Toronto, 
      Ontario, Canada.
FAU - Cheung, Angela M
AU  - Cheung AM
AD  - Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
AD  - Institute of Health Policy, Management and Evaluation, University of Toronto, 
      Toronto, Ontario, Canada.
AD  - Division of General Internal Medicine, University Health Network, Toronto, 
      Ontario, Canada.
AD  - Toronto General Research Institute, University Health Network, Toronto, Ontario, 
      Canada.
AD  - Osteoporosis Program and Centre for Excellence in Skeletal Health Assessment, 
      University Health Network, Toronto, Ontario, Canada.
FAU - Casaubon, Leanne K
AU  - Casaubon LK
AD  - Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
AD  - Division of Neurology, University Health Network, Toronto, Ontario, Canada.
FAU - Kapoor, Eshita
AU  - Kapoor E
AD  - Medical Student, Faculty of Medicine, University of Toronto, Toronto, Ontario, 
      Canada.
FAU - Austin, Peter C
AU  - Austin PC
AD  - ICES, Toronto, Canada.
AD  - Institute of Health Policy, Management and Evaluation, University of Toronto, 
      Toronto, Ontario, Canada.
FAU - Kapral, Moira K
AU  - Kapral MK
AD  - ICES, Toronto, Canada.
AD  - Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
AD  - Institute of Health Policy, Management and Evaluation, University of Toronto, 
      Toronto, Ontario, Canada.
AD  - Division of General Internal Medicine, University Health Network, Toronto, 
      Ontario, Canada.
AD  - Toronto General Research Institute, University Health Network, Toronto, Ontario, 
      Canada.
AD  - Osteoporosis Program and Centre for Excellence in Skeletal Health Assessment, 
      University Health Network, Toronto, Ontario, Canada.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - JAMA Neurol
JT  - JAMA neurology
JID - 101589536
SB  - IM
PMC - PMC6515569
COIS- Conflict of Interest Disclosures: Dr Smith reported receiving personal fees from 
      Portola Pharmaceuticals, Alnylam Pharmaceuticals, and UptoDate outside the 
      submitted work. Dr Casaubon reported receiving speaking fees from Bayer, 
      consulting fees from Medtronic, and was a site principal investigator for a 
      clinical trial sponsored by NoNO Inc outside the submitted work. Dr Cheung 
      reported grants from Amgen and personal fees from Amgen and Eli Lilly outside the 
      submitted work. Dr Kapral reported grants from Heart and Stroke Foundation of 
      Canada during the conduct of the study. No other disclosures were reported.
EDAT- 2019/05/14 06:00
MHDA- 2019/05/14 06:01
PMCR- 2020/05/13
CRDT- 2019/05/14 06:00
PHST- 2019/05/14 06:00 [pubmed]
PHST- 2019/05/14 06:01 [medline]
PHST- 2019/05/14 06:00 [entrez]
PHST- 2020/05/13 00:00 [pmc-release]
AID - 2732928 [pii]
AID - noi190027 [pii]
AID - 10.1001/jamaneurol.2019.1114 [doi]
PST - ppublish
SO  - JAMA Neurol. 2019 Aug 1;76(8):925-931. doi: 10.1001/jamaneurol.2019.1114.

PMID- 30983166
OWN - NLM
STAT- MEDLINE
DCOM- 20200205
LR  - 20240720
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Print)
IS  - 2326-5191 (Linking)
VI  - 71
IP  - 9
DP  - 2019 Sep
TI  - A Multicenter, Randomized, Placebo-Controlled Trial of Atorvastatin for the 
      Primary Prevention of Cardiovascular Events in Patients With Rheumatoid 
      Arthritis.
PG  - 1437-1449
LID - 10.1002/art.40892 [doi]
AB  - OBJECTIVE: Rheumatoid arthritis (RA) is associated with increased cardiovascular 
      event (CVE) risk. The impact of statins in RA is not established. We assessed 
      whether atorvastatin is superior to placebo for the primary prevention of CVEs in 
      RA patients. METHODS: A randomized, double-blind, placebo-controlled trial was 
      designed to detect a 32% CVE risk reduction based on an estimated 1.6% per annum 
      event rate with 80% power at P < 0.05. RA patients age >50 years or with a 
      disease duration of >10 years who did not have clinical atherosclerosis, 
      diabetes, or myopathy received atorvastatin 40 mg daily or matching placebo. The 
      primary end point was a composite of cardiovascular death, myocardial infarction, 
      stroke, transient ischemic attack, or any arterial revascularization. Secondary 
      and tertiary end points included plasma lipids and safety. RESULTS: A total of 
      3,002 patients (mean age 61 years; 74% female) were followed up for a median of 
      2.51 years (interquartile range [IQR] 1.90, 3.49 years) (7,827 patient-years). 
      The study was terminated early due to a lower than expected event rate (0.70% per 
      annum). Of the 1,504 patients receiving atorvastatin, 24 (1.6%) experienced a 
      primary end point, compared with 36 (2.4%) of the 1,498 receiving placebo (hazard 
      ratio [HR] 0.66 [95% confidence interval (95% CI) 0.39, 1.11]; P = 0.115 and 
      adjusted HR 0.60 [95% CI 0.32, 1.15]; P = 0.127). At trial end, patients 
      receiving atorvastatin had a mean ± SD low-density lipoprotein (LDL) cholesterol 
      level 0.77 ± 0.04 mmoles/liter lower than those receiving placebo (P < 0.0001). 
      C-reactive protein level was also significantly lower in the atorvastatin group 
      than the placebo group (median 2.59 mg/liter [IQR 0.94, 6.08] versus 3.60 
      mg/liter [IQR 1.47, 7.49]; P < 0.0001). CVE risk reduction per mmole/liter 
      reduction in LDL cholesterol was 42% (95% CI -14%, 70%). The rates of adverse 
      events in the atorvastatin group (n = 298 [19.8%]) and placebo group (n = 292 
      [19.5%]) were similar. CONCLUSION: Atorvastatin 40 mg daily is safe and results 
      in a significantly greater reduction of LDL cholesterol level than placebo in 
      patients with RA. The 34% CVE risk reduction is consistent with the Cholesterol 
      Treatment Trialists' Collaboration meta-analysis of statin effects in other 
      populations.
CI  - © 2019, The Authors. Arthritis & Rheumatology published by Wiley Periodicals, 
      Inc. on behalf of American College of Rheumatology.
FAU - Kitas, George D
AU  - Kitas GD
AD  - Dudley Group NHS Foundation Trust, Russells Hall Hospital, Stourbridge, UK, and 
      Research UK Centre for Epidemiology, Manchester, UK.
FAU - Nightingale, Peter
AU  - Nightingale P
AD  - University of Birmingham, Birmingham, UK.
FAU - Armitage, Jane
AU  - Armitage J
AD  - University of Oxford, Oxford, UK.
FAU - Sattar, Naveed
AU  - Sattar N
AD  - University of Glasgow, Glasgow, UK, and Oxford Centre for Diabetes, Endocrinology 
      and Metabolism, Oxford, UK.
FAU - Belch, Jill J F
AU  - Belch JJF
AD  - University of Dundee and Ninewells Hospital and Medical School, Dundee, UK.
FAU - Symmons, Deborah P M
AU  - Symmons DPM
AD  - Arthritis Research UK Centre for Epidemiology, University of Manchester, and NIHR 
      Manchester Biomedical Research Center, Manchester NHS Foundation Trust, 
      Manchester, UK.
CN  - TRACE RA Consortium
LA  - eng
SI  - ISRCTN/41829447
GR  - MR/P020941/1/MRC_/Medical Research Council/United Kingdom
GR  - 16514/ARC_/Arthritis Research UK/United Kingdom
GR  - MR/K015346/1/MRC_/Medical Research Council/United Kingdom
GR  - 19704/ARC_/Arthritis Research UK/United Kingdom
GR  - SP/14/3/31114/BHF_/British Heart Foundation/United Kingdom
GR  - MC_UU_12026/5/MRC_/Medical Research Council/United Kingdom
GR  - 19704/VAC_/Versus Arthritis/United Kingdom
GR  - SP/08/010/25939/BHF_/British Heart Foundation/United Kingdom
GR  - MC_U137686853/MRC_/Medical Research Council/United Kingdom
GR  - SP/06/001/BHF_/British Heart Foundation/United Kingdom
GR  - MC_UU_12023/14/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
DEP - 20190722
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Anticholesteremic Agents)
RN  - 0 (Cholesterol, LDL)
RN  - A0JWA85V8F (Atorvastatin)
SB  - IM
CIN - Arthritis Rheumatol. 2019 Sep;71(9):1393-1395. doi: 10.1002/art.40891. PMID: 
      30983150
MH  - Aged
MH  - Anticholesteremic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/blood/*complications
MH  - Atorvastatin/*therapeutic use
MH  - Cardiovascular Diseases/etiology/*prevention & control
MH  - Cholesterol, LDL/blood/drug effects
MH  - Double-Blind Method
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Primary Prevention/*methods
MH  - Proportional Hazards Models
MH  - Treatment Outcome
PMC - PMC6771601
FIR - Kitas, George
IR  - Kitas G
FIR - Belch, Jill
IR  - Belch J
FIR - Symmons, Deborah
IR  - Symmons D
FIR - Williams, Hawys
IR  - Williams H
FIR - Vasishta, Shobna
IR  - Vasishta S
FIR - Storey, Rebecca
IR  - Storey R
FIR - Nightingale, Peter
IR  - Nightingale P
FIR - Bruce, Ian
IR  - Bruce I
FIR - Durrington, Paul
IR  - Durrington P
FIR - McInnes, Iain
IR  - McInnes I
FIR - Sattar, Naveed
IR  - Sattar N
FIR - Situnayake, Deva
IR  - Situnayake D
FIR - Struthers, Allan
IR  - Struthers A
FIR - Lowe, Gordon
IR  - Lowe G
FIR - Armitage, Jane
IR  - Armitage J
FIR - Fox, Keith
IR  - Fox K
FIR - Haskard, Dorian
IR  - Haskard D
FIR - Dore, Caroline
IR  - Dore C
FIR - Bosworth, Ailsa
IR  - Bosworth A
FIR - Kitas, George
IR  - Kitas G
FIR - Belch, Jill
IR  - Belch J
FIR - Symmons, Deborah
IR  - Symmons D
FIR - Williams, Hawys
IR  - Williams H
FIR - Frenneaux, Michael
IR  - Frenneaux M
FIR - Edwards, Christopher
IR  - Edwards C
FIR - Emberson, Jonathan
IR  - Emberson J
FIR - Bax, Deborah
IR  - Bax D
FIR - Cobbe, Stuart
IR  - Cobbe S
FIR - Stott, David
IR  - Stott D
FIR - Sturrock, Roger
IR  - Sturrock R
FIR - Macfarlane, Peter
IR  - Macfarlane P
FIR - Klocke, Rainer
IR  - Klocke R
FIR - Pullar, Tom
IR  - Pullar T
FIR - Knight, Susan
IR  - Knight S
FIR - Rowe, Iain
IR  - Rowe I
FIR - Kumar, Pradeep
IR  - Kumar P
FIR - Goodson, Nicky
IR  - Goodson N
FIR - Mulherin, Diarmuid
IR  - Mulherin D
FIR - Brzeski, Micheal
IR  - Brzeski M
FIR - Gardiner, Philip
IR  - Gardiner P
FIR - Situnayake, Deva
IR  - Situnayake D
FIR - Walker, David
IR  - Walker D
FIR - Callaghan, Rob
IR  - Callaghan R
FIR - Allen, Margaret
IR  - Allen M
FIR - McCarey, David
IR  - McCarey D
FIR - George, Emmanuel
IR  - George E
FIR - Deighton, Chris
IR  - Deighton C
FIR - Kirkham, Bruce
IR  - Kirkham B
FIR - Teh, Lee-Suan
IR  - Teh LS
FIR - Luqmani, Raashid
IR  - Luqmani R
FIR - Chakravarty, Kuntal
IR  - Chakravarty K
FIR - Nixon, Jenny
IR  - Nixon J
FIR - Richards, Selwyn
IR  - Richards S
FIR - Scott, David
IR  - Scott D
FIR - Woolf, Tony
IR  - Woolf T
FIR - Prouse, Peter
IR  - Prouse P
FIR - Packham, Jonathan
IR  - Packham J
FIR - Davies, Martin
IR  - Davies M
FIR - DeLord, Denise
IR  - DeLord D
FIR - O'Neill, Terence
IR  - O'Neill T
FIR - Pande, Ira
IR  - Pande I
FIR - Harvie, John
IR  - Harvie J
FIR - Watts, Richard
IR  - Watts R
FIR - Rankin, Elizabeth
IR  - Rankin E
FIR - Papasavvas, George
IR  - Papasavvas G
FIR - Emery, Paul
IR  - Emery P
FIR - Sinha, Arvind
IR  - Sinha A
FIR - Dasgupta, Bhaskar
IR  - Dasgupta B
FIR - Bruce, Ian
IR  - Bruce I
FIR - Creamer, Paul
IR  - Creamer P
FIR - Zoma, Asad
IR  - Zoma A
FIR - Walsh, David
IR  - Walsh D
FIR - Van-Laar, Jaap
IR  - Van-Laar J
FIR - Capps, Nigel
IR  - Capps N
FIR - Cairns, Andrew
IR  - Cairns A
FIR - Marguerie, Christopher
IR  - Marguerie C
FIR - Kumar, Namita
IR  - Kumar N
FIR - Abernethy, Rikki
IR  - Abernethy R
FIR - Lillicrap, Mark
IR  - Lillicrap M
FIR - Ralston, Stuart
IR  - Ralston S
FIR - Makadsi, Raad
IR  - Makadsi R
FIR - Hopkinson, Neil
IR  - Hopkinson N
FIR - Tan, Su
IR  - Tan S
FIR - Akil, Mohammed
IR  - Akil M
FIR - Ahmad, Yasmeen
IR  - Ahmad Y
FIR - Adler, Matthew
IR  - Adler M
FIR - Bukhari, Marwan
IR  - Bukhari M
FIR - Sanders, Paul
IR  - Sanders P
FIR - Roussou, Euthalia
IR  - Roussou E
FIR - Binymin, Khalid
IR  - Binymin K
FIR - Hassan, Alaa
IR  - Hassan A
FIR - Hughes, Rod
IR  - Hughes R
FIR - O'Reilly, David
IR  - O'Reilly D
FIR - Sainsbury, Paul
IR  - Sainsbury P
FIR - Richmond, Ruth
IR  - Richmond R
FIR - Malgorzata, Magliano
IR  - Malgorzata M
FIR - Nisar, Mohammed
IR  - Nisar M
FIR - McEntergart, Ann
IR  - McEntergart A
FIR - Roy, Dipak
IR  - Roy D
FIR - Marks, Jeffrey
IR  - Marks J
FIR - Batley, Michael
IR  - Batley M
FIR - McKenna, Frank
IR  - McKenna F
FIR - Irani, Mike
IR  - Irani M
FIR - Harris, Helen
IR  - Harris H
FIR - Smyth, Anita
IR  - Smyth A
FIR - Tunn, Eddie
IR  - Tunn E
FIR - Young, Adam
IR  - Young A
FIR - Thomas, Joegi
IR  - Thomas J
FIR - Hall, Frances
IR  - Hall F
FIR - Marshall, Tarnya
IR  - Marshall T
FIR - Rao, Chandini
IR  - Rao C
FIR - Baburaj, Krishnan
IR  - Baburaj K
FIR - Dixey, Josh
IR  - Dixey J
FIR - Gendi, Nagui
IR  - Gendi N
FIR - Birrell, Fraser
IR  - Birrell F
FIR - Chelliah, Gladstone
IR  - Chelliah G
FIR - Morgan, Ann
IR  - Morgan A
FIR - Fishman, Daniel
IR  - Fishman D
FIR - Knights, Sally
IR  - Knights S
FIR - Coady, David
IR  - Coady D
FIR - Makadsi, Raad
IR  - Makadsi R
FIR - Smith, Bill
IR  - Smith B
FIR - Harrison, Beverley
IR  - Harrison B
FIR - Walker, David
IR  - Walker D
FIR - Siebert, Stefan
IR  - Siebert S
FIR - Chan, Anthony
IR  - Chan A
FIR - Putchakayala, Kiran
IR  - Putchakayala K
FIR - Al-Ansari, Atheer
IR  - Al-Ansari A
FIR - Gough, Andrew
IR  - Gough A
FIR - Naz, Sophia
IR  - Naz S
FIR - Kumar, Namita
IR  - Kumar N
FIR - Pyne, Dev
IR  - Pyne D
FIR - Mahmud, Taher
IR  - Mahmud T
FIR - Patel, Yusaf
IR  - Patel Y
FIR - Isdale, Amanda
IR  - Isdale A
EDAT- 2019/04/16 06:00
MHDA- 2020/02/06 06:00
PMCR- 2019/10/01
CRDT- 2019/04/16 06:00
PHST- 2018/09/23 00:00 [received]
PHST- 2019/03/12 00:00 [accepted]
PHST- 2019/04/16 06:00 [pubmed]
PHST- 2020/02/06 06:00 [medline]
PHST- 2019/04/16 06:00 [entrez]
PHST- 2019/10/01 00:00 [pmc-release]
AID - ART40892 [pii]
AID - 10.1002/art.40892 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2019 Sep;71(9):1437-1449. doi: 10.1002/art.40892. Epub 2019 
      Jul 22.

PMID- 30886957
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240214
IS  - 2520-1026 (Electronic)
IS  - 2520-1026 (Linking)
VI  - 2
DP  - 2018
TI  - Methotrexate therapy impacts on red cell distribution width and its predictive 
      value for cardiovascular events in patients with rheumatoid arthritis.
PG  - 6
LID - 10.1186/s41927-018-0012-0 [doi]
LID - 6
AB  - BACKGROUND: Methotrexate (MTX) is well known to affect folic acid metabolism, so 
      MTX treatment can result in alterations of mean corpuscular volume (MCV), which 
      may impact on red cell distribution width (RDW), as MCV levels feed into RDW 
      calculation. We thus questioned whether RDW levels and subsequently its 
      diagnostic utility in RA subjects, as reported before, are influenced by ongoing 
      MTX therapy.We assessed the impact of disease modifying drug (DMARD) treatment, 
      especially MTX, on RDW and evaluated their influence on the predictive value of 
      RDW for cardiovascular (CV) events in patients with rheumatoid arthritis (RA). As 
      far as we know, this is the first study evaluating the influence of MTX on RDW. 
      METHODS: Medical treatment, disease activity, laboratory parameters and history 
      of CV events were retrospectively analysed in 385 RA patients at disease onset 
      and at last follow up at our clinic. Additionally, in patients with CV event, 
      data were recorded at last follow up prior the CV event. RESULTS: Disease 
      parameters and laboratory findings associated with a serious vascular event were 
      older age (p < 0,001), longer disease duration (p = 0,002) and a higher RDW at 
      diagnosis (p = 0,025). No differences in RDW levels became evident with any other 
      treatment regimen beside MTX. MTX treated patients had significantly higher RDW 
      compared to subjects without this drug (p < 0,001). In RA patients without MTX 
      treatment, we found RDW level significantly different between those with versus 
      without a CV event, whereas this difference disappeared in subjects receiving 
      MTX. CONCLUSION: MTX impacts on RDW and might therefor reduce its prognostic 
      value for CV events in patients taking MTX, whereas an increased RDW at diagnosis 
      remains an early risk predictor for myocardial infarction and stroke in RA 
      patients.
FAU - Held, Julia
AU  - Held J
AD  - 1Department of Internal Medicine II, Infectious Diseases, Immunology, 
      Rheumatology, Pneumology, Medical University of Innsbruck, Anichstr. 35, A-6020 
      Innsbruck, Austria. ISNI: 0000 0000 8853 2677. GRID: grid.5361.1
FAU - Mosheimer-Feistritzer, Birgit
AU  - Mosheimer-Feistritzer B
AD  - 1Department of Internal Medicine II, Infectious Diseases, Immunology, 
      Rheumatology, Pneumology, Medical University of Innsbruck, Anichstr. 35, A-6020 
      Innsbruck, Austria. ISNI: 0000 0000 8853 2677. GRID: grid.5361.1
FAU - Gruber, Johann
AU  - Gruber J
AD  - 1Department of Internal Medicine II, Infectious Diseases, Immunology, 
      Rheumatology, Pneumology, Medical University of Innsbruck, Anichstr. 35, A-6020 
      Innsbruck, Austria. ISNI: 0000 0000 8853 2677. GRID: grid.5361.1
FAU - Mur, Erich
AU  - Mur E
AD  - 2Department for Physical Medicine and Rehabilitation, University of Innsbruck, 
      Innsbruck, Austria. ISNI: 0000 0001 2151 8122. GRID: grid.5771.4
FAU - Weiss, Günter
AU  - Weiss G
AD  - 1Department of Internal Medicine II, Infectious Diseases, Immunology, 
      Rheumatology, Pneumology, Medical University of Innsbruck, Anichstr. 35, A-6020 
      Innsbruck, Austria. ISNI: 0000 0000 8853 2677. GRID: grid.5361.1
AD  - Christian Doppler Laboratory for Iron Metabolism and Anemia Research, Innsbruck, 
      Austria.
LA  - eng
GR  - TRP 188/FWF_/Austrian Science Fund FWF/Austria
PT  - Journal Article
DEP - 20180307
PL  - England
TA  - BMC Rheumatol
JT  - BMC rheumatology
JID - 101738571
PMC - PMC6390531
OTO - NOTNLM
OT  - Cardiovascular events
OT  - Methotrexate
OT  - Red cell distribution width
OT  - Rheumatoid arthritis
COIS- The study was approved by the Ethics committee at Medical University Innsbruck, 
      Austria (study number AN2014-0277). Patients in the database provided written 
      informed consent, for patients who were retrospectively analysed, no consent to 
      participate was obtained. This was approved by the Ethics committee at Medical 
      University Innsbruck, Austria.Not applicable.The authors declare that they have 
      no competing interests.Springer Nature remains neutral with regard to 
      jurisdictional claims in published maps and institutional affiliations.
EDAT- 2019/03/20 06:00
MHDA- 2019/03/20 06:01
PMCR- 2018/03/07
CRDT- 2019/03/20 06:00
PHST- 2017/11/25 00:00 [received]
PHST- 2018/02/09 00:00 [accepted]
PHST- 2019/03/20 06:00 [entrez]
PHST- 2019/03/20 06:00 [pubmed]
PHST- 2019/03/20 06:01 [medline]
PHST- 2018/03/07 00:00 [pmc-release]
AID - 12 [pii]
AID - 10.1186/s41927-018-0012-0 [doi]
PST - epublish
SO  - BMC Rheumatol. 2018 Mar 7;2:6. doi: 10.1186/s41927-018-0012-0. eCollection 2018.

PMID- 30875456
OWN - NLM
STAT- MEDLINE
DCOM- 20200720
LR  - 20210109
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Print)
IS  - 2151-464X (Linking)
VI  - 72
IP  - 4
DP  - 2020 Apr
TI  - Comparative Risk of Cardiovascular Events With Biologic and Synthetic 
      Disease-Modifying Antirheumatic Drugs in Patients With Rheumatoid Arthritis: A 
      Systematic Review and Meta-Analysis.
PG  - 561-576
LID - 10.1002/acr.23875 [doi]
AB  - OBJECTIVE: We performed a systematic review and meta-analysis to evaluate the 
      comparative effects of tumor necrosis factor inhibitors (TNFi), non-TNFi 
      biologics, and conventional synthetic disease-modifying antirheumatic drugs 
      (csDMARDs) on cardiovascular risk in rheumatoid arthritis (RA). METHODS: Using a 
      systematic search through May 8, 2018, we included 14 observational studies in 
      adults with RA treated with TNFi, non-TNFi biologics, tofacitinib, or csDMARDs, 
      reporting the risk of major adverse cardiovascular events (MACE) or stroke. Only 
      studies reporting active comparators were included. We performed random effects 
      meta-analysis and estimated odds ratios (ORs) and 95% confidence intervals (95% 
      CIs). RESULTS: As compared to TNFi, tocilizumab was associated with a decreased 
      risk of MACE (OR 0.59 [95% CI 0.34-1.00]), whereas csDMARDs were associated with 
      an increased risk of MACE (csDMARDs including methotrexate OR 1.45 [95% CI 
      1.09-1.93]; without methotrexate OR 2.57 [95% CI 1.32-5.00]), without 
      heterogeneity (I(2) = 0%); there was no difference in risk of MACE between 
      abatacept and TNFi (OR 0.89 [95% CI 0.71-1.11]), or between tocilizumab and 
      abatacept (OR 0.81 [0.57-1.16]). Based on 11 cohorts (n = 135,053 patients), as 
      compared to TNFi, csDMARDs were associated with an increased risk of stroke (OR 
      1.17 [95% CI 1.01-1.36]); there was no difference in risk of stroke between 
      different biologics (tocilizumab versus TNFi OR 0.98 [95% CI 0.59-1.61]; 
      abatacept versus TNFi OR 1.08 [0.86-1.34]; tocilizumab versus abatacept OR 0.73 
      [95% CI 0.39-1.38]), without heterogeneity (I(2) = 0%). No comparative studies on 
      cardiovascular risk with tofacitinib were identified. CONCLUSION: Based on 
      meta-analysis, as compared to TNFi, tocilizumab may be associated with a reduced 
      risk of MACE, whereas csDMARDs may be associated with an increased risk of MACE 
      and stroke.
CI  - © 2019, American College of Rheumatology.
FAU - Singh, Siddharth
AU  - Singh S
AD  - University of California San Diego, La Jolla.
FAU - Fumery, Mathurin
AU  - Fumery M
AD  - Amiens University and Hospital and Université de Picardie Jules Verne, Amiens, 
      France.
FAU - Singh, Abha G
AU  - Singh AG
AD  - University of California San Diego, La Jolla.
FAU - Singh, Namrata
AU  - Singh N
AUID- ORCID: 0000-0001-7149-363X
AD  - University of Washington, Seattle.
FAU - Prokop, Larry J
AU  - Prokop LJ
AD  - Mayo Clinic, Rochester, Minnesota.
FAU - Dulai, Parambir S
AU  - Dulai PS
AD  - University of California San Diego, La Jolla.
FAU - Sandborn, William J
AU  - Sandborn WJ
AD  - University of California San Diego, La Jolla.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AUID- ORCID: 0000-0002-8907-8976
AD  - University of Alabama at Birmingham.
LA  - eng
GR  - K23 DK117058/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Systematic Review
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
SB  - IM
MH  - Antirheumatic Agents/*adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Biological Products/*adverse effects/therapeutic use
MH  - Cardiovascular Diseases/*chemically induced
MH  - Humans
MH  - Risk
PMC - PMC6745288
MID - NIHMS1016510
EDAT- 2019/03/16 06:00
MHDA- 2020/07/21 06:00
PMCR- 2020/09/15
CRDT- 2019/03/16 06:00
PHST- 2018/07/27 00:00 [received]
PHST- 2019/03/05 00:00 [accepted]
PHST- 2019/03/16 06:00 [pubmed]
PHST- 2020/07/21 06:00 [medline]
PHST- 2019/03/16 06:00 [entrez]
PHST- 2020/09/15 00:00 [pmc-release]
AID - 10.1002/acr.23875 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2020 Apr;72(4):561-576. doi: 10.1002/acr.23875.

PMID- 30791646
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231109
IS  - 2076-3271 (Electronic)
IS  - 2076-3271 (Linking)
VI  - 7
IP  - 2
DP  - 2019 Feb 20
TI  - Assessment of Cardiovascular Disease Risk and Therapeutic Patterns among Urban 
      Black Rheumatoid Arthritis Patients.
LID - 10.3390/medsci7020031 [doi]
LID - 31
AB  - Rheumatoid arthritis (RA) patients have nearly twice the risk of cardiovascular 
      disease (CVD) compared to the general population. We aimed to assess, in a 
      predominantly Black population, the prevalence of traditional and RA-specific CVD 
      risk factors and therapeutic patterns. Utilizing ICD codes, we identified 503 RA 
      patients ≥18 years old who were seen from 2010 to 2017. Of them, 88.5% were 
      Black, 87.9% were women and 29.4% were smokers. CVD risk factors (obesity, 
      diabetes, hypertension, dyslipidemia) were higher than in previously reported 
      White RA cohorts. Eighty-seven percent of the patients had at least one 
      traditional CVD risk factor, 37% had three or more traditional CVD risk factors 
      and 58% had RA-specific risk factors (seropositive RA, >10 years of disease, 
      joint erosions, elevated inflammatory markers, extra-articular disease, body mass 
      index (BMI) < 20). CV outcomes (coronary artery disease/myocardial infarction, 
      heart failure, atrial fibrillation and stroke) were comparable to published 
      reports. Higher steroid use, which increases CVD risk, and lesser utilization of 
      biologics (decrease CV risk) were also observed. Our Black RA cohort had higher 
      rates of traditional CVD risk factors, in addition to chronic inflammation from 
      aggressive RA, which places our patients at a higher risk for CVD outcomes, 
      calling for revised risk stratification strategies and effective interventions to 
      address comorbidities in this vulnerable population.
FAU - McFarlane, Isabel M
AU  - McFarlane IM
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA. 
      Isabel.McFarlane@downstate.edu.
FAU - Zhaz Leon, Su Yien
AU  - Zhaz Leon SY
AD  - Samaritan Medical Center Department of Rheumatology, Watertown, NY 13601, USA. 
      szhaz@shsny.com.
FAU - Bhamra, Manjeet S
AU  - Bhamra MS
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Burza, Aaliya
AU  - Burza A
AD  - Department of Medicine, Division of Pulmonary and Critical Care State, SUNY 
      Downstate Medical Center/Health + Hospitals Kings County, Brooklyn, NY 11201, 
      USA. Aaliya.Burza@downstate.edu.
FAU - Waite, Stephen Anthony
AU  - Waite SA
AD  - Department of Radiology SUNY Downstate Medical Center/Health + Hospitals Kings 
      County, Brooklyn, NY 11201, USA. Stephen.Waite@downstate.edu.
FAU - Rodriguez Alvarez, Milena
AU  - Rodriguez Alvarez M
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Koci, Kristaq
AU  - Koci K
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Taklalsingh, Nicholas
AU  - Taklalsingh N
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Kaplan, Ian
AU  - Kaplan I
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Pathiparampil, Joshy
AU  - Pathiparampil J
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Kabani, Naureen
AU  - Kabani N
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Watler, Elsie
AU  - Watler E
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Sorrento, Cristina S
AU  - Sorrento CS
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Frefer, Mosab
AU  - Frefer M
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Vaitkus, Vytas
AU  - Vaitkus V
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Green, Jason
AU  - Green J
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Matthew, Keron
AU  - Matthew K
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Arroyo-Mercado, Fray
AU  - Arroyo-Mercado F
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Lyo, Helen
AU  - Lyo H
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Soliman, Faisal
AU  - Soliman F
AD  - Department of Geriatrics, New York Presbyterian Brooklyn Methodist Hospital, 
      Brooklyn, NY 11201, USA. fas9051@nyp.org.
FAU - Sanchez, Randolph A
AU  - Sanchez RA
AD  - Department of Rheumatology, Hahnemann Hospital, Philadelphia, PA 19019, USA. 
      Randysanchez2011@gmail.com.
FAU - Reyes, Felix M
AU  - Reyes FM
AD  - Department of Family and Social Medicine, Montefiore Medical Center Albert 
      Einstein College of Medicine, Bronx, NY 10468, USA. freyesv@montefiore.org.
FAU - Ozeri, David J
AU  - Ozeri DJ
AD  - Sheba Medical Center, Tel Aviv 6100000, Israel. david.ozeri@sheba.health.gov.il.
FAU - Dronamraju, Veena
AU  - Dronamraju V
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Trevisonno, Michael
AU  - Trevisonno M
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Grant, Christon
AU  - Grant C
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Clerger, Guerrier
AU  - Clerger G
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Amin, Khabbab
AU  - Amin K
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Freeman, Latoya
AU  - Freeman L
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Dawkins, Makeda
AU  - Dawkins M
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Lopez, Diana Lenis
AU  - Lopez DL
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Smerling, Jonathan
AU  - Smerling J
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Gondal, Irfan
AU  - Gondal I
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Dellinger, Elaine
AU  - Dellinger E
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Paltoo, Karen
AU  - Paltoo K
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Bhat, Hina
AU  - Bhat H
AD  - Department of Medicine, Division of Rheumatology SUNY Downstate Medical 
      Center/Health + Hospitals Kings County, Brooklyn, NY 11201, USA.
FAU - Kolla, Srinivas
AU  - Kolla S
AD  - Department of Radiology SUNY Downstate Medical Center/Health + Hospitals Kings 
      County, Brooklyn, NY 11201, USA.
LA  - eng
PT  - Journal Article
DEP - 20190220
PL  - Switzerland
TA  - Med Sci (Basel)
JT  - Medical sciences (Basel, Switzerland)
JID - 101629322
PMC - PMC6410013
OTO - NOTNLM
OT  - cardiovascular outcomes
OT  - erosive disease
OT  - extra-articular manifestations
OT  - rheumatoid arthritis
OT  - rheumatoid arthritis specific risk factors
OT  - seropositive rheumatoid arthritis
OT  - therapeutic patterns
OT  - traditional risk factors
COIS- The authors declare no conflict of interest.
EDAT- 2019/02/23 06:00
MHDA- 2019/02/23 06:01
PMCR- 2019/02/20
CRDT- 2019/02/23 06:00
PHST- 2018/12/26 00:00 [received]
PHST- 2019/01/27 00:00 [revised]
PHST- 2019/01/27 00:00 [accepted]
PHST- 2019/02/23 06:00 [entrez]
PHST- 2019/02/23 06:00 [pubmed]
PHST- 2019/02/23 06:01 [medline]
PHST- 2019/02/20 00:00 [pmc-release]
AID - medsci7020031 [pii]
AID - medsci-07-00031 [pii]
AID - 10.3390/medsci7020031 [doi]
PST - epublish
SO  - Med Sci (Basel). 2019 Feb 20;7(2):31. doi: 10.3390/medsci7020031.

PMID- 30742401
STAT- Publisher
CTDT- 20190211
PB  - National Center for Biotechnology Information (US)
DP  - 2012
TI  - Piroxicam Therapy and CYP2C9 Genotype.
BTI - Medical Genetics Summaries
AB  - Piroxicam (brand name Feldene) is a nonsteroidal anti-inflammatory drug (NSAID) 
      used to treat osteoarthritis and rheumatoid arthritis. Piroxicam provides pain 
      relief and reduces inflammation. Piroxicam is primarily metabolized by CYP2C9. 
      Individuals who lack CYP2C9 activity (“CYP2C9 poor metabolizers”) have an 
      increased exposure to piroxicam, and an increased risk of side effects. Like all 
      NSAIDs, piroxicam increases the risk of serious cardiovascular events, including 
      myocardial infarction and stroke, and serious gastrointestinal (GI) adverse 
      events such as bleeding, ulceration, and perforation. The standard dose of 
      piroxicam for osteoarthritis and rheumatoid arthritis in adults is 20 mg once 
      daily. But for all patients, the lowest effective dose of piroxicam should be 
      used for the shortest length of time, consistent with the treatment goals of each 
      individual (1). The FDA-approved drug label for piroxicam states that a dose 
      reduction should be considered in “patients who are known or suspected to be poor 
      CYP2C9 metabolizers based on genotype or previous history/experience with other 
      CYP2C9 substrates (such as warfarin and phenytoin)”. Dose reductions should be 
      considered because these patients may have abnormally high plasma levels of 
      piroxicam caused by reduced metabolic clearance. However, specific dose 
      reductions based on CYP2C9 phenotype are not provided (Table 1) (1). As for all 
      NSAIDs, piroxicam is contraindicated in patients with a known hypersensitivity, a 
      history of asthma, urticaria, or other allergic-type reactions after taking 
      aspirin or another NSAID, and following coronary artery bypass graft (CABG) 
      surgery. Piroxicam should also be avoided by pregnant women starting at 30 weeks 
      gestation.
FED - Pratt, Victoria M
ED  - Pratt VM
AD  - Adjunct Professor, Clinical Pharmacology, Indiana University School of Medicine, 
      Indianapolis, IN 46202
AD  - Director, Scientific Affairs Pharmacogenetics, Agena Bioscience, San Diego CA 
      92121
FED - Scott, Stuart A
ED  - Scott SA
AD  - Professor, Department of Pathology Stanford University, Palo Alto, CA 94305
AD  - Director, Stanford Medicine Clinical Genomics Laboratory, Stanford, CA 94305
FED - Pirmohamed, Munir
ED  - Pirmohamed M
AD  - David Weatherall Chair of Medicine and UK National Health Service Chair of 
      Pharmacogenetics, University of Liverpool, Liverpool, UK
AD  - Director, MRC Centre for Drug Safety Science and Wolfson Centre for Personalized 
      Medicine, University of Liverpool, Liverpool, UK
AD  - Director, Health Data Research UK North, Liverpool, UK
FED - Esquivel, Bernard
ED  - Esquivel B
AD  - CEO, GenXys, Vancouver, BC V6B 1B8, Canada
AD  - VP, Clinical Innovation, ixlayer, San Francisco, CA 94105
FED - Kattman, Brandi L
ED  - Kattman BL
AD  - Chief, Medical Genetics and Human Variation, National Center for Biotechnology 
      Information (NCBI), National Library of Medicine, National Institutes of Health, 
      Bethesda, MD 20894
FED - Malheiro, Adriana J
ED  - Malheiro AJ
AD  - Project Lead, Medical Genetics and Human Variation, National Center for 
      Biotechnology Information (NCBI), National Library of Medicine, National 
      Institutes of Health, Bethesda, MD 20894
FAU - Dean, Laura
AU  - Dean L
AD  - NCBI
LA  - eng
PT  - Review
PT  - Book Chapter
PL  - Bethesda (MD)
OTO - NLM
OT  - piroxicam
OT  - piroxicam response
OT  - Feldene
OT  - CYP2C9
EDAT- 2019/02/11 00:00
CRDT- 2019/02/11 00:00
AID - NBK537367 [bookaccession]

PMID- 30742399
STAT- Publisher
CTDT- 20190211
PB  - National Center for Biotechnology Information (US)
DP  - 2012
TI  - Flurbiprofen Therapy and CYP2C9 Genotype.
BTI - Medical Genetics Summaries
AB  - Flurbiprofen (brand name Ansaid) is a nonsteroidal anti-inflammatory drug 
      (NSAID). Tablets and skin patches are used in the management of osteoarthritis 
      and rheumatoid arthritis. Flurbiprofen provides pain relief and reduces 
      inflammation. Flurbiprofen eye drops (brand name Ocufen) may also be used to 
      prevent miosis (excessive constriction of the pupil) during eye operations; e.g., 
      cataract surgery. Flurbiprofen is primarily metabolized by CYP2C9. Individuals 
      who lack CYP2C9 activity (CYP2C9 poor metabolizers) have an increased exposure to 
      flurbiprofen, and an increased risk of side effects. Like all NSAIDs, 
      flurbiprofen increases the risk of serious cardiovascular events, including 
      myocardial infarction and stroke, and serious gastrointestinal (GI) adverse 
      events such as bleeding, ulceration, and perforation, which may be fatal. The 
      recommended starting dose of flurbiprofen tablets in adults is 200–300 mg per 
      day, divided for administration 2, 3, or 4 times a day. But for all patients, the 
      lowest effective dose of flurbiprofen should be used for the shortest length of 
      time, consistent with the treatment goals of each individual. The FDA-approved 
      drug label for flurbiprofen states that the dose of flurbiprofen should be 
      reduced in “patients who are known or suspected to be poor CYP2C9 metabolizers 
      based on genotype or previous history/experience with other CYP2C9 substrates 
      (such as warfarin and phenytoin)” (Table 1). This dose reduction is to avoid the 
      abnormally high plasma levels of flurbiprofen in these patients caused by reduced 
      metabolic clearance. However, specific dose reductions based on CYP2C9 phenotype 
      are not provided (1). As for all NSAIDs, flurbiprofen is contraindicated in 
      patients with a known hypersensitivity; a history of asthma, urticaria, or other 
      allergic-type reactions after taking aspirin or another NSAID; and for coronary 
      artery bypass graft (CABG) surgery. Flurbiprofen should also be avoided by 
      pregnant women starting at 30 weeks gestation (1).
FED - Pratt, Victoria M
ED  - Pratt VM
AD  - Adjunct Professor, Clinical Pharmacology, Indiana University School of Medicine, 
      Indianapolis, IN 46202
AD  - Director, Scientific Affairs Pharmacogenetics, Agena Bioscience, San Diego CA 
      92121
FED - Scott, Stuart A
ED  - Scott SA
AD  - Professor, Department of Pathology Stanford University, Palo Alto, CA 94305
AD  - Director, Stanford Medicine Clinical Genomics Laboratory, Stanford, CA 94305
FED - Pirmohamed, Munir
ED  - Pirmohamed M
AD  - David Weatherall Chair of Medicine and UK National Health Service Chair of 
      Pharmacogenetics, University of Liverpool, Liverpool, UK
AD  - Director, MRC Centre for Drug Safety Science and Wolfson Centre for Personalized 
      Medicine, University of Liverpool, Liverpool, UK
AD  - Director, Health Data Research UK North, Liverpool, UK
FED - Esquivel, Bernard
ED  - Esquivel B
AD  - CEO, GenXys, Vancouver, BC V6B 1B8, Canada
AD  - VP, Clinical Innovation, ixlayer, San Francisco, CA 94105
FED - Kattman, Brandi L
ED  - Kattman BL
AD  - Chief, Medical Genetics and Human Variation, National Center for Biotechnology 
      Information (NCBI), National Library of Medicine, National Institutes of Health, 
      Bethesda, MD 20894
FED - Malheiro, Adriana J
ED  - Malheiro AJ
AD  - Project Lead, Medical Genetics and Human Variation, National Center for 
      Biotechnology Information (NCBI), National Library of Medicine, National 
      Institutes of Health, Bethesda, MD 20894
FAU - Dean, Laura
AU  - Dean L
AD  - NCBI
LA  - eng
PT  - Review
PT  - Book Chapter
PL  - Bethesda (MD)
OTO - NLM
OT  - flurbiprofen
OT  - flurbiprofen response
OT  - Ansaid
OT  - Ocufen
OT  - CYP2C9
EDAT- 2019/02/11 00:00
CRDT- 2019/02/11 00:00
AID - NBK537365 [bookaccession]

PMID- 30729371
OWN - NLM
STAT- MEDLINE
DCOM- 20191203
LR  - 20210226
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 38
IP  - 5
DP  - 2019 May
TI  - Exploring metabolic and inflammatory abnormalities in rheumatoid arthritis 
      patients developing stroke disease: a case-control study using electronic medical 
      record data in northern China.
PG  - 1401-1411
LID - 10.1007/s10067-019-04440-5 [doi]
AB  - OBJECTIVES: Intend to investigate the roles of serum lipids, inflammatory 
      markers, and serological status in rheumatoid arthritis and stroke patients by 
      using case-control study. MATERIALS AND METHODS: Clinical data were retrieved 
      from the electronic medical record of the First Affiliated Hospital of China 
      Medical University during January 2011 to March 2018. The obtained data were 
      categorized into case groups and three control groups, in the ratios of 1:2, 
      respectively, with all matching age and gender. Multinomial logistic regression 
      analysis and restricted cubic spline were conducted examining the associations 
      between serum lipids, inflammatory markers, serological status, and the risk of 
      stroke among RA patients. RESULTS: The present studies included 1057 study 
      subjects. The elevated ESR, LDL-C levels, and much higher CRP levels ≥ 230 mg/L 
      were independent risk factors for RA patients in developing stroke. Furthermore, 
      we found that ESR and LDL-C levels could exhibit a linear association with the 
      risk of comorbid stroke while CRP level had a nonlinearity association with 
      stroke risk among RA patients. CONCLUSIONS: A close monitoring is required for RA 
      patients with dyslipidemia and elevated inflammatory markers, and the primary 
      stroke preventive strategies should be directed against these risk factors.
FAU - Xin, Fangran
AU  - Xin F
AD  - Department of Clinical Epidemiology and Evidence-based medicine, The First 
      Affiliated Hospital of China Medical University, No.155, Nan Jing Bei Street, 
      Shenyang, 110001, Liaoning Province, China.
FAU - Fu, Lingyu
AU  - Fu L
AD  - Department of Clinical Epidemiology and Evidence-based medicine, The First 
      Affiliated Hospital of China Medical University, No.155, Nan Jing Bei Street, 
      Shenyang, 110001, Liaoning Province, China. fulingyucmu@sina.com.
AD  - Department of Medical Record Management Center, The First Affiliated Hospital, 
      China Medical University, Shenyang, China. fulingyucmu@sina.com.
FAU - Liu, Haina
AU  - Liu H
AD  - Department of Rheumatology, The First Affiliated Hospital, China Medical 
      University, Shenyang, China.
FAU - Xu, Yunwei
AU  - Xu Y
AD  - Department of Medical Record Management Center, The First Affiliated Hospital, 
      China Medical University, Shenyang, China.
FAU - Wei, Tingting
AU  - Wei T
AD  - Department of Clinical Epidemiology and Evidence-based medicine, The First 
      Affiliated Hospital of China Medical University, No.155, Nan Jing Bei Street, 
      Shenyang, 110001, Liaoning Province, China.
FAU - Chen, Meng
AU  - Chen M
AD  - Department of Clinical Epidemiology and Evidence-based medicine, The First 
      Affiliated Hospital of China Medical University, No.155, Nan Jing Bei Street, 
      Shenyang, 110001, Liaoning Province, China.
LA  - eng
GR  - ChiCTR1800017343/The prognosis risk model for rheumatoid arthritis based on 
      integrated clinical and genetic data by using bayesian/
PT  - Journal Article
DEP - 20190207
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
RN  - 0 (Biomarkers)
RN  - 0 (Lipids)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*blood/complications
MH  - Biomarkers/blood
MH  - Blood Sedimentation
MH  - Brain Ischemia/*blood/complications
MH  - C-Reactive Protein/*analysis
MH  - China
MH  - Dyslipidemias/*blood/complications
MH  - Electronic Health Records
MH  - Female
MH  - Humans
MH  - Inflammation/blood/complications
MH  - Lipids/blood
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Risk Factors
MH  - Stroke/*blood/complications
OTO - NOTNLM
OT  - Dyslipidemia
OT  - Inflammatory marker
OT  - Rheumatoid arthritis
OT  - Serum lipids
OT  - Stroke
EDAT- 2019/02/08 06:00
MHDA- 2019/12/04 06:00
CRDT- 2019/02/08 06:00
PHST- 2018/09/24 00:00 [received]
PHST- 2019/01/14 00:00 [accepted]
PHST- 2018/12/24 00:00 [revised]
PHST- 2019/02/08 06:00 [pubmed]
PHST- 2019/12/04 06:00 [medline]
PHST- 2019/02/08 06:00 [entrez]
AID - 10.1007/s10067-019-04440-5 [pii]
AID - 10.1007/s10067-019-04440-5 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2019 May;38(5):1401-1411. doi: 10.1007/s10067-019-04440-5. Epub 
      2019 Feb 7.

PMID- 30707391
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2198-6576 (Print)
IS  - 2198-6584 (Electronic)
IS  - 2198-6576 (Linking)
VI  - 6
IP  - 1
DP  - 2019 Mar
TI  - Adverse Events in Giant Cell Arteritis and Rheumatoid Arthritis Patient 
      Populations: Analyses of Tocilizumab Clinical Trials and Claims Data.
PG  - 77-88
LID - 10.1007/s40744-019-0139-5 [doi]
AB  - INTRODUCTION: The safety profile of tocilizumab (TCZ) in patients with rheumatoid 
      arthritis (RA) is well established. TCZ was approved to treat giant cell 
      arteritis (GCA) in 2017 in the USA and Europe, and its safety profile in patients 
      with GCA continues to be defined. The objective of this analysis was to examine 
      incidence rates (IRs) of adverse events of special interest (AESI) occurring 
      during the TCZ clinical development program and in healthcare claims data in 
      patients with GCA or RA. METHODS: TCZ-naïve patients with GCA or RA were 
      identified in the MarketScan administrative healthcare claims database. 
      TCZ-treated patients with GCA from the GiACTA trial and TCZ-treated patients with 
      RA from pooled clinical trial data were analyzed. The IRs of AESI (AESI IRs) were 
      calculated for all cohorts. In the claims cohorts, risks of AESI were estimated 
      using Poisson regression. RESULTS: TCZ-naïve claims cohorts comprised 4804 
      patients with GCA [mean (standard deviation) age 73.4 (9.8) years; follow-up 3.9 
      (3.1) years] and 15,164 patients with RA [age 60.3 (8.2) years; follow-up, 4.5 
      (2.8) years]. TCZ-treated clinical trial cohorts comprised 149 patients with GCA 
      [age 69.5 (8.4) years; exposure approx. 138 patient-years (PY)] and 7647 with RA 
      [age 52 (12.6) years; exposure approx. 22,394 PY]. The IRs of infections, stroke, 
      malignancies, myocardial infarction, and gastrointestinal perforations in the GCA 
      claims cohort exceeded those in the RA claims cohort; the risk of AESI (adjusted 
      for age and glucocorticoid use) was higher in patients with GCA than in those 
      with RA. Similar patterns to the claims cohorts in terms of the AESI IRs were 
      observed in clinical trial cohorts, although the number of events was limited in 
      the GCA trial cohort. CONCLUSION: Higher IRs of AESI were observed in patients 
      with GCA versus those with RA in both TCZ-naïve and -treated cohorts. Differences 
      in underlying disease, age, and glucocorticoid use may influence AESI incidence, 
      irrespective of intervention. FUNDING: This study was funded by F. Hoffmann-La 
      Roche Ltd and Genentech, Inc. Article processing charges were funded by F. 
      Hoffmann-La Roche Ltd. Plain language summary is available for this article.
FAU - Gale, Sara
AU  - Gale S
AD  - Genentech, Inc, South San Francisco, CA, USA. gale.sara@gene.com.
FAU - Trinh, Huong
AU  - Trinh H
AD  - Genentech, Inc, South San Francisco, CA, USA.
FAU - Tuckwell, Katie
AU  - Tuckwell K
AD  - Genentech, Inc, South San Francisco, CA, USA.
FAU - Collinson, Neil
AU  - Collinson N
AD  - Roche Products, Ltd, Welwyn Garden City, UK.
FAU - Stone, John H
AU  - Stone JH
AD  - Massachusetts General Hospital, Boston, MA, USA.
FAU - Sarsour, Khaled
AU  - Sarsour K
AD  - Genentech, Inc, South San Francisco, CA, USA.
FAU - Pei, Jinglan
AU  - Pei J
AD  - Genentech, Inc, South San Francisco, CA, USA.
FAU - Best, Jennie
AU  - Best J
AD  - Genentech, Inc, South San Francisco, CA, USA.
FAU - Birchwood, Christine
AU  - Birchwood C
AD  - Genentech, Inc, South San Francisco, CA, USA.
FAU - Mohan, Shalini V
AU  - Mohan SV
AD  - Genentech, Inc, South San Francisco, CA, USA.
LA  - eng
PT  - Journal Article
DEP - 20190201
PL  - England
TA  - Rheumatol Ther
JT  - Rheumatology and therapy
JID - 101674543
PMC - PMC6393272
OTO - NOTNLM
OT  - Giant cell arteritis
OT  - Rheumatoid arthritis
OT  - Rheumatology
OT  - Safety
OT  - Tocilizumab
EDAT- 2019/02/02 06:00
MHDA- 2019/02/02 06:01
PMCR- 2019/02/01
CRDT- 2019/02/02 06:00
PHST- 2018/11/06 00:00 [received]
PHST- 2019/02/02 06:00 [pubmed]
PHST- 2019/02/02 06:01 [medline]
PHST- 2019/02/02 06:00 [entrez]
PHST- 2019/02/01 00:00 [pmc-release]
AID - 10.1007/s40744-019-0139-5 [pii]
AID - 139 [pii]
AID - 10.1007/s40744-019-0139-5 [doi]
PST - ppublish
SO  - Rheumatol Ther. 2019 Mar;6(1):77-88. doi: 10.1007/s40744-019-0139-5. Epub 2019 
      Feb 1.

PMID- 30684090
OWN - NLM
STAT- MEDLINE
DCOM- 20191231
LR  - 20200309
IS  - 1534-6242 (Electronic)
IS  - 1523-3804 (Linking)
VI  - 21
IP  - 2
DP  - 2019 Jan 25
TI  - Rheumatoid Arthritis: Atherosclerosis Imaging and Cardiovascular Risk Assessment 
      Using Machine and Deep Learning-Based Tissue Characterization.
PG  - 7
LID - 10.1007/s11883-019-0766-x [doi]
AB  - PURPOSE OF THE REVIEW: Rheumatoid arthritis (RA) is a chronic, autoimmune disease 
      which may result in a higher risk of cardiovascular (CV) events and stroke. 
      Tissue characterization and risk stratification of patients with rheumatoid 
      arthritis are a challenging problem. Risk stratification of RA patients using 
      traditional risk factor-based calculators either underestimates or overestimates 
      the CV risk. Advancements in medical imaging have facilitated early and accurate 
      CV risk stratification compared to conventional cardiovascular risk calculators. 
      RECENT FINDING: In recent years, a link between carotid atherosclerosis and 
      rheumatoid arthritis has been widely discussed by multiple studies. Imaging the 
      carotid artery using 2-D ultrasound is a noninvasive, economic, and efficient 
      imaging approach that provides an atherosclerotic plaque tissue-specific image. 
      Such images can help to morphologically characterize the plaque type and 
      accurately measure vital phenotypes such as media wall thickness and wall 
      variability. Intelligence-based paradigms such as machine learning- and deep 
      learning-based techniques not only automate the risk characterization process but 
      also provide an accurate CV risk stratification for better management of RA 
      patients. This review provides a brief understanding of the pathogenesis of RA 
      and its association with carotid atherosclerosis imaged using the B-mode 
      ultrasound technique. Lacunas in traditional risk scores and the role of machine 
      learning-based tissue characterization algorithms are discussed and could 
      facilitate cardiovascular risk assessment in RA patients. The key takeaway points 
      from this review are the following: (i) inflammation is a common link between RA 
      and atherosclerotic plaque buildup, (ii) carotid ultrasound is a better choice to 
      characterize the atherosclerotic plaque tissues in RA patients, and (iii) 
      intelligence-based paradigms are useful for accurate tissue characterization and 
      risk stratification of RA patients.
FAU - Khanna, Narendra N
AU  - Khanna NN
AD  - Department of Cardiology, Indraprastha Apollo Hospitals, New Delhi, India.
FAU - Jamthikar, Ankush D
AU  - Jamthikar AD
AD  - Department of Electronics and Communication Engineering, Visvesvaraya National 
      Institute of Technology, Nagpur, Maharashtra, India.
FAU - Gupta, Deep
AU  - Gupta D
AD  - Department of Electronics and Communication Engineering, Visvesvaraya National 
      Institute of Technology, Nagpur, Maharashtra, India.
FAU - Piga, Matteo
AU  - Piga M
AD  - Department of Rheumatology, University Clinic and AOU of Cagliari, Cagliari, 
      Italy.
FAU - Saba, Luca
AU  - Saba L
AD  - Department of Radiology, University of Cagliari, Cagliari, Italy.
FAU - Carcassi, Carlo
AU  - Carcassi C
AD  - Department of Genetics, University of Cagliari, Cagliari, Italy.
FAU - Giannopoulos, Argiris A
AU  - Giannopoulos AA
AD  - Department of Medicine, Imperial College London, London, UK.
FAU - Nicolaides, Andrew
AU  - Nicolaides A
AD  - Department of Vascular Surgery, Imperial College London, London, UK.
AD  - Vascular Diagnostic Center, University of Cyprus, Nicosia, Cyprus.
FAU - Laird, John R
AU  - Laird JR
AD  - Heart and Vascular Institute, Adventist Health St. Helena, St. Helena, CA, USA.
FAU - Suri, Harman S
AU  - Suri HS
AD  - Brown University, Providence, RI, USA.
FAU - Mavrogeni, Sophie
AU  - Mavrogeni S
AD  - Cardiology Clinic, Onassis Cardiac Surgery Center, Athens, Greece.
FAU - Protogerou, A D
AU  - Protogerou AD
AD  - Cardiovascular Prevention Unit, Department of Pathophysiology, NKU of Athens, 
      Athens, Greece.
FAU - Sfikakis, Petros
AU  - Sfikakis P
AD  - Rheumatology Unit, Laikon University Hospital, Athens, Greece.
AD  - Medical School, National Kapodistrian University of Athens, Athens, Greece.
FAU - Kitas, George D
AU  - Kitas GD
AD  - Arthritis Research UK Centre for Epidemiology, Manchester University, Manchester, 
      UK.
AD  - Research and Development, Academic Affairs, Dudley Group NHS Foundation Trust, 
      Dudley, UK.
FAU - Suri, Jasjit S
AU  - Suri JS
AD  - Stroke Monitoring and Diagnostic Division, AtheroPoint™, Roseville, CA, USA. 
      Jasjit.Suri@atheropoint.com.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20190125
PL  - United States
TA  - Curr Atheroscler Rep
JT  - Current atherosclerosis reports
JID - 100897685
SB  - IM
MH  - Arthritis, Rheumatoid/*complications/pathology
MH  - Atherosclerosis/*diagnostic imaging/*etiology
MH  - Carotid Arteries/pathology
MH  - Carotid Artery Diseases/*diagnostic imaging/*etiology
MH  - *Deep Learning
MH  - Humans
MH  - Inflammation/complications/metabolism
MH  - Plaque, Atherosclerotic/diagnostic imaging/etiology/metabolism
MH  - Risk Assessment
MH  - Risk Factors
MH  - Tomography, Optical Coherence
MH  - Ultrasonography
OTO - NOTNLM
OT  - Atherosclerosis
OT  - Cardiovascular risk assessment
OT  - Carotid ultrasound
OT  - Deep learning
OT  - Machine learning
OT  - Optical coherence tomography
OT  - Rheumatoid arthritis
OT  - Tissue characterization
EDAT- 2019/01/27 06:00
MHDA- 2020/01/01 06:00
CRDT- 2019/01/27 06:00
PHST- 2019/01/27 06:00 [entrez]
PHST- 2019/01/27 06:00 [pubmed]
PHST- 2020/01/01 06:00 [medline]
AID - 10.1007/s11883-019-0766-x [pii]
AID - 10.1007/s11883-019-0766-x [doi]
PST - epublish
SO  - Curr Atheroscler Rep. 2019 Jan 25;21(2):7. doi: 10.1007/s11883-019-0766-x.

PMID- 30663869
OWN - NLM
STAT- MEDLINE
DCOM- 20200106
LR  - 20231012
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Print)
IS  - 2326-5191 (Linking)
VI  - 71
IP  - 7
DP  - 2019 Jul
TI  - Cardiovascular Safety During Treatment With Baricitinib in Rheumatoid Arthritis.
PG  - 1042-1055
LID - 10.1002/art.40841 [doi]
AB  - OBJECTIVE: To assess the frequency of cardiovascular and venous thromboembolic 
      events in clinical studies of baricitinib, an oral, selective JAK1 and JAK2 
      inhibitor approved in more than 50 countries for the treatment of 
      moderately-to-severely active rheumatoid arthritis (RA). METHODS: Data were 
      pooled from 9 RA studies. Placebo comparison up to 24 weeks included data from 6 
      studies. Randomized dose comparison between baricitinib doses of 2 mg and 4 mg 
      used data from 4 studies and from the associated long-term extension study. The 
      data analysis set designated "All-bari-RA" included all baricitinib exposures at 
      any dose. RESULTS: Overall, 3,492 RA patients received baricitinib (7,860 
      patient-years of exposure). No imbalance compared to the placebo group was seen 
      in the incidence of major adverse cardiovascular events (MACE) (incidence rates 
      [IRs] of 0.5 per 100 patient-years for placebo and 0.8 per 100 patient-years for 
      4 mg baricitinib), arterial thrombotic events (ATE) (IRs of 0.5 per 100 
      patient-years for placebo and 0.5 per 100 patient-years for 4 mg baricitinib), or 
      congestive heart failure (CHF) broad term (IRs of 4.3 per 100 patient-years for 
      placebo and 2.4 per 100 patient-years for 4 mg baricitinib). Deep vein thrombosis 
      (DVT)/pulmonary embolism (PE) were reported in 0 of 1,070 patients treated with 
      placebo and 6 of 997 patients treated with 4 mg baricitinib during the 
      placebo-controlled period; these events were serious in 2 of 6 patients, while 
      all 6 had risk factors and 1 patient developed DVT/PE after discontinuation of 
      the study drug. In the 2 mg-4 mg-extended data analysis set, IRs of DVT/PE were 
      comparable between the doses across event types (IRs of 0.5 per 100 patient-years 
      in those receiving 2 mg baricitinib and 0.6 per 100 patient-years in those 
      receiving 4 mg baricitinib). In the All-bari-RA data analysis set, the rates were 
      stable over time, with an IR of DVT/PE of 0.5 per 100 patient-years. CONCLUSION: 
      In RA clinical trials, no association was found between baricitinib treatment and 
      the incidence of MACE, ATE, or CHF. With regard to incidence of DVT/PE, 6 events 
      occurred in patients treated with 4 mg baricitinib, but no cases of DVT/PE were 
      reported in the placebo group. During longer-term evaluation, the incidence of 
      DVT/PE was similar between the baricitinib dose groups, with consistent IR values 
      over time, and this was similar to the rates previously reported in patients with 
      RA.
CI  - © 2019 Eli Lilly and Company. Arthritis & Rheumatology published by Wiley 
      Periodicals, Inc. on behalf of American College of Rheumatology.
FAU - Taylor, Peter C
AU  - Taylor PC
AD  - University of Oxford, Oxford, UK.
FAU - Weinblatt, Michael E
AU  - Weinblatt ME
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Burmester, Gerd R
AU  - Burmester GR
AD  - Charité Universitätsmedizin Berlin, Berlin, Germany.
FAU - Rooney, Terence P
AU  - Rooney TP
AD  - Eli Lilly and Company, Indianapolis, Indiana.
FAU - Witt, Sarah
AU  - Witt S
AD  - Eli Lilly and Company, Indianapolis, Indiana.
FAU - Walls, Chad D
AU  - Walls CD
AD  - Eli Lilly and Company, Indianapolis, Indiana.
FAU - Issa, Maher
AU  - Issa M
AD  - Eli Lilly and Company, Indianapolis, Indiana.
FAU - Salinas, Claudia A
AU  - Salinas CA
AD  - Eli Lilly and Company, Indianapolis, Indiana.
FAU - Saifan, Chadi
AU  - Saifan C
AD  - Eli Lilly and Company, Indianapolis, Indiana.
FAU - Zhang, Xin
AU  - Zhang X
AD  - Eli Lilly and Company, Indianapolis, Indiana.
FAU - Cardoso, Anabela
AU  - Cardoso A
AD  - Eli Lilly and Company, Indianapolis, Indiana.
FAU - González-Gay, Miguel A
AU  - González-Gay MA
AD  - Hospital Universitario Marqués de Valdecilla, IDIVAL and University of Cantabria, 
      Santander, Spain, and University of the Witwatersrand, Johannesburg, South 
      Africa.
FAU - Takeuchi, Tsutomu
AU  - Takeuchi T
AD  - Keio University School of Medicine, Tokyo, Japan.
LA  - eng
GR  - Eli Lilly and Company/International
GR  - Incyte Corporation/International
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190525
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Azetidines)
RN  - 0 (Janus Kinase Inhibitors)
RN  - 0 (Purines)
RN  - 0 (Pyrazoles)
RN  - 0 (Sulfonamides)
RN  - ISP4442I3Y (baricitinib)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Azetidines/*therapeutic use
MH  - Cardiovascular Diseases/*epidemiology/mortality
MH  - Clinical Trials as Topic
MH  - Female
MH  - Heart Failure/epidemiology
MH  - Humans
MH  - Janus Kinase Inhibitors/*therapeutic use
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology
MH  - Pulmonary Embolism/epidemiology
MH  - Purines
MH  - Pyrazoles
MH  - Stroke/epidemiology
MH  - Sulfonamides/*therapeutic use
MH  - Thrombosis/epidemiology
MH  - Venous Thrombosis/epidemiology
PMC - PMC6618316
EDAT- 2019/01/22 06:00
MHDA- 2020/01/07 06:00
PMCR- 2019/07/10
CRDT- 2019/01/22 06:00
PHST- 2018/07/19 00:00 [received]
PHST- 2019/01/15 00:00 [accepted]
PHST- 2019/01/22 06:00 [pubmed]
PHST- 2020/01/07 06:00 [medline]
PHST- 2019/01/22 06:00 [entrez]
PHST- 2019/07/10 00:00 [pmc-release]
AID - ART40841 [pii]
AID - 10.1002/art.40841 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2019 Jul;71(7):1042-1055. doi: 10.1002/art.40841. Epub 2019 
      May 25.

PMID- 30656399
OWN - NLM
STAT- MEDLINE
DCOM- 20191002
LR  - 20200225
IS  - 1435-1250 (Electronic)
IS  - 0340-1855 (Linking)
VI  - 78
IP  - 3
DP  - 2019 Apr
TI  - [Cardiovascular comorbidities in rheumatoid arthritis].
PG  - 221-227
LID - 10.1007/s00393-018-0584-5 [doi]
AB  - Approximately 80% of patients with rheumatoid arthritis (RA) suffer from 
      comorbidities including more than 50% from cardiovascular (CV) diseases. 
      Inflammatory activity is the main factor connecting RA with atherosclerosis, 
      coronary heart disease, stroke, thromboembolic events and heart failure. 
      Altogether these affect RA patients twice as frequently as the general population 
      and CV events are the major cause of death in RA. Besides inflammatory activity, 
      which can be reduced or eliminated by optimal treatment and controlling the RA 
      activity, traditional CV risk factors also contribute to the total CV risk. These 
      risk factors, such as hypertension, diabetes and hyperlipidemia can also be found 
      more frequently in RA patients but often remain undetected and untreated for a 
      long time. Reducing this deficit means improvement of the life expectancy for RA 
      patients, which has been demonstrated in studies by treatment of 
      hyperlipoproteinemia. Among the drugs used for RA treatment non-steroidal 
      antirheumatic drugs and glucocorticoids increase the CV risk if used in the long 
      term. Hydroxychloroquine, methotrexate and biologics on the other hand are able 
      to dramatically reduce the risk. Elevated CV risks of inflammatory rheumatic 
      diseases are widely unknown in primary care. Therefore, the rheumatologist should 
      be responsible for assessment of risk factors but in real life motivation to do 
      so is relatively low. Some studies could demonstrate that using nursing-based 
      standardized assessment is an excellent opportunity to reduce these deficits. 
      Depending on the individual risk reassessment should take place every 1-5 years.
FAU - Krüger, K
AU  - Krüger K
AD  - Rheumatologisches Praxiszentrum, St. Bonifatius Str. 5, 81541, München, 
      Deutschland. Klaus.krueger@med.uni-muenchen.de.
FAU - Nüßlein, H
AU  - Nüßlein H
AD  - Gemeinschaftspraxis für Rheumatologie, Nürnberg, Deutschland.
LA  - ger
PT  - Journal Article
PT  - Review
TT  - Kardiovaskuläre Komorbiditäten bei rheumatoider Arthritis.
PL  - Germany
TA  - Z Rheumatol
JT  - Zeitschrift fur Rheumatologie
JID - 0414162
RN  - 0 (Antirheumatic Agents)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - *Antirheumatic Agents
MH  - *Arthritis, Rheumatoid/epidemiology
MH  - *Cardiovascular Diseases/epidemiology
MH  - Comorbidity
MH  - Humans
MH  - Methotrexate
MH  - Risk Factors
OTO - NOTNLM
OT  - Atherosclerosis
OT  - Heart failure
OT  - Inflammation
OT  - Stroke
OT  - Thromboembolic complications
EDAT- 2019/01/19 06:00
MHDA- 2019/10/03 06:00
CRDT- 2019/01/19 06:00
PHST- 2019/01/19 06:00 [pubmed]
PHST- 2019/10/03 06:00 [medline]
PHST- 2019/01/19 06:00 [entrez]
AID - 10.1007/s00393-018-0584-5 [pii]
AID - 10.1007/s00393-018-0584-5 [doi]
PST - ppublish
SO  - Z Rheumatol. 2019 Apr;78(3):221-227. doi: 10.1007/s00393-018-0584-5.

PMID- 30514359
OWN - NLM
STAT- MEDLINE
DCOM- 20191009
LR  - 20231004
IS  - 1478-6362 (Electronic)
IS  - 1478-6354 (Print)
IS  - 1478-6354 (Linking)
VI  - 20
IP  - 1
DP  - 2018 Dec 4
TI  - Prevalence of comorbidities in systemic sclerosis versus rheumatoid arthritis: a 
      comparative, multicenter, matched-cohort study.
PG  - 267
LID - 10.1186/s13075-018-1771-0 [doi]
LID - 267
AB  - BACKGROUND: Comorbidities are common in chronic systemic connective tissue 
      diseases and are associated with adverse outcomes, increased morbidity and 
      mortality. Although the prevalence of comorbidities has been well-studied in 
      isolated diseases, comparative studies between different autoimmune diseases are 
      limited. In this study, we compared the prevalence of common comorbidities 
      between patients with systemic sclerosis (SSc) and patients with rheumatoid 
      arthritis (RA). METHODS: Between 2016 and 2017, 408 consecutive patients with 
      SSc, aged 59 ± 13 years (87% women), were matched 1:1 for age and gender with 408 
      patients with RA; mean disease duration was 10 ± 8 and 9 ± 8 years, respectively. 
      Rates of cardiovascular risk factors, coronary artery disease, stroke, chronic 
      obstructive pulmonary disease (COPD), osteoporosis, neoplasms and depression were 
      compared between the two cohorts. RESULTS: The prevalence of dyslipidemia (18.4% 
      vs 30.1%, p = 0.001) and diabetes mellitus (5.6% vs 11.8%, p = 0.007) and body 
      mass index (p = 0.001) were lower in SSc compared to RA, while there was no 
      difference in arterial hypertension or smoking. While there was a trend for lower 
      prevalence of ischemic stroke in SSc than in RA (1.1% vs 3.2%, p = 0.085), 
      coronary artery disease was comparable (2.7% vs 3.7%). No differences were found 
      between patients with SSc and patients with RA in the prevalence of COPD (5.2% vs 
      3.7%), osteoporosis (24% vs 22%) or neoplasms overall (1.1% vs 1.7%); however 
      lung cancer was the most prevalent cancer in SSc (7/17, 41%), whereas hematologic 
      malignancies (7/19, 36%) and breast cancer (7/19, 36%) predominated in RA. 
      Depression was more prevalent in SSc (22% vs 12%, p = 0.001), especially in 
      diffuse SSc. CONCLUSIONS: Despite the prevalence of dyslipidemia and diabetes 
      mellitus in SSc being almost half that in RA, the cardiovascular comorbidity 
      burden appears to be similar in both. The overall prevalence of neoplasms is no 
      higher in SSc than in RA, but SSc has a more negative impact on quality of life, 
      as clearly, more SSc patients develop depression compared to patients with RA.
FAU - Panopoulos, Stylianos
AU  - Panopoulos S
AD  - Joint Rheumatology Program, 1st Department of Propedeutic Internal 
      Medicine-Rheumatology Unit, National and Kapodistrian University of Athens, 
      School of Medicine, Laikon General Hospital, Athens, Greece.
FAU - Tektonidou, Maria
AU  - Tektonidou M
AD  - Joint Rheumatology Program, 1st Department of Propedeutic Internal 
      Medicine-Rheumatology Unit, National and Kapodistrian University of Athens, 
      School of Medicine, Laikon General Hospital, Athens, Greece.
FAU - Drosos, Alexandros A
AU  - Drosos AA
AD  - Rheumatology Clinic, Department of Internal Medicine, Medical School University 
      of Ioannina, Ioannina, Greece.
FAU - Liossis, Stamatis-Nick
AU  - Liossis SN
AD  - Division of Rheumatology, University of Patras Medical School, Patras University 
      Hospital, Patras, Greece.
FAU - Dimitroulas, Theodoros
AU  - Dimitroulas T
AD  - 4th Department of Medicine, Aristotle University, Thessaloniki, Greece.
FAU - Garyfallos, Alexandros
AU  - Garyfallos A
AD  - 4th Department of Medicine, Aristotle University, Thessaloniki, Greece.
FAU - Sakkas, Lazaros
AU  - Sakkas L
AD  - Department of Rheumatology and Clinical Immunology, School of Health Sciences, 
      University of Thessaly, Larissa, Greece.
FAU - Boumpas, Dimitrios
AU  - Boumpas D
AD  - Joint Rheumatology Program, 4th Department of Medicine, National and Kapodistrian 
      University of Athens, School of Medicine, Attikon University Hospital, Athens, 
      Greece.
FAU - Voulgari, Paraskevi V
AU  - Voulgari PV
AD  - Rheumatology Clinic, Department of Internal Medicine, Medical School University 
      of Ioannina, Ioannina, Greece.
FAU - Daoussis, Dimitrios
AU  - Daoussis D
AD  - Division of Rheumatology, University of Patras Medical School, Patras University 
      Hospital, Patras, Greece.
FAU - Thomas, Konstantinos
AU  - Thomas K
AD  - Joint Rheumatology Program, Clinical Immunology-Rheumatology Unit, 2nd Department 
      of Medicine and Laboratory, National and Kapodistrian University of Athens, 
      School of Medicine, Hippokration General Hospital, 114 Vass. Sophias Ave, 115 27, 
      Athens, Greece.
FAU - Georgiopoulos, Georgios
AU  - Georgiopoulos G
AD  - Joint Rheumatology Program, Clinical Immunology-Rheumatology Unit, 2nd Department 
      of Medicine and Laboratory, National and Kapodistrian University of Athens, 
      School of Medicine, Hippokration General Hospital, 114 Vass. Sophias Ave, 115 27, 
      Athens, Greece.
FAU - Vosvotekas, Georgios
AU  - Vosvotekas G
AD  - 1st Department of Medicine, Aristotle University of Thessaloniki, School of 
      Medicine, University General Hospital of Thessaloniki AHEPA, Thessaloniki, 
      Greece.
FAU - Vassilopoulos, Dimitrios
AU  - Vassilopoulos D
AD  - Joint Rheumatology Program, Clinical Immunology-Rheumatology Unit, 2nd Department 
      of Medicine and Laboratory, National and Kapodistrian University of Athens, 
      School of Medicine, Hippokration General Hospital, 114 Vass. Sophias Ave, 115 27, 
      Athens, Greece. dvassilop@med.uoa.gr.
FAU - Sfikakis, Petros P
AU  - Sfikakis PP
AD  - Joint Rheumatology Program, 1st Department of Propedeutic Internal 
      Medicine-Rheumatology Unit, National and Kapodistrian University of Athens, 
      School of Medicine, Laikon General Hospital, Athens, Greece.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20181204
PL  - England
TA  - Arthritis Res Ther
JT  - Arthritis research & therapy
JID - 101154438
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Cohort Studies
MH  - Comorbidity
MH  - Coronary Artery Disease/epidemiology
MH  - Diabetes Mellitus/epidemiology
MH  - Dyslipidemias/epidemiology
MH  - Female
MH  - Greece/epidemiology
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Osteoporosis/epidemiology
MH  - Prevalence
MH  - Pulmonary Disease, Chronic Obstructive/epidemiology
MH  - Quality of Life
MH  - Risk Assessment/*methods/*statistics & numerical data
MH  - Risk Factors
MH  - Scleroderma, Systemic/*epidemiology
PMC - PMC6280404
OTO - NOTNLM
OT  - Cardiovascular diseases
OT  - Comorbidities
OT  - Depression
OT  - Neoplasms
OT  - Rheumatoid arthritis
OT  - Systemic sclerosis
COIS- ETHICS APPROVAL AND CONSENT TO PARTICIPATE: Ethical approval was provided by the 
      local institutional boards of participating centers and informed consent was 
      provided by all patients before their inclusion in the study. CONSENT FOR 
      PUBLICATION: Not applicable. COMPETING INTERESTS: The authors declare that they 
      have no competing interests. PUBLISHER’S NOTE: Springer Nature remains neutral 
      with regard to jurisdictional claims in published maps and institutional 
      affiliations.
EDAT- 2018/12/06 06:00
MHDA- 2019/10/11 06:00
PMCR- 2018/12/04
CRDT- 2018/12/06 06:00
PHST- 2018/09/06 00:00 [received]
PHST- 2018/11/19 00:00 [accepted]
PHST- 2018/12/06 06:00 [entrez]
PHST- 2018/12/06 06:00 [pubmed]
PHST- 2019/10/11 06:00 [medline]
PHST- 2018/12/04 00:00 [pmc-release]
AID - 10.1186/s13075-018-1771-0 [pii]
AID - 1771 [pii]
AID - 10.1186/s13075-018-1771-0 [doi]
PST - epublish
SO  - Arthritis Res Ther. 2018 Dec 4;20(1):267. doi: 10.1186/s13075-018-1771-0.

PMID- 30484352
OWN - NLM
STAT- MEDLINE
DCOM- 20191212
LR  - 20191217
IS  - 1439-7609 (Electronic)
IS  - 1439-7595 (Linking)
VI  - 29
IP  - 5
DP  - 2019 Sep
TI  - Higher risk of hospitalized infection, cardiovascular disease, and fracture in 
      patients with rheumatoid arthritis determined using the Japanese health insurance 
      database.
PG  - 788-794
LID - 10.1080/14397595.2018.1519889 [doi]
AB  - Objective: To evaluate the risk of hospitalized infection (HI), cardiovascular 
      disease (CVD), stroke, and fracture in rheumatoid arthritis (RA) patients 
      compared with non-RA patients using the Japanese health insurance database. 
      Method: Among individuals aged ≥18 years, RA cases were defined to have one RA 
      diagnostic code and receiving ≥1 disease-modifying antirheumatic drug between 
      2005 and 2013 (n = 6,712). Age-, sex-, calendar year of the observation start-, 
      and observation length-matched non-RA cases were selected at 1:5 (n = 33,560). 
      Hazard ratios (HRs) were calculated using the time-dependent Cox regression 
      analysis. Results: Median age of the patients was 52.0 years. The incidence rates 
      of HI, CVD, and fracture in the RA group were 2.42/100 person-years (PY), 
      4.94/1,000 PY, and 10.59/1,000 PY. The crude incidence rate ratios (95% CI) (RA 
      vs. non-RA) for HI, CVD, and fracture were 2.47 (2.20-2.77), 1.89 (1.49-2.41), 
      and 3.35 (2.80-4.02). The adjusted HR (95% CI) (RA vs. non-RA) was significantly 
      elevated (HI, 1.74 [1.52-1.99], CVD, 1.38 [1.04-1.85], and fracture, 1.88 
      (1.54-2.31)]. Conclusion: The relatively young RA population had significantly 
      higher risks of these complications than the non-RA, indicating importance of 
      prevention of them even at young ages in clinical settings.
FAU - Kasai, Shoko
AU  - Kasai S
AUID- ORCID: 0000-0001-8856-5660
AD  - Department of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo 
      Medical and Dental University , Tokyo , Japan.
FAU - Sakai, Ryoko
AU  - Sakai R
AD  - Division of Epidemiology and Pharmacoepidemiology of Rheumatic Diseases, 
      Department of Rheumatology, School of Medicine, Tokyo Women's Medical University 
      , Tokyo , Japan.
FAU - Koike, Ryuji
AU  - Koike R
AD  - Department of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo 
      Medical and Dental University , Tokyo , Japan.
FAU - Kohsaka, Hitoshi
AU  - Kohsaka H
AD  - Department of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo 
      Medical and Dental University , Tokyo , Japan.
FAU - Miyasaka, Nobuyuki
AU  - Miyasaka N
AD  - Tokyo Medical and Dental University , Tokyo , Japan.
FAU - Harigai, Masayoshi
AU  - Harigai M
AD  - Division of Epidemiology and Pharmacoepidemiology of Rheumatic Diseases, 
      Department of Rheumatology, School of Medicine, Tokyo Women's Medical University 
      , Tokyo , Japan.
LA  - eng
PT  - Journal Article
DEP - 20181128
PL  - England
TA  - Mod Rheumatol
JT  - Modern rheumatology
JID - 100959226
SB  - IM
EIN - Mod Rheumatol. 2019 Sep;29(5):v. doi: 10.1080/14397595.2018.1562101. PMID: 
      30964353
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Cardiovascular Diseases/*epidemiology
MH  - Female
MH  - Fractures, Bone/*epidemiology
MH  - Hospitalization/statistics & numerical data
MH  - Humans
MH  - Infections/*epidemiology
MH  - Insurance, Health/statistics & numerical data
MH  - Japan
MH  - Male
MH  - Middle Aged
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - epidemiology
OT  - fracture
OT  - infection
OT  - rheumatoid arthritis
OT  - stroke
EDAT- 2018/11/30 06:00
MHDA- 2019/12/18 06:00
CRDT- 2018/11/29 06:00
PHST- 2018/11/30 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
PHST- 2018/11/29 06:00 [entrez]
AID - 10.1080/14397595.2018.1519889 [doi]
PST - ppublish
SO  - Mod Rheumatol. 2019 Sep;29(5):788-794. doi: 10.1080/14397595.2018.1519889. Epub 
      2018 Nov 28.

PMID- 30470476
OWN - NLM
STAT- MEDLINE
DCOM- 20190717
LR  - 20191210
IS  - 1958-5578 (Electronic)
IS  - 0040-5957 (Linking)
VI  - 74
IP  - 2
DP  - 2019 Apr
TI  - The systematic case-referent method.
PG  - 199-207
LID - S0040-5957(18)30241-5 [pii]
LID - 10.1016/j.therap.2018.09.073 [doi]
AB  - The systematic case-referent method is a special case-referent design originally 
      developed for pharmacoepidemiologic research purposes. It consists in the 
      systematic collection of series of incident cases of various disorders and the 
      assembling of a general reference pool, from which "controls" are secondarily 
      selected to be matched to specific cases. Both series are collected independently 
      from each other and with no a priori hypothesis to be investigated. The reference 
      pool can be either general or limited to a subpopulation, representative of the 
      source population of the cases. Based on clinical recruitment of cases and 
      referents, the design allows a very high specificity of diagnosis and 
      documentation of clinical variables. All cases and referents are systematically 
      documented on all treatments received before the incidence of the cases or before 
      identification of referents. This documentation is done preferentially using 
      objective sources assembled independently (linkage to claims data, medical 
      records, pharmacy records, prescription records, hospital discharge letters). It 
      can be completed with patients' interviews using standardised research tools, in 
      particular for over-the-counter drug use and self-medication, and for the 
      documentation of adherence to treatment and specific time-windows of exposure. 
      Likewise, all cases and all referents are systematically documented on a series 
      of risk factors, which are common to most epidemiological studies and are not 
      hypothesis-dependent. Whenever the documentation of a confounding factor specific 
      to the disease at hand is necessary, additional questionnaires can be applied to 
      all or a sample of patients. The method has been successfully implemented for the 
      pharmacoepidemiologic study of myocardial infarction, stroke, lupus, multiple 
      sclerosis, rheumatoid arthritis, Guillain Barré syndrome, idiopathic 
      thrombocytopenic purpura, type 1 diabetes mellitus, suicide attempts, breast 
      cancer, and other disorders, for the analysis of the risk or preventing action of 
      NSAIDs, statins, antiplatelet agents, anticoagulants, insulins, vaccines and 
      other drugs.
CI  - Copyright © 2018. Published by Elsevier Masson SAS.
FAU - Grimaldi-Bensouda, Lamiae
AU  - Grimaldi-Bensouda L
AD  - Service de pharmacologie - UF de pharmaco-épidémiologie, hôpital 
      Raymond-Poincaré, groupe hospitalier Paris, Île-de-France Ouest, AP-HP, UFR des 
      sciences de la santé Simone-Veil, université Versailles Saint-Quentin, 2, avenue 
      de la Source-de-la-Bièvre, 78180 Montigny-le-Bretonneux, France. Electronic 
      address: Lamiae.grimaldi@aphp.fr.
FAU - Abenhaim, Lucien
AU  - Abenhaim L
AD  - London School of Hygiene and Tropical Medicine, LA Risk Research, London EC1R 
      5BD, United Kingdom.
LA  - eng
PT  - Journal Article
DEP - 20181026
PL  - France
TA  - Therapie
JT  - Therapie
JID - 0420544
RN  - 0 (Nonprescription Drugs)
SB  - IM
MH  - Case-Control Studies
MH  - *Confounding Factors, Epidemiologic
MH  - Humans
MH  - Incidence
MH  - Nonprescription Drugs/administration & dosage/adverse effects
MH  - Pharmacoepidemiology/*methods
MH  - *Research Design
MH  - Risk Factors
MH  - Self Medication/adverse effects/methods
MH  - Surveys and Questionnaires
OTO - NOTNLM
OT  - Case-control
OT  - Epidemiologic design
OT  - Pharmacoepidemiology
OT  - Selection of controls
OT  - Systematic case-referent
EDAT- 2018/11/25 06:00
MHDA- 2019/07/18 06:00
CRDT- 2018/11/25 06:00
PHST- 2018/07/09 00:00 [received]
PHST- 2018/09/21 00:00 [accepted]
PHST- 2018/11/25 06:00 [pubmed]
PHST- 2019/07/18 06:00 [medline]
PHST- 2018/11/25 06:00 [entrez]
AID - S0040-5957(18)30241-5 [pii]
AID - 10.1016/j.therap.2018.09.073 [doi]
PST - ppublish
SO  - Therapie. 2019 Apr;74(2):199-207. doi: 10.1016/j.therap.2018.09.073. Epub 2018 
      Oct 26.

PMID- 30353563
OWN - NLM
STAT- MEDLINE
DCOM- 20190501
LR  - 20211204
IS  - 1932-8737 (Electronic)
IS  - 0160-9289 (Print)
IS  - 0160-9289 (Linking)
VI  - 42
IP  - 1
DP  - 2019 Jan
TI  - Association of galectin-3 with markers of myocardial function, atherosclerosis, 
      and vascular fibrosis in patients with rheumatoid arthritis.
PG  - 62-68
LID - 10.1002/clc.23105 [doi]
AB  - BACKGROUND: Galectin-3 has emerged as a promising novel biomarker of 
      cardiovascular fibrosis in patients with cardiovascular diseases. HYPOTHESIS: We 
      investigated whether galectin-3 correlates with markers of vascular fibrosis, 
      subclinical atherosclerosis, and cardiac function in patients with rheumatoid 
      arthritis (RA), a disease accompanied by high cardiovascular risk. METHODS: RA 
      and non-RA individuals underwent applanation tonometry, carotid ultrasound, and 
      impedance cardiography, to obtain markers of arterial stiffness, subclinical 
      atherosclerosis, and myocardial function, respectively. Cardiovascular risk was 
      estimated from the Framingham Heart Study. Serum levels of galectin-3 were 
      determined by enzyme-linked immunosorbent assay. RESULTS: Galectin-3 was elevated 
      in RA patients (n = 85) compared to controls (n = 39), but this difference was no 
      longer significant after adjustment for the presence of cardiovascular 
      comorbidities. In the univariate analysis, galectin-3 significantly correlated 
      with markers of vascular stiffness (including pulse wave velocity, central blood 
      pressure, central and peripheral pulse pressure, and total arterial compliance); 
      atherosclerosis (carotid intima-media thickness); myocardial blood flow (cardiac 
      output, stroke volume) and contractibility (acceleration and velocity index); 
      systemic vascular resistance, and estimated cardiovascular risk. Multivariate 
      analysis models revealed an independent association between galectin-3 and both 
      cardiac output (β = -0.274, P = 0.039), as well as systemic vascular resistance 
      (β = 0.266, P = 0.039). CONCLUSIONS: In a relatively well-controlled cohort of RA 
      patients with low-grade systemic inflammation and long-standing disease, serum 
      galectin-3 might be useful as a marker of cardiac function and cardiovascular 
      fibrosis.
CI  - © 2018 Wiley Periodicals, Inc.
FAU - Anyfanti, Panagiota
AU  - Anyfanti P
AD  - 3rd Department of Internal Medicine, Papageorgiou Hospital, Aristotle University 
      of Thessaloniki, Thessaloniki, Greece.
FAU - Gkaliagkousi, Eugenia
AU  - Gkaliagkousi E
AUID- ORCID: 0000-0002-6324-2475
AD  - 3rd Department of Internal Medicine, Papageorgiou Hospital, Aristotle University 
      of Thessaloniki, Thessaloniki, Greece.
FAU - Gavriilaki, Eleni
AU  - Gavriilaki E
AD  - 3rd Department of Internal Medicine, Papageorgiou Hospital, Aristotle University 
      of Thessaloniki, Thessaloniki, Greece.
FAU - Triantafyllou, Areti
AU  - Triantafyllou A
AD  - 3rd Department of Internal Medicine, Papageorgiou Hospital, Aristotle University 
      of Thessaloniki, Thessaloniki, Greece.
FAU - Dolgyras, Panagiotis
AU  - Dolgyras P
AD  - 3rd Department of Internal Medicine, Papageorgiou Hospital, Aristotle University 
      of Thessaloniki, Thessaloniki, Greece.
FAU - Galanopoulou, Vasiliki
AU  - Galanopoulou V
AD  - Rheumatology Department, Papageorgiou Hospital, Aristotle University of 
      Thessaloniki, Thessaloniki, Greece.
FAU - Aslanidis, Spyros
AU  - Aslanidis S
AD  - Rheumatology Department, 2nd Propedeutic Department of Internal Medicine, 
      Hippokration Hospital, Aristotle University of Thessaloniki, Thessaloniki, 
      Greece.
FAU - Douma, Stella
AU  - Douma S
AD  - 3rd Department of Internal Medicine, Papageorgiou Hospital, Aristotle University 
      of Thessaloniki, Thessaloniki, Greece.
LA  - eng
PT  - Journal Article
DEP - 20181127
PL  - United States
TA  - Clin Cardiol
JT  - Clinical cardiology
JID - 7903272
RN  - 0 (Biomarkers)
RN  - 0 (Blood Proteins)
RN  - 0 (Galectin 3)
RN  - 0 (Galectins)
RN  - 0 (LGALS3 protein, human)
SB  - IM
MH  - Arthritis, Rheumatoid/blood/*complications
MH  - Atherosclerosis/*blood/diagnosis/etiology
MH  - Biomarkers/blood
MH  - Blood Pressure
MH  - Blood Proteins
MH  - Cardiography, Impedance
MH  - Carotid Artery Diseases/*blood/diagnosis/etiology
MH  - Carotid Artery, Common/diagnostic imaging/physiopathology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Fibrosis/blood/diagnosis/etiology
MH  - Galectin 3/*blood
MH  - Galectins
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Contraction/*physiology
MH  - Prognosis
MH  - Stroke Volume/*physiology
MH  - Ultrasonography
MH  - *Vascular Stiffness
PMC - PMC6436501
OTO - NOTNLM
OT  - galectin-3
OT  - myocardial function
OT  - rheumatoid arthritis
OT  - vascular stiffness
EDAT- 2018/10/26 06:00
MHDA- 2019/05/02 06:00
PMCR- 2018/11/27
CRDT- 2018/10/25 06:00
PHST- 2018/07/18 00:00 [received]
PHST- 2018/10/14 00:00 [revised]
PHST- 2018/10/17 00:00 [accepted]
PHST- 2018/10/26 06:00 [pubmed]
PHST- 2019/05/02 06:00 [medline]
PHST- 2018/10/25 06:00 [entrez]
PHST- 2018/11/27 00:00 [pmc-release]
AID - CLC23105 [pii]
AID - 10.1002/clc.23105 [doi]
PST - ppublish
SO  - Clin Cardiol. 2019 Jan;42(1):62-68. doi: 10.1002/clc.23105. Epub 2018 Nov 27.

PMID- 30285854
OWN - NLM
STAT- MEDLINE
DCOM- 20190114
LR  - 20230928
IS  - 1741-7015 (Electronic)
IS  - 1741-7015 (Linking)
VI  - 16
IP  - 1
DP  - 2018 Oct 4
TI  - Racial differences in comorbidity profile among patients with chronic obstructive 
      pulmonary disease.
PG  - 178
LID - 10.1186/s12916-018-1159-7 [doi]
LID - 178
AB  - BACKGROUND: Chronic obstructive pulmonary disease (COPD) is often accompanied by 
      multiple comorbidities, which are associated with an increased risk of 
      exacerbation, a poor health-related quality of life, and high mortality. However, 
      differences in comorbidity profile by race and ethnicity in COPD patients have 
      not been fully elucidated. METHODS: Participants aged 40 to 79 years with 
      spirometry-defined COPD from the U.S. National Health and Nutrition Examination 
      Survey (NHANES) (2007-2012) and from the Korea NHANES (2007-2015) were analyzed 
      to compare the prevalence of comorbidities by race and ethnicity group. 
      Comorbidities were defined using questionnaire data, physical exams, and 
      laboratory tests. RESULTS: Non-Hispanic Whites had the highest prevalence of 
      dyslipidemia (65.5%), myocardial infarction (6.2%), osteoarthritis (40.1%), and 
      osteoporosis (13.6%), while non-Hispanic Blacks had the highest prevalence of 
      asthma (24.0%), hypertension (70.2%), stroke (7.3%), diabetes mellitus (DM) 
      (23.3%), anemia (16.4%), and rheumatoid arthritis (11.9%). Compared to 
      non-Hispanic Whites, non-Hispanic Blacks had a significantly higher prevalence of 
      hypertension, stroke, DM, anemia, and rheumatoid arthritis after adjusting for 
      age, sex, body mass index, and smoking status, while Hispanics had a 
      significantly higher prevalence of DM and anemia, and Koreans had significantly 
      lower prevalences of all comorbidities except stroke, DM, and anemia. 
      CONCLUSIONS: COPD-related comorbidities varied significantly by race and 
      ethnicity, and different strategies may be required for the optimal management of 
      COPD and its comorbidities in different race and ethnicity groups.
FAU - Lee, Hyun
AU  - Lee H
AD  - Division of Pulmonary Medicine and Allergy, Department of Internal Medicine, 
      Hanyang University College of Medicine, Seoul, South Korea.
FAU - Shin, Sun Hye
AU  - Shin SH
AD  - Division of Pulmonary and Critical Care Medicine, Department of Medicine, Samsung 
      Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea.
FAU - Gu, Seonhye
AU  - Gu S
AD  - Center for Clinical Epidemiology, Samsung Medical Center, Seoul, South Korea.
FAU - Zhao, Di
AU  - Zhao D
AD  - Department of Epidemiology and Welch Center for Prevention, Epidemiology, and 
      Clinical Research, Johns Hopkins University Bloomberg School of Public Health, 
      Baltimore, MD, USA.
FAU - Kang, Danbee
AU  - Kang D
AD  - Center for Clinical Epidemiology, Samsung Medical Center, Seoul, South Korea.
AD  - Department of Clinical Research Design and Evaluation, SAIHST, Sungkyunkwan 
      University, Seoul, South Korea.
FAU - Joi, Yeong Rae
AU  - Joi YR
AD  - Center for Clinical Epidemiology, Samsung Medical Center, Seoul, South Korea.
FAU - Suh, Gee Young
AU  - Suh GY
AD  - Division of Pulmonary and Critical Care Medicine, Department of Medicine, Samsung 
      Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea.
FAU - Pastor-Barriuso, Roberto
AU  - Pastor-Barriuso R
AD  - National Center for Epidemiology, Instituto de Salud Carlos III, and Consortium 
      for Biomedical Research in Epidemiology and Public Health (CIBERESP), Madrid, 
      Spain.
FAU - Guallar, Eliseo
AU  - Guallar E
AD  - Department of Clinical Research Design and Evaluation, SAIHST, Sungkyunkwan 
      University, Seoul, South Korea.
AD  - Department of Epidemiology and Welch Center for Prevention, Epidemiology, and 
      Clinical Research, Johns Hopkins University Bloomberg School of Public Health, 
      Baltimore, MD, USA.
FAU - Cho, Juhee
AU  - Cho J
AD  - Center for Clinical Epidemiology, Samsung Medical Center, Seoul, South Korea.
AD  - Department of Clinical Research Design and Evaluation, SAIHST, Sungkyunkwan 
      University, Seoul, South Korea.
AD  - Department of Epidemiology and Welch Center for Prevention, Epidemiology, and 
      Clinical Research, Johns Hopkins University Bloomberg School of Public Health, 
      Baltimore, MD, USA.
FAU - Park, Hye Yun
AU  - Park HY
AD  - Division of Pulmonary and Critical Care Medicine, Department of Medicine, Samsung 
      Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea. 
      hyeyunpark@skku.edu.
LA  - eng
PT  - Journal Article
DEP - 20181004
PL  - England
TA  - BMC Med
JT  - BMC medicine
JID - 101190723
SB  - IM
MH  - Adult
MH  - Aged
MH  - *Comorbidity
MH  - Cross-Sectional Studies
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Nutrition Surveys
MH  - Prevalence
MH  - Pulmonary Disease, Chronic Obstructive/*epidemiology
MH  - Quality of Life
MH  - Republic of Korea/epidemiology
MH  - United States
PMC - PMC6171244
OTO - NOTNLM
OT  - COPD
OT  - Comorbidity
OT  - Ethnicity
OT  - Race
COIS- ETHICS APPROVAL AND CONSENT TO PARTICIPATE: As we used publicly available data, 
      our institutions waived the need for ethical approval. The original U.S. NHANES 
      and KNHANES surveys we used were approved by the relevant institutional review 
      boards and all participants provided written, informed consent. CONSENT FOR 
      PUBLICATION: Not applicable. COMPETING INTERESTS: HYP has received lecture fees 
      from AstraZeneca, Novartis, and Boehringer-Ingelheim. HL, SHS, SG, DZ, DK, YRJ, 
      GYS, RP, EG, and JC have no competing interests to declare. PUBLISHER’S NOTE: 
      Springer Nature remains neutral with regard to jurisdictional claims in published 
      maps and institutional affiliations.
EDAT- 2018/10/05 06:00
MHDA- 2019/01/15 06:00
PMCR- 2018/10/04
CRDT- 2018/10/05 06:00
PHST- 2018/01/13 00:00 [received]
PHST- 2018/08/22 00:00 [accepted]
PHST- 2018/10/05 06:00 [entrez]
PHST- 2018/10/05 06:00 [pubmed]
PHST- 2019/01/15 06:00 [medline]
PHST- 2018/10/04 00:00 [pmc-release]
AID - 10.1186/s12916-018-1159-7 [pii]
AID - 1159 [pii]
AID - 10.1186/s12916-018-1159-7 [doi]
PST - epublish
SO  - BMC Med. 2018 Oct 4;16(1):178. doi: 10.1186/s12916-018-1159-7.

PMID- 30209695
OWN - NLM
STAT- MEDLINE
DCOM- 20190618
LR  - 20190618
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 37
IP  - 11
DP  - 2018 Nov
TI  - Risk of adverse outcomes in patients with rheumatoid arthritis hospitalized for 
      stroke-a cross-sectional study.
PG  - 2917-2926
LID - 10.1007/s10067-018-4287-8 [doi]
AB  - Specific data regarding the full range of stroke outcomes among patients with 
      rheumatoid arthritis (RA) are lacking. This study aimed to investigate outcomes 
      in RA patients hospitalized for a stroke. The study retrieved data from the 
      Taiwan Longitudinal Health Insurance Database 2005. We identified 26,336 patients 
      who were hospitalized for stroke treatment. Of these patients, 736 patients with 
      a prior diagnosis of RA before the index hospitalization were selected as the 
      study group. We selected 2208 age-sex-matched patients without RA as the 
      comparison group. We performed conditional logistic regressions to calculate odds 
      ratios (ORs) for in-hospital mortality and secondary diagnoses of pneumonia, 
      urinary tract infections (UTIs), peptic ulcers, acute respiratory failure, and 
      the use of mechanical ventilation to compare RA patients and comparison patients. 
      We also compared the length of stay (LOS) and hospitalization costs between 
      patients with RA and comparison patients. We found that RA patients had a 
      significantly increased risk of peptic ulcer during the stroke hospitalization 
      (OR = 1.52, 95% CI = 1.05-2.20). However, there were no significant differences 
      between patients with RA and comparison patients in terms of in-hospital 
      mortality, pneumonia, UTIs, acute respiratory failure, or the use of mechanical 
      ventilation. Furthermore, the LOS of stroke hospitalization did not differ 
      between the two groups. We concluded that RA patients hospitalized for a stroke 
      do not have a significantly different risk of in-hospital mortality, pneumonia, 
      UTIs, and mechanical ventilator use, but they have a higher risk of peptic 
      ulcers. Additionally, among patients with a subarachnoid/intracerebral 
      hemorrhagic stroke, RA patients were more likely to have received mechanical 
      ventilation than comparison patients (adjusted OR = 1.89, 95% CI = 1.14-3.15).
FAU - Kang, Jiunn-Horng
AU  - Kang JH
AD  - Department of Physical Medicine and Rehabilitation, Taipei Medical University 
      Hospital, Taipei, Taiwan.
AD  - Department of Physical Medicine and Rehabilitation, School of Medicine, College 
      of Medicine, Taipei Medical University, Taipei, Taiwan.
FAU - Xirasagar, Sudha
AU  - Xirasagar S
AD  - Department of Health Services Policy and Management, Arnold School of Public 
      Health, University of South Carolina, Columbia, SC, USA.
FAU - Lin, Herng-Ching
AU  - Lin HC
AUID- ORCID: 0000-0003-4661-959X
AD  - School of Health Care Administration, Taipei Medical University, 250 Wu-Hsing St, 
      Taipei, 110, Taiwan. henry11111@tmu.edu.tw.
AD  - Sleep Research Center, Taipei Medical University Hospital, Taipei, Taiwan. 
      henry11111@tmu.edu.tw.
FAU - Kao, Pai-Feng
AU  - Kao PF
AD  - Department of Internal Medicine, School of Medicine, College of Medicine, Taipei 
      Medical University, Taipei, Taiwan.
AD  - Division of Cardiology, Department of Internal Medicine, Shuang Ho Hospital, 
      Taipei Medical University Taipei, Taipei, Taiwan.
FAU - Sung, Li-Chin
AU  - Sung LC
AD  - Department of Internal Medicine, School of Medicine, College of Medicine, Taipei 
      Medical University, Taipei, Taiwan.
AD  - Division of Cardiology, Department of Internal Medicine, Shuang Ho Hospital, 
      Taipei Medical University Taipei, Taipei, Taiwan.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20180912
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
SB  - IM
EIN - Clin Rheumatol. 2019 May;38(5):1533. doi: 10.1007/s10067-019-04531-3. PMID: 
      31286290
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*complications
MH  - Comorbidity
MH  - Cross-Sectional Studies
MH  - Databases, Factual
MH  - Female
MH  - Hospital Mortality/*trends
MH  - Humans
MH  - Length of Stay/*statistics & numerical data
MH  - Logistic Models
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - Stroke/*epidemiology/mortality
MH  - Taiwan/epidemiology
OTO - NOTNLM
OT  - Cardiovascular risk
OT  - Epidemiology
OT  - Rheumatoid arthritis
OT  - Stroke
EDAT- 2018/09/14 06:00
MHDA- 2019/06/19 06:00
CRDT- 2018/09/14 06:00
PHST- 2018/05/28 00:00 [received]
PHST- 2018/09/03 00:00 [accepted]
PHST- 2018/08/27 00:00 [revised]
PHST- 2018/09/14 06:00 [pubmed]
PHST- 2019/06/19 06:00 [medline]
PHST- 2018/09/14 06:00 [entrez]
AID - 10.1007/s10067-018-4287-8 [pii]
AID - 10.1007/s10067-018-4287-8 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2018 Nov;37(11):2917-2926. doi: 10.1007/s10067-018-4287-8. Epub 
      2018 Sep 12.

PMID- 30175897
OWN - NLM
STAT- MEDLINE
DCOM- 20200228
LR  - 20200228
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Linking)
VI  - 71
IP  - 8
DP  - 2019 Aug
TI  - Tocilizumab and the Risk of Cardiovascular Disease: Direct Comparison Among 
      Biologic Disease-Modifying Antirheumatic Drugs for Rheumatoid Arthritis Patients.
PG  - 1004-1018
LID - 10.1002/acr.23737 [doi]
AB  - OBJECTIVE: Multiple studies have shown seemingly unfavorable changes in lipid 
      profiles associated with interleukin-6 receptor (IL-6R) antagonists and some 
      other therapies for rheumatoid arthritis. The aim of this study was to assess the 
      real-world cardiovascular disease (CVD) risk associated with tocilizumab, the 
      first anti-IL-6R medication approved for the treatment of RA. METHODS: We 
      conducted a cohort study using 2006-2015 Medicare and MarketScan claims for 
      patients with RA in whom treatment with biologic disease-modifying antirheumatic 
      drugs was initiated after January 1, 2010. The primary outcome was a composite of 
      myocardial infarction, stroke, and fatal CVD, assessed using a validated method. 
      The influence of potential confounding due to RA disease activity was assessed in 
      a subgroup analysis (~5-10% of biologic therapy initiations) using the 
      multi-biomarker disease activity (MBDA) score. RESULTS: A total of 88,463 
      patients with RA were included. The crude incidence rate (IR) per 1,000 
      patient-years for composite CVD events among Medicare patients ranged from 11.8 
      (95% confidence interval [95% CI] 9.7-14.4) for etanercept users to 17.3 (95% CI 
      15.2-19.7) for infliximab users. The crude IR for pooled users of a tumor 
      necrosis factor inhibitor was 15.0 (95% CI 13.9-16.3). Compared to tocilizumab, 
      the corresponding adjusted hazard ratios (HRs) were 1.01 (95% CI 0.79-1.28) for 
      abatacept, 1.16 (95% CI 0.89-1.53) for rituximab, 1.10 (95% CI 0.80-1.51) for 
      etanercept, 1.33 (95% CI 0.99-1.80) for adalimumab, and 1.61 (95% CI 1.22-2.12) 
      for infliximab. There were no statistically significant differences in the risk 
      of CVD between tocilizumab and any other biologic when MarketScan data were used. 
      Results were robust in numerous subgroup analyses and after external adjustment 
      to control for RA disease activity in the subgroup of patients with linked MBDA 
      test results (n = 4,156). CONCLUSION: Tocilizumab was associated with a CVD risk 
      comparable to that for etanercept as well as a number of other biologics used for 
      the treatment of RA.
CI  - © 2018, American College of Rheumatology.
FAU - Xie, Fenglong
AU  - Xie F
AD  - University of Alabama, Birmingham.
FAU - Yun, Huifeng
AU  - Yun H
AD  - University of Alabama, Birmingham.
FAU - Levitan, Emily B
AU  - Levitan EB
AD  - University of Alabama, Birmingham.
FAU - Muntner, Paul
AU  - Muntner P
AD  - University of Alabama, Birmingham.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AUID- ORCID: 0000-0002-8907-8976
AD  - University of Alabama, Birmingham.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Antirheumatic Agents)
RN  - I031V2H011 (tocilizumab)
SB  - IM
MH  - Antibodies, Monoclonal, Humanized/*adverse effects
MH  - Antirheumatic Agents/*adverse effects
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Cardiovascular Diseases/*epidemiology
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - United States
EDAT- 2018/09/04 06:00
MHDA- 2020/02/29 06:00
CRDT- 2018/09/04 06:00
PHST- 2018/03/12 00:00 [received]
PHST- 2018/08/21 00:00 [accepted]
PHST- 2018/09/04 06:00 [pubmed]
PHST- 2020/02/29 06:00 [medline]
PHST- 2018/09/04 06:00 [entrez]
AID - 10.1002/acr.23737 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2019 Aug;71(8):1004-1018. doi: 10.1002/acr.23737.

PMID- 30086795
OWN - NLM
STAT- MEDLINE
DCOM- 20190514
LR  - 20190514
IS  - 1478-6362 (Electronic)
IS  - 1478-6354 (Print)
IS  - 1478-6354 (Linking)
VI  - 20
IP  - 1
DP  - 2018 Aug 7
TI  - Biologics and cardiovascular events in inflammatory arthritis: a prospective 
      national cohort study.
PG  - 171
LID - 10.1186/s13075-018-1669-x [doi]
LID - 171
AB  - BACKGROUND: Inflammatory arthritides including rheumatoid arthritis (RA), 
      psoriatic arthritis (PsA) and ankylosing spondylitis (AS) are associated with 
      increased risk of cardiovascular disease. This process may be driven by systemic 
      inflammation, and the use of tumour necrosis factor (TNF) inhibitors could 
      therefore potentially reduce cardiovascular risk by reducing this inflammatory 
      burden. The aims of this study were to evaluate whether the risk of 
      cardiovascular events (CVEs) in patients with inflammatory arthritis is 
      associated with treatment with anti-TNF therapy, compared with other biologics or 
      non-biologic therapy, and to compare the CVE risk between participants with RA, 
      PsA and AS. METHODS: Data from consecutive participants in the Australian 
      Rheumatology Association Database with RA, PsA and AS from September 2001 to 
      January 2015 were included in the study. The Cox proportional hazards model using 
      the counting process with time-varying covariates tested for risk of having CVEs, 
      defined as angina, myocardial infarction, coronary artery bypass graft, 
      percutaneous coronary intervention, other heart disease, stroke/transient 
      ischaemic attack or death from cardiovascular causes. The model was adjusted for 
      age, sex, diagnosis, methotrexate use, prednisone use, non-steroidal 
      anti-inflammatory use, smoking, alcohol consumption, hypertension, 
      hyperlipidaemia, diabetes and functional status (Health Assessment Questionnaire 
      Disability Score). RESULTS: There were 4140 patients included in the analysis, 
      totalling 19,627 patient-years. After multivariate adjustment, the CVE risk was 
      reduced with anti-TNF use (HR 0.85, 95% CI 0.76-0.95) or other biologic therapies 
      (HR 0.81, 95% CI 0.70-0.95), but not in those who had ceased biologic therapy (HR 
      0.96, 95% CI 0.83-1.11). After adjustment, no significant difference in CVE risk 
      was observed between participants with RA and PsA (HR 0.92, 95% CI 0.77-1.10) or 
      AS (HR 1.14, 95% CI 0.96-1.36). CONCLUSIONS: Current biologic use was associated 
      with a reduction in major CVEs. No reduction in CVE risk was seen in those who 
      had ceased biologic therapy. After adjustment, the CVE risk was not significantly 
      different between RA, AS or PsA.
FAU - Lee, Joshua L
AU  - Lee JL
AD  - Sydney Medical School, University of Sydney, Sydney, Australia.
FAU - Sinnathurai, Premarani
AU  - Sinnathurai P
AUID- ORCID: 0000-0002-8142-1274
AD  - Sydney Medical School, University of Sydney, Sydney, Australia. 
      Premarani.Sinnathurai@health.nsw.gov.au.
AD  - Institute of Bone and Joint Research, Kolling Institute, Northern Sydney Local 
      Health District, St Leonards, NSW, Australia. 
      Premarani.Sinnathurai@health.nsw.gov.au.
AD  - Department of Rheumatology, Royal North Shore Hospital, Reserve Road, St 
      Leonards, NSW, 2065, Australia. Premarani.Sinnathurai@health.nsw.gov.au.
FAU - Buchbinder, Rachelle
AU  - Buchbinder R
AD  - Monash Department of Clinical Epidemiology, Cabrini Institute, Melbourne, VIC, 
      Australia.
AD  - Centre of Cardiovascular Research & Education in Therapeutics, School of Public 
      Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia.
FAU - Hill, Catherine
AU  - Hill C
AD  - Department of Rheumatology, The Queen Elizabeth Hospital, Adelaide, SA, 
      Australia.
AD  - University of Adelaide, Adelaide, SA, Australia.
FAU - Lassere, Marissa
AU  - Lassere M
AD  - School of Public Health and Community Medicine, University of New South Wales, 
      Sydney, NSW, Australia.
AD  - Rheumatology Department, St George Hospital, Sydney, NSW, Australia.
FAU - March, Lyn
AU  - March L
AD  - Sydney Medical School, University of Sydney, Sydney, Australia.
AD  - Institute of Bone and Joint Research, Kolling Institute, Northern Sydney Local 
      Health District, St Leonards, NSW, Australia.
AD  - Department of Rheumatology, Royal North Shore Hospital, Reserve Road, St 
      Leonards, NSW, 2065, Australia.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180807
PL  - England
TA  - Arthritis Res Ther
JT  - Arthritis research & therapy
JID - 101154438
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antirheumatic Agents/*adverse effects
MH  - Arthritis, Psoriatic/*drug therapy
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Cardiovascular Diseases/*epidemiology
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Proportional Hazards Models
MH  - Spondylitis, Ankylosing/*drug therapy
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
PMC - PMC6081907
OTO - NOTNLM
OT  - Ankylosing spondylitis
OT  - Biologicals
OT  - Cardiovascular disease
OT  - Psoriatic arthritis
OT  - Rheumatoid arthritis
COIS- ETHICAL APPROVAL AND CONSENT TO PARTICIPATE: Twenty ethics committees and 
      organisations have granted approval for the ARAD across each state in Australia 
      (New South Wales: Northern Sydney Local Health District, Cancer Council NSW; 
      Victoria: Cabrini Health, Monash University, Royal Children’s Hospital, St 
      Vincent’s Hospital, Cancer Council Victoria; Queensland: Queensland Government; 
      South Australia: The South Australian Department of Health and Ageing, Women’s 
      and Children’s Hospital SA Health Network; Western Australia: Department of 
      Health WA, Fiona Stanley Hospital, Rockingham General Hospital, Royal Perth 
      Hospital, Southern Metropolitan Health Service, Government of WA; Tasmania: 
      Tasmania Health, University of Tasmania; Australian Capital Territory: ACT Health 
      and Community Care). Approval has also been granted by the Australian Institute 
      of Health and Welfare, the Australian Government Department of Health and the 
      Department of Defence and Veterans’ Affairs, the cancer registry in each state 
      (New South Wales, Victoria, Queensland, South Australia, Western Australia, 
      Tasmania, Australian Capital Territory, Northern Territory) and the National 
      Cancer Statistics Clearing House. All participants provide informed consent. 
      CONSENT FOR PUBLICATION: Not applicable. COMPETING INTERESTS: The authors declare 
      that they have no competing interests. PUBLISHER’S NOTE: Springer Nature remains 
      neutral with regard to jurisdictional claims in published maps and institutional 
      affiliations.
EDAT- 2018/08/09 06:00
MHDA- 2019/05/15 06:00
PMCR- 2018/08/07
CRDT- 2018/08/09 06:00
PHST- 2018/02/27 00:00 [received]
PHST- 2018/07/12 00:00 [accepted]
PHST- 2018/08/09 06:00 [entrez]
PHST- 2018/08/09 06:00 [pubmed]
PHST- 2019/05/15 06:00 [medline]
PHST- 2018/08/07 00:00 [pmc-release]
AID - 10.1186/s13075-018-1669-x [pii]
AID - 1669 [pii]
AID - 10.1186/s13075-018-1669-x [doi]
PST - epublish
SO  - Arthritis Res Ther. 2018 Aug 7;20(1):171. doi: 10.1186/s13075-018-1669-x.

PMID- 30051403
OWN - NLM
STAT- MEDLINE
DCOM- 20190306
LR  - 20190306
IS  - 0065-2598 (Print)
IS  - 0065-2598 (Linking)
VI  - 1065
DP  - 2018
TI  - Sex-Specific Cardiovascular Comorbidities with Associations in Dermatologic and 
      Rheumatic Disorders.
PG  - 489-509
LID - 10.1007/978-3-319-77932-4_30 [doi]
AB  - Cardiology, dermatology, and rheumatology form a fascinating triad. Many skin and 
      joint disorders are associated with cardiovascular comorbidities because they 
      share etiologic elements. Female predominance is often remarkable and likely 
      related to autoimmune pathology. Although studies have shown that X-encoded genes 
      may be involved in the differences in immunity between males and females, other 
      studies have also shown that sex chromosomes are irrelevant and that estrogens 
      and androgens are responsible for the differences. The elevated immune activity 
      in females provides a beneficial position in coping with a pathogenic stimulus 
      but may also enhance their susceptibility to autoimmunity. The complexity of the 
      immune system and its role as a defensive force against infection requires an 
      armamentarium to precisely identify and selectively control inflammatory 
      processes or cells which promote atherosclerosis. On the other hand, the 
      inflammation in skin diseases seems to be an active source of diverse 
      proinflammatory cytokines and chemokines which can predispose to cardiovascular 
      comorbidities. Also, it has been shown that comorbidity disproportionately 
      accelerates risk in women.The skin offers a readily available window to 
      facilitate detection of risk factors or even to assist the diagnostic process 
      regarding a variety of disorders, including those with cardiovascular 
      involvement. Current imaging techniques provide exquisite capabilities for 
      diagnosing and possibly even counteracting atherosclerotic plaque formation, 
      before serious cardiovascular events occur. Combining imaging approaches (such as 
      videocapillaroscopy, intravascular ultrasound, and FDG positron emission 
      tomography) with insights based on immunology will likely accelerate advances in 
      this area.We review major dermatologic manifestations and rheumatologic disorders 
      which are associated with cardiac and vascular abnormalities. In particular we 
      discuss sex-specific aspects concerning incidence and severity of cardiovascular 
      disease associated with systemic sclerosis, rheumatoid arthritis, systemic lupus 
      erythematosus, psoriasis, atopic dermatitis, and hidradenitis suppurativa.
FAU - Kerkhof, Peter L M
AU  - Kerkhof PLM
AUID- ORCID: 0000-0001-9488-633X
AD  - Department of Radiology and Nuclear Medicine, Amsterdam Cardiovascular Sciences, 
      VU University Medical Center, Amsterdam, The Netherlands. plm.kerkhof@VUmc.nl.
FAU - Khamaganova, Irina
AU  - Khamaganova I
AUID- ORCID: 0000-0003-2942-8812
AD  - Department of Skin Diseases & Cosmetology, Pirogov Russian National Research 
      Medical University, Moscow, Russia.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Adv Exp Med Biol
JT  - Advances in experimental medicine and biology
JID - 0121103
RN  - 0 (Inflammation Mediators)
SB  - IM
MH  - Cardiovascular Diseases/diagnosis/*epidemiology/immunology/physiopathology
MH  - Cardiovascular System/immunology/*physiopathology
MH  - Comorbidity
MH  - Female
MH  - Health Status Disparities
MH  - *Hemodynamics
MH  - Humans
MH  - Incidence
MH  - Inflammation Mediators/immunology
MH  - Male
MH  - Prevalence
MH  - Rheumatic Diseases/diagnosis/*epidemiology/immunology/physiopathology
MH  - Risk Factors
MH  - Sex Characteristics
MH  - Sex Factors
MH  - Skin Diseases/diagnosis/*epidemiology/immunology/physiopathology
MH  - *Vascular Stiffness
MH  - *Ventricular Function
OTO - NOTNLM
OT  - Ankylosing spondylitis
OT  - Atopic dermatitis
OT  - Cardio-dermatology
OT  - Carotid intima-media thickness
OT  - Heart failure
OT  - Hidradenitis suppurativa
OT  - Immune-mediated inflammatory disease
OT  - Inflammasome
OT  - Inflammation imaging
OT  - Inflammatory bowel disease
OT  - Ischemic heart disease
OT  - Nailfold videocapillaroscopy
OT  - Neutrophil extracellular trap
OT  - PET scan
OT  - Psoriasis
OT  - Pulse wave velocity
OT  - Review
OT  - Rheumatoid arthritis
OT  - Rosacea
OT  - Sex hormones
OT  - Sex-specific risk factors
OT  - Stroke
OT  - Systemic lupus erythematosus
OT  - Systemic sclerosis
EDAT- 2018/07/28 06:00
MHDA- 2019/03/07 06:00
CRDT- 2018/07/28 06:00
PHST- 2018/07/28 06:00 [entrez]
PHST- 2018/07/28 06:00 [pubmed]
PHST- 2019/03/07 06:00 [medline]
AID - 10.1007/978-3-319-77932-4_30 [doi]
PST - ppublish
SO  - Adv Exp Med Biol. 2018;1065:489-509. doi: 10.1007/978-3-319-77932-4_30.

PMID- 29971194
OWN - NLM
STAT- MEDLINE
DCOM- 20181126
LR  - 20200602
IS  - 2160-8288 (Electronic)
IS  - 2160-8288 (Linking)
VI  - 8
DP  - 2018
TI  - Conditions Associated with Essential Tremor in Veterans: A Potential Role for 
      Chronic Stress.
PG  - 517
LID - 10.7916/D8VD8FF5 [doi]
LID - 517
AB  - BACKGROUND: Increased depression, hearing loss, dementia, alcoholism, and 
      mortality in essential tremor patients remain unexplained. We investigated 
      whether conditions associated with tremor are linked to chronic stress. METHODS: 
      The FY2013 Veterans Affairs database was queried for 38 selected dual diagnosis 
      combinations in 5,854,223 veterans aged 21-95 years. RESULTS: Post-traumatic 
      stress disorder, anxiety, and depression were the most common psychiatric 
      diagnoses in tremor patients, with the odds ratio exceeding 2 in all 15-year 
      cohorts. Depending on age, patients with essential tremor were more likely than 
      those without to have obsessive-compulsive disorder, bipolar illness, 
      schizophrenia, use tobacco and abuse alcohol, have hypertension, obesity, 
      hyperlipidemia, diabetes, vitamin D deficiency, coronary and cerebrovascular 
      diseases, congestive heart failure, stroke, asthma, hypothyroidism, irritable 
      bowel syndrome, renal insufficiency, alcoholic liver disease, hearing loss, 
      glaucoma, macular degeneration, migraine, epilepsy, idiopathic polyneuropathy, 
      history of head trauma, and 'Alzheimer's dementia. In contrast, lung and 
      colorectal cancer, amyotrophic lateral sclerosis, psychostimulant abuse, and 
      rheumatoid arthritis were not more common. DISCUSSION: Post-traumatic stress 
      disorder, anxiety, and depression, strongly associated with essential tremor, are 
      known risk factors for poor health habits, tobacco use and alcohol abuse; 
      collectively these are risk factors for vascular disease, with further negative 
      health consequences for multiple organ systems. As essential tremor is associated 
      with all these conditions, we propose that chronic stress is not only responsible 
      for the conditions associated with tremor but in some cases itself directly and 
      indirectly induces essential tremor, so that tremor and poor health share a 
      common cause.
FAU - Handforth, Adrian
AU  - Handforth A
AD  - Neurology Service, Veterans Affairs Greater Los Angeles Healthcare System, Los 
      Angeles, CA, USA.
FAU - Parker, Gail A
AU  - Parker GA
AD  - Knowledge Management, Veterans Affairs Greater Los Angeles Healthcare System, Los 
      Angeles, CA, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20180517
PL  - England
TA  - Tremor Other Hyperkinet Mov (N Y)
JT  - Tremor and other hyperkinetic movements (New York, N.Y.)
JID - 101569493
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Chronic Disease
MH  - Cohort Studies
MH  - Essential Tremor/*complications/*epidemiology
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Mood Disorders/complications/epidemiology
MH  - Personality Disorders/complications/epidemiology
MH  - Risk Factors
MH  - Stress, Psychological/complications/epidemiology
MH  - Substance-Related Disorders/complications/epidemiology
MH  - *Veterans/psychology
MH  - Young Adult
PMC - PMC6026277
OTO - NOTNLM
OT  - Essential tremor
OT  - affective disorders
OT  - drug abuse
OT  - epidemiology
OT  - personality disorder
COIS- Funding: The authors were supported by Veterans Affairs. Conflict of Interests: 
      The authors report no conflict of interest. Ethics Statement: This study was 
      reviewed and approved by the authors' institutional ethics committee and was 
      performed in accordance with the ethical standards detailed in the Declaration of 
      Helsinki, with waived consent and authorization for review of medical records.
EDAT- 2018/07/05 06:00
MHDA- 2018/11/27 06:00
PMCR- 2018/05/17
CRDT- 2018/07/05 06:00
PHST- 2017/10/02 00:00 [received]
PHST- 2018/04/06 00:00 [accepted]
PHST- 2018/07/05 06:00 [entrez]
PHST- 2018/07/05 06:00 [pubmed]
PHST- 2018/11/27 06:00 [medline]
PHST- 2018/05/17 00:00 [pmc-release]
AID - 10.7916/D8VD8FF5 [doi]
PST - epublish
SO  - Tremor Other Hyperkinet Mov (N Y). 2018 May 17;8:517. doi: 10.7916/D8VD8FF5. 
      eCollection 2018.

PMID- 29915769
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 2249-4863 (Print)
IS  - 2278-7135 (Electronic)
IS  - 2249-4863 (Linking)
VI  - 7
IP  - 1
DP  - 2018 Jan-Feb
TI  - Rhupus syndrome and Chiari's network.
PG  - 249-251
LID - 10.4103/jfmpc.jfmpc_197_17 [doi]
AB  - A 69-year-old female patient was admitted to our clinic with photosensitivity, 
      symmetric erosive polyarthritis, and cutaneous vasculitis of lower extremities. 
      Rhupus syndrome was diagnosed, and Chiari's network in the right atrium and 
      interatrial septum patent foramen ovale was achieved on transthoracic and 
      transesophageal echocardiography. If it is thought that increased prevalence of 
      antiphospholipid antibodies in patients with rhupus, this congenital remnant is 
      important for the thrombosis risk, cardiac event, and stroke. The association of 
      both diseases may lead to more serious events and cause worse prognosis. Here, 
      our aim is to present a 69-year-old female patient with rhupus syndrome 
      presenting with cutaneous vasculitis and Chiari's network in the right atrium.
FAU - Sargin, Gokhan
AU  - Sargin G
AD  - Department of Rheumatology, Medical Faculty, Adnan Menderes University, Aydin, 
      Turkey.
FAU - Senturk, Taskin
AU  - Senturk T
AD  - Department of Rheumatology, Medical Faculty, Adnan Menderes University, Aydin, 
      Turkey.
FAU - Cildag, Songul
AU  - Cildag S
AD  - Department of Rheumatology, Medical Faculty, Adnan Menderes University, Aydin, 
      Turkey.
LA  - eng
PT  - Case Reports
PL  - India
TA  - J Family Med Prim Care
JT  - Journal of family medicine and primary care
JID - 101610082
PMC - PMC5958579
OTO - NOTNLM
OT  - Chiari's network
OT  - rheumatoid arthritis
OT  - rhupus syndrome
OT  - systemic lupus erythematosus
COIS- There are no conflicts of interest.
EDAT- 2018/06/20 06:00
MHDA- 2018/06/20 06:01
PMCR- 2018/01/01
CRDT- 2018/06/20 06:00
PHST- 2018/06/20 06:00 [entrez]
PHST- 2018/06/20 06:00 [pubmed]
PHST- 2018/06/20 06:01 [medline]
PHST- 2018/01/01 00:00 [pmc-release]
AID - JFMPC-7-249 [pii]
AID - 10.4103/jfmpc.jfmpc_197_17 [doi]
PST - ppublish
SO  - J Family Med Prim Care. 2018 Jan-Feb;7(1):249-251. doi: 
      10.4103/jfmpc.jfmpc_197_17.

PMID- 29861211
OWN - NLM
STAT- MEDLINE
DCOM- 20190506
LR  - 20190506
IS  - 1728-7731 (Electronic)
IS  - 1726-4901 (Linking)
VI  - 81
IP  - 9
DP  - 2018 Sep
TI  - The effect of rheumatoid arthritis on the risk of cerebrovascular disease and 
      coronary artery disease in young adults.
PG  - 772-780
LID - S1726-4901(18)30119-9 [pii]
LID - 10.1016/j.jcma.2018.03.009 [doi]
AB  - BACKGROUND: Only a few studies have investigated the affect of rheumatoid 
      arthritis (RA) on the risk of cerebrovascular disease (CVD)/coronary artery 
      disease (CAD) in young adults. This study, therefore, examined the association 
      between RA and the risk of CVD/CAD in young adults and the interaction effects 
      between cardiovascular risk factors and RA on the risk of CVD/CAD. METHODS: Data 
      regarding 52,840 subjects (10,568 patients with RA and 42,272 age-, sex-, 
      urbanization-, and income-matched non-RA controls) were collected from the 
      National Health Insurance Research Database (NHIRD) in 2006. All subjects were 
      followed until a CVD or CAD diagnosis, or death, or December 31, 2011. The hazard 
      ratios (HRs) of CVD/CAD were estimated using Cox proportional hazard models. The 
      interaction effects between cardiovascular risk factors and RA on the risk of 
      CVD/CAD were assessed using additive and multiplicative models. RESULTS: RA 
      increased the risk of CVD/CAD in young adults, especially those at risk of 
      ischemic stroke (adjusted HR, 3.48; 95% confidence interval (CI), 2.16-5.61). 
      Even without comorbidity at baseline, patients with RA still had a 2.35-fold 
      greater risk of CVD/CAD relative to those without RA. RA and hypertension 
      interacted positively on the risk of CVD/CAD. The highest CVD/CAD risk was found 
      in patients with RA and hypertension (HR, 9.08; 95% CI, 7.22-11.41) relative to 
      subjects without RA and hypertension. CONCLUSION: RA is an independent risk 
      factor for CVD/CAD in young adults. The government should develop policies for 
      preventing early onset hypertension to reduce the incidence of CVD/CAD among 
      young patients with RA.
CI  - Copyright © 2018. Published by Elsevier Taiwan LLC.
FAU - Chen, Yih-Ru
AU  - Chen YR
AD  - School of Public Health, College of Public Health, Taipei Medical University, 
      Taipei, Taiwan, ROC.
FAU - Hsieh, Fang-I
AU  - Hsieh FI
AD  - School of Public Health, College of Public Health, Taipei Medical University, 
      Taipei, Taiwan, ROC.
FAU - Chang, Chi-Ching
AU  - Chang CC
AD  - Department of Internal Medicine, School of Medicine, College of Medicine, Taipei 
      Medical University, Taipei, Taiwan, ROC; Division of Rheumatology, Immunology and 
      Allergy, Department of Internal Medicine, Taipei Medical University Hospital, 
      Taipei, Taiwan, ROC.
FAU - Chi, Nai-Fang
AU  - Chi NF
AD  - Department of Neurology, Shuang Ho Hospital, Taipei, Taiwan, ROC.
FAU - Wu, Hsin-Chiao
AU  - Wu HC
AD  - School of Public Health, College of Public Health, Taipei Medical University, 
      Taipei, Taiwan, ROC.
FAU - Chiou, Hung-Yi
AU  - Chiou HY
AD  - School of Public Health, College of Public Health, Taipei Medical University, 
      Taipei, Taiwan, ROC. Electronic address: hychiou@tmu.edu.tw.
LA  - eng
PT  - Journal Article
DEP - 20180601
PL  - Netherlands
TA  - J Chin Med Assoc
JT  - Journal of the Chinese Medical Association : JCMA
JID - 101174817
SB  - IM
MH  - Adult
MH  - Arthritis, Rheumatoid/*complications
MH  - Cerebrovascular Disorders/*etiology
MH  - Coronary Artery Disease/*etiology
MH  - Female
MH  - Humans
MH  - Male
MH  - Patient Outcome Assessment
MH  - Proportional Hazards Models
MH  - Risk Factors
MH  - Young Adult
OTO - NOTNLM
OT  - Cerebrovascular disorders
OT  - Coronary artery disease
OT  - Hypertension
OT  - Rheumatoid arthritis
EDAT- 2018/06/05 06:00
MHDA- 2019/05/07 06:00
CRDT- 2018/06/05 06:00
PHST- 2017/11/01 00:00 [received]
PHST- 2018/03/21 00:00 [accepted]
PHST- 2018/06/05 06:00 [pubmed]
PHST- 2019/05/07 06:00 [medline]
PHST- 2018/06/05 06:00 [entrez]
AID - S1726-4901(18)30119-9 [pii]
AID - 10.1016/j.jcma.2018.03.009 [doi]
PST - ppublish
SO  - J Chin Med Assoc. 2018 Sep;81(9):772-780. doi: 10.1016/j.jcma.2018.03.009. Epub 
      2018 Jun 1.

PMID- 29860668
OWN - NLM
STAT- MEDLINE
DCOM- 20181030
LR  - 20181114
IS  - 1432-1459 (Electronic)
IS  - 0340-5354 (Linking)
VI  - 265
IP  - 8
DP  - 2018 Aug
TI  - Rheumatoid arthritis significantly increased recurrence risk after ischemic 
      stroke/transient ischemic attack.
PG  - 1810-1818
LID - 10.1007/s00415-018-8885-9 [doi]
AB  - The effect of RA on recurrent stroke is unknown. Therefore, we examined effects 
      of rheumatoid arthritis (RA) on risk of stroke recurrence and investigated the 
      interaction between RA and traditional cardiovascular risk factors on recurrence 
      risk after ischemic stroke (IS) or transient ischemic attack (TIA). Of 3190 
      patients with IS or TIA recruited in this cohort study, 638 were comorbid with RA 
      and 2552 without RA. Stroke recurrence, RA, lifestyle, lipid variables and other 
      comorbidities were identified through linkage between a nationwide stroke 
      database in Taiwan and the National Health Insurance claims database. Cox 
      proportional hazard models with competing risk adjustment were used to evaluate 
      the relationship between RA and recurrent stroke. Patients with RA showed a 
      significantly increased risk of recurrent stroke, particular in recurrent IS/TIA. 
      The increased risk of recurrent IS/TIA in RA patients may through the changes of 
      triglycerides (TG)/high-density lipoprotein cholesterol (HDL-C) ratio. A positive 
      additive interaction was observed between RA and current smoking on the risk of 
      recurrent IS/TIA. Significantly increased risks for recurrent IS/TIA were 
      observed among RA patients who smoked > 40 years or those who smoked > 20 
      cigarettes/day. This study provides the first evidence that RA significantly 
      increased recurrence IS/TIA risk. The changes of TG/HDL-C ratio may play some 
      roles in the recurrence IS/TIA risk in RA patients. In addition, our results 
      suggest that smoking increases the risk of recurrent IS/TIA in RA patients and 
      reinforces the need for aggressive smoking cessation efforts in RA patients.
FAU - Chen, Yih-Ru
AU  - Chen YR
AD  - School of Public Health, College of Public Health, Taipei Medical University, No. 
      250, Wuxing Street, Taipei City, 110, Taiwan.
FAU - Hsieh, Fang-I
AU  - Hsieh FI
AD  - School of Public Health, College of Public Health, Taipei Medical University, No. 
      250, Wuxing Street, Taipei City, 110, Taiwan.
FAU - Lien, Li-Ming
AU  - Lien LM
AD  - Department of Neurology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.
AD  - School of Medicine, College of Medicine, Taipei Medical University, Taipei, 
      Taiwan.
FAU - Hu, Chaur-Jong
AU  - Hu CJ
AD  - School of Medicine, College of Medicine, Taipei Medical University, Taipei, 
      Taiwan.
AD  - Department of Neurology, Shuang Ho Hospital, Taipei, Taiwan.
FAU - Jeng, Jiann-Shing
AU  - Jeng JS
AD  - Stroke Center and Department of Neurology, National Taiwan University Hospital, 
      Taipei, Taiwan.
FAU - Peng, Giia-Sheun
AU  - Peng GS
AD  - Department of Neurology, Tri-Service General Hospital, National Defense Medical 
      Center, Taipei, Taiwan.
FAU - Tang, Sung-Chun
AU  - Tang SC
AD  - Stroke Center and Department of Neurology, National Taiwan University Hospital, 
      Taipei, Taiwan.
FAU - Chi, Nai-Fang
AU  - Chi NF
AD  - Department of Neurology, Shuang Ho Hospital, Taipei, Taiwan.
FAU - Sung, Yueh-Feng
AU  - Sung YF
AD  - Department of Neurology, Tri-Service General Hospital, National Defense Medical 
      Center, Taipei, Taiwan.
FAU - Chiou, Hung-Yi
AU  - Chiou HY
AD  - School of Public Health, College of Public Health, Taipei Medical University, No. 
      250, Wuxing Street, Taipei City, 110, Taiwan. hychiou@tmu.edu.tw.
LA  - eng
GR  - MOHW105-TDU-B-212-133018/The Ministry of Health and Welfare, Taiwan/
GR  - NSC 100-2811-B-038-018/Ministry of Science and Technology, Taiwan (TW)/
GR  - NSC 101-2314-B-038-043-MY3/Ministry of Science and Technology, Taiwan (TW)/
GR  - NSC 102-2314-B-038-041/Ministry of Science and Technology, Taiwan (TW)/
GR  - MOST 104-2314-B-038-069/Ministry of Science and Technology, Taiwan (TW)/
PT  - Journal Article
DEP - 20180602
PL  - Germany
TA  - J Neurol
JT  - Journal of neurology
JID - 0423161
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications/*epidemiology
MH  - Brain Ischemia/*complications/*epidemiology
MH  - Cohort Studies
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Pilot Projects
MH  - Proportional Hazards Models
MH  - Recurrence
MH  - Risk Factors
MH  - Smoking/epidemiology
MH  - Stroke/*complications/*epidemiology
MH  - Taiwan
OTO - NOTNLM
OT  - Lipid
OT  - Rheumatoid arthritis
OT  - Smoking
OT  - Stroke recurrence
EDAT- 2018/06/04 06:00
MHDA- 2018/10/31 06:00
CRDT- 2018/06/04 06:00
PHST- 2018/04/02 00:00 [received]
PHST- 2018/04/24 00:00 [accepted]
PHST- 2018/04/23 00:00 [revised]
PHST- 2018/06/04 06:00 [pubmed]
PHST- 2018/10/31 06:00 [medline]
PHST- 2018/06/04 06:00 [entrez]
AID - 10.1007/s00415-018-8885-9 [pii]
AID - 10.1007/s00415-018-8885-9 [doi]
PST - ppublish
SO  - J Neurol. 2018 Aug;265(8):1810-1818. doi: 10.1007/s00415-018-8885-9. Epub 2018 
      Jun 2.

PMID- 29856128
OWN - NLM
STAT- MEDLINE
DCOM- 20200102
LR  - 20200102
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Linking)
VI  - 71
IP  - 4
DP  - 2019 Apr
TI  - Incidence and Risk of Glucocorticoid-Associated Adverse Effects in Patients With 
      Rheumatoid Arthritis.
PG  - 498-511
LID - 10.1002/acr.23611 [doi]
AB  - OBJECTIVE: Using the UK Clinical Practice Research Datalink, we examined the 
      incidence of glucocorticoid (GC)-related serious adverse events (SAEs) in 
      rheumatoid arthritis (RA) and non-RA patients and quantified the risk of SAEs in 
      patients with RA. METHODS: We matched incident patients with RA to an age- and 
      sex-matched, non-RA comparison group of equal size. In a cohort analysis, we 
      estimated incidence rates (IRs) and IR ratios (IRRs) for GC-related AEs (i.e., 
      diabetes mellitus [DM], osteoporosis, fractures, glaucoma, hypertension, 
      gastrointestinal [GI] perforation or bleeding, thrombotic stroke or myocardial 
      infarction [MI], or death), stratified by GC use. We conducted a series of nested 
      case-control analyses among patients with RA, evaluating the effects of 
      increasing cumulative and average daily GC dose. Cases of each outcome were 
      matched to controls for age, sex, and general practice. We calculated adjusted 
      odds ratios (ORs) with 95% confidence intervals (95% CIs) for each outcome. 
      RESULTS: Patients with RA had a higher incidence for all investigated SAEs except 
      glaucoma, compared to non-RA patients. IRRs were greater in those patients 
      prescribed a GC than in those without. In patients with RA, GCs were associated 
      with an elevated risk of DM (adjusted OR 1.33 [95% CI 1.14-1.56]), osteoporosis 
      (adjusted OR 1.41 [95% CI 1.25-1.59]), thrombotic stroke or MI (adjusted OR 1.28 
      [95% CI 1.07-1.52]), serious infection (adjusted OR 1.28 [95% CI 1.11-1.48]), and 
      death (adjusted OR 1.33 [95% CI 1.19-1.48]). There was a trend of increasing risk 
      with increasing cumulative and average daily GC dose for all outcomes other than 
      glaucoma, hypertension, and GI perforations or bleeding (P < 0.05). CONCLUSION: 
      Patients with RA had an increased incidence of GC-related AEs. Increasing 
      cumulative and average daily GC doses were found to be associated with an 
      increasing risk of developing an AE.
CI  - © 2018, American College of Rheumatology.
FAU - Wilson, Jessica C
AU  - Wilson JC
AD  - University of Basel, Basel, Switzerland.
FAU - Sarsour, Khaled
AU  - Sarsour K
AD  - Genentech, South San Francisco, California.
FAU - Gale, Sara
AU  - Gale S
AD  - Genentech, South San Francisco, California.
FAU - Pethö-Schramm, Attila
AU  - Pethö-Schramm A
AD  - F. Hoffmann-La Roche, Basel, Switzerland.
FAU - Jick, Susan S
AU  - Jick SS
AD  - Boston University School of Public Health, Lexington, Massachusetts.
FAU - Meier, Christoph R
AU  - Meier CR
AD  - University of Basel and University Hospital Basel, Basel, Switzerland, and Boston 
      Collaborative Drug Surveillance Program, Lexington, Massachusetts.
LA  - eng
GR  - F. Hoffmann-La Roche and Genentech, Inc./International
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 0 (Glucocorticoids)
SB  - IM
MH  - Arthritis, Rheumatoid/*drug therapy/mortality
MH  - Cardiovascular Diseases/*chemically induced/epidemiology
MH  - Case-Control Studies
MH  - Diabetes Mellitus/*chemically induced/epidemiology
MH  - Female
MH  - Gastrointestinal Hemorrhage/chemically induced/epidemiology
MH  - Glaucoma/chemically induced/epidemiology
MH  - Glucocorticoids/*adverse effects
MH  - Humans
MH  - Incidence
MH  - Intestinal Perforation/chemically induced/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Osteoporosis/*chemically induced/epidemiology
MH  - United Kingdom/epidemiology
EDAT- 2018/06/02 06:00
MHDA- 2020/01/03 06:00
CRDT- 2018/06/02 06:00
PHST- 2017/10/04 00:00 [received]
PHST- 2018/05/29 00:00 [accepted]
PHST- 2018/06/02 06:00 [pubmed]
PHST- 2020/01/03 06:00 [medline]
PHST- 2018/06/02 06:00 [entrez]
AID - 10.1002/acr.23611 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2019 Apr;71(4):498-511. doi: 10.1002/acr.23611.

PMID- 29799667
OWN - NLM
STAT- MEDLINE
DCOM- 20200102
LR  - 20211001
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Print)
IS  - 2151-464X (Linking)
VI  - 71
IP  - 4
DP  - 2019 Apr
TI  - Subsequent Cardiovascular Events Among Patients With Rheumatoid Arthritis, 
      Psoriatic Arthritis, or Psoriasis: Patterns of Disease-Modifying Antirheumatic 
      Drug Treatment.
PG  - 512-520
LID - 10.1002/acr.23609 [doi]
AB  - OBJECTIVE: To examine disease-modifying antirheumatic drug (DMARD) treatments and 
      estimate the risk of a subsequent cardiovascular (CV) event following an initial 
      CV event in patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), 
      or psoriasis. METHODS: We analyzed data from MarketScan claims databases (January 
      1, 2006 to June 30, 2015) for adults with RA, PsA, or psoriasis and an 
      initial/index CV event (acute myocardial infarction, stroke, or coronary 
      revascularization) while receiving DMARDs (tumor necrosis factor inhibitor [TNFi] 
      biologic DMARDs [bDMARDs], conventional synthetic DMARDs [csDMARDs], or non-TNFi 
      bDMARDs). We studied DMARD treatment patterns following the index event and rates 
      of subsequent CV events. We used Cox regression to investigate predictors of 
      DMARD discontinuation and risk factors for subsequent CV events. RESULTS: Among 
      10,254 patients, 15.3% discontinued and 15.5% switched DMARD therapy after the 
      index CV event. Independent predictors of DMARD discontinuation included a 
      psoriasis diagnosis, renal disease, hypertension, heart failure, diabetes 
      mellitus, older age, and baseline csDMARD or non-TNFi bDMARD use (versus TNFi 
      bDMARDs). Rates per 1,000 patient-years of subsequent events were 75.2 (95% 
      confidence interval [95% CI] 54.4-96.0) for patients taking TNFi bDMARDs, 83.6 
      (95% CI 53.3-113.9) for csDMARDs, and 122.4 (95% CI 60.6-184.3) for non-TNFi 
      bDMARDs. A diagnosis of RA (versus psoriasis) and heart failure at baseline, but 
      not a DMARD pattern after the index event, were independently associated with an 
      increased risk of subsequent CV event. CONCLUSION: In this large nationwide 
      study, nearly one-third of patients with RA, PsA, or psoriasis switched or 
      discontinued DMARD therapy following a CV event. There was no association between 
      DMARD class and the risk of a subsequent CV event.
CI  - © 2018, The Authors. Arthritis Care & Research published by Wiley Periodicals, 
      Inc. on behalf of American College of Rheumatology.
FAU - Sparks, Jeffrey A
AU  - Sparks JA
AUID- ORCID: 0000-0002-5556-4618
AD  - Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
FAU - Lesperance, Tamara
AU  - Lesperance T
AD  - DOCS Global Inc., North Wales, Pennsylvania.
FAU - Accortt, Neil A
AU  - Accortt NA
AD  - Amgen Inc., Thousand Oaks, California.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
LA  - eng
GR  - K23 AR069688/AR/NIAMS NIH HHS/United States
GR  - L30 AR066953/AR/NIAMS NIH HHS/United States
GR  - Amgen Inc./International
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Antirheumatic Agents/*administration & dosage
MH  - Arthritis, Psoriatic/*complications/drug therapy
MH  - Arthritis, Rheumatoid/*complications/drug therapy
MH  - Cardiovascular Diseases/*etiology
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Practice Patterns, Physicians'
MH  - Recurrence
MH  - Retrospective Studies
PMC - PMC6252288
MID - NIHMS970964
EDAT- 2018/05/26 06:00
MHDA- 2020/01/03 06:00
PMCR- 2019/07/01
CRDT- 2018/05/26 06:00
PHST- 2017/12/07 00:00 [received]
PHST- 2018/05/22 00:00 [accepted]
PHST- 2018/05/26 06:00 [pubmed]
PHST- 2020/01/03 06:00 [medline]
PHST- 2018/05/26 06:00 [entrez]
PHST- 2019/07/01 00:00 [pmc-release]
AID - ACR23609 [pii]
AID - 10.1002/acr.23609 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2019 Apr;71(4):512-520. doi: 10.1002/acr.23609.

PMID- 29764964
OWN - NLM
STAT- MEDLINE
DCOM- 20191114
LR  - 20191114
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
VI  - 45
IP  - 9
DP  - 2018 Aug
TI  - Cardiovascular (CV) Risk after Initiation of Abatacept versus TNF Inhibitors in 
      Rheumatoid Arthritis Patients with and without Baseline CV Disease.
PG  - 1240-1248
LID - 10.3899/jrheum.170926 [doi]
AB  - OBJECTIVE: To evaluate the cardiovascular safety of abatacept (ABA) versus tumor 
      necrosis factor inhibitors (TNFi) in rheumatoid arthritis (RA) patients with and 
      without underlying cardiovascular disease (CVD). METHODS: We identified RA 
      patients with and without baseline CVD who initiated ABA or TNFi by using data 
      from 2 large US insurance claims databases: Medicare (2008-2013) and Truven 
      MarketScan (2006-2015). After stratifying by baseline CVD, ABA initiators were 
      1:1 propensity score (PS) matched to TNFi initiators to control for > 60 baseline 
      covariates. Cox proportional hazards regression estimated the HR and 95% CI for a 
      composite endpoint of CVD including myocardial infarction, stroke/transient 
      ischemic stroke, or coronary revascularization in the PS-matched cohorts. HR from 
      2 databases were combined through an inverse variance-weighted fixed-effects 
      model. RESULTS: We included 6102 PS-matched pairs of ABA and TNFi initiators from 
      Medicare and 6934 pairs from MarketScan. Of these, 35.3% in Medicare and 14.0% in 
      MarketScan had baseline CVD. HR (95% CI) for composite CVD in the overall ABA 
      group versus TNFi was 0.67 (0.55-0.81) in Medicare and 1.08 (0.83-1.41) in 
      MarketScan with the combined HR of 0.79 (0.67-0.92). Among patients with baseline 
      CVD, the HR (95% CI) was 0.71 (0.55-0.92) in Medicare and 1.02 (0.68-1.51) in 
      MarketScan, with the combined HR of 0.79 (0.64-0.98). CONCLUSION: In this large 
      cohort of publicly or privately insured patients with RA in the United States, 
      ABA was associated with a 20% reduced risk of CVD versus TNFi. While this 
      observational study is subject to potential residual confounding, our results 
      were consistent in patients with baseline CVD.
FAU - Jin, Yinzhu
AU  - Jin Y
AD  - From the Division of Pharmacoepidemiology and Pharmacoeconomics, and Division of 
      Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard 
      Medical School, Boston, Massachusetts, USA; Division of Rheumatology, Department 
      of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, South 
      Korea.
AD  - Y. Jin, MS, MPH, Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham 
      and Women's Hospital, Harvard Medical School; E.H. Kang, MD, PhD, MPH, Division 
      of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, 
      Harvard Medical School, and Division of Rheumatology, Department of Internal 
      Medicine, Seoul National University Bundang Hospital; G. Brill, MS, Division of 
      Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard 
      Medical School; R.J. Desai, PhD, Division of Pharmacoepidemiology and 
      Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School; S.C. 
      Kim, MD, ScD, MSCE, Division of Pharmacoepidemiology and Pharmacoeconomics, and 
      Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 
      Harvard Medical School.
FAU - Kang, Eun Ha
AU  - Kang EH
AD  - From the Division of Pharmacoepidemiology and Pharmacoeconomics, and Division of 
      Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard 
      Medical School, Boston, Massachusetts, USA; Division of Rheumatology, Department 
      of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, South 
      Korea.
AD  - Y. Jin, MS, MPH, Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham 
      and Women's Hospital, Harvard Medical School; E.H. Kang, MD, PhD, MPH, Division 
      of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, 
      Harvard Medical School, and Division of Rheumatology, Department of Internal 
      Medicine, Seoul National University Bundang Hospital; G. Brill, MS, Division of 
      Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard 
      Medical School; R.J. Desai, PhD, Division of Pharmacoepidemiology and 
      Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School; S.C. 
      Kim, MD, ScD, MSCE, Division of Pharmacoepidemiology and Pharmacoeconomics, and 
      Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 
      Harvard Medical School.
FAU - Brill, Gregory
AU  - Brill G
AD  - From the Division of Pharmacoepidemiology and Pharmacoeconomics, and Division of 
      Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard 
      Medical School, Boston, Massachusetts, USA; Division of Rheumatology, Department 
      of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, South 
      Korea.
AD  - Y. Jin, MS, MPH, Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham 
      and Women's Hospital, Harvard Medical School; E.H. Kang, MD, PhD, MPH, Division 
      of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, 
      Harvard Medical School, and Division of Rheumatology, Department of Internal 
      Medicine, Seoul National University Bundang Hospital; G. Brill, MS, Division of 
      Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard 
      Medical School; R.J. Desai, PhD, Division of Pharmacoepidemiology and 
      Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School; S.C. 
      Kim, MD, ScD, MSCE, Division of Pharmacoepidemiology and Pharmacoeconomics, and 
      Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 
      Harvard Medical School.
FAU - Desai, Rishi J
AU  - Desai RJ
AD  - From the Division of Pharmacoepidemiology and Pharmacoeconomics, and Division of 
      Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard 
      Medical School, Boston, Massachusetts, USA; Division of Rheumatology, Department 
      of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, South 
      Korea.
AD  - Y. Jin, MS, MPH, Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham 
      and Women's Hospital, Harvard Medical School; E.H. Kang, MD, PhD, MPH, Division 
      of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, 
      Harvard Medical School, and Division of Rheumatology, Department of Internal 
      Medicine, Seoul National University Bundang Hospital; G. Brill, MS, Division of 
      Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard 
      Medical School; R.J. Desai, PhD, Division of Pharmacoepidemiology and 
      Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School; S.C. 
      Kim, MD, ScD, MSCE, Division of Pharmacoepidemiology and Pharmacoeconomics, and 
      Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 
      Harvard Medical School.
FAU - Kim, Seoyoung C
AU  - Kim SC
AD  - From the Division of Pharmacoepidemiology and Pharmacoeconomics, and Division of 
      Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Harvard 
      Medical School, Boston, Massachusetts, USA; Division of Rheumatology, Department 
      of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, South 
      Korea. skim62@partners.org.
AD  - Y. Jin, MS, MPH, Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham 
      and Women's Hospital, Harvard Medical School; E.H. Kang, MD, PhD, MPH, Division 
      of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, 
      Harvard Medical School, and Division of Rheumatology, Department of Internal 
      Medicine, Seoul National University Bundang Hospital; G. Brill, MS, Division of 
      Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, Harvard 
      Medical School; R.J. Desai, PhD, Division of Pharmacoepidemiology and 
      Pharmacoeconomics, Brigham and Women's Hospital, Harvard Medical School; S.C. 
      Kim, MD, ScD, MSCE, Division of Pharmacoepidemiology and Pharmacoeconomics, and 
      Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 
      Harvard Medical School. skim62@partners.org.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180515
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 7D0YB67S97 (Abatacept)
SB  - IM
MH  - Abatacept/*adverse effects/therapeutic use
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Antirheumatic Agents/*adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy/epidemiology
MH  - Biological Products/*adverse effects/therapeutic use
MH  - Cardiovascular Diseases/*epidemiology/etiology
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Registries
MH  - Risk
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
MH  - United States
OTO - NOTNLM
OT  - BIOLOGIC DISEASE-MODIFYING ANTIRHEUMATIC DRUGS
OT  - CARDIOVASCULAR DISEASES
OT  - COMPARATIVE SAFETY RESEARCH
OT  - RHEUMATOID ARTHRITIS
EDAT- 2018/05/17 06:00
MHDA- 2019/11/15 06:00
CRDT- 2018/05/17 06:00
PHST- 2018/02/12 00:00 [accepted]
PHST- 2018/05/17 06:00 [pubmed]
PHST- 2019/11/15 06:00 [medline]
PHST- 2018/05/17 06:00 [entrez]
AID - jrheum.170926 [pii]
AID - 10.3899/jrheum.170926 [doi]
PST - ppublish
SO  - J Rheumatol. 2018 Aug;45(9):1240-1248. doi: 10.3899/jrheum.170926. Epub 2018 May 
      15.

PMID- 29673963
OWN - NLM
STAT- MEDLINE
DCOM- 20190110
LR  - 20190110
IS  - 1532-866X (Electronic)
IS  - 0049-0172 (Linking)
VI  - 48
IP  - 3
DP  - 2018 Dec
TI  - No difference in cardiovascular risk of tocilizumab versus abatacept for 
      rheumatoid arthritis: A multi-database cohort study.
PG  - 399-405
LID - S0049-0172(17)30810-7 [pii]
LID - 10.1016/j.semarthrit.2018.03.012 [doi]
AB  - OBJECTIVES: While tocilizumab may increase serum lipid levels, recent studies do 
      not suggest a link between tocilizumab use and clinical cardiovascular risk in 
      patients with rheumatoid arthritis (RA). METHODS: To compare cardiovascular 
      safety of tocilizumab with abatacept, we conducted a cohort study using data from 
      Medicare (2010-2013), IMS PharMetrics (2011-2014) and MarketScan (2011-6/2015). 
      RA patients aged ≥18 years who newly started tocilizumab or abatacept entered the 
      cohort on the day of their first use of tocilizumab or abatacept after a 
      continuous enrollment period for ≥365 days. The primary outcome was a composite 
      cardiovascular endpoint of hospitalization for myocardial infarction or stroke. 
      To control for more than 60 confounders, tocilizumab starters were propensity 
      score (PS)-matched to abatacept starters with a variable ratio of 1:3 within each 
      database. A fixed-effects model combined database-specific hazard ratios (HR). 
      RESULTS: We included 6237 tocilizumab starters PS-matched to 14,685 abatacept 
      starters in all three databases. Mean age was 72 years in Medicare, 51 in 
      PharMetrics and 53 in MarketScan. The incidence rate of the composite 
      cardiovascular events per 100 person-years ranged from 0.37 (PharMetrics) to 1.64 
      (Medicare) in the tocilizumab group and from 0.59 (PharMetrics) to 1.69 
      (Medicare) in the abatacept group. The risk of the composite cardiovascular 
      events was similar between the two groups across all three databases, with a 
      combined HR of 0.82 (95% CI: 0.55-1.22) in tocilizumab versus abatacept starters. 
      CONCLUSIONS: This multi-database cohort study found no difference in the risk of 
      cardiovascular events in RA patients who newly started tocilizumab versus 
      abatacept.
CI  - Copyright © 2018 Elsevier Inc. All rights reserved.
FAU - Kim, Seoyoung C
AU  - Kim SC
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, 1620 Tremont Street, Suite 3030, Boston, MA 02120; Division of 
      Rheumatology, Immunology and Allergy; Brigham and Women's Hospital, Boston, MA 
      02115. Electronic address: skim62@partners.org.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, 1620 Tremont Street, Suite 3030, Boston, MA 02120; Division of 
      Rheumatology, Immunology and Allergy; Brigham and Women's Hospital, Boston, MA 
      02115.
FAU - Rogers, James R
AU  - Rogers JR
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, 1620 Tremont Street, Suite 3030, Boston, MA 02120.
FAU - Gale, Sara
AU  - Gale S
AD  - Genentech, a Member of the Roche Group, South San Francisco, CA 94080.
FAU - Klearman, Micki
AU  - Klearman M
AD  - Genentech, a Member of the Roche Group, South San Francisco, CA 94080.
FAU - Sarsour, Khaled
AU  - Sarsour K
AD  - Genentech, a Member of the Roche Group, South San Francisco, CA 94080.
FAU - Schneeweiss, Sebastian
AU  - Schneeweiss S
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, 1620 Tremont Street, Suite 3030, Boston, MA 02120.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180322
PL  - United States
TA  - Semin Arthritis Rheum
JT  - Seminars in arthritis and rheumatism
JID - 1306053
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - 7D0YB67S97 (Abatacept)
RN  - I031V2H011 (tocilizumab)
SB  - IM
MH  - Abatacept/*adverse effects/therapeutic use
MH  - Aged
MH  - Aged, 80 and over
MH  - Antibodies, Monoclonal, Humanized/*adverse effects/therapeutic use
MH  - Antirheumatic Agents/*adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Biological Products/*adverse effects/therapeutic use
MH  - Cohort Studies
MH  - Databases, Factual
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/chemically induced/*epidemiology
MH  - Stroke/chemically induced/*epidemiology
MH  - United States
OTO - NOTNLM
OT  - Abatacept
OT  - Biologic therapy
OT  - Cardiovascular disease
OT  - Rheumatoid arthritis
OT  - Tocilizumab
EDAT- 2018/04/21 06:00
MHDA- 2019/01/11 06:00
CRDT- 2018/04/21 06:00
PHST- 2017/12/13 00:00 [received]
PHST- 2018/03/02 00:00 [revised]
PHST- 2018/03/21 00:00 [accepted]
PHST- 2018/04/21 06:00 [pubmed]
PHST- 2019/01/11 06:00 [medline]
PHST- 2018/04/21 06:00 [entrez]
AID - S0049-0172(17)30810-7 [pii]
AID - 10.1016/j.semarthrit.2018.03.012 [doi]
PST - ppublish
SO  - Semin Arthritis Rheum. 2018 Dec;48(3):399-405. doi: 
      10.1016/j.semarthrit.2018.03.012. Epub 2018 Mar 22.

PMID- 29600936
OWN - NLM
STAT- MEDLINE
DCOM- 20181126
LR  - 20181202
IS  - 0392-856X (Print)
IS  - 0392-856X (Linking)
VI  - 36 Suppl 112
IP  - 3
DP  - 2018 May-Jun
TI  - Association between primary Sjögren's syndrome, cardiovascular and 
      cerebrovascular disease: a systematic review and meta-analysis.
PG  - 190-197
AB  - OBJECTIVES: Acute systemic inflammation and chronic systemic vasculitis are 
      associated with endothelial dysfunction and atherosclerotic plaque formation. 
      Studies on cardiovascular or cerebrovascular events in primary Sjögren's syndrome 
      (pSS) are limited, with conflicting results. This meta-analysis aimed to explore 
      the risk of cardiovascular and cerebrovascular disease in pSS. METHODS: A 
      comprehensive search of the MEDLINE and EMBASE databases was performed from date 
      of inception through August 2017. The inclusion criterion was observational 
      studies evaluating the association between pSS and cardiovascular disease or 
      cerebrovascular event. Outcomes are diagnosis of ischaemic heart disease, 
      myocardial infarction, ischaemic stroke or haemorrhagic stroke. The pooled odds 
      ratio (OR) of the cerebrovascular event or cardiovascular disease and their 95% 
      confidence interval (CI) were calculated using a random-effect meta-analysis to 
      compare risk between patients with pSS and controls. The between-study 
      heterogeneity of effect-size was quantified using the Q statistic and I2. 
      RESULTS: Data were extracted from 10 observational studies involving 165,291 
      subjects. Pooled result demonstrated a significant increase in risk of having 
      cardiovascular disease or cerebrovascular event in pSS patients compared with 
      controls (OR=1.28; 95% CI: 0.11-1.46, p value<0.01, I2=68%). Subgroup analyses 
      showed no difference in risk for cerebrovascular event (OR=1.31; 95% CI: 
      0.96-1.79, p value=0.09, I2=71%), but an increased risk of cardiovascular disease 
      (OR=1.30; 95% CI: 1.09-1.55, p value=0.003, I2=74%). CONCLUSIONS: Our study has 
      shown an increased risk of cardiovascular or cerebrovascular disease in patients 
      with pSS. These results support multiple studies' finding of increased arterial 
      stiffness in patients with pSS.
FAU - Yong, Wai Chung
AU  - Yong WC
AD  - Department of Internal Medicine, Greenfield Family Medicine, Baystate Franklin 
      Medical Center, Greenfield, MA, USA.
FAU - Sanguankeo, Anawin
AU  - Sanguankeo A
AD  - Division of Nephrology, Johns Hopkins University School of Medicine, Baltimore, 
      MD, USA; and Department of Preventive and Social Medicine, Faculty of Medicine 
      Siriraj Hospital, Mahidol University, Bangkok, Thailand. asangua1@jhmi.edu.
FAU - Upala, Sikarin
AU  - Upala S
AD  - Section of Endocrinology, Diabetes and Metabolism, Department of Medicine, 
      University of Chicago, USA; and Department of Preventive and Social Medicine, 
      Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Review
PT  - Systematic Review
DEP - 20180319
PL  - Italy
TA  - Clin Exp Rheumatol
JT  - Clinical and experimental rheumatology
JID - 8308521
SB  - IM
MH  - Adult
MH  - Aged
MH  - Cardiovascular Diseases/diagnosis/*epidemiology
MH  - Cerebrovascular Disorders/diagnosis/*epidemiology
MH  - Chi-Square Distribution
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Observational Studies as Topic
MH  - Odds Ratio
MH  - Prognosis
MH  - Risk Assessment
MH  - Risk Factors
MH  - Sjogren's Syndrome/diagnosis/*epidemiology
EDAT- 2018/03/31 06:00
MHDA- 2018/11/27 06:00
CRDT- 2018/03/31 06:00
PHST- 2017/09/04 00:00 [received]
PHST- 2017/11/20 00:00 [accepted]
PHST- 2018/03/31 06:00 [pubmed]
PHST- 2018/11/27 06:00 [medline]
PHST- 2018/03/31 06:00 [entrez]
AID - 12208 [pii]
PST - ppublish
SO  - Clin Exp Rheumatol. 2018 May-Jun;36 Suppl 112(3):190-197. Epub 2018 Mar 19.

PMID- 29575885
OWN - NLM
STAT- MEDLINE
DCOM- 20180427
LR  - 20180427
IS  - 1898-2263 (Electronic)
IS  - 1232-1966 (Linking)
VI  - 25
IP  - 1
DP  - 2018 Mar 14
TI  - Periodontal condition in patients of the specialist Outpatient Clinics at the 
      Institute of Rural Health in Lublin, Poland.
PG  - 9-12
LID - 72562 [pii]
LID - 10.5604/12321966.1227649 [doi]
AB  - INTRODUCTION: Periodontal disease is a chronic inflammation which, if remains 
      untreated, can lead to the loss of teeth and supporting structures. Evidence data 
      support the relationship of periodontal disease with the development and course 
      of diseases such as heart attack, stroke, hypertension, chronic renal diseases, 
      rheumatoid arthritis or diabetes. OBJECTIVE: The aim of the study was to conduct 
      an assessment of periodontal status and periodontal needs in people from the 
      rural environment who were patients of selected specialist outpatient clinics at 
      the Institute of Rural Health in Lublin, Poland. MATERIAL AND METHODS: The 
      examined population included 450 patients. The Community Periodontal Index of 
      Treatment Needs, which is a measure of the assessment of the selected periodontal 
      symptoms incidence, was used. The obtained data was discussed and analyzed with 
      Chi-square test. RESULTS: The data obtained revealed that a healthy periodontium 
      occurred only in 5.1% of respondents, tartar in 41.6%, pathological pockets of 
      3.5-5.5 mm in 23.6%, and pockets deeper than 5.5 mm in 5.8% of patients. Most 
      people with healthy periodontium were in the youngest age group. In the analyzed 
      group, 7.1% of patients required specialized comprehensive periodontal treatment, 
      and only 6.5% of the examined persons did not show any need for periodontal 
      treatment. CONCLUSIONS: Patients of specialist clinics of the Institute of Rural 
      Health who formed the analyzed group, had affected periodontium which required 
      comprehensive periodontal treatment. The alarmingly high percentage of people 
      over 55 years of age with advanced periodontopathy may translate into an 
      increased risk of cause-and-effect incidence of systemic diseases.
FAU - Pawłowicz, Agnieszka
AU  - Pawłowicz A
AD  - Department of Conservative Dentistry and Endodontics, Medical University of 
      Lublin, Poland.
FAU - Bachanek, Teresa
AU  - Bachanek T
AD  - Department of Conservative Dentistry and Endodontics, Medical University of 
      Lublin, Poland.
FAU - Klijer, Magdalena
AU  - Klijer M
AD  - Department of Conservative Dentistry and Endodontics, Medical University of 
      Lublin, Poland.
FAU - Chałas, Renata
AU  - Chałas R
AD  - Department of Conservative Dentistry and Endodontics, Medical University of 
      Lublin, Poland. renata.chalas@umlub.pl.
LA  - eng
PT  - Journal Article
DEP - 20161228
PL  - Poland
TA  - Ann Agric Environ Med
JT  - Annals of agricultural and environmental medicine : AAEM
JID - 9500166
SB  - IM
MH  - Adult
MH  - Ambulatory Care Facilities/*statistics & numerical data
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Outpatients/statistics & numerical data
MH  - Periodontal Diseases/*epidemiology
MH  - Periodontal Index
MH  - Poland/epidemiology
MH  - Rural Health/*statistics & numerical data
OTO - NOTNLM
OT  - Community Periodontal Index of Treatment Needs (CPITN)
OT  - periodontal diseases
OT  - systemic diseases
EDAT- 2018/03/27 06:00
MHDA- 2018/04/28 06:00
CRDT- 2018/03/27 06:00
PHST- 2018/03/27 06:00 [entrez]
PHST- 2018/03/27 06:00 [pubmed]
PHST- 2018/04/28 06:00 [medline]
AID - 72562 [pii]
AID - 10.5604/12321966.1227649 [doi]
PST - ppublish
SO  - Ann Agric Environ Med. 2018 Mar 14;25(1):9-12. doi: 10.5604/12321966.1227649. 
      Epub 2016 Dec 28.

PMID- 29560750
OWN - NLM
STAT- MEDLINE
DCOM- 20181023
LR  - 20181023
IS  - 1651-2006 (Electronic)
IS  - 1401-7431 (Linking)
VI  - 52
IP  - 4
DP  - 2018 Aug
TI  - Association of non-invasive hemodynamics with arterial stiffness in rheumatoid 
      arthritis.
PG  - 171-176
LID - 10.1080/14017431.2018.1453943 [doi]
AB  - OBJECTIVES: Arterial stiffness has emerged as a surrogate marker of 
      cardiovascular disease. We investigated the role of myocardial performance and 
      hemodynamic parameters in arterial stiffness in patients with rheumatoid 
      arthritis (RA), which is accompanied by excess cardiovascular risk. DESIGN: 
      Arterial stiffness was evaluated with pulse wave velocity (PWV) in RA patients 
      and controls. Cardiac and hemodynamic characterization was based on impedance 
      cardiography. Cardiovascular risk factors, inflammatory markers and 
      disease-related parameters were assessed. RESULTS: PWV (8.2 ± 2.1 vs 7.4 ± 1.4 
      m/s, p = .016) was higher among RA patients (n = 104) compared to controls 
      (n = 52). In the RA group, PWV correlated with markers of cardiac contractibility 
      (acceleration and velocity index), myocardial blood flow (cardiac output and 
      stroke volume), preload (thoracic fluid content) and afterload (systemic vascular 
      resistance) (p < .05 for all). PWV tended to increase with decreasing oxygen 
      delivery to the myocardium (r = 0.055), as well as with shortening of the 
      ejection duration of the left ventricle (p = .058). However, these associations 
      no longer remained significant after adjustment for classical cardiovascular risk 
      factors, inflammation and corticosteroid use, which were independently associated 
      with PWV. CONCLUSIONS: Among patients with RA, arterial stiffness appears as the 
      composite of cardiovascular risk factors and inflammation, while corticosteroid 
      use emerges as an additional adverse factor.
FAU - Anyfanti, Panagiota
AU  - Anyfanti P
AD  - a 3rd Department of Internal Medicine , Papageorgiou Hospital, Aristotle 
      University of Thessaloniki , Thessaloniki , Greece.
FAU - Triantafyllou, Areti
AU  - Triantafyllou A
AD  - a 3rd Department of Internal Medicine , Papageorgiou Hospital, Aristotle 
      University of Thessaloniki , Thessaloniki , Greece.
FAU - Gkaliagkousi, Eugenia
AU  - Gkaliagkousi E
AD  - a 3rd Department of Internal Medicine , Papageorgiou Hospital, Aristotle 
      University of Thessaloniki , Thessaloniki , Greece.
FAU - Koletsos, Nikolaos
AU  - Koletsos N
AD  - a 3rd Department of Internal Medicine , Papageorgiou Hospital, Aristotle 
      University of Thessaloniki , Thessaloniki , Greece.
FAU - Aslanidis, Spyros
AU  - Aslanidis S
AD  - b Rheumatology Department-2nd Propedeutic Department of Internal Medicine , 
      Hippokration Hospital, Aristotle University of Thessaloniki , Thessaloniki , 
      Greece.
FAU - Douma, Stella
AU  - Douma S
AD  - a 3rd Department of Internal Medicine , Papageorgiou Hospital, Aristotle 
      University of Thessaloniki , Thessaloniki , Greece.
LA  - eng
PT  - Journal Article
DEP - 20180321
PL  - England
TA  - Scand Cardiovasc J
JT  - Scandinavian cardiovascular journal : SCJ
JID - 9708377
RN  - 0 (Adrenal Cortex Hormones)
RN  - 0 (Inflammation Mediators)
SB  - IM
MH  - Adrenal Cortex Hormones/adverse effects
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications/diagnosis/drug therapy/physiopathology
MH  - Cardiography, Impedance
MH  - Cardiovascular Diseases/diagnosis/*etiology/physiopathology
MH  - Case-Control Studies
MH  - Chi-Square Distribution
MH  - Female
MH  - *Hemodynamics
MH  - Humans
MH  - Inflammation Mediators/blood
MH  - Linear Models
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Myocardial Contraction
MH  - Pulse Wave Analysis
MH  - Risk Factors
MH  - Stroke Volume
MH  - *Vascular Stiffness
MH  - Ventricular Function, Left
OTO - NOTNLM
OT  - Arterial stiffness
OT  - hemodynamic parameters
OT  - impedance cardiography
OT  - myocardial function
OT  - rheumatoid arthritis
EDAT- 2018/03/22 06:00
MHDA- 2018/10/24 06:00
CRDT- 2018/03/22 06:00
PHST- 2018/03/22 06:00 [pubmed]
PHST- 2018/10/24 06:00 [medline]
PHST- 2018/03/22 06:00 [entrez]
AID - 10.1080/14017431.2018.1453943 [doi]
PST - ppublish
SO  - Scand Cardiovasc J. 2018 Aug;52(4):171-176. doi: 10.1080/14017431.2018.1453943. 
      Epub 2018 Mar 21.

PMID- 29554376
OWN - NLM
STAT- MEDLINE
DCOM- 20180716
LR  - 20180716
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 57
IP  - 6
DP  - 2018 Jun 1
TI  - High-sensitivity cardiac troponin I is a biomarker for occult coronary plaque 
      burden and cardiovascular events in patients with rheumatoid arthritis.
PG  - 1080-1088
LID - 10.1093/rheumatology/key057 [doi]
AB  - OBJECTIVES: Patients with RA display greater occult coronary atherosclerosis 
      burden and experience higher cardiovascular morbidity and mortality compared with 
      controls. We here explored whether pro-inflammatory cytokines and 
      high-sensitivity cardiac troponin I (hs-cTnI), a biomarker of myocardial injury, 
      correlated with plaque burden and cardiovascular events (CVEs) in RA. METHODS: We 
      evaluated 150 patients with 64-slice coronary CT angiography. Coronary artery 
      calcium, number of segments with plaque (segment involvement score), stenotic 
      severity and plaque burden were assessed. Lesions were described as 
      non-calcified, mixed or fully calcified. Blood levels of hs-cTnI and 
      pro-inflammatory cytokines were assessed during coronary CT angiography. Subjects 
      were followed over 60 (s.d. 26) months for both ischaemic [cardiac death, 
      non-fatal myocardial infarction (MI), stroke, peripheral arterial ischaemia] and 
      non-ischaemic (new-onset heart failure hospitalization) CVEs. RESULTS: Plasma 
      hs-cTnI correlated with all coronary plaque outcomes (P < 0.01). Elevated hs-cTnI 
      (⩾1.5 pg/ml) further associated with significant calcification, extensive 
      atherosclerosis, obstructive plaque and any advanced mixed or calcified plaques 
      after adjustments for cardiac risk factors or Framingham D'Agostino scores (all P 
      < 0.05). Eleven patients suffered a CVE (1.54/100 patient-years), eight ischaemic 
      and three non-ischaemic. Elevated hs-cTnI predicted all CVE risk independent of 
      demographics, cardiac risk factors and prednisone use (P = 0.03). Conversely, low 
      hs-cTnI presaged a lower risk for both extensive atherosclerosis (P < 0.05) and 
      incident CVEs (P = 0.037). CONCLUSION: Plasma hs-cTnI independently associated 
      with occult coronary plaque burden, composition and long-term incident CVEs in 
      patients with RA. Low hs-cTnI forecasted a lower risk for both extensive 
      atherosclerosis as well as CVEs. hs-cTnI may therefore optimize cardiovascular 
      risk stratification in RA.
FAU - Karpouzas, George A
AU  - Karpouzas GA
AD  - Division of Rheumatology, Harbor-UCLA Medical Center and Los Angeles Biomedical 
      Research Institute, Torrance, CA, USA.
FAU - Estis, Joel
AU  - Estis J
AD  - Singulex, Alameda, CA, USA.
FAU - Rezaeian, Panteha
AU  - Rezaeian P
AD  - Division of Cardiology, Harbor-UCLA Medical Center and Los Angeles Biomedical 
      Research Institute, Torrance, CA, USA.
FAU - Todd, John
AU  - Todd J
AD  - Singulex, Alameda, CA, USA.
FAU - Budoff, Matthew J
AU  - Budoff MJ
AD  - Division of Cardiology, Harbor-UCLA Medical Center and Los Angeles Biomedical 
      Research Institute, Torrance, CA, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
RN  - 0 (Biomarkers)
RN  - 0 (Troponin I)
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/blood/*complications
MH  - Biomarkers/blood
MH  - Computed Tomography Angiography
MH  - Coronary Angiography
MH  - Coronary Artery Disease/*blood/diagnosis/etiology
MH  - Coronary Vessels/*diagnostic imaging
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Multidetector Computed Tomography/methods
MH  - Plaque, Atherosclerotic/*blood/diagnosis/etiology
MH  - Prospective Studies
MH  - Troponin I/*blood
EDAT- 2018/03/20 06:00
MHDA- 2018/07/17 06:00
CRDT- 2018/03/20 06:00
PHST- 2017/10/04 00:00 [received]
PHST- 2018/03/20 06:00 [pubmed]
PHST- 2018/07/17 06:00 [medline]
PHST- 2018/03/20 06:00 [entrez]
AID - 4937703 [pii]
AID - 10.1093/rheumatology/key057 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2018 Jun 1;57(6):1080-1088. doi: 
      10.1093/rheumatology/key057.

PMID- 29548675
OWN - NLM
STAT- MEDLINE
DCOM- 20190625
LR  - 20190625
IS  - 1879-1913 (Electronic)
IS  - 0002-9149 (Linking)
VI  - 121
IP  - 10
DP  - 2018 May 15
TI  - Effect on Risk of Stroke and Acute Myocardial Infarction of Nonselective 
      Nonsteroidal Anti-Inflammatory Drugs in Patients With Rheumatoid Arthritis.
PG  - 1271-1277
LID - S0002-9149(18)30189-9 [pii]
LID - 10.1016/j.amjcard.2018.01.044 [doi]
AB  - There are still debates on the association of increased cardiovascular risk with 
      the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in patients with 
      rheumatoid arthritis (RA) because of inconsistent results. Therefore, our study 
      aims to evaluate the transient effects of selective and nonselective NSAIDs on 
      the risk of stroke and acute myocardial infarction (AMI) in patients with RA. We 
      conducted a case-crossover study of 5,921 stroke or AMI patients with 
      co-morbidity of RA. All cases were identified from the Taiwan National Health 
      Insurance Database between January 1, 2006, and December 31, 2011, according to 
      the International Classification of Diseases, 9th Revision and Clinical 
      Modification diagnosis codes from inpatient claims. The index date was defined as 
      the date of hospitalization for stroke or AMI. Exposure to NSAIDs was compared 
      during a case period (1 to 30 days before the index date) with a control period 
      (91 to 120 days before the index date). The adjusted odds ratios (ORs) of stroke 
      and AMI were estimated using conditional logistic regression models. Our results 
      showed that overall NSAIDs use increased the risk of stroke by 1.40-fold (95% 
      confidence interval [CI] 1.25 to 1.56) and risk of AMI by 1.73-fold (95% CI 1.29 
      to 2.32). After classifying NSAIDs into selective and nonselective groups, only 
      nonselective NSAIDs use significantly increased the risks of stroke (adjusted OR 
      1.39; 95% CI 1.25 to 1.55) and AMI (adjusted OR 1.82; 95% CI 1.37 to 2.41), 
      respectively. In conclusion, nonselective NSAIDs were associated with an 
      increased risk of both stroke and AMI in patients with RA.
CI  - Copyright © 2018 Elsevier Inc. All rights reserved.
FAU - Chen, Yih-Ru
AU  - Chen YR
AD  - School of Public Health, College of Public Health, Taipei Medical University, 
      Taipei, Taiwan.
FAU - Hsieh, Fang-I
AU  - Hsieh FI
AD  - School of Public Health, College of Public Health, Taipei Medical University, 
      Taipei, Taiwan.
FAU - Chang, Chi-Ching
AU  - Chang CC
AD  - Department of Internal Medicine, School of Medicine, College of Medicine, Taipei 
      Medical University, Taipei, Taiwan; Division of Rheumatology, Immunology and 
      Allergy, Department of Internal Medicine, Taipei Medical University Hospital, 
      Taipei, Taiwan.
FAU - Chi, Nai-Fang
AU  - Chi NF
AD  - Department of Neurology, Shuang Ho Hospital, Taipei, Taiwan.
FAU - Wu, Hsin-Chiao
AU  - Wu HC
AD  - School of Public Health, College of Public Health, Taipei Medical University, 
      Taipei, Taiwan.
FAU - Chiou, Hung-Yi
AU  - Chiou HY
AD  - School of Public Health, College of Public Health, Taipei Medical University, 
      Taipei, Taiwan. Electronic address: hychiou@tmu.edu.tw.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180212
PL  - United States
TA  - Am J Cardiol
JT  - The American journal of cardiology
JID - 0207277
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 144O8QL0L1 (Diclofenac)
RN  - 367589PJ2C (Mefenamic Acid)
RN  - JCX84Q7J1L (Celecoxib)
RN  - VG2QF83CGL (Meloxicam)
RN  - WK2XYI10QM (Ibuprofen)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Anti-Inflammatory Agents, Non-Steroidal/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy/epidemiology
MH  - Celecoxib/therapeutic use
MH  - Diclofenac/therapeutic use
MH  - Female
MH  - Humans
MH  - Ibuprofen/therapeutic use
MH  - Logistic Models
MH  - Male
MH  - Mefenamic Acid/therapeutic use
MH  - Meloxicam/therapeutic use
MH  - Middle Aged
MH  - Myocardial Infarction/*epidemiology
MH  - Odds Ratio
MH  - Risk Factors
MH  - Stroke/*epidemiology
EDAT- 2018/03/20 06:00
MHDA- 2019/06/27 06:00
CRDT- 2018/03/18 06:00
PHST- 2017/10/03 00:00 [received]
PHST- 2018/01/20 00:00 [revised]
PHST- 2018/01/30 00:00 [accepted]
PHST- 2018/03/20 06:00 [pubmed]
PHST- 2019/06/27 06:00 [medline]
PHST- 2018/03/18 06:00 [entrez]
AID - S0002-9149(18)30189-9 [pii]
AID - 10.1016/j.amjcard.2018.01.044 [doi]
PST - ppublish
SO  - Am J Cardiol. 2018 May 15;121(10):1271-1277. doi: 10.1016/j.amjcard.2018.01.044. 
      Epub 2018 Feb 12.

PMID- 29514802
OWN - NLM
STAT- MEDLINE
DCOM- 20190806
LR  - 20220330
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Print)
IS  - 0003-4967 (Linking)
VI  - 77
IP  - 7
DP  - 2018 Jul
TI  - Novel gene variants associated with cardiovascular disease in systemic lupus 
      erythematosus and rheumatoid arthritis.
PG  - 1063-1069
LID - 10.1136/annrheumdis-2017-212614 [doi]
AB  - OBJECTIVES: Patients with systemic lupus erythematosus (SLE) and rheumatoid 
      arthritis (RA) have increased risk of cardiovascular disease (CVD). We 
      investigated whether single nucleotide polymorphisms (SNPs) at autoimmunity risk 
      loci were associated with CVD in SLE and RA. METHODS: Patients with SLE (n=1045) 
      were genotyped using the 200K Immunochip SNP array (Illumina). The allele 
      frequency was compared between patients with and without different manifestations 
      of CVD. Results were replicated in a second SLE cohort (n=1043) and in an RA 
      cohort (n=824). We analysed publicly available genetic data from general 
      population, performed electrophoretic mobility shift assays and measured cytokine 
      levels and occurrence of antiphospholipid antibodies (aPLs). RESULTS: We 
      identified two new putative risk loci associated with increased risk for CVD in 
      two SLE populations, which remained after adjustment for traditional CVD risk 
      factors. An IL19 risk allele, rs17581834(T) was associated with stroke/myocardial 
      infarction (MI) in SLE (OR 2.3 (1.5 to 3.4), P=8.5×10(-5)) and RA (OR 2.8 (1.4 to 
      5.6), P=3.8×10(-3)), meta-analysis (OR 2.5 (2.0 to 2.9), P=3.5×10(-7)), but not 
      in population controls. The IL19 risk allele affected protein binding, and SLE 
      patients with the risk allele had increased levels of plasma-IL10 (P=0.004) and 
      aPL (P=0.01). An SRP54-AS1 risk allele, rs799454(G) was associated with 
      stroke/transient ischaemic attack in SLE (OR 1.7 (1.3 to 2.2), P=2.5×10(-5)) but 
      not in RA. The SRP54-AS1 risk allele is an expression quantitative trait locus 
      for four genes. CONCLUSIONS: The IL19 risk allele was associated with stroke/MI 
      in SLE and RA, but not in the general population, indicating that shared immune 
      pathways may be involved in the CVD pathogenesis in inflammatory rheumatic 
      diseases.
CI  - © Article author(s) (or their employer(s) unless otherwise stated in the text of 
      the article) 2018. All rights reserved. No commercial use is permitted unless 
      otherwise expressly granted.
FAU - Leonard, Dag
AU  - Leonard D
AD  - Department of Medical Sciences, Science for Life Laboratory, Rheumatology, 
      Uppsala University, Uppsala, Sweden.
FAU - Svenungsson, Elisabet
AU  - Svenungsson E
AD  - Department of Medicine, Rheumatology Unit, Karolinska Institutet, Karolinska 
      University Hospital, Stockholm, Sweden.
FAU - Dahlqvist, Johanna
AU  - Dahlqvist J
AD  - Department of Medical Biochemistry and Microbiology, Science for Life Laboratory, 
      Uppsala University, Uppsala, Sweden.
FAU - Alexsson, Andrei
AU  - Alexsson A
AD  - Department of Medical Sciences, Science for Life Laboratory, Rheumatology, 
      Uppsala University, Uppsala, Sweden.
FAU - Ärlestig, Lisbeth
AU  - Ärlestig L
AD  - Department of Public Health and Clinical Medicine/Rheumatology, Umeå University, 
      Umeå, Sweden.
FAU - Taylor, Kimberly E
AU  - Taylor KE
AD  - University of California, San Francisco, Rosalind Russell/Ephraim P. Engleman 
      Rheumatology Research Center, San Francisco, California, USA.
FAU - Sandling, Johanna K
AU  - Sandling JK
AD  - Department of Medical Sciences, Science for Life Laboratory, Rheumatology, 
      Uppsala University, Uppsala, Sweden.
FAU - Bengtsson, Christine
AU  - Bengtsson C
AD  - Department of Public Health and Clinical Medicine/Rheumatology, Umeå University, 
      Umeå, Sweden.
FAU - Frodlund, Martina
AU  - Frodlund M
AD  - Department of Clinical and Experimental Medicine, Linköping University, 
      Linköping, Sweden.
FAU - Jönsen, Andreas
AU  - Jönsen A
AD  - Department of Rheumatology, Skåne University Hospital, Lund, Sweden.
FAU - Eketjäll, Susanna
AU  - Eketjäll S
AD  - Cardiovascular and Metabolic Diseases, Innovative Medicines and Early Development 
      Biotech Unit, AstraZeneca, Integrated Cardio Metabolic Centre, Karolinska 
      Institutet, Stockholm, Sweden.
FAU - Jensen-Urstad, Kerstin
AU  - Jensen-Urstad K
AD  - Department of Clinical Physiology, Södersjukhuset, Karolinska Institutet, 
      Stockholm, Sweden.
FAU - Gunnarsson, Iva
AU  - Gunnarsson I
AD  - Department of Medicine, Rheumatology Unit, Karolinska Institutet, Karolinska 
      University Hospital, Stockholm, Sweden.
FAU - Sjöwall, Christopher
AU  - Sjöwall C
AUID- ORCID: 0000-0003-0900-2048
AD  - Department of Clinical and Experimental Medicine, Linköping University, 
      Linköping, Sweden.
FAU - Bengtsson, Anders A
AU  - Bengtsson AA
AD  - Department of Rheumatology, Skåne University Hospital, Lund, Sweden.
FAU - Eloranta, Maija-Leena
AU  - Eloranta ML
AD  - Department of Medical Sciences, Science for Life Laboratory, Rheumatology, 
      Uppsala University, Uppsala, Sweden.
FAU - Syvänen, Ann-Christine
AU  - Syvänen AC
AD  - Department of Medical Sciences, Science for Life Laboratory, Molecular Medicine, 
      Uppsala University, Uppsala, Sweden.
FAU - Rantapää-Dahlqvist, Solbritt
AU  - Rantapää-Dahlqvist S
AD  - Department of Public Health and Clinical Medicine/Rheumatology, Umeå University, 
      Umeå, Sweden.
FAU - Criswell, Lindsey A
AU  - Criswell LA
AD  - University of California, San Francisco, Rosalind Russell/Ephraim P. Engleman 
      Rheumatology Research Center, San Francisco, California, USA.
FAU - Rönnblom, Lars
AU  - Rönnblom L
AD  - Department of Medical Sciences, Science for Life Laboratory, Rheumatology, 
      Uppsala University, Uppsala, Sweden.
LA  - eng
GR  - P30 AR070155/AR/NIAMS NIH HHS/United States
GR  - P60 AR053308/AR/NIAMS NIH HHS/United States
GR  - UL1 TR000004/TR/NCATS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20180307
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (IL19 protein, human)
RN  - 0 (Interleukins)
RN  - 0 (SRP54 protein, human)
RN  - 0 (Signal Recognition Particle)
CIN - Ann Transl Med. 2018 Nov;6(Suppl 1):S14. doi: 10.21037/atm.2018.09.25. PMID: 
      30613589
CIN - Ann Transl Med. 2018 Nov;6(Suppl 1):S44. doi: 10.21037/atm.2018.09.67. PMID: 
      30613619
MH  - Age Distribution
MH  - Alleles
MH  - Arthritis, Rheumatoid/epidemiology/*genetics/physiopathology
MH  - Cardiovascular Diseases/epidemiology/*genetics/physiopathology
MH  - Case-Control Studies
MH  - Comorbidity
MH  - Female
MH  - Gene Frequency
MH  - Genetic Predisposition to Disease/*epidemiology
MH  - Genetic Variation
MH  - Humans
MH  - Incidence
MH  - Interleukins
MH  - Lupus Erythematosus, Systemic/epidemiology/*genetics/physiopathology
MH  - Male
MH  - Polymorphism, Single Nucleotide/*genetics
MH  - Prognosis
MH  - Reference Values
MH  - Severity of Illness Index
MH  - Sex Distribution
MH  - Signal Recognition Particle/genetics
PMC - PMC6029634
OTO - NOTNLM
OT  - rheumatoid arthritis
COIS- Competing interests: None declared.
EDAT- 2018/03/09 06:00
MHDA- 2019/08/07 06:00
PMCR- 2018/07/03
CRDT- 2018/03/09 06:00
PHST- 2017/10/30 00:00 [received]
PHST- 2018/02/16 00:00 [revised]
PHST- 2018/02/19 00:00 [accepted]
PHST- 2018/03/09 06:00 [pubmed]
PHST- 2019/08/07 06:00 [medline]
PHST- 2018/03/09 06:00 [entrez]
PHST- 2018/07/03 00:00 [pmc-release]
AID - annrheumdis-2017-212614 [pii]
AID - 10.1136/annrheumdis-2017-212614 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2018 Jul;77(7):1063-1069. doi: 10.1136/annrheumdis-2017-212614. 
      Epub 2018 Mar 7.

PMID- 29430085
OWN - NLM
STAT- MEDLINE
DCOM- 20180905
LR  - 20181113
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 2017
DP  - 2017
TI  - Protective Effects of Methotrexate against Proatherosclerotic Cytokines: A Review 
      of the Evidence.
PG  - 9632846
LID - 10.1155/2017/9632846 [doi]
LID - 9632846
AB  - There is good epidemiological evidence that patients with autoimmune rheumatic 
      disease states, particularly rheumatoid arthritis, have an increased risk of 
      cardiovascular morbidity and mortality when compared to the general population. 
      The presence of a chronic systemic proinflammatory state in this patient group 
      disrupts the structural and functional integrity of the endothelium and the 
      arterial wall, favouring the onset and progression of atherosclerosis. A 
      significant role in the detrimental effects of inflammation on endothelial 
      function and vascular homeostasis is played by specific proatherosclerotic 
      cytokines such as tumour necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and 
      interleukin-6 (IL-6). Recent systematic reviews and meta-analyses have shown that 
      treatment with methotrexate, a first-line disease-modifying antirheumatic drug 
      (DMARD), is associated with a significant reduction in atherosclerosis-mediated 
      cardiovascular events, such as myocardial infarction and stroke, and mortality, 
      when compared to other DMARDs. This suggests that methotrexate might exert 
      specific protective effects against vascular inflammation and atherosclerosis in 
      the context of autoimmune rheumatic disease. This review discusses the available 
      evidence regarding the potential antiatherosclerotic effects of methotrexate 
      through the inhibition of TNF-α, IL-1, and IL-6 and provides suggestions for 
      future experimental and human studies addressing this issue.
FAU - Mangoni, Arduino A
AU  - Mangoni AA
AUID- ORCID: 0000-0001-8699-1412
AD  - Department of Clinical Pharmacology, College of Medicine and Public Health, 
      Flinders Medical Centre, Flinders University, Adelaide, SA, Australia.
FAU - Zinellu, Angelo
AU  - Zinellu A
AUID- ORCID: 0000-0002-8396-0968
AD  - Department of Biomedical Sciences, University of Sassari, Sassari, Italy.
FAU - Sotgia, Salvatore
AU  - Sotgia S
AUID- ORCID: 0000-0002-3717-3437
AD  - Department of Biomedical Sciences, University of Sassari, Sassari, Italy.
FAU - Carru, Ciriaco
AU  - Carru C
AUID- ORCID: 0000-0002-6985-4907
AD  - Department of Biomedical Sciences, University of Sassari, Sassari, Italy.
AD  - Quality Control Unit, University Hospital of Sassari (AOUSS), Sassari, Italy.
FAU - Piga, Matteo
AU  - Piga M
AD  - Rheumatology Unit, University Clinic and AOU of Cagliari, Cagliari, Italy.
FAU - Erre, Gian Luca
AU  - Erre GL
AUID- ORCID: 0000-0001-6818-7666
AD  - Rheumatology Unit, Department of Clinical and Experimental Medicine, University 
      Hospital of Sassari (AOUSS), Sassari, Italy.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20171221
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - K72T3FS567 (Adenosine)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - AMP-Activated Protein Kinases/physiology
MH  - Adenosine/metabolism
MH  - Atherosclerosis/*drug therapy/immunology
MH  - Cytokines/*antagonists & inhibitors/physiology
MH  - Endothelium, Vascular/physiology
MH  - Humans
MH  - Interleukin-1/antagonists & inhibitors
MH  - Interleukin-6/antagonists & inhibitors
MH  - Methotrexate/adverse effects/*pharmacology/therapeutic use
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
PMC - PMC5753000
EDAT- 2018/02/13 06:00
MHDA- 2018/09/06 06:00
PMCR- 2017/12/21
CRDT- 2018/02/13 06:00
PHST- 2017/07/20 00:00 [received]
PHST- 2017/11/02 00:00 [revised]
PHST- 2017/11/26 00:00 [accepted]
PHST- 2018/02/13 06:00 [entrez]
PHST- 2018/02/13 06:00 [pubmed]
PHST- 2018/09/06 06:00 [medline]
PHST- 2017/12/21 00:00 [pmc-release]
AID - 10.1155/2017/9632846 [doi]
PST - ppublish
SO  - Mediators Inflamm. 2017;2017:9632846. doi: 10.1155/2017/9632846. Epub 2017 Dec 
      21.

PMID- 29421936
OWN - NLM
STAT- MEDLINE
DCOM- 20190128
LR  - 20190128
IS  - 1940-4034 (Electronic)
IS  - 1074-2484 (Print)
IS  - 1074-2484 (Linking)
VI  - 23
IP  - 2
DP  - 2018 Mar
TI  - Cardiorenal Safety of OTC Analgesics.
PG  - 103-118
LID - 10.1177/1074248417751070 [doi]
AB  - Over-the-counter analgesics are used globally for the relief of acute pain. 
      Although effective, these agents can be associated with adverse effects that may 
      limit their use in some people. In the early 2000s, observations from clinical 
      trials of prescription-strength and supratherapeutic doses of nonselective and 
      cyclooxygenase-2-selective nonsteroidal anti-inflammatory drugs (NSAIDs) raised 
      safety concerns regarding the risk of cardiovascular adverse effects with the use 
      of these medications. Subsequently, the US Food and Drug Administration mandated 
      additional study of the cardiovascular safety of NSAIDs for a more comprehensive 
      understanding of their risk. As these data were being collected, and based on a 
      comprehensive review of prescription data and the recommendations of the US Food 
      and Drug Administration Advisory Committee, the warning labels of 
      over-the-counter NSAIDs were updated to emphasize the potential cardiovascular 
      risks of these agents. The recently reported "Prospective Randomized Evaluation 
      of Celecoxib Integrated Safety versus Ibuprofen or Naproxen" (PRECISION) trial, 
      in which participants with osteoarthritis or rheumatoid arthritis and underlying 
      cardiovascular risk factors were treated with prescription-strength celecoxib, 
      ibuprofen, or naproxen, revealed similar rates of cardiovascular events (death 
      from cardiovascular causes including hemorrhagic death, nonfatal myocardial 
      infarction, or nonfatal stroke) among the 3 treatment groups. Although 
      informative, the cardiovascular safety findings derived from PRECISION cannot be 
      extrapolated to the safety of the over-the-counter pain relievers ibuprofen and 
      naproxen, given that the doses used were higher (mean [standard deviation]: 
      ibuprofen, 2045 [246] mg; naproxen, 852 [103] mg) and the durations of use longer 
      (∼20 months) than recommended with over-the-counter use of NSAIDs, which for 
      ibuprofen is up to 10 days. This review discusses the cardiorenal safety of the 
      most commonly used over-the-counter analgesics, ibuprofen, naproxen, and 
      acetaminophen. Available data suggest that there is little cardiovascular risk 
      when over-the-counter formulations of these agents are used as directed in their 
      labels.
FAU - White, William B
AU  - White WB
AUID- ORCID: 0000-0001-8936-967X
AD  - 1 Calhoun Cardiology Center, University of Connecticut School of Medicine, 
      Farmington, CT, USA.
FAU - Kloner, Robert A
AU  - Kloner RA
AD  - 2 HMRI Cardiovascular Research Institute, Huntington Medical Research Institutes, 
      Pasadena, CA, USA.
AD  - 3 Cardiovascular Division, Department of Medicine, Keck School of Medicine, 
      University of Southern California, Los Angeles, CA, USA.
FAU - Angiolillo, Dominick J
AU  - Angiolillo DJ
AD  - 4 Division of Cardiology, University of Florida College of Medicine, 
      Jacksonville, FL, USA.
FAU - Davidson, Michael H
AU  - Davidson MH
AD  - 5 Preventive Cardiology, The University of Chicago Medicine, Chicago, IL, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - J Cardiovasc Pharmacol Ther
JT  - Journal of cardiovascular pharmacology and therapeutics
JID - 9602617
RN  - 0 (Analgesics)
RN  - 0 (Nonprescription Drugs)
RN  - 362O9ITL9D (Acetaminophen)
RN  - 57Y76R9ATQ (Naproxen)
RN  - WK2XYI10QM (Ibuprofen)
SB  - IM
MH  - Acetaminophen/administration & dosage/*adverse effects
MH  - Analgesics/administration & dosage/*adverse effects
MH  - Drug Labeling
MH  - Heart Diseases/*chemically induced/diagnosis/mortality
MH  - Humans
MH  - Ibuprofen/administration & dosage/*adverse effects
MH  - Kidney Diseases/*chemically induced/diagnosis/mortality
MH  - Naproxen/administration & dosage/*adverse effects
MH  - Nonprescription Drugs/administration & dosage/*adverse effects
MH  - Patient Safety
MH  - Risk Assessment
MH  - Risk Factors
PMC - PMC5808827
OTO - NOTNLM
OT  - acetaminophen
OT  - coxibs
OT  - nonsteroidal anti-inflammatory drugs
OT  - over-the-counter
OT  - pain
OT  - safety
COIS- Declaration of Conflicting Interests: The author(s) declared the following 
      potential conflicts of interest with respect to the research, authorship, and/or 
      publication of this article: W. B. White, R. A. Kloner, and M. H. Davidson have 
      been consultants to Pfizer Consumer Healthcare/Wyeth Laboratories. D. J. 
      Angiolillo has received consulting fees or honoraria from Pfizer and Pfizer 
      Consumer Healthcare.
EDAT- 2018/02/10 06:00
MHDA- 2019/01/29 06:00
PMCR- 2018/02/12
CRDT- 2018/02/10 06:00
PHST- 2018/02/10 06:00 [entrez]
PHST- 2018/02/10 06:00 [pubmed]
PHST- 2019/01/29 06:00 [medline]
PHST- 2018/02/12 00:00 [pmc-release]
AID - 10.1177_1074248417751070 [pii]
AID - 10.1177/1074248417751070 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol Ther. 2018 Mar;23(2):103-118. doi: 
      10.1177/1074248417751070.

PMID- 29409152
OWN - NLM
STAT- MEDLINE
DCOM- 20190712
LR  - 20220330
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Linking)
VI  - 70
IP  - 11
DP  - 2018 Nov
TI  - Is Rheumatoid Arthritis a Cardiovascular Risk-Equivalent to Diabetes Mellitus?
PG  - 1694-1699
LID - 10.1002/acr.23535 [doi]
AB  - OBJECTIVE: The 2013 American College of Cardiology/American Heart Association 
      cholesterol treatment guidelines recommend statins for patients with diabetes 
      mellitus ages 40-75 years due to their elevated cardiovascular disease (CVD) 
      risk. We compared the incidence of hospitalized acute myocardial infarction (MI), 
      stroke, and coronary revascularization according to whether patients had diabetes 
      mellitus, rheumatoid arthritis (RA), both, or neither. METHODS: Using 2006-2010 
      private and public health plan claims, we identified 4 mutually exclusive 
      retrospective cohorts ages >40 years: patients with RA and diabetes mellitus, RA 
      only, diabetes mellitus only, or neither condition. Patients with prevalent CVD 
      were excluded. Outcomes included acute MI and stroke, identified from inpatient 
      discharge diagnosis codes, and coronary revascularization from procedure codes. 
      Across the 4 cohorts, we calculated incidence rates (IRs) of the outcomes, 
      standardized to the 2010 US census age and sex distribution. RESULTS: We 
      identified 920,772 eligible participants. The age- and sex-standardized IRs (per 
      1,000 person-years) for MI were highest among patients with RA and diabetes 
      mellitus (IR 12.6 [95% confidence interval (95% CI) 10.7-14.7]), followed by 
      patients with diabetes mellitus only (IR 10.7 [95% CI 10.3-11.0]), RA only (IR 
      5.7 [95% CI 5.2-6.3]), and with neither condition (IR 4.2 [95% CI 4.1-4.3]). 
      CONCLUSION: Findings from the present study suggest that while CVD risk in RA is 
      elevated, it is lower in magnitude compared to the CVD risk associated with 
      diabetes mellitus. Therefore, considering RA a diabetes mellitus risk-equivalent 
      with respect to hyperlipidemia management may not be appropriate.
CI  - © 2018, American College of Rheumatology.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AUID- ORCID: 0000-0002-8907-8976
AD  - University of Alabama at Birmingham.
FAU - Yang, Shuo
AU  - Yang S
AD  - University of Alabama at Birmingham.
FAU - Singh, Jasvinder A
AU  - Singh JA
AUID- ORCID: 0000-0003-3485-0006
AD  - University of Alabama at Birmingham.
FAU - Xie, Fenglong
AU  - Xie F
AD  - University of Alabama at Birmingham.
FAU - Chen, Lang
AU  - Chen L
AD  - University of Alabama at Birmingham.
FAU - Yun, Huifeng
AU  - Yun H
AD  - University of Alabama at Birmingham.
FAU - Muntner, Paul
AU  - Muntner P
AD  - University of Alabama at Birmingham.
FAU - Kent, Shia T
AU  - Kent ST
AD  - University of Alabama at Birmingham.
FAU - Levitan, Emily B
AU  - Levitan EB
AD  - University of Alabama at Birmingham.
FAU - Safford, Monika M
AU  - Safford MM
AD  - University of Alabama at Birmingham.
FAU - Saag, Kenneth G
AU  - Saag KG
AUID- ORCID: 0000-0001-6189-8078
AD  - University of Alabama at Birmingham.
FAU - Zhang, Jie
AU  - Zhang J
AD  - University of Alabama at Birmingham.
LA  - eng
GR  - PCORI/Patient-Centered Outcomes Research Institute/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications
MH  - Cardiovascular Diseases/*etiology
MH  - Diabetes Complications/*etiology
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Risk
EDAT- 2018/02/07 06:00
MHDA- 2019/07/13 06:00
CRDT- 2018/02/07 06:00
PHST- 2017/09/07 00:00 [received]
PHST- 2018/01/30 00:00 [accepted]
PHST- 2018/02/07 06:00 [pubmed]
PHST- 2019/07/13 06:00 [medline]
PHST- 2018/02/07 06:00 [entrez]
AID - 10.1002/acr.23535 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2018 Nov;70(11):1694-1699. doi: 10.1002/acr.23535.

PMID- 29372595
OWN - NLM
STAT- MEDLINE
DCOM- 20181211
LR  - 20181211
IS  - 1756-185X (Electronic)
IS  - 1756-1841 (Linking)
VI  - 21
IP  - 8
DP  - 2018 Aug
TI  - Methotrexate might reduce ischemic stroke in patients with rheumatoid arthritis: 
      a population-based retrospective cohort study.
PG  - 1591-1599
LID - 10.1111/1756-185X.13267 [doi]
AB  - AIM: To investigate the effects of hydroxychloroquine, sulfasalazine and 
      methotrexate on ischemic stroke in patients with rheumatoid arthritis (RA). 
      METHODS: This population-based retrospective cohort study included 7904 RA 
      patients and 15 808 non-RA patients between 2000 and 2010. All of the 
      participants were sampled from the National Health Insurance Research Database 
      (NHIRD) of Taiwan. Using univariate analyses, these two groups of patients were 
      compared to evaluate the differences in disease-modifying anti-rheumatic drugs 
      usage and demographic variables. Cox proportional hazard models and Schoenfeld 
      residuals test were performed to estimate the hazard ratios for ischemic stroke 
      and proportional hazard assumptions of these drugs, respectively. RESULTS: The 
      mean age of participants was about 53 years old, and about 70% of RA patients 
      were women. The hazard ratio for ischemic stroke was 1.21 (95% CI: 1.10-1.34; P < 
      0.01) in the case group compared with the control group, and this significant 
      difference persisted throughout the 10-year period. With respect to RA patients, 
      while hydroxychloroquine showed an insignificant protective effect on ischemic 
      stroke, sulfasalazine and methotrexate were found out to have inconsistent 
      effects during these 10 years. The proportional hazard assumption test of 
      methotrexate at > 0.5 defined daily dose (8.75 mg/week) was violated at a 
      significant level after adjustment (P = 0.0002). CONCLUSIONS: At a dosage of > 
      0.5 defined daily dose, short-term methotrexate might decrease ischemic stroke 
      risk in RA patients, while hydroxychloroquine and sulfasalazine were neutral.
CI  - © 2018 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons 
      Australia, Ltd.
FAU - Tam, Hong-Wei
AU  - Tam HW
AUID- ORCID: 0000-0002-5372-4737
AD  - School of Medicine, Chung Shan Medical University, Tai Chung, Taiwan.
FAU - Chen, Chyong-Mei
AU  - Chen CM
AD  - Institute of Public Health, School of Medicine, National Yang-Ming University, 
      Taipei, Taiwan.
FAU - Leong, Pui-Ying
AU  - Leong PY
AD  - Division of Allergy, Immunology and Rheumatology, Chung Shan Medical University 
      Hospital, Tai Chung, Taiwan.
AD  - Institute of Medicine, Chung Shan Medical University Hospital, Tai Chung, Taiwan.
FAU - Chen, Chao-Hsi
AU  - Chen CH
AD  - School of Medicine, Chung Shan Medical University, Tai Chung, Taiwan.
FAU - Li, Yuan-Chao
AU  - Li YC
AD  - School of Medicine, Chung Shan Medical University, Tai Chung, Taiwan.
FAU - Wang, Yu-Hsun
AU  - Wang YH
AD  - Department of Medical Research, Chung Shan Medical University Hospital, Tai 
      Chung, Taiwan.
FAU - Lin, Li-Chi
AU  - Lin LC
AD  - Division of Allergy, Immunology and Rheumatology, Chung Shan Medical University 
      Hospital, Tai Chung, Taiwan.
AD  - Institute of Medicine, Chung Shan Medical University Hospital, Tai Chung, Taiwan.
AD  - Department of Statistics, Oklahoma State University, Stillwater, OK, USA.
FAU - Chiou, Jeng-Yuan
AU  - Chiou JY
AD  - School of Health Policy and Management, Chung Shan Medical University, Tai Chung, 
      Taiwan.
FAU - Wei, James Cheng-Chung
AU  - Wei JC
AD  - Division of Allergy, Immunology and Rheumatology, Chung Shan Medical University 
      Hospital, Tai Chung, Taiwan.
AD  - Institute of Medicine, Chung Shan Medical University Hospital, Tai Chung, Taiwan.
AD  - Institute of Integrative Medicine, China Medical University, Tai Chung, Taiwan.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20180125
PL  - England
TA  - Int J Rheum Dis
JT  - International journal of rheumatic diseases
JID - 101474930
RN  - 0 (Antirheumatic Agents)
RN  - 3XC8GUZ6CB (Sulfasalazine)
RN  - 4QWG6N8QKH (Hydroxychloroquine)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Antirheumatic Agents/*administration & dosage
MH  - Arthritis, Rheumatoid/diagnosis/*drug therapy/epidemiology
MH  - Databases, Factual
MH  - Female
MH  - Humans
MH  - Hydroxychloroquine/administration & dosage
MH  - Incidence
MH  - Male
MH  - Methotrexate/*administration & dosage
MH  - Middle Aged
MH  - Protective Factors
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Stroke/diagnosis/epidemiology/*prevention & control
MH  - Sulfasalazine/administration & dosage
MH  - Taiwan/epidemiology
MH  - Treatment Outcome
OTO - NOTNLM
OT  - hydroxychloroquine
OT  - ischemic stroke
OT  - methotrexate
OT  - rheumatoid arthritis
OT  - sulfasalazine
EDAT- 2018/01/27 06:00
MHDA- 2018/12/12 06:00
CRDT- 2018/01/27 06:00
PHST- 2018/01/27 06:00 [pubmed]
PHST- 2018/12/12 06:00 [medline]
PHST- 2018/01/27 06:00 [entrez]
AID - 10.1111/1756-185X.13267 [doi]
PST - ppublish
SO  - Int J Rheum Dis. 2018 Aug;21(8):1591-1599. doi: 10.1111/1756-185X.13267. Epub 
      2018 Jan 25.

PMID- 29367417
OWN - NLM
STAT- MEDLINE
DCOM- 20191210
LR  - 20240318
IS  - 2047-9980 (Electronic)
IS  - 2047-9980 (Linking)
VI  - 7
IP  - 3
DP  - 2018 Jan 24
TI  - Comparative Cardiovascular Risk of Abatacept and Tumor Necrosis Factor Inhibitors 
      in Patients With Rheumatoid Arthritis With and Without Diabetes Mellitus: A 
      Multidatabase Cohort Study.
LID - 10.1161/JAHA.117.007393 [doi]
LID - e007393
AB  - BACKGROUND: We examined the cardiovascular risk of abatacept compared with tumor 
      necrosis factor (TNF) inhibitors in patients with rheumatoid arthritis with and 
      without diabetes mellitus (DM). METHODS AND RESULTS: We conducted a cohort study 
      of patients with rheumatoid arthritis who newly started abatacept or TNF 
      inhibitors using claims data from Medicare and MarketScan. The primary outcome 
      was a composite cardiovascular end point of myocardial infarction (MI), 
      stroke/transient ischemic attack, and coronary revascularization. To account for 
      >60 baseline characteristics, abatacept initiators were 1:1 propensity score (PS) 
      matched to TNF initiators in each database. Cox proportional hazards models 
      estimated hazard ratio (HR) and 95% confidence interval (CI) in the PS-matched 
      cohort per database. A fixed-effects meta-analysis pooled database-specific HRs. 
      We included a total of 13 039 PS-matched pairs of abatacept and TNF inhibitor 
      initiators (6103 pairs in Medicare and 6936 pairs in MarketScan). A total of 
      34.7% in Medicare and 19.8% in MarketScan had baseline DM. The HR (95% CI) for 
      the primary outcome associated with abatacept use versus TNF inhibitor was 0.81 
      (0.66-0.99) in Medicare and 0.95 (0.74-1.23) in MarketScan, with a pooled HR of 
      0.86 (95% CI, 0.73-1.01; P=0.3 for heterogeneity). The risk of the primary 
      outcome was lower in abatacept initiators versus TNF inhibitors in the DM 
      subgroup, with a pooled HR of 0.74 (95% CI, 0.57-0.96; P=0.7 for heterogeneity), 
      but not in the non-DM subgroup, with a pooled HR of 0.94 (95% CI, 0.77-1.14; 
      P=0.4 for heterogeneity). CONCLUSIONS: In this large population-based cohort of 
      patients with rheumatoid arthritis, abatacept use appeared to be associated with 
      a modestly reduced cardiovascular risk when compared with TNF inhibitor use, 
      particularly in patients with DM.
CI  - © 2018 The Authors. Published on behalf of the American Heart Association, Inc., 
      by Wiley.
FAU - Kang, Eun Ha
AU  - Kang EH
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Harvard Medical School, Boston, MA.
AD  - Division of Rheumatology, Department of Internal Medicine, Seoul National 
      University Bundang Hospital, Seongnam, South Korea.
FAU - Jin, Yinzhu
AU  - Jin Y
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Harvard Medical School, Boston, MA.
FAU - Brill, Gregory
AU  - Brill G
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Harvard Medical School, Boston, MA.
FAU - Lewey, Jennifer
AU  - Lewey J
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Harvard Medical School, Boston, MA.
AD  - Division of Cardiology, University of Pennsylvania, Philadelphia, PA.
FAU - Patorno, Elisabetta
AU  - Patorno E
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Harvard Medical School, Boston, MA.
FAU - Desai, Rishi J
AU  - Desai RJ
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Harvard Medical School, Boston, MA.
FAU - Kim, Seoyoung C
AU  - Kim SC
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Harvard Medical School, Boston, MA skim62@partners.org.
AD  - Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 
      Harvard Medical School, Boston, MA.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20180124
PL  - England
TA  - J Am Heart Assoc
JT  - Journal of the American Heart Association
JID - 101580524
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 7D0YB67S97 (Abatacept)
SB  - IM
MH  - Abatacept/adverse effects/*therapeutic use
MH  - Administrative Claims, Healthcare
MH  - Aged
MH  - Aged, 80 and over
MH  - Antirheumatic Agents/adverse effects/*therapeutic use
MH  - Arthritis, Rheumatoid/diagnosis/*drug therapy/epidemiology/immunology
MH  - Biological Products/adverse effects/*therapeutic use
MH  - Cardiovascular Diseases/diagnosis/*epidemiology/therapy
MH  - Databases, Factual
MH  - Diabetes Mellitus/diagnosis/*epidemiology
MH  - Female
MH  - Humans
MH  - Ischemic Attack, Transient/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology
MH  - Myocardial Revascularization
MH  - Risk Assessment
MH  - Risk Factors
MH  - Stroke/epidemiology
MH  - Time Factors
MH  - Treatment Outcome
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors/immunology
MH  - United States/epidemiology
PMC - PMC5850244
OTO - NOTNLM
OT  - cardiovascular disease
OT  - comparative effectiveness research
OT  - diabetes mellitus
OT  - rheumatoid arthritis
OT  - treatment
EDAT- 2018/01/26 06:00
MHDA- 2019/12/18 06:00
PMCR- 2018/02/01
CRDT- 2018/01/26 06:00
PHST- 2018/01/26 06:00 [entrez]
PHST- 2018/01/26 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
PHST- 2018/02/01 00:00 [pmc-release]
AID - JAHA.117.007393 [pii]
AID - JAH32896 [pii]
AID - 10.1161/JAHA.117.007393 [doi]
PST - epublish
SO  - J Am Heart Assoc. 2018 Jan 24;7(3):e007393. doi: 10.1161/JAHA.117.007393.

PMID- 29335343
OWN - NLM
STAT- MEDLINE
DCOM- 20191022
LR  - 20191022
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
VI  - 45
IP  - 3
DP  - 2018 Mar
TI  - Association Between Glucocorticoid Exposure and Healthcare Expenditures for 
      Potential Glucocorticoid-related Adverse Events in Patients with Rheumatoid 
      Arthritis.
PG  - 320-328
LID - 10.3899/jrheum.170418 [doi]
AB  - OBJECTIVE: Oral glucocorticoid (OGC) use for rheumatoid arthritis (RA) is debated 
      because of the adverse event (AE) profile of OGC. We evaluated the associations 
      between cumulative doses of OGC and potential OGC-related AE, and quantified the 
      associated healthcare expenditures. METHODS: Using the MarketScan databases, 
      patients ≥ 18 years old who have RA with continuous enrollment from January 1 to 
      December 31, 2012 (baseline), and from January 1 to December 31, 2013 (evaluation 
      period), were identified. Cumulative OGC dose was measured using prescription 
      claims during the baseline period. Potential OGC-related AE (osteoporosis, 
      fracture, aseptic necrosis of the bone, type 2 diabetes, ulcer/gastrointestinal 
      bleeding, cataract, hospitalization for opportunistic infection, myocardial 
      infarction, or stroke) and AE-related expenditures (2013 US$) were gathered 
      during the evaluation period. Multivariable regression models were fitted to 
      estimate OR of AE and incremental costs for patients with AE. RESULTS: There were 
      84,357 patients analyzed, of whom 48% used OGC during the baseline period and 26% 
      had an AE during the evaluation period. A cumulative OGC dose > 1800 mg was 
      associated with an increased risk of any AE compared with no OGC exposure (OR 
      1.19, 99.65% CI 1.09-1.30). Incremental costs per patient with any AE were 
      significantly greater for cumulative OGC dose > 1800 mg compared with no OGC 
      exposure (incremental cost = $3528, 99.65% CI $2402-$4793). CONCLUSION: Chronic 
      exposure to low to medium doses of OGC was associated with significantly 
      increased risk of potential OGC-related AE in patients with RA, and greater 
      cumulative OGC dose was associated with substantially higher AE-related 
      healthcare expenditures among patients with AE.
FAU - Best, Jennie H
AU  - Best JH
AD  - From Genentech Inc., South San Francisco, California; Truven Health Analytics, an 
      IBM Company; Truven Health Analytics, an IBM Company, Cambridge, Massachusetts; 
      University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
AD  - Jennie Best and Khaled Sarsour are employees of Genentech Inc. Amanda Kong and 
      Gregory Lenhart are employees of Truven Health Analytics, which received funding 
      from Genentech Inc. Marni Stott-Miller was an employee of Truven Health Analytics 
      at the time this research was conducted.
AD  - J.H. Best, PhD, Genentech Inc.; A.M. Kong, MPH, Truven Health Analytics; G.M. 
      Lenhart, MS, Truven Health Analytics; K. Sarsour, PhD, MPH, Genentech Inc.; M. 
      Stott-Miller, PhD, MS, Truven Health Analytics; Y. Hwang, MD, University of 
      Pittsburgh.
FAU - Kong, Amanda M
AU  - Kong AM
AD  - From Genentech Inc., South San Francisco, California; Truven Health Analytics, an 
      IBM Company; Truven Health Analytics, an IBM Company, Cambridge, Massachusetts; 
      University of Pittsburgh, Pittsburgh, Pennsylvania, USA. akong@us.ibm.com.
AD  - Jennie Best and Khaled Sarsour are employees of Genentech Inc. Amanda Kong and 
      Gregory Lenhart are employees of Truven Health Analytics, which received funding 
      from Genentech Inc. Marni Stott-Miller was an employee of Truven Health Analytics 
      at the time this research was conducted. akong@us.ibm.com.
AD  - J.H. Best, PhD, Genentech Inc.; A.M. Kong, MPH, Truven Health Analytics; G.M. 
      Lenhart, MS, Truven Health Analytics; K. Sarsour, PhD, MPH, Genentech Inc.; M. 
      Stott-Miller, PhD, MS, Truven Health Analytics; Y. Hwang, MD, University of 
      Pittsburgh. akong@us.ibm.com.
FAU - Lenhart, Gregory M
AU  - Lenhart GM
AD  - From Genentech Inc., South San Francisco, California; Truven Health Analytics, an 
      IBM Company; Truven Health Analytics, an IBM Company, Cambridge, Massachusetts; 
      University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
AD  - Jennie Best and Khaled Sarsour are employees of Genentech Inc. Amanda Kong and 
      Gregory Lenhart are employees of Truven Health Analytics, which received funding 
      from Genentech Inc. Marni Stott-Miller was an employee of Truven Health Analytics 
      at the time this research was conducted.
AD  - J.H. Best, PhD, Genentech Inc.; A.M. Kong, MPH, Truven Health Analytics; G.M. 
      Lenhart, MS, Truven Health Analytics; K. Sarsour, PhD, MPH, Genentech Inc.; M. 
      Stott-Miller, PhD, MS, Truven Health Analytics; Y. Hwang, MD, University of 
      Pittsburgh.
FAU - Sarsour, Khaled
AU  - Sarsour K
AD  - From Genentech Inc., South San Francisco, California; Truven Health Analytics, an 
      IBM Company; Truven Health Analytics, an IBM Company, Cambridge, Massachusetts; 
      University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
AD  - Jennie Best and Khaled Sarsour are employees of Genentech Inc. Amanda Kong and 
      Gregory Lenhart are employees of Truven Health Analytics, which received funding 
      from Genentech Inc. Marni Stott-Miller was an employee of Truven Health Analytics 
      at the time this research was conducted.
AD  - J.H. Best, PhD, Genentech Inc.; A.M. Kong, MPH, Truven Health Analytics; G.M. 
      Lenhart, MS, Truven Health Analytics; K. Sarsour, PhD, MPH, Genentech Inc.; M. 
      Stott-Miller, PhD, MS, Truven Health Analytics; Y. Hwang, MD, University of 
      Pittsburgh.
FAU - Stott-Miller, Marni
AU  - Stott-Miller M
AD  - From Genentech Inc., South San Francisco, California; Truven Health Analytics, an 
      IBM Company; Truven Health Analytics, an IBM Company, Cambridge, Massachusetts; 
      University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
AD  - Jennie Best and Khaled Sarsour are employees of Genentech Inc. Amanda Kong and 
      Gregory Lenhart are employees of Truven Health Analytics, which received funding 
      from Genentech Inc. Marni Stott-Miller was an employee of Truven Health Analytics 
      at the time this research was conducted.
AD  - J.H. Best, PhD, Genentech Inc.; A.M. Kong, MPH, Truven Health Analytics; G.M. 
      Lenhart, MS, Truven Health Analytics; K. Sarsour, PhD, MPH, Genentech Inc.; M. 
      Stott-Miller, PhD, MS, Truven Health Analytics; Y. Hwang, MD, University of 
      Pittsburgh.
FAU - Hwang, Yong
AU  - Hwang Y
AD  - From Genentech Inc., South San Francisco, California; Truven Health Analytics, an 
      IBM Company; Truven Health Analytics, an IBM Company, Cambridge, Massachusetts; 
      University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
AD  - Jennie Best and Khaled Sarsour are employees of Genentech Inc. Amanda Kong and 
      Gregory Lenhart are employees of Truven Health Analytics, which received funding 
      from Genentech Inc. Marni Stott-Miller was an employee of Truven Health Analytics 
      at the time this research was conducted.
AD  - J.H. Best, PhD, Genentech Inc.; A.M. Kong, MPH, Truven Health Analytics; G.M. 
      Lenhart, MS, Truven Health Analytics; K. Sarsour, PhD, MPH, Genentech Inc.; M. 
      Stott-Miller, PhD, MS, Truven Health Analytics; Y. Hwang, MD, University of 
      Pittsburgh.
LA  - eng
PT  - Journal Article
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20180115
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Glucocorticoids)
SB  - IM
CIN - J Rheumatol. 2018 Mar;45(3):293-296. doi: 10.3899/jrheum.171331. PMID: 29496913
MH  - Administration, Oral
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Cohort Studies
MH  - Databases, Factual
MH  - Diabetes Mellitus, Type 2/chemically induced
MH  - Female
MH  - Fractures, Bone/chemically induced
MH  - Glucocorticoids/administration & dosage/*adverse effects/economics/*therapeutic 
      use
MH  - Health Care Costs
MH  - *Health Expenditures
MH  - Humans
MH  - Linear Models
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Myocardial Infarction/chemically induced
MH  - Opportunistic Infections/chemically induced
MH  - Osteoporosis/chemically induced
MH  - Stroke/chemically induced
OTO - NOTNLM
OT  - ADVERSE EFFECTS
OT  - CORTICOSTEROIDS
OT  - GLUCOCORTICOIDS
OT  - HEALTHCARE COSTS
OT  - RHEUMATOID ARTHRITIS
EDAT- 2018/01/18 06:00
MHDA- 2019/10/23 06:00
CRDT- 2018/01/17 06:00
PHST- 2017/09/15 00:00 [accepted]
PHST- 2018/01/18 06:00 [pubmed]
PHST- 2019/10/23 06:00 [medline]
PHST- 2018/01/17 06:00 [entrez]
AID - jrheum.170418 [pii]
AID - 10.3899/jrheum.170418 [doi]
PST - ppublish
SO  - J Rheumatol. 2018 Mar;45(3):320-328. doi: 10.3899/jrheum.170418. Epub 2018 Jan 
      15.

PMID- 29303702
OWN - NLM
STAT- MEDLINE
DCOM- 20180614
LR  - 20180614
IS  - 0392-856X (Print)
IS  - 0392-856X (Linking)
VI  - 36
IP  - 2
DP  - 2018 Mar-Apr
TI  - Comparison of the risks of hospitalisation for cardiovascular events in patients 
      with rheumatoid arthritis treated with tocilizumab and etanercept.
PG  - 310-313
AB  - OBJECTIVES: To verify if tocilizumab (TCZ) is associated with an increased risk 
      of cardiovascular (CV) events compared with etanercept (ETN) in rheumatoid 
      arthritis (RA). METHODS: This is a retrospective cohort study on administrative 
      healthcare databases (AHD) in Italy. Patients were identified using a validated 
      algorithm based on AHD. Exposure to specific drugs was estimated by the drug 
      prescription recorded in the AHD. The occurrence of acute CV events (myocardial 
      infarction, stroke, other CV events) was derived from the hospital discharge 
      forms. The association between TCZ or ETN and CV events was estimated using 
      competing risk models, adjusting for pre-specified confounders. RESULTS: We 
      identified 1,752 subjects with RA, 1,086 treated with ETN and 666 with TCZ. TCZ 
      did not increase the overall risk of acute CV events, even when adjusted for 
      pre-specified confounders (hazard ratio HR 0.95, 95% confidence interval 95%CI 
      0.54-1.66), specifically of acute myocardial infarction (HR 0.39, 95%CI 
      0.15-1.06), stroke (HR 1.44, 95%CI 0.24-8.68) or other CV event (1.07, 95%CI 
      0.59-1.92). CONCLUSIONS: RA patients with TCZ do not have a medium-term excess of 
      CV risk in patients compared with ETN.
FAU - Generali, Elena
AU  - Generali E
AD  - Division of Rheumatology and Clinical Immunology, Humanitas Research Hospital, 
      Rozzano, Italy.
FAU - Carrara, Greta
AU  - Carrara G
AD  - Epidemiology Unit, Italian Society for Rheumatology, Milan, Italy.
FAU - Selmi, Carlo
AU  - Selmi C
AD  - Division of Rheumatology and Clinical Immunology, Humanitas Research Hospital, 
      Rozzano; and BIOMETRA Department, University of Milan, Italy.
FAU - Verstappen, Suzanne M M
AU  - Verstappen SMM
AD  - Arthritis Research UK Centre for Epidemiology, The University of Manchester, UK.
FAU - Zambon, Antonella
AU  - Zambon A
AD  - Department of Statistics and Quantitative Methods, Division of Biostatistics, 
      Epidemiology and Public Health, University of Milano-Bicocca, Milan, Italy.
FAU - Bortoluzzi, Alessandra
AU  - Bortoluzzi A
AD  - Rheumatology Unit, Department of Medical Sciences, University of Ferrara, Italy.
FAU - Silvagni, Ettore
AU  - Silvagni E
AD  - Rheumatology Unit, Department of Medical Sciences, University of Ferrara, Italy.
FAU - Scirè, Carlo Alberto
AU  - Scirè CA
AD  - Epidemiology Unit, Italian Society for Rheumatology, Milan; and Rheumatology 
      Unit, Department of Medical Sciences, University of Ferrara, Italy. 
      c.scire@reumatologia.it.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20171228
PL  - Italy
TA  - Clin Exp Rheumatol
JT  - Clinical and experimental rheumatology
JID - 8308521
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - I031V2H011 (tocilizumab)
RN  - OP401G7OJC (Etanercept)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antibodies, Monoclonal, Humanized/*adverse effects
MH  - Arthritis, Rheumatoid/complications/*drug therapy
MH  - Cardiovascular Diseases/*etiology
MH  - Etanercept/*adverse effects
MH  - Female
MH  - *Hospitalization
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Risk
EDAT- 2018/01/06 06:00
MHDA- 2018/06/15 06:00
CRDT- 2018/01/06 06:00
PHST- 2016/12/09 00:00 [received]
PHST- 2017/08/02 00:00 [accepted]
PHST- 2018/01/06 06:00 [pubmed]
PHST- 2018/06/15 06:00 [medline]
PHST- 2018/01/06 06:00 [entrez]
AID - 11415 [pii]
PST - ppublish
SO  - Clin Exp Rheumatol. 2018 Mar-Apr;36(2):310-313. Epub 2017 Dec 28.

PMID- 29175662
OWN - NLM
STAT- MEDLINE
DCOM- 20180815
LR  - 20180815
IS  - 1879-1336 (Electronic)
IS  - 1054-8807 (Linking)
VI  - 32
DP  - 2018 Jan-Feb
TI  - Comorbidities in relation to fatality of first myocardial infarction.
PG  - 32-37
LID - S1054-8807(17)30139-4 [pii]
LID - 10.1016/j.carpath.2017.11.002 [doi]
AB  - INTRODUCTION: Present knowledge concerning potential associations between 
      comorbidities and the fatality of a first myocardial infarction (MI) is limited. 
      AIM: To identify comorbidities in 45-70-year-old individuals who suffered a first 
      MI and died within 7 days in Stockholm County from 1992-1994. In addition, to 
      assess how each of the comorbidities identified, as well as the number of 
      hospitalizations during the 10-year period prior to the MI, was associated with 
      MI fatality. METHODS: The data collected on our inception cohort of 1984 first 
      MI, of which 524 were fatal within 7 days, were primarily self-reported, 
      proxy-reported by questionnaire and/or extracted from comprehensive national 
      registers. Comorbidities among fatal cases with a prevalence >2% were identified. 
      Risk ratios (with 95% confidence intervals) for the association of MI fatality 
      with number of prior hospitalizations and specific comorbidities were calculated 
      using binomial regression with log link. A structured review of autopsy reports 
      on fatal cases was performed in order to identify additional indicators of 
      comorbidities. RESULTS: After adjusting for sex, age and disposable income, the 
      number of previous hospitalizations was associated with 7-day MI fatality. Of the 
      comorbidities identified as prevalent in fatal cases, the following were 
      associated with 7-day fatality in crude analysis: epilepsy, heart failure, 
      stroke, alcoholism, cancer, renal diseases, asthma, psychiatric diseases, 
      diabetes, and rheumatoid arthritis. Indicators of comorbidities identified from 
      autopsy data included a silent MI, severe atherosclerosis of the abdominal aorta, 
      and hepatic steatosis. Adjustments for sex and age (although not possible for 
      epilepsy and alcoholism), did not substantially alter results. CONCLUSIONS: Our 
      current findings indicate that in connection with a first MI, particular 
      attention should be paid to those with repeated prior hospitalizations and/or 
      epilepsy, heart failure, stroke, alcoholism, cancer, renal diseases, asthma, 
      psychiatric diseases, diabetes and rheumatoid arthritis.
CI  - Copyright © 2017 Elsevier Inc. All rights reserved.
FAU - Quintana, Hedley Knewjen
AU  - Quintana HK
AD  - Unit of Cardiovascular Epidemiology, Institute of Environmental Medicine, 
      Karolinska Institutet, Stockholm, Sweden. Electronic address: 
      Hedley.Quintana@ki.se.
FAU - Janszky, Imre
AU  - Janszky I
AD  - Department of Public Health and General Practice, Norwegian University of Science 
      and Technology, Trondheim, Norway.
FAU - Kanar, Alkass
AU  - Kanar A
AD  - Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
FAU - Gigante, Bruna
AU  - Gigante B
AD  - Unit of Cardiovascular Epidemiology, Institute of Environmental Medicine, 
      Karolinska Institutet, Stockholm, Sweden; Division of Cardiovascular Medicine, 
      Department of Clinical Sciences, Danderyd University Hospital, Danderyd, Sweden.
FAU - Druid, Henrik
AU  - Druid H
AD  - Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
FAU - Ahlbom, Anders
AU  - Ahlbom A
AD  - Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, 
      Stockholm, Sweden.
FAU - de Faire, Ulf
AU  - de Faire U
AD  - Unit of Cardiovascular Epidemiology, Institute of Environmental Medicine, 
      Karolinska Institutet, Stockholm, Sweden; Department of Cardiology, Karolinska 
      University Hospital, Stockholm, Sweden.
FAU - Hallqvist, Johan
AU  - Hallqvist J
AD  - Department of Public Health and Caring Sciences, Family Medicine and Preventive 
      Medicine, Uppsala University, Uppsala, Sweden.
FAU - Leander, Karin
AU  - Leander K
AD  - Unit of Cardiovascular Epidemiology, Institute of Environmental Medicine, 
      Karolinska Institutet, Stockholm, Sweden.
LA  - eng
PT  - Journal Article
DEP - 20171114
PL  - United States
TA  - Cardiovasc Pathol
JT  - Cardiovascular pathology : the official journal of the Society for Cardiovascular 
      Pathology
JID - 9212060
SB  - IM
MH  - Aged
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*epidemiology
MH  - Risk Factors
MH  - Sweden/epidemiology
OTO - NOTNLM
OT  - Comorbidity
OT  - Fatality
OT  - Myocardial infarction
EDAT- 2017/11/28 06:00
MHDA- 2018/08/16 06:00
CRDT- 2017/11/28 06:00
PHST- 2017/05/19 00:00 [received]
PHST- 2017/10/18 00:00 [revised]
PHST- 2017/11/08 00:00 [accepted]
PHST- 2017/11/28 06:00 [pubmed]
PHST- 2018/08/16 06:00 [medline]
PHST- 2017/11/28 06:00 [entrez]
AID - S1054-8807(17)30139-4 [pii]
AID - 10.1016/j.carpath.2017.11.002 [doi]
PST - ppublish
SO  - Cardiovasc Pathol. 2018 Jan-Feb;32:32-37. doi: 10.1016/j.carpath.2017.11.002. 
      Epub 2017 Nov 14.

PMID- 29136635
OWN - NLM
STAT- MEDLINE
DCOM- 20190703
LR  - 20220330
IS  - 1423-0208 (Electronic)
IS  - 0251-5350 (Linking)
VI  - 49
IP  - 3-4
DP  - 2017
TI  - Stroke among Rheumatoid Arthritis Patients: Does Age Matter? A Real-Life Study.
PG  - 99-105
LID - 10.1159/000481992 [doi]
AB  - BACKGROUND/AIMS: Rheumatoid arthritis (RA) is a chronic, debilitating autoimmune 
      disease that affects the joints and it is known to be associated with 
      cardiovascular morbidity. However, the association between RA and stroke among 
      different age groups has not been explored. The objective of our study was to 
      evaluate the association between RA and stroke in different age strata. METHODS: 
      Cross-sectional study, utilizing the database of Israel's largest healthcare 
      provider. The proportion of stroke was compared between patients diagnosed with 
      RA and age- and gender-matched controls. The study sample was divided into 2 age 
      groups: young (≤65 years) and elderly (>65 years). Multivariable analysis was 
      performed using logistic regression. RESULTS: The study included 11,782 RA 
      patients and 57,973 age- and gender-matched controls. RA patients, primarily 
      young, had more cardiovascular risk factors than controls. Stroke rates were 
      significantly elevated among young RA patients in comparison with controls (3.74 
      vs. 2.20%, respectively, p < 0.001). In multivariate analysis, RA was found to be 
      independently associated with stroke (OR 1.18, 95% CI 1.09-1.28). CONCLUSION: RA 
      is independently associated with stroke, especially among RA patients under 65 
      years, for whom cardiovascular risk factors were more prominent. Physicians 
      should advise RA patients to manage their risk factors strictly.
CI  - © 2017 S. Karger AG, Basel.
FAU - Tiosano, Shmuel
AU  - Tiosano S
AD  - Department of Medicine "B", Sheba Medical Center, Tel-Hashomer, Israel.
AD  - Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 
      Israel.
AD  - Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
FAU - Yavne, Yarden
AU  - Yavne Y
AD  - Department of Medicine "B", Sheba Medical Center, Tel-Hashomer, Israel.
AD  - Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 
      Israel.
AD  - Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
FAU - Gendelman, Omer
AU  - Gendelman O
AD  - Department of Medicine "B", Sheba Medical Center, Tel-Hashomer, Israel.
AD  - Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 
      Israel.
AD  - Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
FAU - Watad, Abdulla
AU  - Watad A
AD  - Department of Medicine "B", Sheba Medical Center, Tel-Hashomer, Israel.
AD  - Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 
      Israel.
AD  - Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
FAU - Comaneshter, Doron
AU  - Comaneshter D
AD  - Chief Physician's Office, Clalit Health Services, Tel-Aviv, Israel.
FAU - Shoenfeld, Yehuda
AU  - Shoenfeld Y
AD  - Department of Medicine "B", Sheba Medical Center, Tel-Hashomer, Israel.
AD  - Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, 
      Israel.
AD  - Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
AD  - Incumbent of the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases, 
      Tel-Aviv University, Tel-Aviv, Israel.
FAU - Cohen, Arnon D
AU  - Cohen AD
AD  - Chief Physician's Office, Clalit Health Services, Tel-Aviv, Israel.
AD  - Siaal Research Center for Family Medicine and Primary Care, Faculty of Health 
      Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
FAU - Amital, Daniela
AU  - Amital D
AD  - Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
AD  - Ness-Ziona/Beer-Yaakov Mental Health Center, Beer-Yaakov, Israel.
LA  - eng
PT  - Journal Article
DEP - 20171114
PL  - Switzerland
TA  - Neuroepidemiology
JT  - Neuroepidemiology
JID - 8218700
SB  - IM
MH  - Age Factors
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Comorbidity
MH  - Cross-Sectional Studies
MH  - Databases, Factual
MH  - Female
MH  - Humans
MH  - Israel/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - Stroke/*epidemiology
OTO - NOTNLM
OT  - Age
OT  - Autoimmunity
OT  - Cerebrovascular disease
OT  - Rheumatoid arthritis
OT  - Risk factors
OT  - Stroke
EDAT- 2017/11/15 06:00
MHDA- 2019/07/04 06:00
CRDT- 2017/11/15 06:00
PHST- 2017/07/22 00:00 [received]
PHST- 2017/10/03 00:00 [accepted]
PHST- 2017/11/15 06:00 [pubmed]
PHST- 2019/07/04 06:00 [medline]
PHST- 2017/11/15 06:00 [entrez]
AID - 000481992 [pii]
AID - 10.1159/000481992 [doi]
PST - ppublish
SO  - Neuroepidemiology. 2017;49(3-4):99-105. doi: 10.1159/000481992. Epub 2017 Nov 14.

PMID- 29079568
OWN - NLM
STAT- MEDLINE
DCOM- 20180618
LR  - 20240606
IS  - 2047-9980 (Electronic)
IS  - 2047-9980 (Linking)
VI  - 6
IP  - 11
DP  - 2017 Oct 27
TI  - Comparative Risk of Cardiovascular Outcomes Between Topical and Oral Nonselective 
      NSAIDs in Taiwanese Patients With Rheumatoid Arthritis.
LID - 10.1161/JAHA.117.006874 [doi]
LID - e006874
AB  - BACKGROUND: Topical NSAIDs have less systemic absorption than oral NSAIDs. We 
      examined the risk of cardiovascular events associated with nonselective topical 
      NSAIDs versus oral NSAIDs among patients with rheumatoid arthritis in Taiwan. 
      METHODS AND RESULTS: We conducted a retrospective cohort study that included 
      patients with incident rheumatoid arthritis who were newly starting therapy with 
      nonselective topical NSAIDs or oral NSAIDs. We used the Taiwan National Health 
      Insurance Research Database (NHIRD). The first date patients received either type 
      of NSAID was defined as the index date. NSAID exposures continued until there was 
      a treatment gap of >30 days. The main outcome was composite cardiovascular 
      events, including myocardial infarction, unstable angina, heart failure, stroke, 
      or revascularization. Follow-up was censored at treatment discontinuation, switch 
      or addition of other NSAID category, cardiovascular outcome, death, or the end of 
      the study. Propensity score weighted Cox regression models were used to compare 
      the risk of cardiovascular events between topical NSAIDs and oral NSAIDs. There 
      were 10 758 and 78 056 treatment episodes for topical and oral NSAIDs identified. 
      After weighting by propensity score, the cohorts were well balanced over all 
      covariates. The crude cardiovascular event rate was 1.87 per 100 person-years for 
      topical NSAIDs and 2.14 per 100 person-years for oral NSAIDs. Results of 
      propensity score weighted Cox regression found the topical NSAID group had 36% 
      lower risk for cardiovascular events compared with the oral NSAID group (hazard 
      ratio, 0.64; 95% confidence interval, 0.43-0.95). CONCLUSIONS: We found topical 
      NSAID users experienced a reduced risk of cardiovascular events compared with 
      oral NSAID users. If future studies with a larger sample size and longer 
      follow-up confirm these results, NSAID prescribing might change accordingly.
CI  - © 2017 The Authors. Published on behalf of the American Heart Association, Inc., 
      by Wiley.
FAU - Lin, Tzu-Chieh
AU  - Lin TC
AD  - Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 
      Boston, MA.
AD  - Harvard Medical School, Boston, MA.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 
      Boston, MA.
AD  - Harvard Medical School, Boston, MA.
AD  - Division of Pharmacoepideimiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Boston, MA.
FAU - Tedeschi, Sara K
AU  - Tedeschi SK
AD  - Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 
      Boston, MA.
AD  - Harvard Medical School, Boston, MA.
FAU - Yoshida, Kazuki
AU  - Yoshida K
AD  - Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, 
      Boston, MA.
AD  - Departments of Epidemiology and Biostatistics, Harvard T.H. Chan School of Public 
      Health, Boston, MA.
FAU - Kao Yang, Yea-Huei
AU  - Kao Yang YH
AD  - Health Outcome Research Center, National Cheng Kung University, Tainan, Taiwan 
      yhkao@mail.ncku.edu.tw.
AD  - School of Pharmacy, College of Medicine, Tainan, Taiwan.
AD  - Institute of Clinical Pharmacy and Pharmaceutical Science, National Cheng Kung 
      University, Tainan, Taiwan.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20171027
PL  - England
TA  - J Am Heart Assoc
JT  - Journal of the American Heart Association
JID - 101580524
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
SB  - IM
MH  - Administration, Oral
MH  - Administration, Topical
MH  - Adult
MH  - Aged
MH  - Anti-Inflammatory Agents, Non-Steroidal/*administration & dosage/*adverse effects
MH  - Arthritis, Rheumatoid/diagnosis/*drug therapy/epidemiology
MH  - Cardiovascular Diseases/*chemically induced/diagnosis/epidemiology/prevention & 
      control
MH  - Comparative Effectiveness Research
MH  - Databases, Factual
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Kaplan-Meier Estimate
MH  - Male
MH  - Middle Aged
MH  - Propensity Score
MH  - Proportional Hazards Models
MH  - Retrospective Studies
MH  - Risk Assessment
MH  - Risk Factors
MH  - Taiwan/epidemiology
MH  - Time Factors
MH  - Treatment Outcome
PMC - PMC5721772
OTO - NOTNLM
OT  - NSAIDs
OT  - cardiovascular outcomes
OT  - comparative effectiveness
OT  - pharmacoepidemiology
OT  - rheumatoid arthritis
EDAT- 2017/10/29 06:00
MHDA- 2018/06/19 06:00
PMCR- 2017/11/01
CRDT- 2017/10/29 06:00
PHST- 2017/10/29 06:00 [entrez]
PHST- 2017/10/29 06:00 [pubmed]
PHST- 2018/06/19 06:00 [medline]
PHST- 2017/11/01 00:00 [pmc-release]
AID - JAHA.117.006874 [pii]
AID - JAH32699 [pii]
AID - 10.1161/JAHA.117.006874 [doi]
PST - epublish
SO  - J Am Heart Assoc. 2017 Oct 27;6(11):e006874. doi: 10.1161/JAHA.117.006874.

PMID- 29074035
OWN - NLM
STAT- MEDLINE
DCOM- 20200909
LR  - 20200909
IS  - 1096-0023 (Electronic)
IS  - 1043-4666 (Linking)
VI  - 122
DP  - 2019 Oct
TI  - The IL-12 cytokine family in cardiovascular diseases.
PG  - 154188
LID - S1043-4666(17)30315-0 [pii]
LID - 10.1016/j.cyto.2017.10.010 [doi]
AB  - Cytokines of the Interleukin (IL)-12 family, consisting of IL-12, IL-23, IL-27 
      and IL-35, are important regulators in (chronic) inflammatory disorders such as 
      rheumatoid arthritis and multiple sclerosis, but also in cardiovascular diseases. 
      Cytokines of the IL-12 family consist of two subunits and are known for their 
      regulatory functions in the immunologic response, more specifically in the 
      regulation and differentiation of T-helper (Th) cells such as Th1 and Th17 cells. 
      Binding of these cytokines to its specific heterodimeric receptor results in the 
      activation of the JAK-STAT signaling. Despite similarities in structure, the 
      members of the IL-12 family have diverse, both pro- and anti-inflammatory, 
      effects and functions. Because of the pro-inflammatory effects of IL-12 cytokine 
      family members on immune responses, the IL-12 cytokines have been implicated in 
      the development and progression of cardiovascular diseases such as 
      atherosclerosis, but also in acute cardiovascular syndromes such as myocardial 
      infarction and stroke. For example, patients suffering from cardiovascular 
      disease display increased blood levels of IL-12, IL-23 and IL-27, while decreased 
      IL-35 levels have been linked to a lower cardiovascular risk. In this review, we 
      aim to highlight the current understandings of the IL-12 cytokine family and its 
      specific family members to cardiovascular diseases, including both clinical and 
      experimental studies. We will also discuss the potential of these cytokines as a 
      biomarker in acute cardiovascular syndromes.
CI  - Copyright © 2017 Elsevier Ltd. All rights reserved.
FAU - van der Heijden, T
AU  - van der Heijden T
AD  - Division of BioTherapeutics, LACDR, Leiden University, Leiden, The Netherlands.
FAU - Bot, I
AU  - Bot I
AD  - Division of BioTherapeutics, LACDR, Leiden University, Leiden, The Netherlands.
FAU - Kuiper, J
AU  - Kuiper J
AD  - Division of BioTherapeutics, LACDR, Leiden University, Leiden, The Netherlands. 
      Electronic address: j.kuiper@lacdr.leidenuniv.nl.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171023
PL  - England
TA  - Cytokine
JT  - Cytokine
JID - 9005353
RN  - 0 (Interleukin-23)
RN  - 0 (Interleukin-27)
RN  - 0 (Interleukins)
RN  - 0 (Receptors, Interleukin-12)
RN  - 0 (interleukin-35, human)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
MH  - Animals
MH  - Cardiovascular Diseases/*metabolism/therapy
MH  - Disease Progression
MH  - Humans
MH  - Inflammation/immunology/metabolism/therapy
MH  - Interleukin-12/*metabolism
MH  - Interleukin-23/metabolism
MH  - Interleukin-27/metabolism
MH  - Interleukins/metabolism
MH  - Models, Animal
MH  - Plaque, Atherosclerotic/metabolism/therapy
MH  - Receptors, Interleukin-12/*metabolism
MH  - Signal Transduction/genetics
MH  - Th1 Cells/immunology
MH  - Th17 Cells/immunology
OTO - NOTNLM
OT  - Cardiovascular diseases
OT  - IL-12 family
OT  - IL-23
OT  - IL-27
OT  - IL-35
EDAT- 2017/10/28 06:00
MHDA- 2020/09/10 06:00
CRDT- 2017/10/28 06:00
PHST- 2017/06/27 00:00 [received]
PHST- 2017/10/06 00:00 [revised]
PHST- 2017/10/10 00:00 [accepted]
PHST- 2017/10/28 06:00 [pubmed]
PHST- 2020/09/10 06:00 [medline]
PHST- 2017/10/28 06:00 [entrez]
AID - S1043-4666(17)30315-0 [pii]
AID - 10.1016/j.cyto.2017.10.010 [doi]
PST - ppublish
SO  - Cytokine. 2019 Oct;122:154188. doi: 10.1016/j.cyto.2017.10.010. Epub 2017 Oct 23.

PMID- 29073669
OWN - NLM
STAT- MEDLINE
DCOM- 20190703
LR  - 20190703
IS  - 2333-0384 (Print)
IS  - 2333-0376 (Linking)
VI  - 31
IP  - 4
DP  - 2017 Fall
TI  - Prevalence of Temporomandibular Disorders in Rheumatoid Arthritis and Associated 
      Risk Factors: A Nationwide Study in Taiwan.
PG  - e29-e36
LID - 10.11607/ofph.1917 [doi]
AB  - AIMS: To investigate the association between temporomandibular disorders (TMD) 
      and rheumatoid arthritis (RA), as well as potential risk factors for TMD and the 
      preventive effect of medications on TMD, by using the Taiwan National Health 
      Insurance Research Database. METHODS: In total, 17,317 patients newly diagnosed 
      with RA and 17,317 matched controls without RA were followed up from 2000 to 
      2010. Cox regression was used to determine risk factors for developing TMD. 
      Kaplan-Meier curve with log-rank test was used to determine the cumulative risk 
      of TMD in RA patients and the effects of antirheumatic medications. RESULTS: Cox 
      regression showed a higher risk of developing TMD if patients had RA (adjusted 
      hazard ratio [HR] 2.538, P < .001) and a lower risk if patients were of male 
      gender and elderly (≥ 40 years) in comparison to younger patients (20 to 29 
      years) (P < .01). Patients with insomnia, stroke, and mental disorders had, 
      respectively, 4.756, 6.929, and 9.671 times the number of events of TMD compared 
      to those without diseases (P < .001). No patients with RA treated with 
      disease-modifying antirheumatic drugs (DMARDs) developed TMD after the 11-year 
      follow-up. CONCLUSION: RA patients had 2.538 times the events of TMD compared 
      with non-RA patients during this trial in Taiwan. The other risk factors for 
      developing TMD included female gender, younger age, insomnia, stroke, and mental 
      disorders. The DMARDs had a beneficial effect on prevention of TMD.
FAU - Lin, Ching-Yueh
AU  - Lin CY
FAU - Chung, Chi-Hsiang
AU  - Chung CH
FAU - Chu, Heng-Yi
AU  - Chu HY
FAU - Chen, Liang-Cheng
AU  - Chen LC
FAU - Tu, Kuo-Hsien
AU  - Tu KH
FAU - Tsao, Chang-Huei
AU  - Tsao CH
FAU - Wu, Yung-Tsan
AU  - Wu YT
FAU - Chien, Wu-Chien
AU  - Chien WC
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Oral Facial Pain Headache
JT  - Journal of oral & facial pain and headache
JID - 101624698
RN  - 0 (Antirheumatic Agents)
MH  - Adult
MH  - Aged
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/complications/drug therapy/*epidemiology
MH  - Comorbidity
MH  - Databases, Factual
MH  - Female
MH  - Humans
MH  - Kaplan-Meier Estimate
MH  - Male
MH  - Middle Aged
MH  - Prevalence
MH  - Proportional Hazards Models
MH  - Risk Factors
MH  - Taiwan/epidemiology
MH  - Temporomandibular Joint Disorders/complications/*epidemiology/prevention & 
      control
MH  - Young Adult
EDAT- 2017/10/27 06:00
MHDA- 2019/07/04 06:00
CRDT- 2017/10/27 06:00
PHST- 2017/10/27 06:00 [entrez]
PHST- 2017/10/27 06:00 [pubmed]
PHST- 2019/07/04 06:00 [medline]
AID - 10.11607/ofph.1917 [doi]
PST - ppublish
SO  - J Oral Facial Pain Headache. 2017 Fall;31(4):e29-e36. doi: 10.11607/ofph.1917.

PMID- 29049200
OWN - NLM
STAT- MEDLINE
DCOM- 20171031
LR  - 20220408
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 96
IP  - 42
DP  - 2017 Oct
TI  - Subclinical atherosclerosis and history of cardiovascular events in Italian 
      patients with rheumatoid arthritis: Results from a cross-sectional, multicenter 
      GIRRCS (Gruppo Italiano di Ricerca in Reumatologia Clinica e Sperimentale) study.
PG  - e8180
LID - 10.1097/MD.0000000000008180 [doi]
LID - e8180
AB  - Several studies have pointed out a significant association between rheumatoid 
      arthritis (RA) and accelerated atherosclerosis. At the best of our knowledge, no 
      such study has been carried out in a large Italian series and, in this study, we 
      aimed to investigate the prevalence of both subclinical atherosclerosis and 
      history of cardiovascular events (CVEs), in patients consecutively admitted from 
      January 1, 2015 to December 31, 2015 to Rheumatology Units throughout the whole 
      Italy.Centers members of GIRRCS (Gruppo Italiano di Ricerca in Reumatologia 
      Clinica e Sperimentale) were invited to enrol patients consecutively admitted 
      from January 1, 2015 to December 31, 2015 and satisfying American College of 
      Rheumatology/ European League Against Rheumatism criteria for RA and to 
      investigate each of them for: traditional cardiovascular risk factors: sex, age, 
      smoking habit, total cholesterol, triglycerides, glycaemia, high blood pressure, 
      metabolic syndrome (MS), type 2 diabetes (T2D); RA features: disease duration as 
      assessed from the first symptom, disease activity as evaluated by DAS28, 
      radiographic damage as assessed by hands and feet x-ray, and previous joint 
      surgery; prevalence of both subclinical atherosclerosis and history of CVEs.Eight 
      centers participated to the study. From January 1, 2015 to December 31, 2015, the 
      1176 patients, who had been investigated for all the items, were enrolled in the 
      study. They were mostly women (80.52%), with a median age of 60 years (range, 
      18-91 years), a median disease duration of 12 years (range, 0.8-25 years), 
      seropositive in 69.21%. Nineteen percent were in remission; 17.51% presented low 
      disease activity; 39.45% moderate disease activity; 22.61% high disease 
      activity.Eighty-two patients (6.9%) had a history for CVEs (58 myocardial 
      infarction, 38 heart failure, 10 ischemic transitory attack, and 7 stroke). This 
      figure appears to be lower than that reported worldwide (8.5%). After excluding 
      the 82 patients with a history of CV events, subclinical atherosclerosis was 
      detected in 16% of our patients, (176 patients), a figure lower than that 
      reported worldwide (32.7%) and in previous Italian studies.This is the first 
      Italian multicenter study on subclinical and clinical atherosclerosis in patients 
      with RA. We pointed out a low prevalence of both subclinical atherosclerosis and 
      history of CV events.
FAU - Ruscitti, Piero
AU  - Ruscitti P
AD  - Rheumatology Section, Department of Biotechnological and Applied Clinical 
      Sciences, University of L'Aquila, L'Aquila Clinical Medicine and Rheumatology 
      Department, Campus Bio-Medico University of Rome, Rome Rheumatology Section, 
      Department of Internal Medicine, University of Palermo, Palermo Rheumatology 
      Section, Department of Clinical and Experimental Medicine, Second University of 
      Naples, Naples Rheumatology Section, Department of Medical and Surgical Sciences, 
      University of Foggia Medical School, Foggia Department of Experimental and 
      Clinical Medicine, University of Florence, Florence Rheumatology Section, L. 
      Sacco University Hospital, Milan Systemic Rheumatic and Autoimmune Diseases Unit, 
      Department of Biomedical Sciences and Human Oncology, University of Bari Medical 
      School, Bari, Italy.
FAU - Margiotta, Domenico Paolo Emanuele
AU  - Margiotta DPE
FAU - Macaluso, Federica
AU  - Macaluso F
FAU - Iacono, Daniela
AU  - Iacono D
FAU - D'Onofrio, Francesca
AU  - D'Onofrio F
FAU - Emmi, Giacomo
AU  - Emmi G
FAU - Atzeni, Fabiola
AU  - Atzeni F
FAU - Prete, Marcella
AU  - Prete M
FAU - Perosa, Federico
AU  - Perosa F
FAU - Sarzi-Puttini, Piercarlo
AU  - Sarzi-Puttini P
FAU - Emmi, Lorenzo
AU  - Emmi L
FAU - Cantatore, Francesco Paolo
AU  - Cantatore FP
FAU - Triolo, Giovanni
AU  - Triolo G
FAU - Afeltra, Antonella
AU  - Afeltra A
FAU - Giacomelli, Roberto
AU  - Giacomelli R
FAU - Valentini, Gabriele
AU  - Valentini G
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Observational Study
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
RN  - 0 (Blood Glucose)
RN  - 0 (Triglycerides)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/blood/*complications
MH  - Atherosclerosis/blood/*complications/epidemiology
MH  - Blood Glucose/analysis
MH  - Cardiovascular Diseases/*epidemiology/etiology
MH  - Cholesterol/blood
MH  - Cross-Sectional Studies
MH  - Diabetes Mellitus, Type 2/complications/epidemiology
MH  - Female
MH  - Humans
MH  - Hypertension/complications/epidemiology
MH  - Italy/epidemiology
MH  - Male
MH  - Metabolic Syndrome/complications/epidemiology
MH  - Middle Aged
MH  - Prevalence
MH  - Risk Factors
MH  - Triglycerides/blood
MH  - Young Adult
PMC - PMC5662366
COIS- The authors report no conflicts of interest for this study.
EDAT- 2017/10/20 06:00
MHDA- 2017/11/01 06:00
PMCR- 2017/10/20
CRDT- 2017/10/20 06:00
PHST- 2017/10/20 06:00 [entrez]
PHST- 2017/10/20 06:00 [pubmed]
PHST- 2017/11/01 06:00 [medline]
PHST- 2017/10/20 00:00 [pmc-release]
AID - 00005792-201710200-00038 [pii]
AID - MD-D-17-04881 [pii]
AID - 10.1097/MD.0000000000008180 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2017 Oct;96(42):e8180. doi: 10.1097/MD.0000000000008180.

PMID- 28982826
OWN - NLM
STAT- MEDLINE
DCOM- 20180608
LR  - 20220331
IS  - 2044-6055 (Electronic)
IS  - 2044-6055 (Linking)
VI  - 7
IP  - 10
DP  - 2017 Oct 5
TI  - Beliefs about medicines and non-adherence in patients with stroke, diabetes 
      mellitus and rheumatoid arthritis: a cross-sectional study in China.
PG  - e017293
LID - 10.1136/bmjopen-2017-017293 [doi]
LID - e017293
AB  - OBJECTIVES: To investigate beliefs about medicines and their association with 
      medicine adherence in patients with chronic diseases in China. DESIGN: A 
      cross-sectional questionnaire-based study SETTING: Two large urban hospitals in 
      Hefei and Tianjin, China PARTICIPANTS: Hospital inpatients (313 stroke patients) 
      and outpatients (315 diabetic patients and 339 rheumatoid arthritis (RA) 
      patients) were recruited between January 2014 and September 2014. OUTCOME 
      MEASURES: The Beliefs about Medicines Questionnaire (BMQ), assessing patients' 
      beliefs about the specific medicine (Specific-Necessity and Specific-Concerns) 
      prescribed for their conditions (stroke/diabetes/RA) and more general background 
      beliefs about pharmaceuticals as a class of treatment (BMQ-General Benefit, Harm 
      and Overuse); the Perceived Sensitivity to Medicines scale (PSM) assessed 
      patients' beliefs about how sensitive they were to the effects of medicines and 
      the Medication Adherence Report Scale. The association between non-adherence and 
      beliefs about medicines was assessed using a logistic regression model. RESULTS: 
      Patients with diabetes mellitus had a stronger perceived need for treatment (mean 
      (SD) Specific-Necessity score, 3.75 (0.40)) than patients with stroke (3.69 
      (0.53)) and RA (3.66 (0.44)) (p=0.049). Moderate correlations were observed 
      between Specific-Concerns and General-Overuse, General-Harm and PSM (Pearson 
      correlation coefficients, 0.39, 0.49 and 0.49, respectively, p<0.01). Three 
      hundred and eleven patients were non-adherent to their medicine (159 (51.0%) in 
      the stroke group, 60 (26.7%) in the diabetes mellitus group and 62 (19.8%) in the 
      RA group, p<0.01). Across the whole sample, after adjusting for demographic 
      characteristics, non-adherence was associated with patients who had higher 
      concerns about their medicines (OR, 1.35, 95% CI 1.07 to 1.71) and patients who 
      believed that they were personally sensitive to the effects of medications (OR 
      1.44, 95% CI 1.16 to 1.85). CONCLUSION: The BMQ is a useful tool to identify 
      patients at risk of non-adherence. In the future, adherence intervention studies 
      may use the BMQ to screen for patients who are at risk of non-adherence and to 
      map interventional support.
CI  - © Article author(s) (or their employer(s) unless otherwise stated in the text of 
      the article) 2017. All rights reserved. No commercial use is permitted unless 
      otherwise expressly granted.
FAU - Wei, Li
AU  - Wei L
AD  - Department of Practice and Policy, University College London School of Pharmacy, 
      London, UK.
FAU - Champman, Sarah
AU  - Champman S
AD  - Department of Practice and Policy, University College London School of Pharmacy, 
      London, UK.
AD  - Department of Pharmacy & Pharmacology, University of Bath, Bath, UK.
FAU - Li, Xiaomei
AU  - Li X
AD  - Department of Rheumatology and Immunology, Anhui Provincial Hospital, Anhui 
      Medical University, Hefei, China.
FAU - Li, Xin
AU  - Li X
AD  - Department of Neurology, The Second Hospital, Tianjin Medical University, 
      Tianjin, China.
FAU - Li, Sumei
AU  - Li S
AD  - Department of Endocrinology, Anhui Provincial Hospital, Anhui Medical University, 
      Hefei, China.
FAU - Chen, Ruoling
AU  - Chen R
AD  - Centre for Health and Social Care Improvement, Faculty of Education Health and 
      Wellbeing, University of Wolverhampton, Wolverhampton, UK.
FAU - Bo, Nie
AU  - Bo N
AD  - Department of Practice and Policy, University College London School of Pharmacy, 
      London, UK.
FAU - Chater, Angel
AU  - Chater A
AD  - Department of Practice and Policy, University College London School of Pharmacy, 
      London, UK.
AD  - Centre for Health, Wellbeing and Behaviour Change, Faculty of Education and 
      Sport, University of Bedfordshire, Bedford, UK.
FAU - Horne, Robert
AU  - Horne R
AD  - Department of Practice and Policy, University College London School of Pharmacy, 
      London, UK.
LA  - eng
GR  - G106/1249/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Multicenter Study
DEP - 20171005
PL  - England
TA  - BMJ Open
JT  - BMJ open
JID - 101552874
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - China
MH  - Cross-Sectional Studies
MH  - Diabetes Mellitus/*drug therapy
MH  - Female
MH  - *Health Knowledge, Attitudes, Practice
MH  - Hospitals, Teaching
MH  - Humans
MH  - Logistic Models
MH  - Male
MH  - Medication Adherence/*statistics & numerical data
MH  - Middle Aged
MH  - Self Report
MH  - Severity of Illness Index
MH  - Stroke/*drug therapy
PMC - PMC5640055
OTO - NOTNLM
OT  - beliefs about medicines
OT  - chronic diseases
OT  - medicine non-adherence
COIS- Competing interests: RH declares: (1) Speaker engagements with honoraria and 
      consultancy payments from the pharmaceutical companies; (2) Founder and 
      shareholder of a UCL-Business, university spin-out company (Spoonful of Sugar) 
      providing consultancy on medication-related behaviours to healthcare policy 
      makers, providers and industry; and (3) Originator of BMQ.
EDAT- 2017/10/07 06:00
MHDA- 2018/06/09 06:00
PMCR- 2017/10/05
CRDT- 2017/10/07 06:00
PHST- 2017/10/07 06:00 [entrez]
PHST- 2017/10/07 06:00 [pubmed]
PHST- 2018/06/09 06:00 [medline]
PHST- 2017/10/05 00:00 [pmc-release]
AID - bmjopen-2017-017293 [pii]
AID - 10.1136/bmjopen-2017-017293 [doi]
PST - epublish
SO  - BMJ Open. 2017 Oct 5;7(10):e017293. doi: 10.1136/bmjopen-2017-017293.

PMID- 28877868
OWN - NLM
STAT- MEDLINE
DCOM- 20171213
LR  - 20220408
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Print)
IS  - 0003-4967 (Linking)
VI  - 77
IP  - 1
DP  - 2018 Jan
TI  - Impact of risk factors associated with cardiovascular outcomes in patients with 
      rheumatoid arthritis.
PG  - 48-54
LID - 10.1136/annrheumdis-2017-211735 [doi]
AB  - OBJECTIVES: Patients with rheumatoid arthritis (RA) have an excess risk of 
      cardiovascular disease (CVD). We aimed to assess the impact of CVD risk factors, 
      including potential sex differences, and RA-specific variables on CVD outcome in 
      a large, international cohort of patients with RA. METHODS: In 13 rheumatology 
      centres, data on CVD risk factors and RA characteristics were collected at 
      baseline. CVD outcomes (myocardial infarction, angina, revascularisation, stroke, 
      peripheral vascular disease and CVD death) were collected using standardised 
      definitions. RESULTS: 5638 patients with RA and no prior CVD were included (mean 
      age: 55.3 (SD: 14.0) years, 76% women). During mean follow-up of 5.8 (SD: 4.4) 
      years, 148 men and 241 women developed a CVD event (10-year cumulative incidence 
      20.9% and 11.1%, respectively). Men had a higher burden of CVD risk factors, 
      including increased blood pressure, higher total cholesterol and smoking 
      prevalence than women (all p<0.001). Among the traditional CVD risk factors, 
      smoking and hypertension had the highest population attributable risk (PAR) 
      overall and among both sexes, followed by total cholesterol. The PAR for Disease 
      Activity Score and for seropositivity were comparable in magnitude to the PAR for 
      lipids. A total of 70% of CVD events were attributable to all CVD risk factors 
      and RA characteristics combined (separately 49% CVD risk factors and 30% RA 
      characteristics). CONCLUSIONS: In a large, international cohort of patients with 
      RA, 30% of CVD events were attributable to RA characteristics. This finding 
      indicates that RA characteristics play an important role in efforts to reduce CVD 
      risk among patients with RA.
CI  - © Article author(s) (or their employer(s) unless otherwise stated in the text of 
      the article) 2018. All rights reserved. No commercial use is permitted unless 
      otherwise expressly granted.
FAU - Crowson, Cynthia S
AU  - Crowson CS
AD  - Division of Biomedical Statistics and Informatics, Department of Health Sciences 
      Research, Mayo Clinic, Rochester, Minnesota, USA.
AD  - Division of Rheumatology, Department of Medicine, Mayo Clinic, Rochester, 
      Minnesota, USA.
FAU - Rollefstad, Silvia
AU  - Rollefstad S
AD  - Preventive Cardio-Rheuma Clinic, Department of Rheumatology, Diakonhjemmet 
      Hospital, Oslo, Norway.
FAU - Ikdahl, Eirik
AU  - Ikdahl E
AD  - Preventive Cardio-Rheuma Clinic, Department of Rheumatology, Diakonhjemmet 
      Hospital, Oslo, Norway.
FAU - Kitas, George D
AU  - Kitas GD
AD  - Department of Rheumatology, Dudley Group NHS Foundation Trust, West Midlands, UK.
FAU - van Riel, Piet L C M
AU  - van Riel PLCM
AD  - Department of Rheumatic Diseases, Radboud University Nijmegen Medical Centre, 
      Nijmegen, The Netherlands.
FAU - Gabriel, Sherine E
AU  - Gabriel SE
AD  - Division of Rheumatology, Department of Medicine, Mayo Clinic, Rochester, 
      Minnesota, USA.
AD  - Rutgers Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA.
FAU - Matteson, Eric L
AU  - Matteson EL
AD  - Division of Rheumatology, Department of Medicine, Mayo Clinic, Rochester, 
      Minnesota, USA.
FAU - Kvien, Tore K
AU  - Kvien TK
AD  - Preventive Cardio-Rheuma Clinic, Department of Rheumatology, Diakonhjemmet 
      Hospital, Oslo, Norway.
FAU - Douglas, Karen
AU  - Douglas K
AD  - Department of Rheumatology, Dudley Group NHS Foundation Trust, West Midlands, UK.
FAU - Sandoo, Aamer
AU  - Sandoo A
AD  - Department of Rheumatology, Dudley Group NHS Foundation Trust, West Midlands, UK.
AD  - School of Sport, Health and Exercise Sciences, Bangor University, Bangor, Wales, 
      UK.
FAU - Arts, Elke
AU  - Arts E
AD  - Department of Rheumatic Diseases, Radboud University Nijmegen Medical Centre, 
      Nijmegen, The Netherlands.
FAU - Wållberg-Jonsson, Solveig
AU  - Wållberg-Jonsson S
AD  - Department of Public Health and Clinical Medicine/Rheumatology, University of 
      Umeå, Umeå, Sweden.
FAU - Innala, Lena
AU  - Innala L
AD  - Department of Public Health and Clinical Medicine/Rheumatology, University of 
      Umeå, Umeå, Sweden.
FAU - Karpouzas, George
AU  - Karpouzas G
AD  - Division of Rheumatology, Harbor UCLA Medical Center RHU, Torrance, California, 
      USA.
FAU - Dessein, Patrick H
AU  - Dessein PH
AD  - Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, 
      Faculty of Health Sciences, University of Witwatersrand, Johannesburg, South 
      Africa.
AD  - Rheumatology Division, UniversitairZiekenhuis and Vrije Universiteit, Brussel, 
      Belgium.
FAU - Tsang, Linda
AU  - Tsang L
AD  - Rheumatology Division, UniversitairZiekenhuis and Vrije Universiteit, Brussel, 
      Belgium.
FAU - El-Gabalawy, Hani
AU  - El-Gabalawy H
AD  - Institute of Musculoskeletal Health and Arthritis, University of Manitoba, 
      Winnipeg, Manitoba, Canada.
FAU - Hitchon, Carol
AU  - Hitchon C
AD  - Institute of Musculoskeletal Health and Arthritis, University of Manitoba, 
      Winnipeg, Manitoba, Canada.
FAU - Ramos, Virginia Pascual
AU  - Ramos VP
AD  - Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas 
      y Nutrición Salvador Zubirán, Mexico City, Mexico.
FAU - Yáñez, Irazú Contreras
AU  - Yáñez IC
AD  - Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas 
      y Nutrición Salvador Zubirán, Mexico City, Mexico.
FAU - Sfikakis, Petros P
AU  - Sfikakis PP
AD  - First Department of Propedeutic Medicine, University of Athens, Athens, Greece.
FAU - Zampeli, Evangelia
AU  - Zampeli E
AD  - First Department of Propedeutic Medicine, University of Athens, Athens, Greece.
FAU - Gonzalez-Gay, Miguel A
AU  - Gonzalez-Gay MA
AD  - Division of Rheumatology, Hospital Universitario Marques de Valdecilla, Santander 
      (Cantabria), Spain.
FAU - Corrales, Alfonso
AU  - Corrales A
AD  - Division of Rheumatology, Hospital Universitario Marques de Valdecilla, Santander 
      (Cantabria), Spain.
FAU - Laar, Mart van de
AU  - Laar MV
AD  - Department of Rheumatology and Clinical Immunology, Hospital Medisch Spectrum 
      Twente, Enschede, The Netherlands.
FAU - Vonkeman, Harald E
AU  - Vonkeman HE
AD  - Department of Rheumatology and Clinical Immunology, Hospital Medisch Spectrum 
      Twente, Enschede, The Netherlands.
FAU - Meek, Inger
AU  - Meek I
AD  - Department of Rheumatology and Clinical Immunology, Hospital Medisch Spectrum 
      Twente, Enschede, The Netherlands.
FAU - Semb, Anne Grete
AU  - Semb AG
AD  - Preventive Cardio-Rheuma Clinic, Department of Rheumatology, Diakonhjemmet 
      Hospital, Oslo, Norway.
CN  - A Trans-Atlantic Cardiovascular Consortium for Rheumatoid Arthritis (ATACC-RA)
LA  - eng
GR  - R01 AR046849/AR/NIAMS NIH HHS/United States
PT  - Journal Article
DEP - 20170906
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
CIN - Ann Transl Med. 2018 Nov;6(Suppl 1):S82. doi: 10.21037/atm.2018.10.72. PMID: 
      30613657
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications
MH  - Cardiovascular Diseases/*epidemiology/*etiology
MH  - Cholesterol/blood
MH  - Cohort Studies
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Hypertension/epidemiology/etiology
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Sex Factors
MH  - Smoking/adverse effects/epidemiology
PMC - PMC5726925
MID - NIHMS905817
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - population attributable risk
OT  - rheumatoid arthritis
OT  - risk factor
COIS- Competing interests: CSC reports grants from National Institute of Arthritis and 
      Musculoskeletal and Skin Disease of the National Institutes of Health during the 
      conduct of the study. AGS has received speaker honoraria and/or consulting fee 
      from Merck/Schering-Plough, Abbott, BMS, UCB, Pfizer/Wyeth, Eli Lilly and 
      Hoffmann-La Roche. TKK reports grants and personal fees from AbbVie, BMS, Biogen, 
      Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Hospira/Pfizer, 
      Merck-Serono, MSD, Mundipharma, Novartis, Oktal, Orion Pharma, Roche, Sandoz and 
      UCB. SR, EI, GDK, PLCMvR, SEG, ELM, KD, AS, EA, SW-J, LI, GK, PHD, LT, HE-G, CH, 
      VPR, ICY, PPS, EZ, MAG-G, AC, MvdL, HEV and IM: none declared.
FIR - Colunga, Iris
IR  - Colunga I
FIR - Galarza, Dionicio
IR  - Galarza D
FIR - Azpiri-López, José Ramón
IR  - Azpiri-López JR
FIR - Husni, Elaine
IR  - Husni E
FIR - Overman, Robert
IR  - Overman R
FIR - Fransen, Jaap
IR  - Fransen J
FIR - Rantapää-Dahlqvist, Solbritt
IR  - Rantapää-Dahlqvist S
FIR - Solomon, Daniel
IR  - Solomon D
FIR - Liao, Katherine
IR  - Liao K
EDAT- 2017/09/08 06:00
MHDA- 2017/12/14 06:00
PMCR- 2019/01/01
CRDT- 2017/09/08 06:00
PHST- 2017/05/04 00:00 [received]
PHST- 2017/06/30 00:00 [revised]
PHST- 2017/08/04 00:00 [accepted]
PHST- 2017/09/08 06:00 [pubmed]
PHST- 2017/12/14 06:00 [medline]
PHST- 2017/09/08 06:00 [entrez]
PHST- 2019/01/01 00:00 [pmc-release]
AID - annrheumdis-2017-211735 [pii]
AID - 10.1136/annrheumdis-2017-211735 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2018 Jan;77(1):48-54. doi: 10.1136/annrheumdis-2017-211735. Epub 
      2017 Sep 6.

PMID- 28847852
OWN - NLM
STAT- MEDLINE
DCOM- 20181025
LR  - 20220409
IS  - 1468-201X (Electronic)
IS  - 1355-6037 (Linking)
VI  - 104
IP  - 2
DP  - 2018 Jan
TI  - Association between chronic immune-mediated inflammatory diseases and 
      cardiovascular risk.
PG  - 119-126
LID - 10.1136/heartjnl-2017-311279 [doi]
AB  - OBJECTIVE: To examine the association between chronic immune-mediated diseases 
      (rheumatoid arthritis, systemic lupus erythematosus or the following chronic 
      immune-mediated inflammatory diagnoses groups: inflammatory bowel diseases, 
      inflammatory polyarthropathies, systemic connective tissue disorders and 
      spondylopathies) and the 6-year coronary artery disease, stroke, cardiovascular 
      disease incidence and overall mortality; and to estimate the population 
      attributable fractions for all four end-points for each chronic immune-mediated 
      inflammatory disease. METHODS: Cohort study of individuals aged 35-85 years, with 
      no history of cardiovascular disease from Catalonia (Spain). The coded diagnoses 
      of chronic immune-mediated diseases and cardiovascular diseases were ascertained 
      and registered using validated codes, and date of death was obtained from 
      administrative data. Cox regression models for each outcome according to exposure 
      were fitted to estimate HRs in two models (1) : after adjustment for sex, age, 
      cardiovascular risk factors and (2) further adjusted for drug use. Population 
      attributable fractions were estimated for each exposure. RESULTS: Data were 
      collected from 991 546 participants. The risk of cardiovascular disease was 
      increased in systemic connective tissue disorders (model 1: HR=1.38 (95% CI 1.21 
      to 1.57) and model 2: HR=1.31 (95% CI 1.15 to 1.49)), rheumatoid arthritis 
      (HR=1.43 (95% CI 1.26 to 1.62) and HR=1.31 (95% CI 1.15 to 1.49)) and 
      inflammatory bowel diseases (HR=1.18 (95% CI 1.06 to 1.32) and HR=1.12 (95% CI 
      1.01 to 1.25)). The effect of anti-inflammatory treatment was significant in all 
      instances (HR=1.50 (95% CI 1.24 to 1.81); HR=1.47 (95% CI 1.23 to 1.75); HR=1.43 
      (95% CI 1.19 to 1.73), respectively). The population attributable fractions for 
      all three disorders were 13.4%, 15.7% and 10.7%, respectively. CONCLUSION: 
      Systemic connective tissue disorders and rheumatoid arthritis conferred the 
      highest cardiovascular risk and population impact, followed by inflammatory bowel 
      diseases.
CI  - © Article author(s) (or their employer(s) unless otherwise stated in the text of 
      the article) 2018. All rights reserved. No commercial use is permitted unless 
      otherwise expressly granted.
FAU - Baena-Díez, Jose Miguel
AU  - Baena-Díez JM
AD  - Cardiovascular Epidemiology and Genetics Group, IMIM (Hospital del Mar Medical 
      Research Institute), Barcelona, Spain.
AD  - La Marina Primary Care Centre and Primary Care Research Institute Jordi Gol, 
      Catalan Institute of Health, Barcelona, Spain.
AD  - Consortium for Biomedical Research in Epidemiology and Public Health (CIBERESP), 
      Barcelona, Spain.
FAU - Garcia-Gil, Maria
AU  - Garcia-Gil M
AD  - Primary Care Research Institute Jordi Gol, Girona, Spain.
AD  - Research Unit in Primary Care, Primary Care Services Girona, Catalan Institute of 
      Health (ICS), Girona, Spain.
AD  - Department of Medical Sciences, School of Medicine, University of Girona, Girona, 
      Spain.
FAU - Comas-Cufí, Marc
AU  - Comas-Cufí M
AD  - Primary Care Research Institute Jordi Gol, Girona, Spain.
AD  - Research Unit in Primary Care, Primary Care Services Girona, Catalan Institute of 
      Health (ICS), Girona, Spain.
FAU - Ramos, Rafel
AU  - Ramos R
AD  - Primary Care Research Institute Jordi Gol, Girona, Spain.
AD  - Research Unit in Primary Care, Primary Care Services Girona, Catalan Institute of 
      Health (ICS), Girona, Spain.
AD  - Department of Medical Sciences, School of Medicine, University of Girona, Girona, 
      Spain.
AD  - Biomedical Research Institute, Girona, Spain.
FAU - Prieto-Alhambra, Daniel
AU  - Prieto-Alhambra D
AD  - Musculoskeletal Diseases Research Group (GREMPAL), Primary Care Research 
      Institute Jordi Gol, Universitat Autònoma de Barcelona, Barcelona, Spain.
AD  - Department of Orthopaedics, Rheumatology, and Musculoskeletal Sciences, 
      Musculoskeletal Pharmaco- and Device Epidemiology, University of Oxford, Oxford, 
      UK.
FAU - Salvador-González, Betlem
AU  - Salvador-González B
AD  - Cardiovascular Epidemiology and Genetics Group, IMIM (Hospital del Mar Medical 
      Research Institute), Barcelona, Spain.
AD  - Florida Sud Primary Care Centre and Primary Care Research Institute Jordi Gol, 
      Catalan Institute of Health, L'Hospitalet de Llobregat, Barcelona, Spain.
FAU - Elosua, Roberto
AU  - Elosua R
AD  - Cardiovascular Epidemiology and Genetics Group, IMIM (Hospital del Mar Medical 
      Research Institute), Barcelona, Spain.
FAU - Dégano, Irene R
AU  - Dégano IR
AD  - Cardiovascular Epidemiology and Genetics Group, IMIM (Hospital del Mar Medical 
      Research Institute), Barcelona, Spain.
FAU - Peñafiel, Judith
AU  - Peñafiel J
AD  - Cardiovascular Epidemiology and Genetics Group, IMIM (Hospital del Mar Medical 
      Research Institute), Barcelona, Spain.
FAU - Grau, María
AU  - Grau M
AUID- ORCID: 0000-0003-2807-8136
AD  - Cardiovascular Epidemiology and Genetics Group, IMIM (Hospital del Mar Medical 
      Research Institute), Barcelona, Spain.
AD  - University of Barcelona, Barcelona, Spain.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170828
PL  - England
TA  - Heart
JT  - Heart (British Cardiac Society)
JID - 9602087
SB  - IM
MH  - Adult
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Autoimmunity
MH  - Connective Tissue Diseases/*epidemiology
MH  - *Coronary Artery Disease/diagnosis/mortality
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Inflammatory Bowel Diseases/*epidemiology
MH  - Male
MH  - Proportional Hazards Models
MH  - Risk Assessment
MH  - Risk Factors
MH  - Spain/epidemiology
MH  - Statistics as Topic
MH  - *Stroke/diagnosis/mortality
OTO - NOTNLM
OT  - Arthritis
OT  - Cardiovascular disease
OT  - Connective Tissue Diseases
OT  - Inflammation
OT  - Inflammatory Bowel Diseases
OT  - Spondyloarthritis
COIS- Competing interests: None declared.
EDAT- 2017/08/30 06:00
MHDA- 2018/10/26 06:00
CRDT- 2017/08/30 06:00
PHST- 2017/01/25 00:00 [received]
PHST- 2017/05/30 00:00 [revised]
PHST- 2017/06/07 00:00 [accepted]
PHST- 2017/08/30 06:00 [pubmed]
PHST- 2018/10/26 06:00 [medline]
PHST- 2017/08/30 06:00 [entrez]
AID - heartjnl-2017-311279 [pii]
AID - 10.1136/heartjnl-2017-311279 [doi]
PST - ppublish
SO  - Heart. 2018 Jan;104(2):119-126. doi: 10.1136/heartjnl-2017-311279. Epub 2017 Aug 
      28.

PMID- 28724649
OWN - NLM
STAT- MEDLINE
DCOM- 20180424
LR  - 20181113
IS  - 2047-9980 (Electronic)
IS  - 2047-9980 (Linking)
VI  - 6
IP  - 7
DP  - 2017 Jul 19
TI  - Significant Associations of Neurological Complications of Herpes Zoster With 
      Stroke in Rheumatoid Arthritis Patients.
LID - 10.1161/JAHA.117.006304 [doi]
LID - e006304
AB  - BACKGROUND: Accumulating evidence suggests an increased risk of stroke after 
      herpes zoster (HZ). This risk is elevated in immunocompromised patients. The 
      incidence of HZ in Asia is higher than in Western countries. However, the 
      epidemiology of HZ and HZ-related stroke among rheumatoid arthritis (RA) patients 
      in Asia remains unclear. METHODS AND RESULTS: We conducted a retrospective cohort 
      study using a population-based database to investigate the epidemiology of HZ in 
      RA patients in Taiwan during the period of 2000-2011. A total of 27 609 newly 
      diagnosed and eligible RA cases were identified, and 110 436 non-RA cases were 
      matched for age and sex at a ratio of 4:1. HZ risk increased by 2.53-fold 
      (P<0.0001) in RA patients compared with the general population. Exposure to 
      corticosteroids (adjusted odds ratio=1.73, P<0.0001), adalimumab (adjusted odds 
      ratio=1.61, P=0.002), and rituximab (adjusted odds ratio=2.06, P=0.008) was 
      associated with an increased risk of HZ in RA patients. A significant association 
      between the use of methotrexate or corticosteroids and HZ risk was dose-dependent 
      (P(trend)<0.0001). Elevated risk of stroke was observed in RA patients with HZ 
      (adjusted hazard ratio=1.27, P=0.047), particularly in those with neurological 
      complications (adjusted hazard ratio=1.54, P=0.015). A 2.30-fold significantly 
      increased risk of stroke within 90 days after HZ occurrence was observed in RA 
      patients compared with those without HZ (P=0.02). Furthermore, death risk 
      increased in RA patients with HZ (adjusted hazard ratio=1.18, P=0.026). 
      CONCLUSIONS: The risk of HZ and HZ-related stroke has increased in RA patients. 
      Monitoring the occurrence of HZ in RA patients and preventing HZ-related stroke 
      or mortality during a specific immunosuppressive therapy are important.
CI  - © 2017 The Authors. Published on behalf of the American Heart Association, Inc., 
      by Wiley.
FAU - Liao, Tsai-Ling
AU  - Liao TL
AD  - Department of Medical Research, Taichung Veterans General Hospital, Taichung, 
      Taiwan.
AD  - Rong Hsing Research Center for Translational Medicine, National Chung Hsing 
      University, Taichung, Taiwan.
FAU - Lin, Ching-Heng
AU  - Lin CH
AD  - Department of Medical Research, Taichung Veterans General Hospital, Taichung, 
      Taiwan.
AD  - National Taipei University of Nursing and Health Science, Taipei, Taiwan.
FAU - Chen, Hsin-Hua
AU  - Chen HH
AD  - Department of Medical Research, Taichung Veterans General Hospital, Taichung, 
      Taiwan.
AD  - Division of Allergy, Immunology and Rheumatology, Taichung Veterans General 
      Hospital, Taichung, Taiwan.
AD  - Rong Hsing Research Center for Translational Medicine, National Chung Hsing 
      University, Taichung, Taiwan.
AD  - Faculty of Medicine, National Yang Ming University, Taipei, Taiwan.
FAU - Chen, Yi-Ming
AU  - Chen YM
AD  - Department of Medical Research, Taichung Veterans General Hospital, Taichung, 
      Taiwan.
AD  - Division of Allergy, Immunology and Rheumatology, Taichung Veterans General 
      Hospital, Taichung, Taiwan.
AD  - Rong Hsing Research Center for Translational Medicine, National Chung Hsing 
      University, Taichung, Taiwan.
AD  - Faculty of Medicine, National Yang Ming University, Taipei, Taiwan.
FAU - Lin, Che-Chen
AU  - Lin CC
AD  - Department of Medical Research, Taichung Veterans General Hospital, Taichung, 
      Taiwan.
FAU - Chen, Der-Yuan
AU  - Chen DY
AD  - Department of Internal Medicine and Medical Education, Taichung Veterans General 
      Hospital, Taichung, Taiwan dychen@vghtc.gov.tw.
AD  - Division of Allergy, Immunology and Rheumatology, Taichung Veterans General 
      Hospital, Taichung, Taiwan.
AD  - Rong Hsing Research Center for Translational Medicine, National Chung Hsing 
      University, Taichung, Taiwan.
AD  - Faculty of Medicine, National Yang Ming University, Taipei, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20170719
PL  - England
TA  - J Am Heart Assoc
JT  - Journal of the American Heart Association
JID - 101580524
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Immunosuppressive Agents)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antirheumatic Agents/*adverse effects
MH  - Arthritis, Rheumatoid/diagnosis/*drug therapy/immunology/mortality
MH  - Chi-Square Distribution
MH  - Databases, Factual
MH  - Female
MH  - Herpes Zoster/diagnosis/immunology/mortality/*virology
MH  - Herpesvirus 3, Human/immunology/*pathogenicity
MH  - Host-Pathogen Interactions
MH  - Humans
MH  - Immunocompromised Host
MH  - Immunosuppressive Agents/*adverse effects
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Odds Ratio
MH  - Opportunistic Infections/diagnosis/immunology/mortality/*virology
MH  - Proportional Hazards Models
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Stroke/diagnosis/immunology/mortality/*virology
MH  - Taiwan/epidemiology
MH  - Time Factors
PMC - PMC5586320
OTO - NOTNLM
OT  - herpes zoster
OT  - immunosuppressive therapy
OT  - infectious disease
OT  - nervous system
OT  - neurological complications
OT  - rheumatoid arthritis
OT  - stroke
EDAT- 2017/07/21 06:00
MHDA- 2018/04/25 06:00
PMCR- 2017/07/01
CRDT- 2017/07/21 06:00
PHST- 2017/07/21 06:00 [entrez]
PHST- 2017/07/21 06:00 [pubmed]
PHST- 2018/04/25 06:00 [medline]
PHST- 2017/07/01 00:00 [pmc-release]
AID - JAHA.117.006304 [pii]
AID - JAH32356 [pii]
AID - 10.1161/JAHA.117.006304 [doi]
PST - epublish
SO  - J Am Heart Assoc. 2017 Jul 19;6(7):e006304. doi: 10.1161/JAHA.117.006304.

PMID- 28711461
OWN - NLM
STAT- MEDLINE
DCOM- 20190726
LR  - 20220318
IS  - 2173-5743 (Electronic)
IS  - 2173-5743 (Linking)
VI  - 15
IP  - 2
DP  - 2019 Mar-Apr
TI  - Prevalence of comorbidities in rheumatoid arthritis and evaluation of their 
      monitoring in clinical practice: the spanish cohort of the COMORA study.
PG  - 102-108
LID - S1699-258X(17)30134-1 [pii]
LID - 10.1016/j.reuma.2017.06.002 [doi]
AB  - OBJECTIVES: To describe the prevalence of comorbidities in patients with RA in 
      Spain and discuss their management and implications using data from the Spanish 
      cohort of the multinational study on COMOrbidities in Rheumatoid Arthritis 
      (COMORA). METHODS: This is a national sub-analysis of the COMORA study. We 
      studied the demographics and disease characteristics of 200 adults patients 
      diagnosed with RA (1987 ACR), and routine practices for screening and preventing 
      the following selected comorbidities: cardiovascular, infections, cancer, 
      gastrointestinal, pulmonary, osteoporosis and depression. RESULTS: Patients had a 
      mean age of 58 years and a mean RA duration of 10 years. Mean DAS28 score was 3.3 
      and approximately 25% of patients were in remission (DAS28 <2.6). Forty-four 
      (22%) patients had ≥1 comorbidity, the most frequent being depression (27%) and 
      obesity (26%). A history of myocardial infarction or stroke was observed in 5% 
      and 1% of patients, respectively, and any solid tumor in 6%. Having a Framingham 
      Risk Score >20% (51%), hypercholesterolemia (46%) or hypertension (41%) and 
      smoking (25%) were the most common CV risk factors. For prostate, colon and skin 
      cancers, only 9%, 10% and 18% of patients, respectively, were optimally 
      monitored. Infections were also inadequately managed, with 7% and 17% of patients 
      vaccinated against influenza and pneumococcal, respectively, as was osteoporosis, 
      with 47% of patients supplemented with vitamin D and 56% with a bone densitometry 
      performed. CONCLUSIONS: In Spain, the prevalence of comorbidities and CV risk 
      factors in RA patients with established and advanced disease is relatively high, 
      and their management in clinical daily practice remains suboptimal.
CI  - Copyright © 2017 Elsevier España, S.L.U. and Sociedad Española de Reumatología y 
      Colegio Mexicano de Reumatología. All rights reserved.
FAU - Balsa, Alejandro
AU  - Balsa A
AD  - Hospital Universitario La Paz IdiPAZ, Madrid, Spain. Electronic address: 
      alejandro.balsa@salud.madrid.org.
FAU - Lojo-Oliveira, Leticia
AU  - Lojo-Oliveira L
AD  - Hospital Universitario La Paz IdiPAZ, Madrid, Spain.
FAU - Alperi-López, Mercedes
AU  - Alperi-López M
AD  - Hospital Universitario Central de Asturias, Asturias, Spain.
FAU - García-Manrique, María
AU  - García-Manrique M
AD  - Hospital Parc Taulí, Sabadell, Barcelona, Spain.
FAU - Ordóñez-Cañizares, Carmen
AU  - Ordóñez-Cañizares C
AD  - Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional 
      Universitario de Málaga, Universidad de Málaga, Málaga, Spain.
FAU - Pérez, Lorena
AU  - Pérez L
AD  - Hospital Universitario Infanta Sofía, Universidad Europea de Madrid, Madrid, 
      Spain.
FAU - Ruiz-Esquide, Virginia
AU  - Ruiz-Esquide V
AD  - Hospital Clínic IdiBAPS, Barcelona, Spain.
FAU - Corrales, Alfonso
AU  - Corrales A
AD  - Hospital Universitario Marqués de Valdecilla IDIVAL, Santander, Spain.
FAU - Narváez, Javier
AU  - Narváez J
AD  - IDIBELL-Hospital Universitario de Bellvitge, Barcelona, Spain.
FAU - Rey-Rey, José
AU  - Rey-Rey J
AD  - Hospital Virgen de la Salud, Toledo, Spain.
FAU - Rodríguez-Lozano, Carlos
AU  - Rodríguez-Lozano C
AD  - Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria, 
      Spain.
FAU - Ojeda, Soledad
AU  - Ojeda S
AD  - Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria, 
      Spain.
FAU - Muñoz-Fernández, Santiago
AU  - Muñoz-Fernández S
AD  - Hospital Universitario Infanta Sofía, Universidad Europea de Madrid, Madrid, 
      Spain.
FAU - Nolla, Joan M
AU  - Nolla JM
AD  - IDIBELL-Hospital Universitario de Bellvitge, Barcelona, Spain.
FAU - García-Torrón, José
AU  - García-Torrón J
AD  - Hospital San Pedro de Alcántara, Cáceres, Spain.
FAU - Gamero, Fernando
AU  - Gamero F
AD  - Hospital San Pedro de Alcántara, Cáceres, Spain.
FAU - García-Vicuña, Rosario
AU  - García-Vicuña R
AD  - Hospital Universitario La Princesa, IIS-IP, Madrid, Spain.
FAU - Hernández-Cruz, Blanca
AU  - Hernández-Cruz B
AD  - Hospital Universitario Virgen Macarena, Sevilla, Spain.
FAU - Campos, José
AU  - Campos J
AD  - Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.
FAU - Rosas, José
AU  - Rosas J
AD  - Hospital Marina Baixa de Villajoyosa, Alicante, Spain.
FAU - García-Llorente, José Francisco
AU  - García-Llorente JF
AD  - Hospital de Mendaro, Guipúzcoa, Spain.
FAU - Gómez-Centeno, Antonio
AU  - Gómez-Centeno A
AD  - Hospital Parc Taulí, Sabadell, Barcelona, Spain.
FAU - Cáliz, Rafael
AU  - Cáliz R
AD  - Hospital Virgen de las Nieves, Granada, Spain.
FAU - Sanmartí, Raimon
AU  - Sanmartí R
AD  - Hospital Clínic IdiBAPS, Barcelona, Spain.
FAU - Bermúdez, Alberto
AU  - Bermúdez A
AD  - Hospital Virgen de la Arrixaca, Murcia, Spain.
FAU - Abasolo-Alcázar, Lydia
AU  - Abasolo-Alcázar L
AD  - IdISSC, Hospital Clínico San Carlos, Madrid, Spain.
FAU - Fernández-Nebro, Antonio
AU  - Fernández-Nebro A
AD  - Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional 
      Universitario de Málaga, Universidad de Málaga, Málaga, Spain.
FAU - Rodríguez-Rodríguez, Luis
AU  - Rodríguez-Rodríguez L
AD  - IdISSC, Hospital Clínico San Carlos, Madrid, Spain.
FAU - Marras, Carlos
AU  - Marras C
AD  - Hospital Virgen de la Arrixaca, Murcia, Spain.
FAU - González-Gay, Miguel Ángel
AU  - González-Gay MÁ
AD  - Hospital Universitario Marqués de Valdecilla IDIVAL, Santander, Spain.
FAU - Hmamouchi, Ihsane
AU  - Hmamouchi I
AD  - Hôpital Provincial de Khémisset Laboratoire de Biostatistique, de Recherche 
      Clinique et d'Epidémiologie (LBRCE), Faculté de Médecine et de Pharmacie, 
      Université Mohamed-V, Rabat, Morocco.
FAU - Martín-Mola, Emilio
AU  - Martín-Mola E
AD  - Hospital Universitario La Paz IdiPAZ, Madrid, Spain.
LA  - eng
LA  - spa
PT  - Journal Article
PT  - Multicenter Study
PT  - Observational Study
DEP - 20170712
PL  - Spain
TA  - Reumatol Clin (Engl Ed)
JT  - Reumatologia clinica
JID - 101717526
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Comorbidity
MH  - Cross-Sectional Studies
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Prevalence
MH  - Risk Factors
MH  - Spain/epidemiology
MH  - Young Adult
OTO - NOTNLM
OT  - Artritis reumatoide
OT  - Comorbidities
OT  - Comorbilidades
OT  - Factores de riesgo
OT  - Prevalence
OT  - Prevalencia
OT  - Rheumatoid arthritis
OT  - Risk factors
EDAT- 2017/07/18 06:00
MHDA- 2019/07/28 06:00
CRDT- 2017/07/17 06:00
PHST- 2017/01/03 00:00 [received]
PHST- 2017/06/08 00:00 [revised]
PHST- 2017/06/08 00:00 [accepted]
PHST- 2017/07/18 06:00 [pubmed]
PHST- 2019/07/28 06:00 [medline]
PHST- 2017/07/17 06:00 [entrez]
AID - S1699-258X(17)30134-1 [pii]
AID - 10.1016/j.reuma.2017.06.002 [doi]
PST - ppublish
SO  - Reumatol Clin (Engl Ed). 2019 Mar-Apr;15(2):102-108. doi: 
      10.1016/j.reuma.2017.06.002. Epub 2017 Jul 12.

PMID- 28701103
OWN - NLM
STAT- MEDLINE
DCOM- 20180801
LR  - 20240712
IS  - 1473-2300 (Electronic)
IS  - 0300-0605 (Print)
IS  - 0300-0605 (Linking)
VI  - 46
IP  - 1
DP  - 2018 Jan
TI  - Lipid management among individuals with inflammatory arthritis in the national 
      REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort.
PG  - 62-69
LID - 10.1177/0300060517713591 [doi]
AB  - Objective Hyperlipidemia guidelines do not currently identify inflammatory 
      arthritis (IA) as a cardiovascular disease (CVD) risk factor. We compared 
      hyperlipidemia treatment of individuals with and without IA (rheumatoid 
      arthritis, psoriatic arthritis, or ankylosing spondylitis) in a large national 
      cohort. Methods Participants from the REasons for Geographic And Racial 
      Differences in Stroke (REGARDS) study were classified as having IA (without 
      diabetes or hypertension); diabetes (but no IA); hypertension (but no diabetes or 
      IA); or no IA, diabetes, or hypertension. Multivariable logistic regression 
      models examined the odds of medical treatment among those with hyperlipidemia. 
      Results Thirty-nine participants had IA, 5423 had diabetes, 7534 had 
      hypertension, and 5288 had no diabetes, hypertension, or IA. The fully adjusted 
      odds of treatment were similar between participants with IA and those without IA, 
      hypertension, or diabetes. Participants with diabetes and no IA and participants 
      with hypertension and no IA were twice as likely to be treated for hyperlipidemia 
      as those without IA, diabetes, or hypertension. Conclusion Despite their higher 
      CVD risk, patients with IA were as likely to be treated for hyperlipidemia as 
      those without diabetes, hypertension, or IA. Lipid guidelines should identify IA 
      as a CVD risk factor to improve CVD risk optimization in IA.
FAU - Navarro-Millán, Iris
AU  - Navarro-Millán I
AD  - 1 Joan and Sanford I Weill Medical College of Cornell University, New York, NY, 
      USA.
AD  - 2 Hospital for Speical Surgery, Division of Rheumatology, New York, NY, USA.
FAU - Gamboa, Christopher M
AU  - Gamboa CM
AD  - 3 University of Alabama at Birmingham, Birmingham, AL, USA.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AD  - 3 University of Alabama at Birmingham, Birmingham, AL, USA.
FAU - Safford, Monika M
AU  - Safford MM
AD  - 1 Joan and Sanford I Weill Medical College of Cornell University, New York, NY, 
      USA.
LA  - eng
GR  - R01 HL080477/HL/NHLBI NIH HHS/United States
GR  - U01 NS041588/NS/NINDS NIH HHS/United States
PT  - Journal Article
DEP - 20170712
PL  - England
TA  - J Int Med Res
JT  - The Journal of international medical research
JID - 0346411
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Hypolipidemic Agents)
RN  - 0 (Immunosuppressive Agents)
SB  - IM
MH  - Aged
MH  - Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Psoriatic/*drug therapy/ethnology/metabolism/physiopathology
MH  - Arthritis, Rheumatoid/*drug therapy/ethnology/metabolism/physiopathology
MH  - Black People
MH  - Cohort Studies
MH  - Diabetes Mellitus/*drug therapy/ethnology/metabolism/physiopathology
MH  - Female
MH  - Humans
MH  - Hyperlipidemias/*drug therapy/ethnology/metabolism/physiopathology
MH  - Hypertension/*drug therapy/ethnology/metabolism/physiopathology
MH  - Hypolipidemic Agents/therapeutic use
MH  - Immunosuppressive Agents/therapeutic use
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Odds Ratio
MH  - Risk Factors
MH  - Spondylitis, Ankylosing/*drug therapy/ethnology/metabolism/physiopathology
MH  - Stroke/*drug therapy/ethnology/metabolism/physiopathology
MH  - United States
MH  - White People
MH  - Black or African American
PMC - PMC6011298
OTO - NOTNLM
OT  - Hyperlipidemia
OT  - ankylosing spondylitis
OT  - cardiovascular disease
OT  - inflammatory arthritis
OT  - psoriatic arthritis
OT  - rheumatoid arthritis
EDAT- 2017/07/14 06:00
MHDA- 2018/08/02 06:00
PMCR- 2018/01/01
CRDT- 2017/07/14 06:00
PHST- 2017/07/14 06:00 [pubmed]
PHST- 2018/08/02 06:00 [medline]
PHST- 2017/07/14 06:00 [entrez]
PHST- 2018/01/01 00:00 [pmc-release]
AID - 10.1177_0300060517713591 [pii]
AID - 10.1177/0300060517713591 [doi]
PST - ppublish
SO  - J Int Med Res. 2018 Jan;46(1):62-69. doi: 10.1177/0300060517713591. Epub 2017 Jul 
      12.

PMID- 28678807
OWN - NLM
STAT- MEDLINE
DCOM- 20171006
LR  - 20221207
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 7
DP  - 2017
TI  - Risk of cardiovascular disease in Chinese patients with rheumatoid arthritis: A 
      cross-sectional study based on hospital medical records in 10 years.
PG  - e0180376
LID - 10.1371/journal.pone.0180376 [doi]
LID - e0180376
AB  - OBJECTIVE: Though the risk of cardiovascular disease (CVD) in rheumatoid 
      arthritis (RA) has been established in Western population, little is known about 
      the risk in Chinese people with RA. Our objective was to estimate the risk of CVD 
      in Chinese people with RA using hospital medical records data. METHODS: The 
      inpatients medical record database 2005-2015 of Sichuan provincial people's 
      hospital was examined. All individuals with a primary diagnosis of RA were 
      included as cases, and those of osteoarthritis (OA) were included as controls, 
      which consisted of the unmatched dataset. Then, RA cases and OA controls were 
      matched by sex and age at 1:1 ratio, forming the matched dataset. The morbidity 
      of CVD (including ischemia heart disease (IHD), congestive heart failure (CHF), 
      et al), stroke and arthrosclerosis were extracted from the database, so as the 
      demographic data and comorbidities related to CVD. Multiple logistic regression 
      analysis was used to estimate the risk of CVD in RA adjusted for demographics and 
      comorbidities using the unmatched dataset. Sensitivity analysis was conducted 1) 
      considering interaction terms between RA and comorbidities, and 2) using 
      multivariable conditional logistic regression for the matched dataset. RESULTS: 
      The unmatched dataset comprised of 1824RA cases and 1995 OA controls and the 
      matched dataset comprised of 1022 pairs of sex and age matched RA and OA 
      patients. RA exhibited increased odds of prevalent CVD compared with OA, and the 
      adjusted ORs (95%CIs) for CVD, stroke, IHD, CHF, and atherosclerosis 
      were1.86(1.42-2.43), 1.11(0.71-1.74), 1.47(0.97-2.24), 2.09(1.03-4.22), and 2.49 
      (1.97-3.13), respectively, and was 2.26 (1.29-3.96)for IHD further adjusted for 
      interaction term. The matched dataset analysis found similar results. 
      CONCLUSIONS: Chinese people with RA were approximated 2 times more likely to have 
      CVD, IHD, CHF and atherosclerosis compared with those with OA. The findings 
      justified the need of further longitudinal study to establish the 
      causal-relationship between RA and CVD and to estimate the precise risk in this 
      population.
FAU - Zou, Kun
AU  - Zou K
AUID- ORCID: 0000-0002-2175-2231
AD  - Department of Medical Records and Statistics, Sichuan Academy of Medical Sciences 
      & Sichuan Provincial People's Hospital, Affiliate Hospital of the University of 
      Electronic Science and Technology, Chengdu, China.
AD  - Division of Rheumatology, Orthopedics and Dermatology, School of Medicine, 
      University of Nottingham, Nottingham, United Kingdom.
FAU - Xiao, Fu-Kun
AU  - Xiao FK
AD  - Department of Medical Records and Statistics, Sichuan Academy of Medical Sciences 
      & Sichuan Provincial People's Hospital, Affiliate Hospital of the University of 
      Electronic Science and Technology, Chengdu, China.
FAU - Li, Hong-Ying
AU  - Li HY
AD  - Department of Medical Records and Statistics, Sichuan Academy of Medical Sciences 
      & Sichuan Provincial People's Hospital, Affiliate Hospital of the University of 
      Electronic Science and Technology, Chengdu, China.
FAU - Zhou, Qiao
AU  - Zhou Q
AD  - Department of Rheumatology and Immunology, Sichuan Academy of Medical Sciences & 
      Sichuan Provincial People's Hospital, Affiliate Hospital of the University of 
      Electronic Science and Technology, Chengdu, China.
FAU - Ban, Lu
AU  - Ban L
AD  - Division of Rheumatology, Orthopedics and Dermatology, School of Medicine, 
      University of Nottingham, Nottingham, United Kingdom.
AD  - Division of Epidemiology & Public Health, School of Medicine, University of 
      Nottingham, Nottingham, United Kingdom.
FAU - Yang, Min
AU  - Yang M
AD  - West China Research Center for Rural Health Development, West China School of 
      Public Health, Sichuan University, Chengdu, China.
FAU - Kuo, Chang-Fu
AU  - Kuo CF
AD  - Division of Rheumatology, Orthopedics and Dermatology, School of Medicine, 
      University of Nottingham, Nottingham, United Kingdom.
AD  - Division of Rheumatology, Allergy and Immunology, Chang Gung Memorial Hospital, 
      Taoyuan, Taiwan.
FAU - Zhang, Weiya
AU  - Zhang W
AD  - Division of Rheumatology, Orthopedics and Dermatology, School of Medicine, 
      University of Nottingham, Nottingham, United Kingdom.
LA  - eng
PT  - Journal Article
DEP - 20170705
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*epidemiology/ethnology
MH  - Asian People
MH  - Cardiovascular Diseases/*epidemiology/ethnology
MH  - China/epidemiology
MH  - Comorbidity
MH  - Cross-Sectional Studies
MH  - Female
MH  - Hospital Records/*statistics & numerical data
MH  - Humans
MH  - Logistic Models
MH  - Male
MH  - Medical Records/*statistics & numerical data
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Prevalence
MH  - Risk Factors
MH  - Time Factors
PMC - PMC5498026
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2017/07/06 06:00
MHDA- 2017/10/07 06:00
PMCR- 2017/07/05
CRDT- 2017/07/06 06:00
PHST- 2017/01/05 00:00 [received]
PHST- 2017/06/14 00:00 [accepted]
PHST- 2017/07/06 06:00 [entrez]
PHST- 2017/07/06 06:00 [pubmed]
PHST- 2017/10/07 06:00 [medline]
PHST- 2017/07/05 00:00 [pmc-release]
AID - PONE-D-16-48494 [pii]
AID - 10.1371/journal.pone.0180376 [doi]
PST - epublish
SO  - PLoS One. 2017 Jul 5;12(7):e0180376. doi: 10.1371/journal.pone.0180376. 
      eCollection 2017.

PMID- 28668802
OWN - NLM
STAT- MEDLINE
DCOM- 20180521
LR  - 20220408
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
VI  - 44
IP  - 9
DP  - 2017 Sep
TI  - Anticyclic Citrullinated Peptide Antibodies and Rheumatoid Factor as Risk Factors 
      for 10-year Cardiovascular Morbidity in Patients with Rheumatoid Arthritis: A 
      Large Inception Cohort Study.
PG  - 1325-1330
LID - 10.3899/jrheum.160670 [doi]
AB  - OBJECTIVE: To determine whether anticyclic citrullinated peptide antibodies 
      (anti-CCP) and rheumatoid factor (RF) are risk factors for 10-year cardiovascular 
      disease (CVD) in patients with rheumatoid arthritis (RA). METHODS: Analyses were 
      performed using data from the Nijmegen early RA inception cohort, in which 
      patients with newly diagnosed RA, consecutively included since 1985, were 
      regularly followed up. Anti-CCP and RF were determined at baseline (diagnosis). 
      Outcome was the first cardiovascular disease (CVD) event [ischemic heart disease, 
      nonhemorrhagic cerebrovascular accident (CVA), or peripheral artery disease 
      (PAD)] after baseline as retrieved from physician diagnosis. Fatality was checked 
      against death certificates. Cox regression including correction for baseline 
      confounders was performed to estimate the effect of anti-CCP, RF, and their 
      interaction on 10-year CVD-free survival. RESULTS: Of 929 patients included, 628 
      were anti-CCP-positive and 697 were RF-positive. During followup, with a median 
      of 7.5 years, 162 CV events were observed (101 ischemic heart disease, 45 CVA, 
      and 16 PAD), of which 15 were fatal. The HR(adjusted) for anti-CCP was 1.17 (95% 
      CI 0.82-1.67) and the HR(adjusted) for RF was 1.52 (95% CI 1.00-2.30). The 
      association of RF positivity with CVD was even stronger in the anti-CCP-negative 
      patients: HR(adjusted) 2.09 (95% CI 1.18-3.71). There was no significant 
      interaction (p = 0.098) between anti-CCP and RF. CONCLUSION: Rather than 
      anti-CCP, presence of RF was associated with CVD in this cohort of patients with 
      RA.
FAU - Berendsen, Mike L T
AU  - Berendsen MLT
AD  - From the Department of Rheumatology, Radboud University Medical Centre; 
      Department of Rheumatology, St. Maartenskliniek, Nijmegen; Department of 
      Rheumatology, Bernhoven Hospital, Uden, the Netherlands.
AD  - M.L. Berendsen, MSc, Department of Rheumatology, Radboud University Medical 
      Centre; M.C. van Maaren, MSc, Department of Rheumatology, Radboud University 
      Medical Centre; E.E. Arts, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre; A.A. den Broeder, PhD, Department of Rheumatology, St. 
      Maartenskliniek; C.D. Popa, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre, and Department of Rheumatology, Bernhoven Hospital; J. 
      Fransen, PhD, Department of Rheumatology, Radboud University Medical Centre.
FAU - van Maaren, Marissa C
AU  - van Maaren MC
AD  - From the Department of Rheumatology, Radboud University Medical Centre; 
      Department of Rheumatology, St. Maartenskliniek, Nijmegen; Department of 
      Rheumatology, Bernhoven Hospital, Uden, the Netherlands.
AD  - M.L. Berendsen, MSc, Department of Rheumatology, Radboud University Medical 
      Centre; M.C. van Maaren, MSc, Department of Rheumatology, Radboud University 
      Medical Centre; E.E. Arts, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre; A.A. den Broeder, PhD, Department of Rheumatology, St. 
      Maartenskliniek; C.D. Popa, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre, and Department of Rheumatology, Bernhoven Hospital; J. 
      Fransen, PhD, Department of Rheumatology, Radboud University Medical Centre.
FAU - Arts, Elke E A
AU  - Arts EEA
AD  - From the Department of Rheumatology, Radboud University Medical Centre; 
      Department of Rheumatology, St. Maartenskliniek, Nijmegen; Department of 
      Rheumatology, Bernhoven Hospital, Uden, the Netherlands.
AD  - M.L. Berendsen, MSc, Department of Rheumatology, Radboud University Medical 
      Centre; M.C. van Maaren, MSc, Department of Rheumatology, Radboud University 
      Medical Centre; E.E. Arts, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre; A.A. den Broeder, PhD, Department of Rheumatology, St. 
      Maartenskliniek; C.D. Popa, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre, and Department of Rheumatology, Bernhoven Hospital; J. 
      Fransen, PhD, Department of Rheumatology, Radboud University Medical Centre.
FAU - den Broeder, Alfons A
AU  - den Broeder AA
AD  - From the Department of Rheumatology, Radboud University Medical Centre; 
      Department of Rheumatology, St. Maartenskliniek, Nijmegen; Department of 
      Rheumatology, Bernhoven Hospital, Uden, the Netherlands.
AD  - M.L. Berendsen, MSc, Department of Rheumatology, Radboud University Medical 
      Centre; M.C. van Maaren, MSc, Department of Rheumatology, Radboud University 
      Medical Centre; E.E. Arts, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre; A.A. den Broeder, PhD, Department of Rheumatology, St. 
      Maartenskliniek; C.D. Popa, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre, and Department of Rheumatology, Bernhoven Hospital; J. 
      Fransen, PhD, Department of Rheumatology, Radboud University Medical Centre.
FAU - Popa, Calin D
AU  - Popa CD
AD  - From the Department of Rheumatology, Radboud University Medical Centre; 
      Department of Rheumatology, St. Maartenskliniek, Nijmegen; Department of 
      Rheumatology, Bernhoven Hospital, Uden, the Netherlands. 
      calin.popa@radboudumc.nl.
AD  - M.L. Berendsen, MSc, Department of Rheumatology, Radboud University Medical 
      Centre; M.C. van Maaren, MSc, Department of Rheumatology, Radboud University 
      Medical Centre; E.E. Arts, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre; A.A. den Broeder, PhD, Department of Rheumatology, St. 
      Maartenskliniek; C.D. Popa, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre, and Department of Rheumatology, Bernhoven Hospital; J. 
      Fransen, PhD, Department of Rheumatology, Radboud University Medical Centre. 
      calin.popa@radboudumc.nl.
FAU - Fransen, Jaap
AU  - Fransen J
AD  - From the Department of Rheumatology, Radboud University Medical Centre; 
      Department of Rheumatology, St. Maartenskliniek, Nijmegen; Department of 
      Rheumatology, Bernhoven Hospital, Uden, the Netherlands.
AD  - M.L. Berendsen, MSc, Department of Rheumatology, Radboud University Medical 
      Centre; M.C. van Maaren, MSc, Department of Rheumatology, Radboud University 
      Medical Centre; E.E. Arts, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre; A.A. den Broeder, PhD, Department of Rheumatology, St. 
      Maartenskliniek; C.D. Popa, MD, PhD, Department of Rheumatology, Radboud 
      University Medical Centre, and Department of Rheumatology, Bernhoven Hospital; J. 
      Fransen, PhD, Department of Rheumatology, Radboud University Medical Centre.
LA  - eng
PT  - Journal Article
DEP - 20170701
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Anti-Citrullinated Protein Antibodies)
RN  - 9009-79-4 (Rheumatoid Factor)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Anti-Citrullinated Protein Antibodies/*blood
MH  - Arthritis, Rheumatoid/blood/*complications/immunology
MH  - Cardiovascular Diseases/blood/*etiology/immunology
MH  - Cohort Studies
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Rheumatoid Factor/*blood
MH  - Risk Factors
OTO - NOTNLM
OT  - ANTICYCLIC CITRULLINATED PEPTIDE ANTIBODIES
OT  - CARDIOVASCULAR DISEASE
OT  - RHEUMATOID ARTHRITIS
OT  - RHEUMATOID FACTOR
EDAT- 2017/07/03 06:00
MHDA- 2018/05/22 06:00
CRDT- 2017/07/03 06:00
PHST- 2017/04/26 00:00 [accepted]
PHST- 2017/07/03 06:00 [pubmed]
PHST- 2018/05/22 06:00 [medline]
PHST- 2017/07/03 06:00 [entrez]
AID - jrheum.160670 [pii]
AID - 10.3899/jrheum.160670 [doi]
PST - ppublish
SO  - J Rheumatol. 2017 Sep;44(9):1325-1330. doi: 10.3899/jrheum.160670. Epub 2017 Jul 
      1.

PMID- 28658137
OWN - NLM
STAT- MEDLINE
DCOM- 20170717
LR  - 20220408
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Print)
IS  - 0025-7974 (Linking)
VI  - 96
IP  - 26
DP  - 2017 Jun
TI  - Cardiovascular disease in immune-mediated inflammatory diseases: A 
      cross-sectional analysis of 6 cohorts.
PG  - e7308
LID - 10.1097/MD.0000000000007308 [doi]
LID - e7308
AB  - To analyze in several immune-mediated inflammatory diseases (IMIDs) the influence 
      of demographic and clinical-related variables on the prevalence of cardiovascular 
      disease (CVD), and compare their standardized prevalences.Cross-sectional study, 
      including consecutive patients diagnosed with rheumatoid arthritis, psoriatic 
      arthritis, psoriasis, systemic lupus erythematosus, Crohn disease, or ulcerative 
      colitis, from rheumatology, gastroenterology, and dermatology tertiary care 
      outpatient clinics located throughout Spain, between 2007 and 2010. Our main 
      outcome was defined as previous diagnosis of angina, myocardial infarction, 
      peripheral vascular disease, and/or stroke. Bivariate and multivariate logistic 
      and mixed-effects logistic regression models were performed for each condition 
      and the overall cohort, respectively. Standardized prevalences (in subjects per 
      100 patients, with 95% confidence intervals) were calculated using marginal 
      analysis.We included 9951 patients. For each IMID, traditional cardiovascular 
      risk factors had a different contribution to CVD. Overall, older age, longer 
      disease duration, presence of traditional cardiovascular risk factors, and male 
      sex were independently associated with a higher CVD prevalence. After adjusting 
      for demographic and traditional cardiovascular risk factors, systemic lupus 
      erythematosus exhibited the highest CVD standardized prevalence, followed by 
      rheumatoid arthritis, psoriasis, Crohn disease, psoriatic arthritis, and 
      ulcerative colitis (4.5 [95% confidence interval (CI): 2.2, 6.8], 1.3 [95% CI: 
      0.8, 1.8], 0.9 [95% CI: 0.5, 1.2], 0.8 [95% CI: 0.2, 1.3], 0.6 [95% CI: 0.2, 
      1.0], and 0.5 [95% CI: 0.1, 0.8], respectively).Systemic lupus erythematosus, 
      rheumatoid arthritis, and psoriasis are associated with higher prevalence of CVD 
      compared with other IMIDs. Specific prevention programs should be established in 
      subjects affected with these conditions to prevent CVD.
FAU - Fernández-Gutiérrez, Benjamín
AU  - Fernández-Gutiérrez B
AD  - Rheumatology Department and Instituto de Investigación Sanitaria San Carlos 
      (IdISSC), Hospital Clínico San Carlos, Madrid Rheumatology Research Group, Vall 
      d'Hebron Hospital Research Institute Department of Medicine, University of 
      Barcelona, Barcelona Gastroenterology Department, Hospital Universitario de la 
      Princesa, Instituto de Investigación Sanitaria Princesa (IIS-IP), Madrid Centro 
      de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas 
      (CIBEREHD) Gastroenterology and Hepatology Department, Hospital Universitari 
      Germans Trias i Pujol, Badalona UGC Reumatología, Instituto de Investigación 
      Biomédica de Málaga, Hospital Regional Universitario de Málaga, Universidad de 
      Málaga, Málaga Rheumatology Department, Hospital Clinic and IDIBAPS Dermatology 
      Department, Hospital Universitari Germans Trias i Pujol, Badalona Universidad 
      Autónoma de Barcelona, Barcelona Rheumatology Department, Hospital General 
      Universitario de Guadalajara, Guadalajara Hospital Universitario Reina Sofía, 
      Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Universidad 
      de Córdoba, Córdoba Hospital Clínic de Barcelona and IDIBAPS, Barcelona 
      Dermatology Department Rheumatology Department, Complejo Hospitalario 
      Universitario A Coruña, INIBIC, A Coruña Rheumatology Department, Hospital 
      Universitari de Bellvitge, L'Hospitalet de Llobregat Rheumatology Department, 
      Hospital Universitario Doce de Octubre, Madrid, Spain.
FAU - Perrotti, Pedro P
AU  - Perrotti PP
FAU - Gisbert, Javier P
AU  - Gisbert JP
FAU - Domènech, Eugeni
AU  - Domènech E
FAU - Fernández-Nebro, Antonio
AU  - Fernández-Nebro A
FAU - Cañete, Juan D
AU  - Cañete JD
FAU - Ferrándiz, Carlos
AU  - Ferrándiz C
FAU - Tornero, Jesús
AU  - Tornero J
FAU - García-Sánchez, Valle
AU  - García-Sánchez V
FAU - Panés, Julián
AU  - Panés J
FAU - Fonseca, Eduardo
AU  - Fonseca E
FAU - Blanco, Francisco
AU  - Blanco F
FAU - Rodríguez-Moreno, Jesús
AU  - Rodríguez-Moreno J
FAU - Carreira, Patricia
AU  - Carreira P
FAU - Julià, Antonio
AU  - Julià A
FAU - Marsal, Sara
AU  - Marsal S
FAU - Rodriguez-Rodriguez, Luis
AU  - Rodriguez-Rodriguez L
CN  - IMID Consortium
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Observational Study
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
SB  - IM
MH  - Adult
MH  - Aged
MH  - Cardiovascular Diseases/*complications/*epidemiology
MH  - Cohort Studies
MH  - Cross-Sectional Studies
MH  - Female
MH  - Humans
MH  - Immune System Diseases/*complications/*epidemiology
MH  - Inflammation/complications/epidemiology
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Prevalence
MH  - Risk Factors
MH  - Spain
MH  - Tertiary Care Centers
PMC - PMC5500059
COIS- F.B. reported receiving consultancy fees from Gebro Pharma, and grant support 
      from Bioiberica, MSD, Glaxo, UCB, Roche, Pfizer, Celltrion, Celgene, Amgen, 
      Grunenthal, Sanofi, and Teded-Meiji; J.P.G. reported receiving speaker's, 
      consultancy or grant support from MSD, Abbvie, Hospira, Kern Pharma, Takeda, 
      Janssen, Pfizer, Ferring, Faes Farma, Shire Pharmaceuticals, Dr. Falk Pharma, 
      Chiesi, Casen Fleet, Gebro Pharma, Otsuka Pharmaceutical, and Vifor Pharma; and 
      the remaining authors have no conflicts of interest to disclose.
EDAT- 2017/06/29 06:00
MHDA- 2017/07/18 06:00
PMCR- 2017/06/30
CRDT- 2017/06/29 06:00
PHST- 2017/06/29 06:00 [entrez]
PHST- 2017/06/29 06:00 [pubmed]
PHST- 2017/07/18 06:00 [medline]
PHST- 2017/06/30 00:00 [pmc-release]
AID - 00005792-201706300-00045 [pii]
AID - MD-D-17-01405 [pii]
AID - 10.1097/MD.0000000000007308 [doi]
PST - ppublish
SO  - Medicine (Baltimore). 2017 Jun;96(26):e7308. doi: 10.1097/MD.0000000000007308.

PMID- 28646083
OWN - NLM
STAT- MEDLINE
DCOM- 20180411
LR  - 20190202
IS  - 2044-6055 (Electronic)
IS  - 2044-6055 (Linking)
VI  - 7
IP  - 4
DP  - 2017 Jun 22
TI  - Does depression increase the risk of stroke in patients with rheumatoid 
      arthritis? A population-based cohort study.
PG  - e014233
LID - 10.1136/bmjopen-2016-014233 [doi]
LID - e014233
AB  - OBJECTIVES: Comorbid depression is common and undertreated in patients with 
      rheumatoid arthritis (RA). It remains uncertain whether comorbid depression 
      provoked the risk of poor clinical outcome, stroke in particular, among patients 
      with RA. This work aimed to determine if depression onset during the treatment 
      process increases stroke risk for patients with RA as compared with those with 
      (1) neither RA nor depression, (2) RA only and (3) depression only. DESIGN: A 
      nationwide, population-based cohort study. SETTING: Taiwan's Longitudinal Health 
      Insurance Database. PARTICIPANTS: We identified 8045 subjects with a newly 
      diagnosed RA between 1997 and 2010, together with 32 600 subjects without RA 
      matched by age, gender and index date. All subjects were further divided into 
      four groups based on whether they were diagnosed with comorbid depression during 
      the follow-up period. MAIN OUTCOME MEASURE: The incidence rate and HR for 
      incident stroke were estimated by the end of 2012 using Cox proportional hazard 
      regression. RESULTS: We discovered that patients with RA with the comorbid 
      depression exhibited the highest risk of stroke, with an adjusted HR of 2.18 (95% 
      CI 1.87 to 2.54). Those with RA only or those with depression only still had the 
      higher risk of stroke by 43% and 57% as compared with subjects without either 
      condition. Multivariate analysis showed RA subjects who were male or older, 
      incurred the onset of depression, or had comorbidities such as hypertension, 
      diabetes as well as heart disease, had a greater risk of stroke. CONCLUSIONS: 
      This study cleared up the significant association between RA and the subsequent 
      risk of stroke, and further highlighted that the onset of depression within the 
      treatment process may increase stroke risk for RA subjects. Findings could assist 
      healthcare providers to pinpoint individuals with RA with a higher predisposition 
      of stroke, which could facilitate the provision of appropriate rehabilitation.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://www.bmj.com/company/products-services/rights-and-licensing/.
FAU - Tsai, Tzung-Yi
AU  - Tsai TY
AD  - Department of Medical Research, Dalin Tzuchi Hospital, The Buddhist Tzuchi 
      Medical Foundation, Chiayi, Taiwan.
AD  - Department of Environmental and Occupational Health, College of Medicine, 
      National Cheng Kung University, Tainan, Taiwan.
AD  - Department of Nursing, Tzu Chi University of Science and Technology, Hualien, 
      Taiwan.
FAU - Lu, Ming-Chi
AU  - Lu MC
AD  - Division of Allergy, Immunology and Rheumatology, Dalin Tzuchi Hospital, The 
      Buddhist Tzuchi Medical Foundation, Chiayi, Taiwan.
AD  - School of Medicine, Tzu Chi University, Hualien, Taiwan.
FAU - Livneh, Hanoch
AU  - Livneh H
AD  - Rehabilitation Counseling Program, Portland State University, Portland, Oregon, 
      USA.
FAU - Chiu, Shan-Yun
AU  - Chiu SY
AD  - Department of Nursing, Dalin Tzuchi Hospital, The Buddhist Tzuchi Medical 
      Foundation, Chiayi, Taiwan.
FAU - Lai, Ning-Sheng
AU  - Lai NS
AD  - Division of Allergy, Immunology and Rheumatology, Dalin Tzuchi Hospital, The 
      Buddhist Tzuchi Medical Foundation, Chiayi, Taiwan.
AD  - School of Medicine, Tzu Chi University, Hualien, Taiwan.
FAU - Guo, How-Ran
AU  - Guo HR
AD  - Department of Environmental and Occupational Health, College of Medicine, 
      National Cheng Kung University, Tainan, Taiwan.
AD  - Department of Occupational and Environmental Medicine, National Cheng Kung 
      University Hospital, Tainan, Taiwan.
AD  - Occupational Safety, Health, and Medicine Research Center, National Cheng Kung 
      University, Tainan, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170622
PL  - England
TA  - BMJ Open
JT  - BMJ open
JID - 101552874
SB  - IM
MH  - Adult
MH  - Age Distribution
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications/epidemiology/physiopathology/*psychology
MH  - Cohort Studies
MH  - Comorbidity
MH  - Depression/*complications/epidemiology/physiopathology
MH  - Diabetes Mellitus/epidemiology/physiopathology
MH  - Female
MH  - Heart Diseases/epidemiology/physiopathology
MH  - Humans
MH  - Hypertension/epidemiology/physiopathology
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Proportional Hazards Models
MH  - Risk Factors
MH  - Sex Distribution
MH  - Stroke/epidemiology/*etiology/physiopathology
MH  - Taiwan/epidemiology
PMC - PMC5541340
OTO - NOTNLM
OT  - cohort study
OT  - rheumatoid arthritis
COIS- Competing interests: None declared.
EDAT- 2017/06/25 06:00
MHDA- 2018/04/12 06:00
PMCR- 2017/06/22
CRDT- 2017/06/25 06:00
PHST- 2017/06/25 06:00 [entrez]
PHST- 2017/06/25 06:00 [pubmed]
PHST- 2018/04/12 06:00 [medline]
PHST- 2017/06/22 00:00 [pmc-release]
AID - bmjopen-2016-014233 [pii]
AID - 10.1136/bmjopen-2016-014233 [doi]
PST - epublish
SO  - BMJ Open. 2017 Jun 22;7(4):e014233. doi: 10.1136/bmjopen-2016-014233.

PMID- 28606965
OWN - NLM
STAT- MEDLINE
DCOM- 20171003
LR  - 20220408
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 76
IP  - 10
DP  - 2017 Oct
TI  - Low disease activity (DAS28≤3.2) reduces the risk of first cardiovascular event 
      in rheumatoid arthritis: a time-dependent Cox regression analysis in a large 
      cohort study.
PG  - 1693-1699
LID - 10.1136/annrheumdis-2016-210997 [doi]
AB  - OBJECTIVE: Systemic inflammation appears to contribute to the excess risk of 
      cardiovascular disease (CVD) in rheumatoid arthritis (RA). The objective of this 
      study was to investigate the effect of different levels of disease activity over 
      time, particularly low disease activity and remission, on CVD risk in patients 
      with RA. METHODS: Data from the Nijmegen early RA inception cohort were used. The 
      primary outcome was first CVD events within the first 10 years of follow-up. Cut 
      points of the DAS28 for remission (<2.6) and low (≤3.2), moderate (3.2-5.1) and 
      high (>5.1) disease activity were used. The effect of disease activity on CVD 
      risk was analysed using Cox-proportional hazards regression with DAS28 as a 
      time-dependent covariate and also conventionally with time-averaged DAS28 as the 
      primary dependent variable. RESULTS: Low DAS28 (≤3.2) was significantly 
      associated with a reduced risk of CVD (HR 0.65, 95% CI 0.43 to 0.99) compared 
      with DAS28 >3.2, both when included as a time-dependent covariate and as 
      time-averaged DAS28 ≤3.2 (HR 0.52, 95% CI 0.33 to 0.81). Remission had a modest, 
      non-significant protective effect against CVD (HR 0.67, 95% CI 0.43 to 1.07). 
      CONCLUSION: Results of this study suggest that low disease activity is sufficient 
      to achieve a protective effect against CVD in RA. Apparently, remission defined 
      as DAS28 <2.6 has no additional protective effect against CVD compared with low 
      disease activity. Our results strengthen the use of tight control strategies in 
      daily clinical practice to achieve low stable disease activity or remission in 
      patients with RA as soon as possible.
CI  - © Article author(s) (or their employer(s) unless otherwise stated in the text of 
      the article) 2017. All rights reserved. No commercial use is permitted unless 
      otherwise expressly granted.
FAU - Arts, Elke Ea
AU  - Arts EE
AD  - Department of Rheumatology, Radboud University Medical Center, Nijmegen, The 
      Netherlands.
FAU - Fransen, Jaap
AU  - Fransen J
AD  - Department of Rheumatology, Medicines Evaluation Board, Utrecht, The Netherlands.
FAU - Den Broeder, Alfons A
AU  - Den Broeder AA
AD  - Department of Rheumatology, Sint Maartenskliniek, Nijmegen, The Netherlands.
FAU - van Riel, Piet L C M
AU  - van Riel PLCM
AD  - Department of Rheumatology, Bernhoven, Uden, The Netherlands.
AD  - Department of Rheumatology, Radboud Institute for Health Sciences, IQ healthcare, 
      Radboud University Medical Center, Nijmegen, The Netherlands.
FAU - Popa, Calin D
AU  - Popa CD
AD  - Department of Rheumatology, Radboud University Medical Center, Nijmegen, The 
      Netherlands.
AD  - Department of Rheumatology, Sint Maartenskliniek, Nijmegen, The Netherlands.
LA  - eng
PT  - Journal Article
DEP - 20170612
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
MH  - Acute Coronary Syndrome/epidemiology
MH  - Adult
MH  - Aged
MH  - Angina, Stable/epidemiology
MH  - Arthritis, Rheumatoid/*epidemiology/physiopathology
MH  - Cardiovascular Diseases/*epidemiology
MH  - Female
MH  - Follow-Up Studies
MH  - Heart Failure/epidemiology
MH  - Humans
MH  - Ischemic Attack, Transient/epidemiology
MH  - Kaplan-Meier Estimate
MH  - Male
MH  - Middle Aged
MH  - Netherlands/epidemiology
MH  - Peripheral Arterial Disease/epidemiology
MH  - Proportional Hazards Models
MH  - Prospective Studies
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Stroke/epidemiology
MH  - Time Factors
OTO - NOTNLM
OT  - Cardiovascular Disease
OT  - Disease Activity
OT  - Rheumatoid Arthritis
COIS- Competing interests: None delared.
EDAT- 2017/06/14 06:00
MHDA- 2017/10/04 06:00
CRDT- 2017/06/14 06:00
PHST- 2016/12/19 00:00 [received]
PHST- 2017/03/20 00:00 [revised]
PHST- 2017/05/05 00:00 [accepted]
PHST- 2017/06/14 06:00 [pubmed]
PHST- 2017/10/04 06:00 [medline]
PHST- 2017/06/14 06:00 [entrez]
AID - annrheumdis-2016-210997 [pii]
AID - 10.1136/annrheumdis-2016-210997 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2017 Oct;76(10):1693-1699. doi: 10.1136/annrheumdis-2016-210997. 
      Epub 2017 Jun 12.

PMID- 28601812
OWN - NLM
STAT- MEDLINE
DCOM- 20171204
LR  - 20220129
IS  - 1468-201X (Electronic)
IS  - 1355-6037 (Print)
IS  - 1355-6037 (Linking)
VI  - 103
IP  - 23
DP  - 2017 Dec
TI  - Cardiovascular and type 2 diabetes morbidity and all-cause mortality among 
      diverse chronic inflammatory disorders.
PG  - 1867-1873
LID - 10.1136/heartjnl-2017-311214 [doi]
AB  - OBJECTIVES: The present study aimed to assess the relationship between 
      inflammatory disorders with cardiometabolic diseases and mortality within a 
      community-based population. METHODS: The UK Biobank data were used to conduct two 
      investigations: a cross-sectional study to estimate cardiometabolic risk and a 
      prospective cohort study to estimate mortality risk. Binary regression analyses 
      were used to model the association between coronary heart disease, stroke, type 2 
      diabetes, venous thromboembolism and peripheral artery disease diagnoses with 
      seven inflammatory disorders (eg, rheumatoid arthritis (RA), systemic lupus 
      erythematosus (SLE), psoriasis, ankylosing spondylitis (AS), systemic vasculitis, 
      Crohn's disease and ulcerative colitis (UC)). Cox proportional hazards was used 
      to estimate all-cause and cardiovascular-related mortality. RESULTS: About 4% 
      (n=19, 082) of the study population (n=5 02 641) were diagnosed with a chronic 
      inflammatory disorder. The most common inflammatory disorder was psoriasis 
      (n=6286), and the least common was SLE (n=654). SLE showed the strongest 
      association with multiple (relative risk (RR) 6.36, 95% CI 4.37 to 9.25) risk of 
      cardiometabolic diseases, followed by the RA (RR 1.70, 95% CI 1.59 to 1.83), UC 
      (RR 1.69, 95% CI 1.51 to 1.89), AS (RR 1.28, 95% CI 1.09 to 1.52), vasculitis (RR 
      1.64, 95% CI 1.42-1.90) and psoriasis (RR 1.25, 95% 1.16 to 1.35) disorders. The 
      magnitude of the association was higher among participants prescribed 
      non-steroidal anti-inflammatory drugs or corticosteroids drugs, with multiple 
      cardiometabolic risk being greater within SLE (RR 12.35, 95% CI 7.18 to 21.24), 
      followed by UC (RR 3.81, 95% CI 2.69 to 5.38), Crohn's disease (RR 3.07, 95% CI 
      1.85 to 5.11), RA (RR 3.06, 95% CI 2.44 to 3.85), psoriasis (RR 2.36, 95% CI 1.88 
      to 2.95), AS (RR 2.25, 95% CI 1.48 to 3.41) and vasculitis (RR 1.89, 95% CI 1.28 
      to 2.79). Similar pattern was observed with respect to the cumulative 
      cardiometabolic risk. CONCLUSION: Inflammatory disorders are associated with 
      heightened risk of cardiometabolic events, which may vary by anti-inflammatory 
      therapy and duration. All-cause mortality was also higher among specific 
      inflammatory disorders compared with the absence of inflammatory disorders.
CI  - © Article author(s) (or their employer(s) unless otherwise stated in the text of 
      the article) 2017. All rights reserved. No commercial use is permitted unless 
      otherwise expressly granted.
FAU - Dregan, Alex
AU  - Dregan A
AD  - Department of Primary Care and Public Health Sciences, King's College London, 
      London, UK.
AD  - National Institute for Health Research Biomedical Research Centre, Guy's and St 
      Thomas NHS Foundation Trust, London, UK.
FAU - Chowienczyk, Phil
AU  - Chowienczyk P
AD  - British Foundation Centre, King's College London, London, UK.
FAU - Molokhia, Mariam
AU  - Molokhia M
AD  - Department of Primary Care and Public Health Sciences, King's College London, 
      London, UK.
AD  - National Institute for Health Research Biomedical Research Centre, Guy's and St 
      Thomas NHS Foundation Trust, London, UK.
LA  - eng
GR  - MC_QA137853/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20170610
PL  - England
TA  - Heart
JT  - Heart (British Cardiac Society)
JID - 9602087
RN  - 0 (Adrenal Cortex Hormones)
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
SB  - IM
MH  - Adolescent
MH  - Adrenal Cortex Hormones/therapeutic use
MH  - Adult
MH  - Aged
MH  - Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
MH  - Biological Specimen Banks
MH  - Cardiovascular Diseases/diagnosis/*mortality
MH  - Cause of Death
MH  - Chronic Disease
MH  - Cross-Sectional Studies
MH  - Diabetes Mellitus, Type 2/diagnosis/*mortality
MH  - Female
MH  - Humans
MH  - Inflammation/diagnosis/drug therapy/*mortality
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Odds Ratio
MH  - Prognosis
MH  - Proportional Hazards Models
MH  - Prospective Studies
MH  - Risk Assessment
MH  - Risk Factors
MH  - United Kingdom
MH  - Young Adult
PMC - PMC5749371
OTO - NOTNLM
OT  - Cardiac risk factors and prevention
OT  - Coronary artery disease
OT  - Diabetes
OT  - Stroke
OT  - Systemic inflammatory diseases
COIS- Competing interests: None declared.
EDAT- 2017/06/12 06:00
MHDA- 2017/12/05 06:00
PMCR- 2018/01/02
CRDT- 2017/06/12 06:00
PHST- 2017/01/12 00:00 [received]
PHST- 2017/05/05 00:00 [revised]
PHST- 2017/05/10 00:00 [accepted]
PHST- 2017/06/12 06:00 [pubmed]
PHST- 2017/12/05 06:00 [medline]
PHST- 2017/06/12 06:00 [entrez]
PHST- 2018/01/02 00:00 [pmc-release]
AID - heartjnl-2017-311214 [pii]
AID - 10.1136/heartjnl-2017-311214 [doi]
PST - ppublish
SO  - Heart. 2017 Dec;103(23):1867-1873. doi: 10.1136/heartjnl-2017-311214. Epub 2017 
      Jun 10.

PMID- 28597983
OWN - NLM
STAT- MEDLINE
DCOM- 20170905
LR  - 20231011
IS  - 1469-493X (Electronic)
IS  - 1361-6137 (Linking)
VI  - 6
IP  - 6
DP  - 2017 Jun 9
TI  - Celecoxib for rheumatoid arthritis.
PG  - CD012095
LID - 10.1002/14651858.CD012095.pub2 [doi]
LID - CD012095
AB  - BACKGROUND: Rheumatoid arthritis is a systemic auto-immune disorder that causes 
      widespread and persistent inflammation of the synovial lining of joints and 
      tendon sheaths. Presently, there is no cure for rheumatoid arthritis and 
      treatment focuses on managing symptoms such as pain, stiffness and mobility, with 
      the aim of achieving stable remission and improving mobility. Celecoxib is a 
      selective non-steroidal anti-inflammatory drug (NSAID) used for treatment of 
      people with rheumatoid arthritis. OBJECTIVES: To assess the benefits and harms of 
      celecoxib in people with rheumatoid arthritis. SEARCH METHODS: We searched the 
      Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, Embase and 
      clinical trials registers (ClinicalTrials.gov and the World Health Organization 
      trials portal) to May 18, 2017. We also searched the reference and citation lists 
      of included studies. SELECTION CRITERIA: We included prospective randomized 
      controlled trials (RCTs) that compared oral celecoxib (200 mg and 400 mg daily) 
      versus no intervention, placebo or a traditional NSAID (tNSAID) in people with 
      confirmed rheumatoid arthritis, of any age and either sex. We excluded studies 
      with fewer than 50 participants in each arm or had durations of fewer than four 
      weeks treatment. DATA COLLECTION AND ANALYSIS: We used standard methodological 
      procedures expected by The Cochrane Collaboration. MAIN RESULTS: We included 
      eight RCTs with durations of 4 to 24 weeks, published between 1998 and 2014 that 
      involved a total of 3988 adults (mean age = 54 years), most of whom were women 
      (73%). Participants had rheumatoid arthritis for an average of 9.2 years. All 
      studies were assessed at high or unclear risk of bias in at least one domain. 
      Overall, evidence was assessed as moderate-to-low quality. Five studies were 
      funded by pharmaceutical companies. Celecoxib versus placeboWe included two 
      studies (N = 873) in which participants received 200 mg daily or 400 mg daily or 
      placebo. Participants who received celecoxib showed significant clinical 
      improvement compared with those receiving placebo (15% absolute improvement; 95% 
      CI 7% to 25%; RR 1.53, 95% CI 1.25 to 1.86; number needed to treat to benefit 
      (NNTB) = 7, 95% CI 5 to 13; 2 studies, 873 participants; moderate to low quality 
      evidence).Participants who received celecoxib reported less pain than 
      placebo-treated people (11% absolute improvement; 95% CI 8% to 14%; NNTB = 4, 95% 
      CI 3 to 6; 1 study, 706 participants) but results were inconclusive for 
      improvement in physical function (MD -0.10, 95% CI 0.29 to 0.10; 1 study, 706 
      participants).In the celecoxib group, 15/293 participants developed ulcers, 
      compared with 4/99 in the placebo group (Peto OR 1.26, 95% CI 0.44 to 3.63; 1 
      study, 392 participants; low quality evidence). Nine (of 475) participants in the 
      celecoxib group developed short-term serious adverse events, compared with five 
      (of 231) in the placebo group (Peto OR 0.87 (0.28 to 2.69; 1 study, 706 
      participants; low quality evidence).There were fewer withdrawals among people who 
      received celecoxib (163/475) compared with placebo (130/231) (22% absolute 
      change; 95% CI 16% to 27%; RR 0.61, 95% CI 0.52 to 0.72; 1 study, 706 
      participants).Cardiovascular events (myocardial infarction, stroke) were not 
      reported. However, regulatory agencies warn of increased cardiovascular event 
      risk associated with celecoxib. Celecoxib versus tNSAIDsSeven studies (N = 2930) 
      compared celecoxib and tNSAIDs (amtolmetin guacyl, diclofenac, ibuprofen, 
      meloxicam, nabumetone, naproxen, pelubiprofen); one study included comparisons of 
      both placebo and tNSAIDs (N = 1149).There was a small improvement, which may not 
      be clinically significant, in numbers of participants achieving ACR20 criteria 
      response in the celecoxib group compared to tNSAIDs (4% absolute improvement; 95% 
      CI 0% less improvement to 8% more improvement; RR 1.10, 95% CI 0.99 to 1.23; 4 
      studies, 1981 participants). There was a lack of evidence of difference between 
      participants in the celecoxib and tNSAID groups in terms of pain or physical 
      function. Results were assessed at moderate-to-low quality evidence (downgraded 
      due to risk of bias and inconsistency).People who received celecoxib had a lower 
      incidence of gastroduodenal ulcers ≥ 3 mm (34/870) compared with those who 
      received tNSAIDs (116/698). This corresponded to 12% absolute change (95% CI 11% 
      to 13%; RR 0.22, 95% CI 0.15 to 0.32; 5 studies, 1568 participants; moderate 
      quality evidence). There were 7% fewer withdrawals among people who received 
      celecoxib (95% CI 4% to 9%; RR 0.73, 95% CI 0.62 to 0.86; 6 studies, 2639 
      participants).Results were inconclusive for short-term serious adverse events and 
      cardiovascular events (low quality evidence). There were 17/918 serious adverse 
      events in people taking celecoxib compared to 42/1236 among people who received 
      placebo (Peto OR 0.71; 95% CI 0.39 to 1.28; 5 studies, 2154 participants). 
      Cardiovascular events were reported in both celecoxib and placebo groups in one 
      study (149 participants). AUTHORS' CONCLUSIONS: Celecoxib may improve clinical 
      symptoms, alleviate pain and contribute to little or no difference in physical 
      function compared with placebo. Celecoxib was associated with fewer numbers of 
      participant withdrawals. Results for incidence of gastroduodenal ulcers (≥ 3 mm) 
      and short-term serious adverse events were uncertain; however, there were few 
      reported events for either.Celecoxib may slightly improve clinical symptoms 
      compared with tNSAIDs. Results for reduced pain and improved physical function 
      were uncertain. Particpants taking celecoxib had lower incidence of 
      gastroduodenal ulcers (≥ 3 mm) and there were fewer withdrawals from trials. 
      Results for cardiovascular events and short-term serious adverse events were also 
      uncertain.Uncertainty about the rate of cardiovascular events between celecoxib 
      and tNSAIDs could be due to risk of bias; another factor is that these were 
      small, short-term trials. It has been reported previously that both celecoxib and 
      tNSAIDs increase cardiovascular event rates. Our confidence in results about 
      harms is therefore low. Larger head-to-head clinical trials comparing celecoxib 
      to other tNSAIDs is needed to better inform clinical practice.
FAU - Fidahic, Mahir
AU  - Fidahic M
AD  - Medical faculty, University of Tuzla, Univerzitetska 1, Tuzla, Canton Tuzla, 
      Bosnia and Herzegovina, 75000.
FAU - Jelicic Kadic, Antonia
AU  - Jelicic Kadic A
FAU - Radic, Mislav
AU  - Radic M
FAU - Puljak, Livia
AU  - Puljak L
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PT  - Systematic Review
DEP - 20170609
PL  - England
TA  - Cochrane Database Syst Rev
JT  - The Cochrane database of systematic reviews
JID - 100909747
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - JCX84Q7J1L (Celecoxib)
SB  - IM
UOF - doi: 10.1002/14651858.CD012095
MH  - Anti-Inflammatory Agents, Non-Steroidal/adverse effects/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Celecoxib/adverse effects/*therapeutic use
MH  - Humans
MH  - Myocardial Infarction/chemically induced/epidemiology
MH  - Pain Measurement
MH  - Randomized Controlled Trials as Topic
MH  - Stomach Ulcer/chemically induced/epidemiology
MH  - Stroke/chemically induced/epidemiology
MH  - Treatment Outcome
PMC - PMC6481589
COIS- Mahir Fidahic: no conflict of interest.  Antonia Jelicic Kadic: no conflict of 
      interest.  Mislav Radic: no conflict of interest.  Livia Puljak: no conflict of 
      interest.
EDAT- 2017/06/10 06:00
MHDA- 2017/09/07 06:00
PMCR- 2018/06/09
CRDT- 2017/06/10 06:00
PHST- 2017/06/10 06:00 [pubmed]
PHST- 2017/09/07 06:00 [medline]
PHST- 2017/06/10 06:00 [entrez]
PHST- 2018/06/09 00:00 [pmc-release]
AID - CD012095.pub2 [pii]
AID - 10.1002/14651858.CD012095.pub2 [doi]
PST - epublish
SO  - Cochrane Database Syst Rev. 2017 Jun 9;6(6):CD012095. doi: 
      10.1002/14651858.CD012095.pub2.

PMID- 28536104
OWN - NLM
STAT- MEDLINE
DCOM- 20170619
LR  - 20240607
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Print)
IS  - 0959-8138 (Linking)
VI  - 357
DP  - 2017 May 23
TI  - Development and validation of QRISK3 risk prediction algorithms to estimate 
      future risk of cardiovascular disease: prospective cohort study.
PG  - j2099
LID - 10.1136/bmj.j2099 [doi]
LID - j2099
AB  - Objectives To develop and validate updated QRISK3 prediction algorithms to 
      estimate the 10 year risk of cardiovascular disease in women and men accounting 
      for potential new risk factors.Design Prospective open cohort 
      study.Setting General practices in England providing data for the QResearch 
      database.Participants 1309 QResearch general practices in England: 981 practices 
      were used to develop the scores and a separate set of 328 practices were used to 
      validate the scores. 7.89 million patients aged 25-84 years were in the 
      derivation cohort and 2.67 million patients in the validation cohort. Patients 
      were free of cardiovascular disease and not prescribed statins at 
      baseline.Methods Cox proportional hazards models in the derivation cohort to 
      derive separate risk equations in men and women for evaluation at 10 years. Risk 
      factors considered included those already in QRISK2 (age, ethnicity, deprivation, 
      systolic blood pressure, body mass index, total cholesterol: high density 
      lipoprotein cholesterol ratio, smoking, family history of coronary heart disease 
      in a first degree relative aged less than 60 years, type 1 diabetes, type 2 
      diabetes, treated hypertension, rheumatoid arthritis, atrial fibrillation, 
      chronic kidney disease (stage 4 or 5)) and new risk factors (chronic kidney 
      disease (stage 3, 4, or 5), a measure of systolic blood pressure variability 
      (standard deviation of repeated measures), migraine, corticosteroids, systemic 
      lupus erythematosus (SLE), atypical antipsychotics, severe mental illness, and 
      HIV/AIDs). We also considered erectile dysfunction diagnosis or treatment in men. 
      Measures of calibration and discrimination were determined in the validation 
      cohort for men and women separately and for individual subgroups by age group, 
      ethnicity, and baseline disease status.Main outcome measures Incident 
      cardiovascular disease recorded on any of the following three linked data 
      sources: general practice, mortality, or hospital admission 
      records.Results 363 565 incident cases of cardiovascular disease were identified 
      in the derivation cohort during follow-up arising from 50.8 million person years 
      of observation. All new risk factors considered met the model inclusion criteria 
      except for HIV/AIDS, which was not statistically significant. The models had good 
      calibration and high levels of explained variation and discrimination. In women, 
      the algorithm explained 59.6% of the variation in time to diagnosis of 
      cardiovascular disease (R(2), with higher values indicating more variation), and 
      the D statistic was 2.48 and Harrell's C statistic was 0.88 (both measures of 
      discrimination, with higher values indicating better discrimination). The 
      corresponding values for men were 54.8%, 2.26, and 0.86. Overall performance of 
      the updated QRISK3 algorithms was similar to the QRISK2 
      algorithms.Conclusion Updated QRISK3 risk prediction models were developed and 
      validated. The inclusion of additional clinical variables in QRISK3 (chronic 
      kidney disease, a measure of systolic blood pressure variability (standard 
      deviation of repeated measures), migraine, corticosteroids, SLE, atypical 
      antipsychotics, severe mental illness, and erectile dysfunction) can help enable 
      doctors to identify those at most risk of heart disease and stroke.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://group.bmj.com/group/rights-licensing/permissions.
FAU - Hippisley-Cox, Julia
AU  - Hippisley-Cox J
AD  - Division of Primary Care, University Park, Nottingham NG2 7RD, UK 
      julia.hippisley-cox@nottingham.ac.uk.
FAU - Coupland, Carol
AU  - Coupland C
AD  - Division of Primary Care, University Park, Nottingham NG2 7RD, UK.
FAU - Brindle, Peter
AU  - Brindle P
AD  - Bristol Primary Clinical Commissioning Group and The National Institute for 
      Health Research Collaboration for Leadership in Applied Health Research and Care 
      West (NIHR CLAHRC West) at University Hospitals Bristol NHS Foundation Trust, UK, 
      UK.
LA  - eng
PT  - Journal Article
PT  - Validation Study
DEP - 20170523
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
RN  - 0 (Antipsychotic Agents)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - *Algorithms
MH  - Antipsychotic Agents
MH  - Atrial Fibrillation
MH  - Blood Pressure
MH  - *Cardiovascular Diseases/mortality
MH  - Diabetes Mellitus, Type 2
MH  - Erectile Dysfunction
MH  - Female
MH  - General Practice
MH  - Humans
MH  - Male
MH  - Mental Disorders
MH  - Middle Aged
MH  - Proportional Hazards Models
MH  - Prospective Studies
MH  - Renal Insufficiency, Chronic
MH  - Rheumatic Fever
MH  - Risk Assessment/*methods
MH  - Risk Factors
MH  - United Kingdom
PMC - PMC5441081
COIS- Competing interests: All authors have completed the ICMJE uniform disclosure form 
      at www.icmje.org/coi_disclosure.pdf and declare: JHC is professor of clinical 
      epidemiology at the University of Nottingham and codirector of QResearch a 
      not-for-profit organisation that is a joint partnership between the University of 
      Nottingham and Egton Medical Information Systems (leading commercial supplier of 
      IT for 55% of general practices in the UK). JHC is also a paid director of 
      ClinRisk, which produces open and closed source software to ensure the reliable 
      and updatable implementation of clinical risk algorithms within clinical computer 
      systems to help improve patient care. CC is associate professor of medical 
      statistics at the University of Nottingham and a paid consultant statistician for 
      ClinRisk. PB is partly funded by Health Research Collaboration for Leadership in 
      Applied Health Research and Care West (NIHR CLAHRC West), Bristol Clinical 
      Commissioning Group and the West of England Academic Health Science Network.. 
      This work and any views expressed within it are solely those of the authors and 
      not of any affiliated bodies or organisations.
EDAT- 2017/05/26 06:00
MHDA- 2017/06/20 06:00
PMCR- 2017/01/01
CRDT- 2017/05/25 06:00
PHST- 2017/05/25 06:00 [entrez]
PHST- 2017/05/26 06:00 [pubmed]
PHST- 2017/06/20 06:00 [medline]
PHST- 2017/01/01 00:00 [pmc-release]
AID - hipj036510 [pii]
AID - 10.1136/bmj.j2099 [doi]
PST - epublish
SO  - BMJ. 2017 May 23;357:j2099. doi: 10.1136/bmj.j2099.

PMID- 28483768
OWN - NLM
STAT- MEDLINE
DCOM- 20170821
LR  - 20240327
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Print)
IS  - 0003-4967 (Linking)
VI  - 76
IP  - 9
DP  - 2017 Sep
TI  - Serious adverse events and the risk of stroke in patients with rheumatoid 
      arthritis: results from the German RABBIT cohort.
PG  - 1583-1590
LID - 10.1136/annrheumdis-2017-211209 [doi]
AB  - OBJECTIVE: In the general population, the incidence of stroke is increased 
      following other serious events and hospitalisation. We investigated the impact of 
      serious adverse events on the risk of stroke in patients with rheumatoid 
      arthritis (RA), taking risk factors and treatment into account. METHODS: Using 
      data of the German biologics register RABBIT (Rheumatoid Arthritis: Observation 
      of Biologic Therapy) with 12354 patients with RA, incidence rates (IRs) and risk 
      factors for stroke were investigated using multi-state and Cox proportional 
      hazard models. In addition, in a nested case-control study, all patients with 
      stroke were matched 1:2 to patients with identical baseline risk profile and 
      analysed using a shared frailty model. RESULTS: During follow-up, 166 strokes 
      were reported. The overall IR was 3.2/1000 patient-years (PY) (95% CI 2.7 to 
      3.7). It was higher after a serious adverse event (IR: 9.0 (7.3 to 11.0)), 
      particularly within 30 days after the event (IR: 94.9 (72.6 to 121.9)). The 
      adjusted Cox model showed increased risks of age per 5 years (HR: 1.4 (1.3 to 
      1.5)), hyperlipoproteinaemia (HR: 1.6 (1.0 to 2.5)) and smoking (HR: 1.9 (1.3 to 
      2.6)). The risk decreased with better physical function (HR: 0.9 (0.8 to 0.96)). 
      In the case-control study, 163 patients were matched to 326 controls. Major risk 
      factors for stroke were untreated cardiovascular disease (HR: 3.3 (1.5 to 7.2)) 
      and serious infections (HR:4.4 (1.6 to 12.5)) or other serious adverse events 
      (HR: 2.6 (1.4 to 4.8)). CONCLUSIONS: Incident adverse events, in particular 
      serious infections, and insufficient treatment of cardiovascular diseases are 
      independent drivers of the risk of stroke. Physicians should be aware that 
      patients who experience a serious event are at increased risk of subsequent 
      stroke.
CI  - © Article author(s) (or their employer(s) unless otherwise stated in the text of 
      the article) 2017. All rights reserved. No commercial use is permitted unless 
      otherwise expressly granted.
FAU - Meissner, Y
AU  - Meissner Y
AD  - Epidemiology Unit, German Rheumatism Research Centre, Berlin, Germany.
FAU - Richter, A
AU  - Richter A
AD  - Epidemiology Unit, German Rheumatism Research Centre, Berlin, Germany.
FAU - Manger, B
AU  - Manger B
AD  - Department of Internal Medicine 3 - Rheumatology and Immunology, 
      Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum 
      Erlangen, Erlangen, Germany.
FAU - Tony, H P
AU  - Tony HP
AD  - Medizinische Klinik und Poliklinik II, University Medicine Würzburg, Würzburg, 
      Germany.
FAU - Wilden, E
AU  - Wilden E
AD  - Rheumatologist, Köln, Germany.
FAU - Listing, J
AU  - Listing J
AD  - Epidemiology Unit, German Rheumatism Research Centre, Berlin, Germany.
FAU - Zink, A
AU  - Zink A
AD  - Epidemiology Unit, German Rheumatism Research Centre, Berlin, Germany.
AD  - Charité University Medicine Berlin, Berlin, Germany.
FAU - Strangfeld, A
AU  - Strangfeld A
AD  - Epidemiology Unit, German Rheumatism Research Centre, Berlin, Germany.
LA  - eng
PT  - Journal Article
DEP - 20170508
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - 0 (Cyclohexanones)
RN  - 0 (Phenols)
RN  - 140670-90-2 (xochitloldione)
SB  - IM
MH  - Adult
MH  - Age Factors
MH  - Aged
MH  - Antirheumatic Agents/*adverse effects
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Biological Products
MH  - Cardiovascular Diseases/epidemiology/therapy
MH  - Case-Control Studies
MH  - Cyclohexanones
MH  - Female
MH  - Germany
MH  - Humans
MH  - Hypolipoproteinemias/epidemiology
MH  - Immunocompromised Host
MH  - Incidence
MH  - Infections/epidemiology/*etiology/immunology
MH  - Ischemic Attack, Transient/*epidemiology
MH  - Male
MH  - Middle Aged
MH  - Phenols
MH  - Proportional Hazards Models
MH  - *Registries
MH  - Risk Factors
MH  - Smoking/epidemiology
MH  - Stroke/*epidemiology
PMC - PMC5561376
OTO - NOTNLM
OT  - rheumatoid arthritis – stroke – cerebrovascular events - serious adverse events – 
      multi state models
COIS- Competing interests: YM: no competing interests. AR: honoraria from Pfizer. BM: 
      honoraria for lectures and consulting fees from Abbvie, BMS, MSD, Pfizer, Roche 
      and UCB outside the submitted work. HPT: personal fees from Abbvie, Astra-Zeneca, 
      BMS, Chugai, Janssen, Lilly, MSD, Novartis, Pfizer, Roche and Sanofi outside the 
      submitted work. EW: personal fees from Pfizer outside the submitted work. JL: 
      personal fees from Sandoz and Pfizer outside the submitted work. AZ: grants and 
      personal fees from AbbVie, BMS, MSD, Pfizer, Roche and UCB outside the submitted 
      work. AS: personal fees from BMS, MSD, Pfizer, Roche and Sanofi-Aventis outside 
      the submitted work.
EDAT- 2017/05/10 06:00
MHDA- 2017/08/22 06:00
PMCR- 2017/08/18
CRDT- 2017/05/10 06:00
PHST- 2017/01/26 00:00 [received]
PHST- 2017/03/30 00:00 [revised]
PHST- 2017/04/09 00:00 [accepted]
PHST- 2017/05/10 06:00 [pubmed]
PHST- 2017/08/22 06:00 [medline]
PHST- 2017/05/10 06:00 [entrez]
PHST- 2017/08/18 00:00 [pmc-release]
AID - annrheumdis-2017-211209 [pii]
AID - 10.1136/annrheumdis-2017-211209 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2017 Sep;76(9):1583-1590. doi: 10.1136/annrheumdis-2017-211209. 
      Epub 2017 May 8.

PMID- 28475479
OWN - NLM
STAT- MEDLINE
DCOM- 20180322
LR  - 20180322
IS  - 1743-1328 (Electronic)
IS  - 0161-6412 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Risk of hemorrhagic transformation after ischemic stroke in patients with 
      antiphospholipid antibody syndrome.
PG  - 477-483
LID - 10.1080/01616412.2017.1323382 [doi]
AB  - BACKGROUND AND PURPOSE: Several rheumatologic conditions including systemic lupus 
      erythematosus, antiphospholipid antibody (APS) syndrome, rheumatoid arthritis, 
      and scleroderma are known risk factors for stroke. The risk of hemorrhagic 
      transformation after an acute ischemic stroke (AIS) in these patients is not 
      known. METHODS: We queried the Nationwide Inpatient Sample (NIS) data between 
      2010 and 2012 with ICD 9 diagnostic codes for AIS. The primary outcome was the 
      development of hemorrhagic transformation. Multivariate predictors for 
      hemorrhagic transformation were identified with a logistic regression model. 
      Using SAS 9.2, Survey procedures were used to accommodate for hierarchical two 
      stage cluster design of NIS. RESULTS: APS (OR 2.57, 95% CI 1.14-5.81, p = 0.0228) 
      independently predicted risk of hemorrhagic transformation in multivariate 
      regression analysis. Similarly, in multivariate regression models for the outcome 
      variables of total charges of the hospitalization and length of stay (LOS), 
      patients with APS had the highest charges ($56,286, p = 0.0228) and LOS 
      (3.87 days, p = 0.0164) compared to other co-variates. Univariate analysis showed 
      increased mortality in the APS compared to the non-APS group (11.68% vs. 7.16%, 
      p = 0.0024). CONCLUSION: APS is an independent risk factor for hemorrhagic 
      transformation in both thrombolytic and non-thrombolytic treated patients. APS is 
      also associated with longer length and cost of hospital stay. Further research is 
      warranted to identify the unique risk factors in these patients to identify 
      strategies to reduce the risk of hemorrhagic transformation in this subgroup of 
      the population.
FAU - Mehta, Tapan
AU  - Mehta T
AD  - a Department of Neurology , University of Connecticut Health Center-Hartford 
      Hospital , Hartford , CT , USA.
FAU - Hussain, Mohammed
AU  - Hussain M
AD  - a Department of Neurology , University of Connecticut Health Center-Hartford 
      Hospital , Hartford , CT , USA.
FAU - Sheth, Khushboo
AU  - Sheth K
AD  - b Department of Internal Medicine , University of Connecticut , Farmington , CT , 
      USA.
FAU - Ding, Yuchuan
AU  - Ding Y
AD  - c Department of Neurosurgery , Wayne State University , Detroit , MI , USA.
FAU - McCullough, Louise D
AU  - McCullough LD
AD  - d Department of Neurology , McGovern Medical School, University of Texas Health 
      Science Center , Houston , TX , USA.
LA  - eng
PT  - Journal Article
DEP - 20170505
PL  - England
TA  - Neurol Res
JT  - Neurological research
JID - 7905298
RN  - 0 (Antibodies, Antiphospholipid)
RN  - 0 (Fibrinolytic Agents)
SB  - IM
MH  - Aged
MH  - Antibodies, Antiphospholipid/immunology
MH  - Antiphospholipid Syndrome/*complications/drug therapy
MH  - Brain Ischemia/complications/*drug therapy
MH  - Female
MH  - Fibrinolytic Agents/*therapeutic use
MH  - Hemorrhage/chemically induced/*drug therapy
MH  - Hospitalization/statistics & numerical data
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - Stroke/complications/*drug therapy
MH  - Thrombolytic Therapy/adverse effects
OTO - NOTNLM
OT  - Hemorrhagic transformation
OT  - antiphospholipid antibody
OT  - ischemic stroke
EDAT- 2017/05/06 06:00
MHDA- 2018/03/23 06:00
CRDT- 2017/05/06 06:00
PHST- 2017/05/06 06:00 [pubmed]
PHST- 2018/03/23 06:00 [medline]
PHST- 2017/05/06 06:00 [entrez]
AID - 10.1080/01616412.2017.1323382 [doi]
PST - ppublish
SO  - Neurol Res. 2017 Jun;39(6):477-483. doi: 10.1080/01616412.2017.1323382. Epub 2017 
      May 5.

PMID- 28339992
OWN - NLM
STAT- MEDLINE
DCOM- 20171004
LR  - 20220331
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Print)
IS  - 1462-0324 (Linking)
VI  - 56
IP  - 7
DP  - 2017 Jul 1
TI  - Rheumatoid arthritis-specific cardiovascular risk scores are not superior to 
      general risk scores: a validation analysis of patients from seven countries.
PG  - 1102-1110
LID - 10.1093/rheumatology/kex038 [doi]
AB  - OBJECTIVES: Cardiovascular disease (CVD) risk calculators developed for the 
      general population do not accurately predict CVD events in patients with RA. We 
      sought to externally validate risk calculators recommended for use in patients 
      with RA including the EULAR 1.5 multiplier, the Expanded Cardiovascular Risk 
      Prediction Score for RA (ERS-RA) and QRISK2. METHODS: Seven RA cohorts from UK, 
      Norway, Netherlands, USA, South Africa, Canada and Mexico were combined. Data on 
      baseline CVD risk factors, RA characteristics and CVD outcomes (including 
      myocardial infarction, ischaemic stroke and cardiovascular death) were collected 
      using standardized definitions. Performance of QRISK2, EULAR multiplier and 
      ERS-RA was compared with other risk calculators [American College of 
      Cardiology/American Heart Association (ACC/AHA), Framingham Adult Treatment Panel 
      III Framingham risk score-Adult Treatment Panel (FRS-ATP) and Reynolds Risk 
      Score] using c-statistics and net reclassification index. RESULTS: Among 1796 RA 
      patients without prior CVD [mean ( s . d .) age: 54.0 (14.0) years, 74% female], 
      100 developed CVD events during a mean follow-up of 6.9 years (12430 
      person-years). Estimated CVD risk by ERS-RA [mean ( s . d .) 8.8% (9.8%)] was 
      comparable to FRS-ATP [mean ( s . d .) 9.1% (8.3%)] and Reynolds [mean ( s . d .) 
      9.2% (12.2%)], but lower than ACC/AHA [mean ( s . d .) 9.8% (12.1%)]. QRISK2 
      substantially overestimated risk [mean ( s . d .) 15.5% (13.9%)]. Discrimination 
      was not improved for ERS-RA (c-statistic = 0.69), QRISK2 or EULAR multiplier 
      applied to ACC/AHA compared with ACC/AHA (c-statistic = 0.72 for all) or for 
      FRS-ATP (c-statistic = 0.75). The net reclassification index for ERS-RA was low 
      (-0.8% vs ACC/AHA and 2.3% vs FRS-ATP). CONCLUSION: The QRISK2, EULAR multiplier 
      and ERS-RA algorithms did not predict CVD risk more accurately in patients with 
      RA than CVD risk calculators developed for the general population.
CI  - © The Author 2017. Published by Oxford University Press on behalf of the British 
      Society for Rheumatology. All rights reserved. For Permissions, please email: 
      journals.permissions@oup.com
FAU - Crowson, Cynthia S
AU  - Crowson CS
AD  - Department of Health Sciences Research and Department of Medicine, Mayo Clinic, 
      Rochester, MN.
FAU - Gabriel, Sherine E
AU  - Gabriel SE
AD  - Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
FAU - Semb, Anne Grete
AU  - Semb AG
AD  - Department of Rheumatology, Diakonhjemmet Hospital, Preventive Cardio-Rheuma 
      Clinic, Oslo, Norway.
FAU - van Riel, Piet L C M
AU  - van Riel PLCM
AD  - Department of Rheumatic Diseases, Radboud University Nijmegen Medical Centre, 
      Nijmegen, Netherlands.
FAU - Karpouzas, George
AU  - Karpouzas G
AD  - Division of Rheumatology, Los Angeles Biomedical Research Institute, Harbor UCLA 
      Medical Center RHU, Torrance, CA, USA.
FAU - Dessein, Patrick H
AU  - Dessein PH
AD  - Cardiovascular Pathophysiology and Genomics Research Unit, University of 
      Witwatersrand, Johannesburg, South Africa.
AD  - Rheumatology Division, Universitair Ziekenhuis and Vrije Universiteit, Brussels, 
      Belgium.
FAU - Hitchon, Carol
AU  - Hitchon C
AD  - Department of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
FAU - Pascual-Ramos, Virginia
AU  - Pascual-Ramos V
AD  - Department of Immunology and Rheumatology, Instituto Nacional de Ciencias Médicas 
      y Nutrición Salvador Zubirán, Mexico City, México.
FAU - Kitas, George D
AU  - Kitas GD
AD  - Clinical Research, Unit, Dudley Group NHS Foundation Trust, West Midlands, UK.
CN  - Trans-Atlantic Cardiovascular Consortium for Rheumatoid Arthritis
LA  - eng
GR  - R01 AR046849/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Multicenter Study
PT  - Validation Study
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
SB  - IM
MH  - Adult
MH  - Age Distribution
MH  - Aged
MH  - *Algorithms
MH  - Arthritis, Rheumatoid/*diagnosis/*epidemiology
MH  - Canada
MH  - Cardiovascular Diseases/*diagnosis/*epidemiology
MH  - Cohort Studies
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Internationality
MH  - Male
MH  - Mexico/epidemiology
MH  - Middle Aged
MH  - Netherlands/epidemiology
MH  - Norway/epidemiology
MH  - Predictive Value of Tests
MH  - Prognosis
MH  - Risk Assessment
MH  - Severity of Illness Index
MH  - Sex Distribution
MH  - South Africa/epidemiology
MH  - United Kingdom/epidemiology
MH  - United States/epidemiology
PMC - PMC5850220
OTO - NOTNLM
OT  - cardiovascular disease
OT  - rheumatoid arthritis
OT  - risk assessment
OT  - risk prediction
FIR - Douglas, Karen
IR  - Douglas K
FIR - Sandoo, Aamer
IR  - Sandoo A
FIR - Rollefstad, Silvia
IR  - Rollefstad S
FIR - Ikdahl, Eirik
IR  - Ikdahl E
FIR - Kvien, Tore K
IR  - Kvien TK
FIR - Arts, Elke
IR  - Arts E
FIR - Fransen, Jaap
IR  - Fransen J
FIR - Tsang, Linda
IR  - Tsang L
FIR - El-Gabalawy, Hani
IR  - El-Gabalawy H
FIR - Yáñez, Irazú Contreras
IR  - Yáñez IC
FIR - Matteson, Eric L
IR  - Matteson EL
FIR - Rantapää-Dahlqvist, Solbritt
IR  - Rantapää-Dahlqvist S
FIR - Wållberg-Jonsson, Solveig
IR  - Wållberg-Jonsson S
FIR - Innala, Lena
IR  - Innala L
FIR - Sfikakis, Petros P
IR  - Sfikakis PP
FIR - Zampeli, Evi
IR  - Zampeli E
FIR - Gonzalez-Gay, Miguel
IR  - Gonzalez-Gay MA
FIR - Corrales, Alfonso
IR  - Corrales A
FIR - van de Laar, Mart
IR  - van de Laar M
FIR - Vonkeman, Harald
IR  - Vonkeman H
FIR - Meek, Inger
IR  - Meek I
FIR - Husni, Elaine
IR  - Husni E
FIR - Overman, Robert
IR  - Overman R
FIR - Colunga, Iris
IR  - Colunga I
FIR - Galarza, Dionicio
IR  - Galarza D
EDAT- 2017/03/25 06:00
MHDA- 2017/10/05 06:00
PMCR- 2018/07/01
CRDT- 2017/03/25 06:00
PHST- 2016/09/21 00:00 [received]
PHST- 2017/03/25 06:00 [pubmed]
PHST- 2017/10/05 06:00 [medline]
PHST- 2017/03/25 06:00 [entrez]
PHST- 2018/07/01 00:00 [pmc-release]
AID - 3063745 [pii]
AID - kex038 [pii]
AID - 10.1093/rheumatology/kex038 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2017 Jul 1;56(7):1102-1110. doi: 
      10.1093/rheumatology/kex038.

PMID- 28337386
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2160-200X (Print)
IS  - 2160-200X (Electronic)
IS  - 2160-200X (Linking)
VI  - 7
IP  - 1
DP  - 2017
TI  - Long-term clinical outcomes of patients with rheumatoid arthritis and concomitant 
      coronary artery disease.
PG  - 9-18
AB  - BACKGROUND: Rheumatoid arthritis (RA) is associated with high morbidity and 
      mortality predominately due to increased cardiovascular risk. Few reports are 
      available regarding the management of coronary artery disease (CAD) in RA 
      patients and the long-term clinical outcomes after coronary revascularization. 
      METHODS AND RESULTS: All consecutive patients with RA were identified by 
      retrospective review at a rheumatology tertiary center in Milan, Italy between 
      2001 and 2013. RA patients affected by significant CAD (RA-CAD+) were 
      prospectively followed for major adverse cardiovascular and cerebrovascular 
      events (MACCE) after percutaneous coronary revascularization (RA-PCI), coronary 
      artery bypass grafting (RA-CABG) or medical therapy (RA-MT). Among 936 patients 
      with RA, the presence of clinically significant CAD was found in 5.6% (53 
      patients, RA-CAD+). Of these, 32 patients (60%) underwent PCI (RA-PCI), 10 
      patients (19%) underwent CABG (RA-CABG) and 11 patients (21%) treated with MT 
      (RA-MT). After a mean follow-up of 9±7 years, the rate of MACCE was 56% in RA-PCI 
      patients, 50% in RA-CABG and 27% in RA-MT patients (P=0.184). The high MACCE rate 
      was mainly driven by repeat coronary revascularization (47%) in the RA-PCI group 
      and high rate of strokes (30%) in RA-CABG patients. CONCLUSION: In patients with 
      rheumatoid arthritis and concomitant coronary artery disease (RA-CAD+), we 
      observed at long-term follow-up a high MACCE rate, predominantly in those who 
      underwent coronary revascularization.
FAU - Spartera, Marco
AU  - Spartera M
AD  - Department of Cardiovascular, San Raffaele Scientific Institute Milan, Italy.
FAU - Godino, Cosmo
AU  - Godino C
AD  - Department of Cardiovascular, San Raffaele Scientific Institute Milan, Italy.
FAU - Baldissera, Elena
AU  - Baldissera E
AD  - Unit of Internal Medicine and Clinical Immunology, San Raffaele Scientific 
      Institute Milan, Italy.
FAU - Campochiaro, Corrado
AU  - Campochiaro C
AD  - Unit of Internal Medicine and Clinical Immunology, San Raffaele Scientific 
      Institute Milan, Italy.
FAU - La Spina, Ketty
AU  - La Spina K
AD  - Department of Cardiovascular, San Raffaele Scientific Institute Milan, Italy.
FAU - Aiello, Patrizia
AU  - Aiello P
AD  - Unit of Internal Medicine and Clinical Immunology, San Raffaele Scientific 
      Institute Milan, Italy.
FAU - Salerno, Anna
AU  - Salerno A
AD  - Department of Cardiovascular, San Raffaele Scientific Institute Milan, Italy.
FAU - Cera, Michela
AU  - Cera M
AD  - Department of Cardiovascular, San Raffaele Scientific Institute Milan, Italy.
FAU - Magni, Valeria
AU  - Magni V
AD  - Department of Cardiovascular, San Raffaele Scientific Institute Milan, Italy.
FAU - Jabbour, Richard J
AU  - Jabbour RJ
AD  - Imperial College London London, UK.
FAU - Dagna, Lorenzo
AU  - Dagna L
AD  - Unit of Internal Medicine and Clinical Immunology, San Raffaele Scientific 
      Institute Milan, Italy.
FAU - Tresoldi, Moreno
AU  - Tresoldi M
AD  - Unit of Internal Medicine and Clinical Immunology, San Raffaele Scientific 
      Institute Milan, Italy.
FAU - Cappelletti, Alberto
AU  - Cappelletti A
AD  - Department of Cardiovascular, San Raffaele Scientific Institute Milan, Italy.
FAU - Alfieri, Ottavio
AU  - Alfieri O
AD  - Department of Cardiovascular, San Raffaele Scientific Institute Milan, Italy.
FAU - Colombo, Antonio
AU  - Colombo A
AD  - Department of Cardiovascular, San Raffaele Scientific InstituteMilan, Italy; 
      EMO-GVM Centro Cuore ColumbusMilan, Italy.
FAU - Sabbadini, Maria Grazia
AU  - Sabbadini MG
AD  - Unit of Internal Medicine and Clinical Immunology, San Raffaele Scientific 
      Institute Milan, Italy.
FAU - Margonato, Alberto
AU  - Margonato A
AD  - Department of Cardiovascular, San Raffaele Scientific Institute Milan, Italy.
LA  - eng
PT  - Journal Article
DEP - 20170215
PL  - United States
TA  - Am J Cardiovasc Dis
JT  - American journal of cardiovascular disease
JID - 101569582
PMC - PMC5344967
OTO - NOTNLM
OT  - Coronary artery disease
OT  - coronary artery bypass grafting
OT  - percutaneous coronary intervention
OT  - rheumatoid arthritis
EDAT- 2017/03/25 06:00
MHDA- 2017/03/25 06:01
PMCR- 2017/02/15
CRDT- 2017/03/25 06:00
PHST- 2016/09/07 00:00 [received]
PHST- 2017/01/22 00:00 [accepted]
PHST- 2017/03/25 06:00 [entrez]
PHST- 2017/03/25 06:00 [pubmed]
PHST- 2017/03/25 06:01 [medline]
PHST- 2017/02/15 00:00 [pmc-release]
PST - epublish
SO  - Am J Cardiovasc Dis. 2017 Feb 15;7(1):9-18. eCollection 2017.

PMID- 28290854
OWN - NLM
STAT- MEDLINE
DCOM- 20180824
LR  - 20191113
IS  - 0022-9040 (Print)
IS  - 0022-9040 (Linking)
VI  - 56
IP  - 6
DP  - 2016 Jun
TI  - [Cardiovascular Complications of Rheumatoid Arthritis: Prevalence and 
      Pathogenesis].
PG  - 89-95
AB  - Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with high 
      risk of cardiovascular events. Among main causes of death in RA are: myocardial 
      infarction, cerebrovascular accident, sudden cardiac death, which are determined 
      by the early development and rapid progression of atherosclerotic vascular 
      lesions. According to studies high risk of cardiovascular events is not explained 
      by only classical risk factors. It is assumed that there are additional 
      mechanisms of development of adverse outcomes such as systemic inflammation, 
      increased arterial stiffness, and endothelial dysfunction. In this literature 
      review we present various risk factors of cardiovascular events in patients with 
      RA and their relation to RA pathogenesis.
FAU - Krougly, L B
AU  - Krougly LB
AD  - Myasnikov Clinical Cardiology Institute, Russian Cardiology Research Center, 
      Moscow, Russia.
AD  - V.A. Nasonova Research Institute of Rheumatology, Moscow, Russia.
FAU - Fomicheva, O A
AU  - Fomicheva OA
AD  - Myasnikov Clinical Cardiology Institute, Russian Cardiology Research Center, 
      Moscow, Russia.
AD  - V.A. Nasonova Research Institute of Rheumatology, Moscow, Russia.
FAU - Karpov, Yu A
AU  - Karpov YA
AD  - Myasnikov Clinical Cardiology Institute, Russian Cardiology Research Center, 
      Moscow, Russia.
AD  - V.A. Nasonova Research Institute of Rheumatology, Moscow, Russia.
FAU - Popkova, T V
AU  - Popkova TV
AD  - Myasnikov Clinical Cardiology Institute, Russian Cardiology Research Center, 
      Moscow, Russia.
AD  - V.A. Nasonova Research Institute of Rheumatology, Moscow, Russia.
FAU - Novikova, D S
AU  - Novikova DS
AD  - Myasnikov Clinical Cardiology Institute, Russian Cardiology Research Center, 
      Moscow, Russia.
AD  - V.A. Nasonova Research Institute of Rheumatology, Moscow, Russia.
FAU - Nasonov, E L
AU  - Nasonov EL
AD  - Myasnikov Clinical Cardiology Institute, Russian Cardiology Research Center, 
      Moscow, Russia.
AD  - V.A. Nasonova Research Institute of Rheumatology, Moscow, Russia.
LA  - rus
PT  - Journal Article
PT  - Review
PL  - Russia (Federation)
TA  - Kardiologiia
JT  - Kardiologiia
JID - 0376351
SB  - IM
MH  - Arthritis, Rheumatoid/*complications
MH  - *Cardiovascular Diseases/epidemiology/etiology
MH  - Humans
MH  - Prevalence
MH  - Risk Assessment
MH  - Risk Factors
OTO - NOTNLM
OT  - atherosclerosis
OT  - cardiology
OT  - cardiovascular complications
OT  - myocardial infarction
OT  - rheumatoid arthritis
OT  - rheumatology
OT  - stroke
EDAT- 2017/03/16 06:00
MHDA- 2018/08/25 06:00
CRDT- 2017/03/15 06:00
PHST- 2017/03/15 06:00 [entrez]
PHST- 2017/03/16 06:00 [pubmed]
PHST- 2018/08/25 06:00 [medline]
AID - 10.18565/cardio.2016.6.89-95 [doi]
PST - ppublish
SO  - Kardiologiia. 2016 Jun;56(6):89-95. doi: 10.18565/cardio.2016.6.89-95.

PMID- 28250138
OWN - NLM
STAT- MEDLINE
DCOM- 20180329
LR  - 20220408
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
VI  - 44
IP  - 4
DP  - 2017 Apr
TI  - Primary Prevention of Myocardial Infarction in Rheumatoid Arthritis Using 
      Aspirin: A Case-crossover Study and a Propensity Score-matched Cohort Study.
PG  - 418-424
LID - 10.3899/jrheum.160930 [doi]
AB  - OBJECTIVE: Subjects with rheumatoid arthritis (RA) are at higher risk of 
      developing cardiovascular disease, which is their leading cause of death. 
      Conflicting evidence exists regarding the efficacy of aspirin (ASA) as primary 
      prevention. We evaluated whether a protective association exists between ASA and 
      myocardial infarction (MI) in RA subjects. METHODS: In the United Kingdom, 
      persons age ≥ 60 years receive free ASA by prescription and 75% of use is by 
      prescription. Subjects ≥ 60 years with RA in the population-based The Health 
      Improvement Network database constituted our study population. We excluded 
      patients with history of MI, angina, stroke, peripheral vascular disease, or 
      coronary artery procedures. Our main outcome was the occurrence of fatal and 
      nonfatal MI. We performed a case-crossover study with each subject contributing a 
      hazard period and a control period 90 days prior to the MI. In addition, to 
      minimize confounding by indication, a propensity score (PS)-matched cohort study 
      was performed, considering all patients with RA with an incident prescription of 
      low-dose ASA as our exposed group. RESULTS: We did not find a protective effect 
      in the case-crossover study (OR 1.83, 95% CI 0.71-4.71), with 55 subjects exposed 
      in the hazard period and 44 in the control period. Similarly, among 1836 subjects 
      included in the PS-matched cohort study (918 ASA users and 918 ASA non-users), we 
      did not find a protective effect of low ASA on MI (HR 1.39, 95% CI 0.87-2.23). 
      CONCLUSION: We did not find a protective effect of ASA on MI in patients with RA 
      when used as primary prophylaxis.
FAU - Durán, Josefina
AU  - Durán J
AD  - From the Rheumatology Department, Pontificia Universidad Católica de Chile School 
      of Medicine, Santiago, Chile; Clinical Epidemiology Unit, Boston University 
      School of Medicine, Boston, Massachusetts, USA; Arthritis Research UK 
      Epidemiology Unit, University of Manchester; Manchester UK National Institute for 
      Health Research Biomedical Research Unit, Manchester, UK. jgduran@uc.cl.
AD  - J. Durán, MD, MSc, Rheumatology Department, Pontificia Universidad Católica de 
      Chile School of Medicine, and Clinical Epidemiology Unit, Boston University 
      School of Medicine; C. Peloquin, MPH, Clinical Epidemiology Unit, Boston 
      University School of Medicine; Y. Zhang, DSc, Clinical Epidemiology Unit, Boston 
      University School of Medicine; D.T. Felson, MD, MPH, Clinical Epidemiology Unit, 
      Boston University School of Medicine, and Arthritis Research UK Epidemiology 
      Unit, University of Manchester, and Manchester UK National Institute for Health 
      Research Biomedical Research Unit. jgduran@uc.cl.
FAU - Peloquin, Christine
AU  - Peloquin C
AD  - From the Rheumatology Department, Pontificia Universidad Católica de Chile School 
      of Medicine, Santiago, Chile; Clinical Epidemiology Unit, Boston University 
      School of Medicine, Boston, Massachusetts, USA; Arthritis Research UK 
      Epidemiology Unit, University of Manchester; Manchester UK National Institute for 
      Health Research Biomedical Research Unit, Manchester, UK.
AD  - J. Durán, MD, MSc, Rheumatology Department, Pontificia Universidad Católica de 
      Chile School of Medicine, and Clinical Epidemiology Unit, Boston University 
      School of Medicine; C. Peloquin, MPH, Clinical Epidemiology Unit, Boston 
      University School of Medicine; Y. Zhang, DSc, Clinical Epidemiology Unit, Boston 
      University School of Medicine; D.T. Felson, MD, MPH, Clinical Epidemiology Unit, 
      Boston University School of Medicine, and Arthritis Research UK Epidemiology 
      Unit, University of Manchester, and Manchester UK National Institute for Health 
      Research Biomedical Research Unit.
FAU - Zhang, Yuqing
AU  - Zhang Y
AD  - From the Rheumatology Department, Pontificia Universidad Católica de Chile School 
      of Medicine, Santiago, Chile; Clinical Epidemiology Unit, Boston University 
      School of Medicine, Boston, Massachusetts, USA; Arthritis Research UK 
      Epidemiology Unit, University of Manchester; Manchester UK National Institute for 
      Health Research Biomedical Research Unit, Manchester, UK.
AD  - J. Durán, MD, MSc, Rheumatology Department, Pontificia Universidad Católica de 
      Chile School of Medicine, and Clinical Epidemiology Unit, Boston University 
      School of Medicine; C. Peloquin, MPH, Clinical Epidemiology Unit, Boston 
      University School of Medicine; Y. Zhang, DSc, Clinical Epidemiology Unit, Boston 
      University School of Medicine; D.T. Felson, MD, MPH, Clinical Epidemiology Unit, 
      Boston University School of Medicine, and Arthritis Research UK Epidemiology 
      Unit, University of Manchester, and Manchester UK National Institute for Health 
      Research Biomedical Research Unit.
FAU - Felson, David T
AU  - Felson DT
AD  - From the Rheumatology Department, Pontificia Universidad Católica de Chile School 
      of Medicine, Santiago, Chile; Clinical Epidemiology Unit, Boston University 
      School of Medicine, Boston, Massachusetts, USA; Arthritis Research UK 
      Epidemiology Unit, University of Manchester; Manchester UK National Institute for 
      Health Research Biomedical Research Unit, Manchester, UK.
AD  - J. Durán, MD, MSc, Rheumatology Department, Pontificia Universidad Católica de 
      Chile School of Medicine, and Clinical Epidemiology Unit, Boston University 
      School of Medicine; C. Peloquin, MPH, Clinical Epidemiology Unit, Boston 
      University School of Medicine; Y. Zhang, DSc, Clinical Epidemiology Unit, Boston 
      University School of Medicine; D.T. Felson, MD, MPH, Clinical Epidemiology Unit, 
      Boston University School of Medicine, and Arthritis Research UK Epidemiology 
      Unit, University of Manchester, and Manchester UK National Institute for Health 
      Research Biomedical Research Unit.
LA  - eng
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20170301
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*complications
MH  - Aspirin/*therapeutic use
MH  - Cross-Over Studies
MH  - Databases, Factual
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/complications/*prevention & control
MH  - Platelet Aggregation Inhibitors/*therapeutic use
MH  - Primary Prevention
MH  - Treatment Outcome
MH  - United Kingdom
OTO - NOTNLM
OT  - ASPIRIN
OT  - CARDIOVASCULAR DISEASE
OT  - MYOCARDIAL INFARCTION
OT  - PRIMARY PREVENTION
OT  - PROPHYLAXIS
OT  - RHEUMATOID ARTHRITIS
EDAT- 2017/03/03 06:00
MHDA- 2018/03/30 06:00
CRDT- 2017/03/03 06:00
PHST- 2017/01/04 00:00 [accepted]
PHST- 2017/03/03 06:00 [pubmed]
PHST- 2018/03/30 06:00 [medline]
PHST- 2017/03/03 06:00 [entrez]
AID - jrheum.160930 [pii]
AID - 10.3899/jrheum.160930 [doi]
PST - ppublish
SO  - J Rheumatol. 2017 Apr;44(4):418-424. doi: 10.3899/jrheum.160930. Epub 2017 Mar 1.

PMID- 28245350
OWN - NLM
STAT- MEDLINE
DCOM- 20170817
LR  - 20220318
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Print)
IS  - 2326-5191 (Linking)
VI  - 69
IP  - 6
DP  - 2017 Jun
TI  - Cardiovascular Safety of Tocilizumab Versus Tumor Necrosis Factor Inhibitors in 
      Patients With Rheumatoid Arthritis: A Multi-Database Cohort Study.
PG  - 1154-1164
LID - 10.1002/art.40084 [doi]
AB  - OBJECTIVE: While tocilizumab (TCZ) is known to increase low-density lipoprotein 
      (LDL) cholesterol levels, it is unclear whether TCZ increases cardiovascular risk 
      in patients with rheumatoid arthritis (RA). This study was undertaken to compare 
      the cardiovascular risk associated with receiving TCZ versus tumor necrosis 
      factor inhibitors (TNFi). METHODS: To examine comparative cardiovascular safety, 
      we conducted a cohort study of RA patients who newly started TCZ or TNFi using 
      claims data from Medicare, IMS PharMetrics, and MarketScan. All patients were 
      required to have previously used a different TNFi, abatacept, or tofacitinib. The 
      primary outcome measure was a composite cardiovascular end point of 
      hospitalization for myocardial infarction or stroke. TCZ initiators were 
      propensity score matched to TNFi initiators with a variable ratio of 1:3 within 
      each database, controlling for >65 baseline characteristics. A fixed-effects 
      model combined database-specific hazard ratios (HRs). RESULTS: We included 9,218 
      TCZ initiators propensity score matched to 18,810 TNFi initiators across all 3 
      databases. The mean age was 72 years in Medicare, 51 in PharMetrics, and 53 in 
      MarketScan. Cardiovascular disease was present at baseline in 14.3% of TCZ 
      initiators and 13.5% of TNFi initiators. During the study period (mean ± SD 
      0.9 ± 0.7 years; maximum 4.5 years), 125 composite cardiovascular events 
      occurred, resulting in an incidence rate of 0.52 per 100 person-years for TCZ 
      initiators and 0.59 per 100 person-years for TNFi initiators. The risk of 
      cardiovascular events associated with TCZ use versus TNFi use was similar across 
      all 3 databases, with a combined HR of 0.84 (95% confidence interval 0.56-1.26). 
      CONCLUSION: This multi-database population-based cohort study showed no evidence 
      of an increased cardiovascular risk among RA patients who switched from a 
      different biologic drug or tofacitinib to TCZ versus to a TNFi.
CI  - © 2017, The Authors. Arthritis & Rheumatology published by Wiley Periodicals, 
      Inc. on behalf of American College of Rheumatology.
FAU - Kim, Seoyoung C
AU  - Kim SC
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Rogers, James R
AU  - Rogers JR
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Gale, Sara
AU  - Gale S
AD  - Genentech, South San Francisco, California.
FAU - Klearman, Micki
AU  - Klearman M
AD  - Genentech, South San Francisco, California.
FAU - Sarsour, Khaled
AU  - Sarsour K
AD  - Genentech, South San Francisco, California.
FAU - Schneeweiss, Sebastian
AU  - Schneeweiss S
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170428
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - I031V2H011 (tocilizumab)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antibodies, Monoclonal, Humanized/*adverse effects
MH  - Antirheumatic Agents/*adverse effects
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Cardiovascular Diseases/chemically induced/*epidemiology
MH  - Cohort Studies
MH  - Databases, Factual
MH  - Drug Substitution/adverse effects
MH  - Female
MH  - Hospitalization/statistics & numerical data
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/chemically induced/epidemiology
MH  - Propensity Score
MH  - Proportional Hazards Models
MH  - Risk Factors
MH  - Stroke/chemically induced/epidemiology
MH  - Treatment Outcome
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
PMC - PMC5573926
EDAT- 2017/03/01 06:00
MHDA- 2017/08/18 06:00
PMCR- 2017/08/29
CRDT- 2017/03/01 06:00
PHST- 2016/09/07 00:00 [received]
PHST- 2017/02/23 00:00 [accepted]
PHST- 2017/03/01 06:00 [pubmed]
PHST- 2017/08/18 06:00 [medline]
PHST- 2017/03/01 06:00 [entrez]
PHST- 2017/08/29 00:00 [pmc-release]
AID - ART40084 [pii]
AID - 10.1002/art.40084 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2017 Jun;69(6):1154-1164. doi: 10.1002/art.40084. Epub 2017 
      Apr 28.

PMID- 28229293
OWN - NLM
STAT- MEDLINE
DCOM- 20170526
LR  - 20220321
IS  - 1434-4726 (Electronic)
IS  - 0937-4477 (Linking)
VI  - 274
IP  - 5
DP  - 2017 May
TI  - Age-related hearing loss and dementia: a 10-year national population-based study.
PG  - 2327-2334
LID - 10.1007/s00405-017-4471-5 [doi]
AB  - Age-related hearing loss (ARHL) is postulated to affect dementia. Our study aims 
      to investigate the relationship between ARHL and the prevalence, and 10-year 
      incidence of dementia in the Taiwan National Health Insurance Research Database 
      (NHIRD). We selected patients diagnosed with ARHL from the NHIRD. A comparison 
      cohort comprising of patients without ARHL was frequency-matched by age, sex, and 
      co-morbidities, and the occurrence of dementia was evaluated in both cohorts. The 
      ARHL cohort consisted of 4108 patients with ARHL and the control cohort consisted 
      of 4013 frequency-matched patients without ARHL. The incidence of dementia 
      [hazard ratio (HR), 1.30; 95% confidence interval (CI 1.14-1.49); P = 0.002] was 
      higher among ARHL patients. Cox models showed that being female (HR, 1.34; 95% CI 
      1.07-1.68), as well as having co-morbidities, including chronic liver disease and 
      cirrhosis, rheumatoid arthritis, hypertension, diabetes mellitus, stroke, head 
      injury, chronic kidney disease, coronary artery disease, alcohol 
      abuse/dependence, and tobacco abuse/dependence (HR, 1.27; 95% CI 1.11-1.45), were 
      independent risk factors for dementia in ARHL patients. We found ARHL may be one 
      of the early characteristics of dementia, and patients with hearing loss were at 
      a higher risk of subsequent dementia. Clinicians should be more sensitive to 
      dementia symptoms within the first 2 years following ARHL diagnosis. Further 
      clinical studies of the relationship between dementia and ARHL may be necessary.
FAU - Su, Peijen
AU  - Su P
AD  - Department of Audiology and Speech-Language Pathology, Mackay Medical College, 
      Taipei, Taiwan, Republic of China.
AD  - Department of Family Medicine, Mackay Memorial Hospital, Taipei, Taiwan, Republic 
      of China.
FAU - Hsu, Chih-Chao
AU  - Hsu CC
AD  - Department of Psychiatry, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, 
      Republic of China.
FAU - Lin, Hung-Ching
AU  - Lin HC
AD  - Department of Audiology and Speech-Language Pathology, Mackay Medical College, 
      Taipei, Taiwan, Republic of China.
AD  - Department of Otorhinolaryngology and Head and Neck Surgery, Mackay Medical 
      Hospital, Taipei, Taiwan, Republic of China.
FAU - Huang, Wei-Shin
AU  - Huang WS
AD  - Department of Family Medicine, Mackay Memorial Hospital, Taipei, Taiwan, Republic 
      of China.
FAU - Yang, Tsung-Lin
AU  - Yang TL
AD  - Department of Otolaryngology, National Taiwan University Hospital and National 
      Taiwan University College of Medicine, Taipei, Taiwan, Republic of China.
FAU - Hsu, Wei-Ting
AU  - Hsu WT
AD  - Department of Otorhinolaryngology and Head and Neck Surgery, Mackay Medical 
      Hospital, Taipei, Taiwan, Republic of China.
FAU - Lin, Cheng-Li
AU  - Lin CL
AD  - Management Office for Health Data, China Medical University Hospital, Taichung, 
      Taiwan, Republic of China.
FAU - Hsu, Chung-Yi
AU  - Hsu CY
AD  - Graduate Institute of Clinical Medical Sciences, Center College of Medicine, 
      China Medical University, Taichung, Taiwan, Republic of China.
FAU - Chang, Kuang-Hsi
AU  - Chang KH
AD  - Management Office for Health Data, China Medical University Hospital, Taichung, 
      Taiwan, Republic of China. s76881072@yahoo.com.tw.
AD  - Department of Public Health, China Medical University, Taichung, Taiwan, Republic 
      of China. s76881072@yahoo.com.tw.
FAU - Hsu, Yi-Chao
AU  - Hsu YC
AD  - Institute of Biomedical Sciences, Mackay Medical College, No.46, Sec. 3, 
      Zhongzheng Rd., Sanzhi Dist., New Taipei City, 252, Taiwan, Republic of China. 
      hsuyc@mmc.edu.tw.
LA  - eng
PT  - Journal Article
DEP - 20170222
PL  - Germany
TA  - Eur Arch Otorhinolaryngol
JT  - European archives of oto-rhino-laryngology : official journal of the European 
      Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the 
      German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
JID - 9002937
SB  - IM
MH  - Aged
MH  - Cohort Studies
MH  - Comorbidity
MH  - *Dementia/diagnosis/epidemiology
MH  - Diabetes Mellitus/epidemiology
MH  - Female
MH  - Humans
MH  - Hypertension/epidemiology
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - *Presbycusis/diagnosis/epidemiology
MH  - Prevalence
MH  - Proportional Hazards Models
MH  - Risk Factors
MH  - Taiwan/epidemiology
OTO - NOTNLM
OT  - Age-related hearing loss
OT  - Dementia
OT  - NHIRD
OT  - Presbycusis
OT  - Sensory hearing loss
EDAT- 2017/02/24 06:00
MHDA- 2017/05/27 06:00
CRDT- 2017/02/24 06:00
PHST- 2016/08/13 00:00 [received]
PHST- 2017/01/18 00:00 [accepted]
PHST- 2017/02/24 06:00 [pubmed]
PHST- 2017/05/27 06:00 [medline]
PHST- 2017/02/24 06:00 [entrez]
AID - 10.1007/s00405-017-4471-5 [pii]
AID - 10.1007/s00405-017-4471-5 [doi]
PST - ppublish
SO  - Eur Arch Otorhinolaryngol. 2017 May;274(5):2327-2334. doi: 
      10.1007/s00405-017-4471-5. Epub 2017 Feb 22.

PMID- 28065772
OWN - NLM
STAT- MEDLINE
DCOM- 20170822
LR  - 20220317
IS  - 1555-7162 (Electronic)
IS  - 0002-9343 (Print)
IS  - 0002-9343 (Linking)
VI  - 130
IP  - 6
DP  - 2017 Jun
TI  - Multimorbidity in Middle-Aged Adults with Cerebral Palsy.
PG  - 744.e9-744.e15
LID - S0002-9343(16)31304-3 [pii]
LID - 10.1016/j.amjmed.2016.11.044 [doi]
AB  - OBJECTIVE: Individuals with cerebral palsy have less lean body mass, greater 
      relative adiposity, and lower fitness and physical activity participation, and 
      yet the prevalence of age-related multimorbidity in this population has yet to be 
      established. The study objective was to examine the prevalence of 
      lifestyle-related chronic conditions and multimorbidity in a sample of 
      middle-aged adults with cerebral palsy. METHODS: A clinic-based sample of 
      middle-aged adults with cerebral palsy was examined using Electronic Medical 
      Records Search Engine software. Our cohort included 435 individuals aged 40 to 60 
      years, with an International Classification of Diseases, Clinical Modification, 
      9th and 10th Revisions Diagnosis Code for cerebral palsy. Prevalence of 12 
      chronic conditions was evaluated, including existing diagnoses or historical 
      record of osteopenia/osteoporosis, myocardial infarction, stroke, coronary artery 
      disease, impaired glucose tolerance/type 2 diabetes, other cardiovascular 
      conditions, rheumatoid arthritis, osteoarthritis, asthma, emphysema, 
      prehypertension/hypertension, and hyperlipidemia. Multivariate logistic models 
      were used to estimate multimorbidity (ie, ≥2 chronic conditions), adjusting for 
      age, sex, smoking status, obesity, and Gross Motor Function Classification System 
      (GMFCS). RESULTS: There were 137 unique multimorbidity combinations. 
      Multimorbidity was significantly more prevalent among obese versus nonobese 
      individuals for both GMFCS I-III (75.8% vs 53.6%) and GMFCS IV-V (79.0% vs 
      64.2%), but was also significantly higher in nonobese individuals with GMFCS IV-V 
      (64.2%) compared with nonobese individuals with GMFCS I-III (53.6%). Both the 
      obesity status (odds ratio, 2.20; 95% confidence interval, 1.32-2.79) and the 
      GMFCS IV-V category (odds ratio, 1.81; 95% confidence interval, 1.32-3.68) were 
      independently associated with multimorbidity. CONCLUSIONS: Middle-aged adults 
      with cerebral palsy have high estimates of multimorbidity; both obesity and 
      higher GMFCS levels are independently associated with greater risk.
CI  - Copyright © 2017 Elsevier Inc. All rights reserved.
FAU - Cremer, Nicole
AU  - Cremer N
AD  - University of Michigan, University of Michigan Medical School, Ann Arbor.
FAU - Hurvitz, Edward A
AU  - Hurvitz EA
AD  - Department of Physical Medicine & Rehabilitation, University of Michigan, Ann 
      Arbor.
FAU - Peterson, Mark D
AU  - Peterson MD
AD  - Department of Physical Medicine & Rehabilitation, University of Michigan, Ann 
      Arbor. Electronic address: mdpeterz@med.umich.edu.
LA  - eng
GR  - K01 HD074706/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20170105
PL  - United States
TA  - Am J Med
JT  - The American journal of medicine
JID - 0267200
SB  - IM
MH  - Adult
MH  - Asthma/epidemiology
MH  - Bone Diseases, Metabolic/epidemiology
MH  - Cardiovascular Diseases/epidemiology
MH  - Cerebral Palsy/*epidemiology
MH  - Comorbidity
MH  - Cross-Sectional Studies
MH  - Humans
MH  - Middle Aged
MH  - Obesity/epidemiology
MH  - Osteoarthritis/epidemiology
MH  - Osteoporosis/epidemiology
MH  - Prevalence
MH  - Sex Factors
PMC - PMC5502778
MID - NIHMS873075
OTO - NOTNLM
OT  - Cerebral palsy
OT  - Diabetes
OT  - Hypertension
OT  - Multimorbidity
OT  - Obesity
OT  - Osteoporosis
COIS- Conflict of Interest: Nicole Cremer has no financial disclosures. Edward A. 
      Hurvitz has no financial disclosures. Mark D. Peterson has no financial 
      disclosures.
EDAT- 2017/01/10 06:00
MHDA- 2017/08/23 06:00
PMCR- 2017/07/10
CRDT- 2017/01/10 06:00
PHST- 2016/10/26 00:00 [received]
PHST- 2016/11/22 00:00 [revised]
PHST- 2016/11/30 00:00 [accepted]
PHST- 2017/01/10 06:00 [pubmed]
PHST- 2017/08/23 06:00 [medline]
PHST- 2017/01/10 06:00 [entrez]
PHST- 2017/07/10 00:00 [pmc-release]
AID - S0002-9343(16)31304-3 [pii]
AID - 10.1016/j.amjmed.2016.11.044 [doi]
PST - ppublish
SO  - Am J Med. 2017 Jun;130(6):744.e9-744.e15. doi: 10.1016/j.amjmed.2016.11.044. Epub 
      2017 Jan 5.

PMID- 28025216
OWN - NLM
STAT- MEDLINE
DCOM- 20181024
LR  - 20220409
IS  - 2055-6845 (Electronic)
VI  - 3
IP  - 2
DP  - 2017 Apr 1
TI  - Hydroxychloroquine for the prevention of recurrent cardiovascular events in 
      myocardial infarction patients: rationale and design of the OXI trial.
PG  - 92-97
LID - 10.1093/ehjcvp/pvw035 [doi]
AB  - BACKGROUND: Inflammation of the arterial wall plays a central role in the 
      pathogenesis of atherosclerosis. Among patients with rheumatic diseases, 
      anti-rheumatic medication reduces the incidence of cardiovascular (CV) diseases, 
      but only few studies have addressed their cardioprotective effects on patients 
      with no rheumatic diseases. Hydroxychloroquine (HCQ) is an anti-rheumatic drug 
      commonly used in the treatment of rheumatoid arthritis and systemic lupus 
      erythematosus. In addition to its anti-inflammatory properties, HCQ reduces 
      cholesterol levels and the risk of type II diabetes, and has also anti-platelet 
      effects. DESIGN: The OXI trial is an event-driven trial that will randomize 2500 
      patients hospitalized for myocardial infarction (MI). Participants will receive 
      active HCQ or placebo for at least 12 months, and until 350 CV events are 
      confirmed. The primary trial endpoint is the composite of death, MI, 
      hospitalization for unstable angina, urgent percutaneous coronary intervention, 
      and urgent coronary artery bypass grafting. Secondary trial endpoints are the 
      primary end point plus stroke, the effect of HCQ treatment on lipids, on the 
      incidence of Type 2 diabetes, on the level of haemoglobin A1c, and on 
      inflammatory parameters. A 6 months placebo-controlled safety pilot trial with 
      200 patients is currently ongoing to assess the safety of HCQ in the setting of 
      MI. SUMMARY: The OXI trial will determine whether treatment with HCQ, as compared 
      with placebo, will reduce recurrent CV events among MI patients. If positive, 
      then the OXI trial would provide an entirely novel multitarget approach for the 
      secondary prevention of atherosclerotic cardiovascular diseases (ACVD).
CI  - Published on behalf of the European Society of Cardiology. All rights reserved. © 
      The Author 2016. For Permissions, please email: journals.permissions@oup.com.
FAU - Hartman, Otto
AU  - Hartman O
AD  - Heart and Lung Center, University of Helsinki and Helsinki University Hospital, 
      PL 340, 00029 HUS, Finland.
FAU - Kovanen, Petri T
AU  - Kovanen PT
AD  - Wihuri Research Institute, Biomedicum Helsinki, Haartmaninkatu 8, Helsinki 00290, 
      Finland.
FAU - Lehtonen, Jukka
AU  - Lehtonen J
AD  - Heart and Lung Center, University of Helsinki and Helsinki University Hospital, 
      PL 340, 00029 HUS, Finland.
FAU - Eklund, Kari K
AU  - Eklund KK
AD  - Department of Rheumatology, University of Helsinki and Helsinki University 
      Hospital, PL 340, 00029 HUS, Helsinki, Finland.
FAU - Sinisalo, Juha
AU  - Sinisalo J
AD  - Heart and Lung Center, University of Helsinki and Helsinki University Hospital, 
      PL 340, 00029 HUS, Finland.
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Eur Heart J Cardiovasc Pharmacother
JT  - European heart journal. Cardiovascular pharmacotherapy
JID - 101669491
RN  - 0 (Antirheumatic Agents)
RN  - 4QWG6N8QKH (Hydroxychloroquine)
SB  - IM
CIN - Eur Heart J Cardiovasc Pharmacother. 2017 Apr 1;3(2):98. doi: 
      10.1093/ehjcvp/pvw046. PMID: 28025215
CIN - Eur Heart J Cardiovasc Pharmacother. 2017 Apr 1;3(2):99. doi: 
      10.1093/ehjcvp/pvw050. PMID: 28069608
MH  - Antirheumatic Agents/therapeutic use
MH  - Atherosclerosis/etiology/*prevention & control
MH  - Double-Blind Method
MH  - Humans
MH  - Hydroxychloroquine/*therapeutic use
MH  - Myocardial Infarction/*complications
MH  - Pilot Projects
MH  - Recurrence
MH  - Secondary Prevention/*methods
OTO - NOTNLM
OT  - Acute coronary syndrome
OT  - Anti-inflammatory
OT  - Atherosclerosis
OT  - Coronary artery disease
OT  - Hydroxychloroquine
OT  - Myocardial infarction
OT  - inflammation
EDAT- 2016/12/28 06:00
MHDA- 2018/10/26 06:00
CRDT- 2016/12/28 06:00
PHST- 2016/09/08 00:00 [received]
PHST- 2016/11/28 00:00 [accepted]
PHST- 2016/12/28 06:00 [pubmed]
PHST- 2018/10/26 06:00 [medline]
PHST- 2016/12/28 06:00 [entrez]
AID - pvw035 [pii]
AID - 10.1093/ehjcvp/pvw035 [doi]
PST - ppublish
SO  - Eur Heart J Cardiovasc Pharmacother. 2017 Apr 1;3(2):92-97. doi: 
      10.1093/ehjcvp/pvw035.

PMID- 27959716
OWN - NLM
STAT- MEDLINE
DCOM- 20170110
LR  - 20220410
IS  - 1533-4406 (Electronic)
IS  - 0028-4793 (Linking)
VI  - 375
IP  - 26
DP  - 2016 Dec 29
TI  - Cardiovascular Safety of Celecoxib, Naproxen, or Ibuprofen for Arthritis.
PG  - 2519-29
LID - 10.1056/NEJMoa1611593 [doi]
AB  - BACKGROUND: The cardiovascular safety of celecoxib, as compared with nonselective 
      nonsteroidal antiinflammatory drugs (NSAIDs), remains uncertain. METHODS: 
      Patients who required NSAIDs for osteoarthritis or rheumatoid arthritis and were 
      at increased cardiovascular risk were randomly assigned to receive celecoxib, 
      ibuprofen, or naproxen. The goal of the trial was to assess the noninferiority of 
      celecoxib with regard to the primary composite outcome of cardiovascular death 
      (including hemorrhagic death), nonfatal myocardial infarction, or nonfatal 
      stroke. Noninferiority required a hazard ratio of 1.12 or lower, as well as an 
      upper 97.5% confidence limit of 1.33 or lower in the intention-to-treat 
      population and of 1.40 or lower in the on-treatment population. Gastrointestinal 
      and renal outcomes were also adjudicated. RESULTS: A total of 24,081 patients 
      were randomly assigned to the celecoxib group (mean [±SD] daily dose, 209±37 mg), 
      the naproxen group (852±103 mg), or the ibuprofen group (2045±246 mg) for a mean 
      treatment duration of 20.3±16.0 months and a mean follow-up period of 34.1±13.4 
      months. During the trial, 68.8% of the patients stopped taking the study drug, 
      and 27.4% of the patients discontinued follow-up. In the intention-to-treat 
      analyses, a primary outcome event occurred in 188 patients in the celecoxib group 
      (2.3%), 201 patients in the naproxen group (2.5%), and 218 patients in the 
      ibuprofen group (2.7%) (hazard ratio for celecoxib vs. naproxen, 0.93; 95% 
      confidence interval [CI], 0.76 to 1.13; hazard ratio for celecoxib vs. ibuprofen, 
      0.85; 95% CI, 0.70 to 1.04; P<0.001 for noninferiority in both comparisons). In 
      the on-treatment analysis, a primary outcome event occurred in 134 patients in 
      the celecoxib group (1.7%), 144 patients in the naproxen group (1.8%), and 155 
      patients in the ibuprofen group (1.9%) (hazard ratio for celecoxib vs. naproxen, 
      0.90; 95% CI, 0.71 to 1.15; hazard ratio for celecoxib vs. ibuprofen, 0.81; 95% 
      CI, 0.65 to 1.02; P<0.001 for noninferiority in both comparisons). The risk of 
      gastrointestinal events was significantly lower with celecoxib than with naproxen 
      (P=0.01) or ibuprofen (P=0.002); the risk of renal events was significantly lower 
      with celecoxib than with ibuprofen (P=0.004) but was not significantly lower with 
      celecoxib than with naproxen (P=0.19). CONCLUSIONS: At moderate doses, celecoxib 
      was found to be noninferior to ibuprofen or naproxen with regard to 
      cardiovascular safety. (Funded by Pfizer; ClinicalTrials.gov number, NCT00346216 
      .).
FAU - Nissen, Steven E
AU  - Nissen SE
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Yeomans, Neville D
AU  - Yeomans ND
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Lüscher, Thomas F
AU  - Lüscher TF
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Libby, Peter
AU  - Libby P
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Husni, M Elaine
AU  - Husni ME
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Graham, David Y
AU  - Graham DY
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Borer, Jeffrey S
AU  - Borer JS
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Wisniewski, Lisa M
AU  - Wisniewski LM
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Wolski, Katherine E
AU  - Wolski KE
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Wang, Qiuqing
AU  - Wang Q
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Menon, Venu
AU  - Menon V
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Ruschitzka, Frank
AU  - Ruschitzka F
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Gaffney, Michael
AU  - Gaffney M
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Beckerman, Bruce
AU  - Beckerman B
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Berger, Manuela F
AU  - Berger MF
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Bao, Weihang
AU  - Bao W
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
FAU - Lincoff, A Michael
AU  - Lincoff AM
AD  - From the Cleveland Clinic, Cleveland (S.E.N., M.E.H., L.M.W., K.E.W., Q.W., V.M., 
      A.M.L.); Western Sydney University, Campbelltown, NSW, Australia (N.D.Y.); 
      Brigham and Women's Hospital, Harvard Medical School, Boston (D.H.S., P.L.); 
      University Hospital Zurich, Zurich, Switzerland (T.F.L., F.R.); Baylor College of 
      Medicine, Veterans Affairs Medical Center, Houston (D.Y.G.); and State University 
      of New York, Downstate Health Sciences Center (J.S.B.) and Pfizer (M.G., B.B., 
      M.F.B., W.B.), New York.
CN  - PRECISION Trial Investigators
LA  - eng
SI  - ClinicalTrials.gov/NCT00346216
GR  - P30 DK056338/DK/NIDDK NIH HHS/United States
PT  - Comment
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
DEP - 20161113
PL  - United States
TA  - N Engl J Med
JT  - The New England journal of medicine
JID - 0255562
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
RN  - 57Y76R9ATQ (Naproxen)
RN  - JCX84Q7J1L (Celecoxib)
RN  - WK2XYI10QM (Ibuprofen)
SB  - IM
CIN - N Engl J Med. 2016 Dec 29;375(26):2595-6. doi: 10.1056/NEJMe1614257. PMID: 
      28029923
CIN - N Engl J Med. 2017 Apr 6;376(14):1389. doi: 10.1056/NEJMc1702534. PMID: 28379792
CON - N Engl J Med. 2017 Apr 6;376(14):1389. doi: 10.1056/NEJMc1702534. PMID: 28379792
CIN - Internist (Berl). 2017 Aug;58(8):863-865. doi: 10.1007/s00108-017-0260-x. PMID: 
      28534137
MH  - Aged
MH  - Anti-Inflammatory Agents, Non-Steroidal/*adverse effects/therapeutic use
MH  - Arthritis/*drug therapy
MH  - Cardiovascular Diseases/*chemically induced/mortality
MH  - Celecoxib/*adverse effects/therapeutic use
MH  - Cyclooxygenase 2 Inhibitors/*adverse effects/therapeutic use
MH  - Female
MH  - Gastrointestinal Diseases/chemically induced
MH  - Humans
MH  - Ibuprofen/*adverse effects/therapeutic use
MH  - Intention to Treat Analysis
MH  - Kidney Diseases/chemically induced
MH  - Male
MH  - Middle Aged
MH  - Naproxen/*adverse effects/therapeutic use
MH  - Risk
FIR - Fleming, Thomas R
IR  - Fleming TR
FIR - Brophy, James
IR  - Brophy J
FIR - Crofford, Leslie J
IR  - Crofford LJ
FIR - Peura, David A
IR  - Peura DA
FIR - Kerr, David R
IR  - Kerr DR
FIR - Krum, Henry
IR  - Krum H
FIR - Anwaruddin, Saif
IR  - Anwaruddin S
FIR - Askari, Arman
IR  - Askari A
FIR - Baranowski, Bryan
IR  - Baranowski B
FIR - Bashian, Gregory
IR  - Bashian G
FIR - Benjamin, Terri-Ann
IR  - Benjamin TA
FIR - Brener, Sorin
IR  - Brener S
FIR - Cavender, Matthew
IR  - Cavender M
FIR - Chenier, Michael
IR  - Chenier M
FIR - Chhatriwalla, Adnan
IR  - Chhatriwalla A
FIR - Coleman, Corey
IR  - Coleman C
FIR - Cremer, Paul
IR  - Cremer P
FIR - Downey, Ross
IR  - Downey R
FIR - Galla, John
IR  - Galla J
FIR - Jones, Brandon
IR  - Jones B
FIR - Kanderian, Anne
IR  - Kanderian A
FIR - Kwon, Deborah
IR  - Kwon D
FIR - Lahoud, Rony
IR  - Lahoud R
FIR - Lappe, Jason
IR  - Lappe J
FIR - Lau, Evan
IR  - Lau E
FIR - Lazar, Lawrence
IR  - Lazar L
FIR - Meadows, Telly
IR  - Meadows T
FIR - Shishehbor, Mehdi
IR  - Shishehbor M
FIR - William, Amila Dilusha
IR  - William AD
FIR - Wu, Willis
IR  - Wu W
FIR - Zardkoohi, Omeed
IR  - Zardkoohi O
FIR - Gupta, Rishi
IR  - Gupta R
FIR - Sharma, Jitendra
IR  - Sharma J
FIR - Shields, Robert
IR  - Shields R
FIR - Sila, Cathy
IR  - Sila C
FIR - Sweeney, Patrick
IR  - Sweeney P
FIR - Truong, Vincent V
IR  - Truong VV
FIR - Uchino, Ken
IR  - Uchino K
FIR - Falk, Gary
IR  - Falk G
FIR - Kandiel, Ahmed
IR  - Kandiel A
FIR - Philpott, Jessica
IR  - Philpott J
FIR - Qadeer, Mohammed A
IR  - Qadeer MA
FIR - Stevens, Tyler
IR  - Stevens T
FIR - Thota, Prashanthi
IR  - Thota P
FIR - Vargo, John
IR  - Vargo J
FIR - Wang, Yinghong Mimi
IR  - Wang YM
FIR - Akhtar, Mateen
IR  - Akhtar M
FIR - Austin, Bethany
IR  - Austin B
FIR - Cantillon, Daniel
IR  - Cantillon D
FIR - Cauthen, Clay
IR  - Cauthen C
FIR - Cavalcante, Joao L
IR  - Cavalcante JL
FIR - Dahiya, Arun
IR  - Dahiya A
FIR - Goldberg, Adam
IR  - Goldberg A
FIR - Gorodeski, Eiran
IR  - Gorodeski E
FIR - Kaminski, Matthew
IR  - Kaminski M
FIR - Lai, James E
IR  - Lai JE
FIR - Tarakji, Khaldoun
IR  - Tarakji K
FIR - Underwood, Donald
IR  - Underwood D
FIR - Atanasovski, Ilijia
IR  - Atanasovski I
FIR - Balog, Craig
IR  - Balog C
FIR - Bash, Dianna
IR  - Bash D
FIR - Becker, Matthew
IR  - Becker M
FIR - Brown, Kimberly
IR  - Brown K
FIR - Bruce, Antoinette
IR  - Bruce A
FIR - Davey, Deborah
IR  - Davey D
FIR - D’Angelo, Patricia
IR  - D’Angelo P
FIR - Fabry, Liz
IR  - Fabry L
FIR - Gladish, Debbie
IR  - Gladish D
FIR - Hodge, Patricia
IR  - Hodge P
FIR - Klancar, Rosemary
IR  - Klancar R
FIR - Lamovsky, Lisa
IR  - Lamovsky L
FIR - Moore, Betty
IR  - Moore B
FIR - Myers, Karen
IR  - Myers K
FIR - Pasca, Narcis
IR  - Pasca N
FIR - Pothier, Claire
IR  - Pothier C
FIR - Prcela, Lisa
IR  - Prcela L
FIR - Rodriguez, Robin
IR  - Rodriguez R
FIR - Scebbi, Tambria
IR  - Scebbi T
FIR - Schnauffer, Maura
IR  - Schnauffer M
FIR - Suchar, Linda
IR  - Suchar L
FIR - Theodos, Gus
IR  - Theodos G
FIR - Wang, Thomas
IR  - Wang T
FIR - Ali-Akhtar, Samia
IR  - Ali-Akhtar S
FIR - Anderson, Tricia
IR  - Anderson T
FIR - Baker, Karen C
IR  - Baker KC
FIR - Collins, Suzanne
IR  - Collins S
FIR - DeShields, Rosetta
IR  - DeShields R
FIR - Fasano, Christine
IR  - Fasano C
FIR - Fayyad, Rana
IR  - Fayyad R
FIR - Goldfarb, Heidi
IR  - Goldfarb H
FIR - Gomez, Myrna
IR  - Gomez M
FIR - Graham, Tameika
IR  - Graham T
FIR - Guilds-Zamarka, Linda
IR  - Guilds-Zamarka L
FIR - Herman, Vivian
IR  - Herman V
FIR - Holmes, Debra
IR  - Holmes D
FIR - Hua, Yue Lisa
IR  - Hua YL
FIR - Iorga, Dinu
IR  - Iorga D
FIR - Ivanac, Karen
IR  - Ivanac K
FIR - Krapf, Sinde
IR  - Krapf S
FIR - Liepins, Adrian
IR  - Liepins A
FIR - Marquino, Valerie
IR  - Marquino V
FIR - McDonagh, Tom
IR  - McDonagh T
FIR - Mihalik, Carol
IR  - Mihalik C
FIR - Miranda, Cesar
IR  - Miranda C
FIR - Nemeth, Mary Anne
IR  - Nemeth MA
FIR - Nguyen, Ha
IR  - Nguyen H
FIR - Pagano, Maria
IR  - Pagano M
FIR - Pressler, Milton L
IR  - Pressler ML
FIR - Ratigan, Mary Kay
IR  - Ratigan MK
FIR - Shine, Erlande
IR  - Shine E
FIR - Simpson, Tamara
IR  - Simpson T
FIR - Spolnik, Anna
IR  - Spolnik A
FIR - Sullivan, Beth
IR  - Sullivan B
FIR - Tantiongco, Elsa S
IR  - Tantiongco ES
FIR - Tarakhonych, Oleksandr I
IR  - Tarakhonych OI
FIR - Wang, Xu
IR  - Wang X
FIR - Wilson, Daniel
IR  - Wilson D
FIR - Wisemandle, Wayne
IR  - Wisemandle W
FIR - Xia, Richard Feng
IR  - Xia RF
FIR - Zhang, Richard
IR  - Zhang R
FIR - Berger, Christina
IR  - Berger C
FIR - Brock, Aksana
IR  - Brock A
FIR - Brink, Karin
IR  - Brink K
FIR - Byrd, Priscilla
IR  - Byrd P
FIR - Cabrera, Desmond
IR  - Cabrera D
FIR - Caleen, Regan
IR  - Caleen R
FIR - Cavin, Serena
IR  - Cavin S
FIR - Crutchfield, Jeannetta
IR  - Crutchfield J
FIR - Dallas, Brian
IR  - Dallas B
FIR - Dawood, Shabnam
IR  - Dawood S
FIR - Dey, Matthew
IR  - Dey M
FIR - DiLiberti, John
IR  - DiLiberti J
FIR - D’Souza, Sharyn
IR  - D’Souza S
FIR - Edwards, Catherine
IR  - Edwards C
FIR - Finn, Amy
IR  - Finn A
FIR - Gardiner, Sarah
IR  - Gardiner S
FIR - Garrett, Angela
IR  - Garrett A
FIR - Gauley, Julie
IR  - Gauley J
FIR - Goldman, Betsy
IR  - Goldman B
FIR - Gross, Jamie
IR  - Gross J
FIR - Hinnant, Kevin
IR  - Hinnant K
FIR - Horwhat, Amy
IR  - Horwhat A
FIR - Houle, Philippe
IR  - Houle P
FIR - Humphreys, Kristina
IR  - Humphreys K
FIR - Iles, Janet
IR  - Iles J
FIR - Kimball, Matthew
IR  - Kimball M
FIR - Kisly, Marek
IR  - Kisly M
FIR - Kopcha, Stacy
IR  - Kopcha S
FIR - Krishnan, Subha
IR  - Krishnan S
FIR - Lloyd, Wendy
IR  - Lloyd W
FIR - Lopez, Gaston
IR  - Lopez G
FIR - Lowe, Kaye
IR  - Lowe K
FIR - Machado, Adriane
IR  - Machado A
FIR - Martin, Erin
IR  - Martin E
FIR - Martin, Joy
IR  - Martin J
FIR - Nene, Madhura
IR  - Nene M
FIR - Oren, Miriam
IR  - Oren M
FIR - Pompilio, Renata
IR  - Pompilio R
FIR - Schimmel, Jamie
IR  - Schimmel J
FIR - Shah, Shivani
IR  - Shah S
FIR - Simari, Leticia
IR  - Simari L
FIR - Singh, Angad
IR  - Singh A
FIR - Steflik, Christie
IR  - Steflik C
FIR - Thompson, Karyn
IR  - Thompson K
FIR - Toledo, Renata
IR  - Toledo R
FIR - Welborne, Caren
IR  - Welborne C
FIR - Whitt, John
IR  - Whitt J
FIR - Williamson, Mark
IR  - Williamson M
FIR - Wright, Ella-Mai
IR  - Wright EM
FIR - Zarate, Julia
IR  - Zarate J
FIR - Zucker, Janet
IR  - Zucker J
FIR - Bradick, April
IR  - Bradick A
FIR - Bustamente, Linda Taylor
IR  - Bustamente LT
FIR - Harris, Kasu
IR  - Harris K
FIR - Smith, Tam
IR  - Smith T
FIR - Bossingham, David
IR  - Bossingham D
FIR - Buchanan, Russell
IR  - Buchanan R
FIR - Colquhoun, David
IR  - Colquhoun D
FIR - De Looze, Ferdinandus
IR  - De Looze F
FIR - Karrasch, Jeff
IR  - Karrasch J
FIR - Huttenmeister, Robyn
IR  - Huttenmeister R
FIR - Day, Deborah
IR  - Day D
FIR - Healy, Bridget
IR  - Healy B
FIR - Pryor, Pauline
IR  - Pryor P
FIR - Hall, Stephen
IR  - Hall S
FIR - Littlejohn, Geoffrey
IR  - Littlejohn G
FIR - Russo, Marc
IR  - Russo M
FIR - Taylor, Andrew
IR  - Taylor A
FIR - Will, Robert
IR  - Will R
FIR - Azevedo, Mário
IR  - Azevedo M
FIR - Baaklini, Cesar
IR  - Baaklini C
FIR - Borba, Victoria
IR  - Borba V
FIR - Brenol, Joao Carlos
IR  - Brenol JC
FIR - Castro, Marise
IR  - Castro M
FIR - Castro, Fabio
IR  - Castro F
FIR - Cavalcanti, Fernando
IR  - Cavalcanti F
FIR - Helfenstein Fonseca, Francisco Antonio
IR  - Helfenstein Fonseca FA
FIR - Gomes, Marco
IR  - Gomes M
FIR - Guimaraes, Swami
IR  - Guimaraes S
FIR - Keiserman, Mauro
IR  - Keiserman M
FIR - Kochen, Jussara
IR  - Kochen J
FIR - Lanna, Cristina
IR  - Lanna C
FIR - Levy, Roger
IR  - Levy R
FIR - Lomonte, Andrea
IR  - Lomonte A
FIR - Marcolino, Flora
IR  - Marcolino F
FIR - Eliaschewitz, Freddy
IR  - Eliaschewitz F
FIR - Melazzi, Ana Claudia
IR  - Melazzi AC
FIR - Moriguchi, Emilio
IR  - Moriguchi E
FIR - Marques Neto, Joao Francisco
IR  - Marques Neto JF
FIR - Neto, Ernesto
IR  - Neto E
FIR - Pinto, Maurilio
IR  - Pinto M
FIR - Provenza, Jose
IR  - Provenza J
FIR - Radominski, Sebastiao
IR  - Radominski S
FIR - Roimicher, Luis
IR  - Roimicher L
FIR - Saraiva, Jose Francisco
IR  - Saraiva JF
FIR - Scotton, Antonio
IR  - Scotton A
FIR - Simon, Julio
IR  - Simon J
FIR - Sousa, Antonio
IR  - Sousa A
FIR - Sebba Barroso de Souza Souza, Weimar Kunz
IR  - Sebba Barroso de Souza Souza WK
FIR - Ximenes, Antonio
IR  - Ximenes A
FIR - Adachi, Jonathan
IR  - Adachi J
FIR - Aggarwal, Naresh
IR  - Aggarwal N
FIR - Attie, Nabil
IR  - Attie N
FIR - Baker, Milton
IR  - Baker M
FIR - Barkhuizen, Frederick
IR  - Barkhuizen F
FIR - Kooy, Jacobus
IR  - Kooy J
FIR - Bartlett, John
IR  - Bartlett J
FIR - Beauchesne, Andre
IR  - Beauchesne A
FIR - Bernstein, Ira
IR  - Bernstein I
FIR - Bhamjee, Hassen
IR  - Bhamjee H
FIR - Bose, Sabyasachi
IR  - Bose S
FIR - Bowler, William
IR  - Bowler W
FIR - Campbell, Ian
IR  - Campbell I
FIR - Chaulk, Domino Roy
IR  - Chaulk DR
FIR - Chouinard, Guy
IR  - Chouinard G
FIR - Collingwood, John
IR  - Collingwood J
FIR - Conter, Howard
IR  - Conter H
FIR - Corey, John
IR  - Corey J
FIR - Craig, Brian
IR  - Craig B
FIR - Dauth, Pierre
IR  - Dauth P
FIR - Dufresne, Maurice
IR  - Dufresne M
FIR - Dzongowski, Peter
IR  - Dzongowski P
FIR - Faraawi, Rafat
IR  - Faraawi R
FIR - Filteau, Pierre
IR  - Filteau P
FIR - Garceau, Claude
IR  - Garceau C
FIR - Gorfinkel, Iris
IR  - Gorfinkel I
FIR - Grant, Eric
IR  - Grant E
FIR - Hart, Randy
IR  - Hart R
FIR - Henein, Sam
IR  - Henein S
FIR - Hudon, Catherine
IR  - Hudon C
FIR - Fortin, Martin
IR  - Fortin M
FIR - Jasey, Gregory
IR  - Jasey G
FIR - Kanani, Subodh
IR  - Kanani S
FIR - Keegan, Philippa
IR  - Keegan P
FIR - Kendler, David
IR  - Kendler D
FIR - Khraishi, Majed
IR  - Khraishi M
FIR - O'Keefe, Dennis
IR  - O'Keefe D
FIR - Lasko, Benjamin
IR  - Lasko B
FIR - Lavoie, Normand
IR  - Lavoie N
FIR - Karsh, Jacob
IR  - Karsh J
FIR - Li, John
IR  - Li J
FIR - Lichtenstein, Tersia
IR  - Lichtenstein T
FIR - Hudson, Neil
IR  - Hudson N
FIR - Lowe, Derek
IR  - Lowe D
FIR - Luterman, Maynard
IR  - Luterman M
FIR - Luton, Robert
IR  - Luton R
FIR - Maranda, Claude
IR  - Maranda C
FIR - McCarthy, Timothy
IR  - McCarthy T
FIR - Misik, Karl
IR  - Misik K
FIR - Morin, Frederic
IR  - Morin F
FIR - Mutrie, John
IR  - Mutrie J
FIR - Taylor, Steven
IR  - Taylor S
FIR - Nagpal, Rohit
IR  - Nagpal R
FIR - O'Mahony, William
IR  - O'Mahony W
FIR - O'Mahony, Michael
IR  - O'Mahony M
FIR - Pesant, Yves
IR  - Pesant Y
FIR - Rodrigues, Jude
IR  - Rodrigues J
FIR - Salter, Timothy
IR  - Salter T
FIR - Saunders, Kevin
IR  - Saunders K
FIR - Schacter, Gordon
IR  - Schacter G
FIR - Senaratne, Manohara
IR  - Senaratne M
FIR - Skeith, Kenneth
IR  - Skeith K
FIR - Sussman, Jack
IR  - Sussman J
FIR - Syan, Swaran
IR  - Syan S
FIR - Syan, Gurcharan
IR  - Syan G
FIR - Thorne, J
IR  - Thorne J
FIR - Tsoukas, George
IR  - Tsoukas G
FIR - Velji, Azim
IR  - Velji A
FIR - Zidel, Brian
IR  - Zidel B
FIR - Arango, Carmen
IR  - Arango C
FIR - Gomez, Juan
IR  - Gomez J
FIR - Jannaut, Maria
IR  - Jannaut M
FIR - Botero Lopez, Rodrigo
IR  - Botero Lopez R
FIR - Pinto Penaranda, Luis
IR  - Pinto Penaranda L
FIR - Ramirez, Gerardo
IR  - Ramirez G
FIR - Molina Restrepo, Jose
IR  - Molina Restrepo J
FIR - Badilla-Gomez, Alvaro
IR  - Badilla-Gomez A
FIR - Cespedes-Vargas, Javier
IR  - Cespedes-Vargas J
FIR - Garzona-Meseguer, Fernando
IR  - Garzona-Meseguer F
FIR - Gutreiman-Goldberg, Mortjay
IR  - Gutreiman-Goldberg M
FIR - Lainez-Ventosilla, Alberto
IR  - Lainez-Ventosilla A
FIR - Monge-Zeledon, Pablo
IR  - Monge-Zeledon P
FIR - Moya-Rodriguez, Javier
IR  - Moya-Rodriguez J
FIR - Oeding-Bermudez, Oscar
IR  - Oeding-Bermudez O
FIR - Poveda-Fernandez, Jonathan
IR  - Poveda-Fernandez J
FIR - Saenz-Castro, Ricardo
IR  - Saenz-Castro R
FIR - Vinocour-Fornieri, Mary
IR  - Vinocour-Fornieri M
FIR - Lam, Yat Yin
IR  - Lam YY
FIR - Wai-Kwok, Gabriel
IR  - Wai-Kwok G
FIR - Lee, Stephen
IR  - Lee S
FIR - Mok, Chi-Chiu
IR  - Mok CC
FIR - Abud-Mendoza, Carlos
IR  - Abud-Mendoza C
FIR - Avila Armengol, Hilario
IR  - Avila Armengol H
FIR - Carmona-Furusho, Luis
IR  - Carmona-Furusho L
FIR - Enkerlin-Pauwells, Hermann
IR  - Enkerlin-Pauwells H
FIR - Garcia-De La Torre, Ignacio
IR  - Garcia-De La Torre I
FIR - Garcia-Lopez, Rafael
IR  - Garcia-Lopez R
FIR - Cardiel Rios, Mario
IR  - Cardiel Rios M
FIR - Hernandez-Paz, Roberto
IR  - Hernandez-Paz R
FIR - Martinez-Osuna, Pindaro
IR  - Martinez-Osuna P
FIR - Ochoa-Ortega, Luis
IR  - Ochoa-Ortega L
FIR - Robles-San Roman, Manuel
IR  - Robles-San Roman M
FIR - Saldate-Alonso, Maria
IR  - Saldate-Alonso M
FIR - Guerra Bautista, Generoso
IR  - Guerra Bautista G
FIR - Trujillo, Rita
IR  - Trujillo R
FIR - Vega Espinoza, Luis
IR  - Vega Espinoza L
FIR - Berrocal Kasay, Alfredo Enrique
IR  - Berrocal Kasay AE
FIR - Ravelo Hernandez, Jorge
IR  - Ravelo Hernandez J
FIR - Kuroiwa, Rita
IR  - Kuroiwa R
FIR - Leon-Portocarrero, Manuel
IR  - Leon-Portocarrero M
FIR - Morales Olazabal, Luis
IR  - Morales Olazabal L
FIR - Eullaran, Ronald
IR  - Eullaran R
FIR - Lanzon, Allan
IR  - Lanzon A
FIR - Lichauco, Juan Javier
IR  - Lichauco JJ
FIR - Li-Yu, Julie
IR  - Li-Yu J
FIR - Navarra, Sandra
IR  - Navarra S
FIR - Ramiterre, Edgar
IR  - Ramiterre E
FIR - Salido, Evelyn
IR  - Salido E
FIR - Tan, Perry
IR  - Tan P
FIR - Chen, Der-Yuan
IR  - Chen DY
FIR - Chen, Hsiang-Cheng
IR  - Chen HC
FIR - Lai, Jenn-Haung
IR  - Lai JH
FIR - Chen, Pei-Chih
IR  - Chen PC
FIR - Chen, Hung-An
IR  - Chen HA
FIR - Hsu, Ping-Ning
IR  - Hsu PN
FIR - Lai, Ning-Sheng
IR  - Lai NS
FIR - Lin, Hsiao-yi
IR  - Lin HY
FIR - Luo, Shue-Fen
IR  - Luo SF
FIR - Tsai, Wen-Chan
IR  - Tsai WC
FIR - Tsay, Gregory
IR  - Tsay G
FIR - Bula, Larysa
IR  - Bula L
FIR - Danyliuk, Svitlana
IR  - Danyliuk S
FIR - Lysenko, Grygorii
IR  - Lysenko G
FIR - Ignatenko, Grygoriy
IR  - Ignatenko G
FIR - Karpenko, Oleksandr
IR  - Karpenko O
FIR - Kononenko, Lyudmyla
IR  - Kononenko L
FIR - Koshlia, Volodymyr
IR  - Koshlia V
FIR - Kovalenko, Volodymyr
IR  - Kovalenko V
FIR - Kuryata, Olexandr
IR  - Kuryata O
FIR - Nikirenkov, Yuriy
IR  - Nikirenkov Y
FIR - Parkhomenko, Oleksandr
IR  - Parkhomenko O
FIR - Petrov, Andriy
IR  - Petrov A
FIR - Shpyleva, Nataliya
IR  - Shpyleva N
FIR - Svintsitskyy, Anatoliy
IR  - Svintsitskyy A
FIR - Tseluyko, Vira
IR  - Tseluyko V
FIR - Tykhonova, Susanna
IR  - Tykhonova S
FIR - Vizir, Vadym
IR  - Vizir V
FIR - Voloshyn, Oleksandr
IR  - Voloshyn O
FIR - Yagensky, Andriy
IR  - Yagensky A
FIR - Abalos-Galito, Marietta
IR  - Abalos-Galito M
FIR - Adams, John
IR  - Adams J
FIR - Adelizzi, Angela
IR  - Adelizzi A
FIR - Adetola, Adegbenga
IR  - Adetola A
FIR - Adler, Patrick
IR  - Adler P
FIR - Aelion, Jacob
IR  - Aelion J
FIR - Ahmed, Shilpi
IR  - Ahmed S
FIR - Akerson, Mark
IR  - Akerson M
FIR - Akpunonu, Basil
IR  - Akpunonu B
FIR - Aldrich, Jose
IR  - Aldrich J
FIR - Hernandez, Pedro
IR  - Hernandez P
FIR - Allaw, Mohammed
IR  - Allaw M
FIR - Alloway, Jeffrey
IR  - Alloway J
FIR - Alper, Jeffrey
IR  - Alper J
FIR - Alvarado, Odilon
IR  - Alvarado O
FIR - Alvarez, German
IR  - Alvarez G
FIR - Alwine, Lawrence
IR  - Alwine L
FIR - Amador, Pamela
IR  - Amador P
FIR - Anagnostis, George
IR  - Anagnostis G
FIR - Anderson, Jerome
IR  - Anderson J
FIR - Anderson, Marshall
IR  - Anderson M
FIR - Andrawis, Nabil
IR  - Andrawis N
FIR - Andron, Richard
IR  - Andron R
FIR - Apaliski, Stephen
IR  - Apaliski S
FIR - Arora, Ramesh
IR  - Arora R
FIR - Asher, Ronald
IR  - Asher R
FIR - Nielsen, Mark
IR  - Nielsen M
FIR - Ashley, Robert
IR  - Ashley R
FIR - Atiee, George
IR  - Atiee G
FIR - Awasty, Vivek
IR  - Awasty V
FIR - Ayesu, Kwabena
IR  - Ayesu K
FIR - Bacon, James
IR  - Bacon J
FIR - Eaton, Gregory
IR  - Eaton G
FIR - Baer, William
IR  - Baer W
FIR - Bakdash, Wa'el
IR  - Bakdash WA
FIR - Baker, Jeffrey
IR  - Baker J
FIR - Ballard, Thomas
IR  - Ballard T
FIR - Baraf, Herbert
IR  - Baraf H
FIR - Barber, Mark
IR  - Barber M
FIR - Bari, Abdul
IR  - Bari A
FIR - Barkhuizen, Andre
IR  - Barkhuizen A
FIR - Barnes, Robert
IR  - Barnes R
FIR - Baron, Scott
IR  - Baron S
FIR - Barringer, Thomas
IR  - Barringer T
FIR - Cromwell, William
IR  - Cromwell W
FIR - Wise, Daniel
IR  - Wise D
FIR - Bays, Harold
IR  - Bays H
FIR - Beach, James
IR  - Beach J
FIR - Beasley, Richard
IR  - Beasley R
FIR - Izzo, Mark
IR  - Izzo M
FIR - Bedel, Gary
IR  - Bedel G
FIR - Bedoya, Ricardo
IR  - Bedoya R
FIR - Bennett, Michael
IR  - Bennett M
FIR - Berenguer, Ramon
IR  - Berenguer R
FIR - Beretta, James
IR  - Beretta J
FIR - Berkowitz, Richard
IR  - Berkowitz R
FIR - Bhat, Anupama
IR  - Bhat A
FIR - Bhuchar, Subodh
IR  - Bhuchar S
FIR - Bland, Veita
IR  - Bland V
FIR - Blaze, Kenneth
IR  - Blaze K
FIR - Blecker, Edgar
IR  - Blecker E
FIR - Geiger, Ralph
IR  - Geiger R
FIR - Block, Bradley
IR  - Block B
FIR - Bloom, Allan
IR  - Bloom A
FIR - Boccalandro, Fernando
IR  - Boccalandro F
FIR - Bockow, Barry
IR  - Bockow B
FIR - Bookbinder, Stephen
IR  - Bookbinder S
FIR - Borenstein, David
IR  - Borenstein D
FIR - Bowers, Brian
IR  - Bowers B
FIR - Englebrecht, James
IR  - Englebrecht J
FIR - Bowling, Bruce
IR  - Bowling B
FIR - Brabham, David
IR  - Brabham D
FIR - Williams, Sheryl
IR  - Williams S
FIR - Brandon, Donald
IR  - Brandon D
FIR - Brautigam, Donald
IR  - Brautigam D
FIR - Bredlau, Clayton
IR  - Bredlau C
FIR - Hartman, Randy
IR  - Hartman R
FIR - Brkic-Vukotic, Ognjenka
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FIR - Brockmyre, Andrew
IR  - Brockmyre A
FIR - Brodsky, Alan
IR  - Brodsky A
FIR - Brogan, Terri-Ann
IR  - Brogan TA
FIR - Broker, Robert
IR  - Broker R
FIR - Brooks, Michael
IR  - Brooks M
FIR - Bruce, Tami
IR  - Bruce T
FIR - Brunner, Richard
IR  - Brunner R
FIR - Brus, William
IR  - Brus W
FIR - Brusky, John
IR  - Brusky J
FIR - Bruya, Timothy
IR  - Bruya T
FIR - Burack, David
IR  - Burack D
FIR - Burchenal, Joseph
IR  - Burchenal J
FIR - Buynak, Robert
IR  - Buynak R
FIR - Caciolo, Barbara
IR  - Caciolo B
FIR - Cader, Cas
IR  - Cader C
FIR - Campbell, Joe
IR  - Campbell J
FIR - Rask, Patrick
IR  - Rask P
FIR - Urbach, Daniel
IR  - Urbach D
FIR - Campolo, Michael
IR  - Campolo M
FIR - Capo, James
IR  - Capo J
FIR - Cappleman, John
IR  - Cappleman J
FIR - Card, John
IR  - Card J
FIR - Cardona, Jose
IR  - Cardona J
FIR - Marquez, Farid
IR  - Marquez F
FIR - Carr, George
IR  - Carr G
FIR - Carr, Albert
IR  - Carr A
FIR - Castro-Skoglund, Jenecsis
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FIR - Chachar, Mushtaque
IR  - Chachar M
FIR - Chakerian, Maia
IR  - Chakerian M
FIR - Chandler, John
IR  - Chandler J
FIR - Chappel, Christopher
IR  - Chappel C
FIR - Chen, Michael
IR  - Chen M
FIR - Cheung, Deanna
IR  - Cheung D
FIR - Chilka, Sapna
IR  - Chilka S
FIR - Chintanadilok, Jirayos
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FIR - Chodock, Allen
IR  - Chodock A
FIR - Christensen, Tom
IR  - Christensen T
FIR - Christina, Melanie
IR  - Christina M
FIR - Chuang, Rita
IR  - Chuang R
FIR - Clark, Lisa
IR  - Clark L
FIR - Clower, James
IR  - Clower J
FIR - Clunn, Amy
IR  - Clunn A
FIR - Cohen, Stanley
IR  - Cohen S
FIR - Cohen, Kenneth
IR  - Cohen K
FIR - Cohen, Robert
IR  - Cohen R
FIR - Collins, Paul
IR  - Collins P
FIR - Collins, Harry
IR  - Collins H
FIR - Connery, Lisa
IR  - Connery L
FIR - McArthur, Robert
IR  - McArthur R
FIR - Conte, John
IR  - Conte J
FIR - Cordero, Abner
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FIR - Lassiter, James
IR  - Lassiter J
FIR - Cornett, George
IR  - Cornett G
FIR - Beavins, Jill
IR  - Beavins J
FIR - Coulter, Franklin
IR  - Coulter F
FIR - Courtnage, Susan
IR  - Courtnage S
FIR - Cowen, Peter
IR  - Cowen P
FIR - Cox, William
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FIR - Coy, Kevin
IR  - Coy K
FIR - Margolis, James
IR  - Margolis J
FIR - Creamer, Michael
IR  - Creamer M
FIR - Cruz, Jairo
IR  - Cruz J
FIR - Cullen, Kathleen
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FIR - Benson, Dalton
IR  - Benson D
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IR  - Curtis J
FIR - Cyrus, Tillmann
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FIR - Chinn, Joseph
IR  - Chinn J
FIR - Nakhle, Samer
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FIR - Dahdul, Adnan
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FIR - Daly, Erik
IR  - Daly E
FIR - Milton, Ami
IR  - Milton A
FIR - Dandillaya, Ramprasad
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IR  - Davida A
FIR - Davis, Cedrice
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FIR - Dawes, Kenneth
IR  - Dawes K
FIR - Rubeiz, George
IR  - Rubeiz G
FIR - Burbano De Lara, Jose
IR  - Burbano De Lara J
FIR - Dean, Julius
IR  - Dean J
FIR - Short, William
IR  - Short W
FIR - Deane, Peter
IR  - Deane P
FIR - DeGarmo, Ronald
IR  - DeGarmo R
FIR - DeHart, Drake
IR  - DeHart D
FIR - DeHaven, Ruth
IR  - DeHaven R
FIR - Delgado, John
IR  - Delgado J
FIR - Deluccia, William
IR  - Deluccia W
FIR - Dennis, David
IR  - Dennis D
FIR - Maldonado-Garcia, Carolyn
IR  - Maldonado-Garcia C
FIR - Sanchez, Sigrid
IR  - Sanchez S
FIR - Szczesny, Michael
IR  - Szczesny M
FIR - Vendetti, Gina
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FIR - Denny, Dolph
IR  - Denny D
FIR - Desai, Vikas
IR  - Desai V
FIR - DeSantis, Michael
IR  - DeSantis M
FIR - Desir, Deborah
IR  - Desir D
FIR - Detweiler, Robert
IR  - Detweiler R
FIR - Diab, Isam
IR  - Diab I
FIR - Diaz, Joseph
IR  - Diaz J
FIR - Dice, John
IR  - Dice J
FIR - Elizalde, Araceli
IR  - Elizalde A
FIR - Hosler, Mirie
IR  - Hosler M
FIR - Dietz, Frederick
IR  - Dietz F
FIR - DiGiovanna, Michael
IR  - DiGiovanna M
FIR - Dikranian, Ara
IR  - Dikranian A
FIR - Doris, James
IR  - Doris J
FIR - Downs, Brandon
IR  - Downs B
FIR - Montgomery, Marcia
IR  - Montgomery M
FIR - Doyle, Natalie
IR  - Doyle N
FIR - Dreyfus, James
IR  - Dreyfus J
FIR - D'Souza, Veemal
IR  - D'Souza V
FIR - Kaner, David
IR  - Kaner D
FIR - Livingston, David
IR  - Livingston D
FIR - Dua, Anit
IR  - Dua A
FIR - Dugano-Daphnis, Pamela
IR  - Dugano-Daphnis P
FIR - DuMontier, Gary
IR  - DuMontier G
FIR - Dunmyer, Shelly
IR  - Dunmyer S
FIR - Dunn, Michael
IR  - Dunn M
FIR - Dunn, Leonard
IR  - Dunn L
FIR - Dunteman, Edwin
IR  - Dunteman E
FIR - Dushkin, Holly
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FIR - Baron, Mira
IR  - Baron M
FIR - Kravitz, Alan
IR  - Kravitz A
FIR - Tresser, Nancy
IR  - Tresser N
FIR - Wine, Alan
IR  - Wine A
FIR - Eade, Joel
IR  - Eade J
FIR - East, Cara
IR  - East C
FIR - Eberly, John
IR  - Eberly J
FIR - Corbett, Bernard
IR  - Corbett B
FIR - Eddy, Richard
IR  - Eddy R
FIR - Edris, Marwan
IR  - Edris M
FIR - Edwards, James
IR  - Edwards J
FIR - Edwards, William
IR  - Edwards W
FIR - Eider, Wendy
IR  - Eider W
FIR - El Sayad, Nabil
IR  - El Sayad N
FIR - Elasmar, Imad
IR  - Elasmar I
FIR - Elijah, Rochelle
IR  - Elijah R
FIR - Ellison, William
IR  - Ellison W
FIR - Engel, Edward
IR  - Engel E
FIR - Engel, Eli
IR  - Engel E
FIR - Yang, Chwi-Young
IR  - Yang CY
FIR - Erickson, Bernard
IR  - Erickson B
FIR - Ettlinger, Robert
IR  - Ettlinger R
FIR - Evanko, David
IR  - Evanko D
FIR - Evans, Paul
IR  - Evans P
FIR - O’Neill, Dennis
IR  - O’Neill D
FIR - Everett, Carlos
IR  - Everett C
FIR - Guerrero, Victor
IR  - Guerrero V
FIR - Eyzaguirre, Robert
IR  - Eyzaguirre R
FIR - Fairfax, Michael
IR  - Fairfax M
FIR - Fallows, Christopher
IR  - Fallows C
FIR - Farag, Azmi
IR  - Farag A
FIR - Farrington, Cecil
IR  - Farrington C
FIR - Fedor, Robert
IR  - Fedor R
FIR - Feinberg, Howard
IR  - Feinberg H
FIR - Feldman, Gary
IR  - Feldman G
FIR - Feldman, Bryan
IR  - Feldman B
FIR - Ashrafzadeh, Ali
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FIR - Feliciano, Elpidio
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FIR - DeWitt, MIcheal
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FIR - Fenton, Ira
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IR  - Fernando R
FIR - Firek, Anthony
IR  - Firek A
FIR - Fiechtner, Justus
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IR  - Fiel T
FIR - Fields, Harold
IR  - Fields H
FIR - Fields, Carolyn
IR  - Fields C
FIR - Figueredo, Romel
IR  - Figueredo R
FIR - Fiorillo, Timothy
IR  - Fiorillo T
FIR - Fisher, George
IR  - Fisher G
FIR - Fitz-Patrick, David
IR  - Fitz-Patrick D
FIR - Flatt, Jerrold
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FIR - Fleischer, Leslie
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IR  - Flint K
FIR - Collins, Ronald
IR  - Collins R
FIR - Flippo, Gregory
IR  - Flippo G
FIR - Savage, Perry
IR  - Savage P
FIR - Folkerth, Steven
IR  - Folkerth S
FIR - Ford, Theresa Lawrence
IR  - Ford TL
FIR - Forney, Bruce
IR  - Forney B
FIR - Forstot, Joseph
IR  - Forstot J
FIR - Franco, Miguel
IR  - Franco M
FIR - Francyk, David
IR  - Francyk D
FIR - Fraser, Neil
IR  - Fraser N
FIR - Fraser, Asad
IR  - Fraser A
FIR - Freed, Robert
IR  - Freed R
FIR - Freiburger, Jared
IR  - Freiburger J
FIR - Fruchter, Gerald
IR  - Fruchter G
FIR - Gabra, Nashwa
IR  - Gabra N
FIR - Gamarra, Lewis
IR  - Gamarra L
FIR - Gaona, Raul
IR  - Gaona R
FIR - Garcia, Bernard
IR  - Garcia B
FIR - Casanova, Rene
IR  - Casanova R
FIR - Garcia, Hiram
IR  - Garcia H
FIR - Gebhardt, Scott
IR  - Gebhardt S
FIR - Iezzi, Alan
IR  - Iezzi A
FIR - Shepard, Roland
IR  - Shepard R
FIR - Heiman, David
IR  - Heiman D
FIR - George, William
IR  - George W
FIR - George, Anu
IR  - George A
FIR - Gerrish, Catherine
IR  - Gerrish C
FIR - Gibbs, Rose
IR  - Gibbs R
FIR - Gillespie, Eve
IR  - Gillespie E
FIR - Gimbel, Joseph
IR  - Gimbel J
FIR - Gladstein, Geoffrey
IR  - Gladstein G
FIR - Glickfield, William
IR  - Glickfield W
FIR - Godbole, Narendra
IR  - Godbole N
FIR - Goldberg, Marc
IR  - Goldberg M
FIR - Goldberger, Edward
IR  - Goldberger E
FIR - Gonzalez, Emilio
IR  - Gonzalez E
FIR - Gonzalez, Manuel
IR  - Gonzalez M
FIR - Gopalani, Salim
IR  - Gopalani S
FIR - Gorman, Darrell
IR  - Gorman D
FIR - Grant, David
IR  - Grant D
FIR - Gray, William
IR  - Gray W
FIR - Greco, Gina
IR  - Greco G
FIR - Sissleman, Stephen
IR  - Sissleman S
FIR - Greenberg, Jerry
IR  - Greenberg J
FIR - Grena, Paul
IR  - Grena P
FIR - Gresh, John
IR  - Gresh J
FIR - Griffin, Robert
IR  - Griffin R
FIR - Schnitz, William
IR  - Schnitz W
FIR - Willis, Larry
IR  - Willis L
FIR - Griffin, Carl
IR  - Griffin C
FIR - Griffin, Jason
IR  - Griffin J
FIR - Grossman, Colby
IR  - Grossman C
FIR - Grubb, Stephen
IR  - Grubb S
FIR - Gudipati, Rao
IR  - Gudipati R
FIR - Gupta, Rajendra
IR  - Gupta R
FIR - Gupta, Ramesh
IR  - Gupta R
FIR - Guskiewicz, Robert
IR  - Guskiewicz R
FIR - Hack, Terrence
IR  - Hack T
FIR - Hackshaw, Kevin
IR  - Hackshaw K
FIR - Hall, Arthur
IR  - Hall A
FIR - Hamilton, Maxine
IR  - Hamilton M
FIR - Hamm, David
IR  - Hamm D
FIR - Hare, Ester
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FIR - Harper, Wayne
IR  - Harper W
FIR - Harris, Lisa
IR  - Harris L
FIR - Harrison, Boyde
IR  - Harrison B
FIR - Hart, Terence
IR  - Hart T
FIR - Haskel, Ethan
IR  - Haskel E
FIR - Headley, David
IR  - Headley D
FIR - Hearne, Archie
IR  - Hearne A
FIR - Heigerick, G
IR  - Heigerick G
FIR - Henry, Bruce
IR  - Henry B
FIR - Herman, Lee
IR  - Herman L
FIR - Hermann, Mark
IR  - Hermann M
FIR - Herring, Robert
IR  - Herring R
FIR - Herrod, John
IR  - Herrod J
FIR - Hershberger, Vernon
IR  - Hershberger V
FIR - Herzog, William
IR  - Herzog W
FIR - Hill, John
IR  - Hill J
FIR - Hilliard, General
IR  - Hilliard G
FIR - Hochman, Eric
IR  - Hochman E
FIR - Hole, Susan
IR  - Hole S
FIR - Holgado, Maynard
IR  - Holgado M
FIR - Aiken, Robert
IR  - Aiken R
FIR - Holkesvik, Reid
IR  - Holkesvik R
FIR - Holt, Peter
IR  - Holt P
FIR - Horn, Curtis
IR  - Horn C
FIR - Horner, Stanley
IR  - Horner S
FIR - House, Angela
IR  - House A
FIR - Howard, Timothy
IR  - Howard T
FIR - Howell, Mary
IR  - Howell M
FIR - Howell, James
IR  - Howell J
FIR - Hufman, Stephen
IR  - Hufman S
FIR - Hughes, William
IR  - Hughes W
FIR - Hunter, Robert
IR  - Hunter R
FIR - Diener, Carl
IR  - Diener C
FIR - Slaski, Andrew
IR  - Slaski A
FIR - Hussain, Murtaza
IR  - Hussain M
FIR - Hymowitz, Richard
IR  - Hymowitz R
FIR - Igleburger, James
IR  - Igleburger J
FIR - Ince, Carlos
IR  - Ince C
FIR - Ismail, Younus
IR  - Ismail Y
FIR - Jackson, Timothy
IR  - Jackson T
FIR - Jacobs, William
IR  - Jacobs W
FIR - Goldman, Brian
IR  - Goldman B
FIR - Jaffe, Kenneth
IR  - Jaffe K
FIR - Jakes, James
IR  - Jakes J
FIR - Janovitz, Richard
IR  - Janovitz R
FIR - Jauch, Werner
IR  - Jauch W
FIR - Jenkins, John
IR  - Jenkins J
FIR - Johnson, Carol
IR  - Johnson C
FIR - Johnson, Claudia
IR  - Johnson C
FIR - Jonas, Beth
IR  - Jonas B
FIR - Jones, Richard
IR  - Jones R
FIR - Jordan, Rebecca
IR  - Jordan R
FIR - Kabour, Ameer
IR  - Kabour A
FIR - Kades, Wagdy
IR  - Kades W
FIR - Kaell, Alan
IR  - Kaell A
FIR - Kafka, Shelly
IR  - Kafka S
FIR - Kalen, Vicki
IR  - Kalen V
FIR - Kamdar, Bina
IR  - Kamdar B
FIR - Kantaros, Louis
IR  - Kantaros L
FIR - Jafar, Mumtazuddin
IR  - Jafar M
FIR - Kapil, Sanjiv
IR  - Kapil S
FIR - Karras, Dean
IR  - Karras D
FIR - Hutchins, Robert
IR  - Hutchins R
FIR - Kashif, Ahmad
IR  - Kashif A
FIR - Kashou, Hisham
IR  - Kashou H
FIR - Katz, Arnold
IR  - Katz A
FIR - Kaufmann, Robert
IR  - Kaufmann R
FIR - Conlin, Michael
IR  - Conlin M
FIR - Kay, Jennifer
IR  - Kay J
FIR - Kaye, William
IR  - Kaye W
FIR - Levin, Robert
IR  - Levin R
FIR - Kelly, Richard
IR  - Kelly R
FIR - Kempf, Kevin
IR  - Kempf K
FIR - Burch, Francis
IR  - Burch F
FIR - Kennedy, Alastair
IR  - Kennedy A
FIR - Kenney, Howard
IR  - Kenney H
FIR - Kenton, David
IR  - Kenton D
FIR - Kerzner, Boris
IR  - Kerzner B
FIR - Kesselbrenner, Michael
IR  - Kesselbrenner M
FIR - Khalifa, Ammar
IR  - Khalifa A
FIR - Abuerreish, Muna
IR  - Abuerreish M
FIR - Khan, Saleem
IR  - Khan S
FIR - Khan, Jalil
IR  - Khan J
FIR - Khan, Bobby
IR  - Khan B
FIR - Khetan, Shishir
IR  - Khetan S
FIR - Kilpatrick, Frank
IR  - Kilpatrick F
FIR - Kutz, Douglad
IR  - Kutz D
FIR - Kim, Andrew
IR  - Kim A
FIR - Kimelheim, Robert
IR  - Kimelheim R
FIR - King, Charles
IR  - King C
FIR - Kinnaman, Stephanie
IR  - Kinnaman S
FIR - Kirby, William
IR  - Kirby W
FIR - Kirstein, Judith
IR  - Kirstein J
FIR - Kistler, Charles
IR  - Kistler C
FIR - Kivitz, Alan
IR  - Kivitz A
FIR - Klein, Steven
IR  - Klein S
FIR - Kliger, Morris
IR  - Kliger M
FIR - Kluge, Ronica
IR  - Kluge R
FIR - Knapp, William
IR  - Knapp W
FIR - Lucas, Mel
IR  - Lucas M
FIR - Knee, C
IR  - Knee C
FIR - Kneller, George
IR  - Kneller G
FIR - Kobylinski, Sabina
IR  - Kobylinski S
FIR - Risser, Joseph
IR  - Risser J
FIR - Kolba, Karen
IR  - Kolba K
FIR - Korff, Gary
IR  - Korff G
FIR - Kosinski, Edward
IR  - Kosinski E
FIR - Krichmar, Perry
IR  - Krichmar P
FIR - Krumian, Razmig
IR  - Krumian R
FIR - Portnoy, Edward
IR  - Portnoy E
FIR - Kumar, Mariananda
IR  - Kumar M
FIR - Fellows, Chistopher
IR  - Fellows C
FIR - Kumar, Ullattil
IR  - Kumar U
FIR - Kohli, Nandini
IR  - Kohli N
FIR - Kwon, Elise
IR  - Kwon E
FIR - Ladner, Timothy
IR  - Ladner T
FIR - Lambert, Jarvis
IR  - Lambert J
FIR - Lamothe, Mario
IR  - Lamothe M
FIR - Lang, Robert
IR  - Lang R
FIR - Laramee, Christine
IR  - Laramee C
FIR - Larrain, German
IR  - Larrain G
FIR - Lawson, Jeffrey
IR  - Lawson J
FIR - Leach, Charles
IR  - Leach C
FIR - Lee, Tat
IR  - Lee T
FIR - Leggett, Richard
IR  - Leggett R
FIR - Lenzmeier, Thomas
IR  - Lenzmeier T
FIR - Leung, Lester
IR  - Leung L
FIR - Levinsky, Dale
IR  - Levinsky D
FIR - Levinson, Lawrence
IR  - Levinson L
FIR - Lewis, David
IR  - Lewis D
FIR - Lidman, Roger
IR  - Lidman R
FIR - Lieberman, Donald
IR  - Lieberman D
FIR - Lim, Esther
IR  - Lim E
FIR - Parikh, Naresh
IR  - Parikh N
FIR - Wyatt, David
IR  - Wyatt D
FIR - Linden, Dennis
IR  - Linden D
FIR - Littlefield, Ronald
IR  - Littlefield R
FIR - Long, John
IR  - Long J
FIR - Long, William
IR  - Long W
FIR - Longshaw, Kevin
IR  - Longshaw K
FIR - Lorraine, Richard
IR  - Lorraine R
FIR - Losoya, Gerardo
IR  - Losoya G
FIR - Lowe, John
IR  - Lowe J
FIR - Lozman, Philip
IR  - Lozman P
FIR - Lubin, Barry
IR  - Lubin B
FIR - Ludivico, Charles
IR  - Ludivico C
FIR - Lunseth, Paul
IR  - Lunseth P
FIR - Paraskevopoulos, Nektaria
IR  - Paraskevopoulos N
FIR - Rusterholtz, Lori Ann
IR  - Rusterholtz LA
FIR - Lutz, Kevin
IR  - Lutz K
FIR - Lynch, Michael
IR  - Lynch M
FIR - MacCarter, Daryl
IR  - MacCarter D
FIR - MacGillivray, Brian
IR  - MacGillivray B
FIR - Madsen, Lisa
IR  - Madsen L
FIR - Maduakolam, Chinedu
IR  - Maduakolam C
FIR - Magargle, Rodney
IR  - Magargle R
FIR - Maggiacomo, Frank
IR  - Maggiacomo F
FIR - Makarowski, William
IR  - Makarowski W
FIR - Mandel, David
IR  - Mandel D
FIR - Manlove-Simmons, Kris
IR  - Manlove-Simmons K
FIR - Hodge, Rasean
IR  - Hodge R
FIR - Manning, Deborah
IR  - Manning D
FIR - Marcadis, Abe
IR  - Marcadis A
FIR - Marino, Louis
IR  - Marino L
FIR - Marks, Steven
IR  - Marks S
FIR - O’Reilly, Terry
IR  - O’Reilly T
FIR - Martin, Kenneth
IR  - Martin K
FIR - Martinez, Juvenal
IR  - Martinez J
FIR - Marwah, Rajendra
IR  - Marwah R
FIR - Matar, Fadi
IR  - Matar F
FIR - Mathews, Steven
IR  - Mathews S
FIR - Mathur, Rameshwar
IR  - Mathur R
FIR - Mazzone, Frank
IR  - Mazzone F
FIR - McCormick, Brian
IR  - McCormick B
FIR - McCurley, LeeRoy
IR  - McCurley L
FIR - McDermott, Edward
IR  - McDermott E
FIR - McDonald, David
IR  - McDonald D
FIR - McElya, Martin
IR  - McElya M
FIR - McFarland, Mairus
IR  - McFarland M
FIR - McGrew, Frank
IR  - McGrew F
FIR - McIntosh, Marvin
IR  - McIntosh M
FIR - McKenzie, Wilfred
IR  - McKenzie W
FIR - McLaurin, Brent
IR  - McLaurin B
FIR - McLean, Barry
IR  - McLean B
FIR - McRae, Jon
IR  - McRae J
FIR - Surratt, Darrekk
IR  - Surratt D
FIR - Mefford, Ivan
IR  - Mefford I
FIR - Mehta, Daksha
IR  - Mehta D
FIR - Mehta, Praful
IR  - Mehta P
FIR - Mehta, Chandrakant
IR  - Mehta C
FIR - Meka, Ajay
IR  - Meka A
FIR - Meli, James
IR  - Meli J
FIR - Merritt, Brock
IR  - Merritt B
FIR - Michlin, Bernard
IR  - Michlin B
FIR - Mihills, Cody
IR  - Mihills C
FIR - Mikhail, Magdy
IR  - Mikhail M
FIR - Milas, John
IR  - Milas J
FIR - Miller, James
IR  - Miller J
FIR - Miller, Sam
IR  - Miller S
FIR - Miller, Jeffrey
IR  - Miller J
FIR - Miller, Gary
IR  - Miller G
FIR - Miller, David
IR  - Miller D
FIR - Miller, Paul
IR  - Miller P
FIR - Mills, Richard
IR  - Mills R
FIR - Minkowitz, Harold
IR  - Minkowitz H
FIR - Miranda, Francisco
IR  - Miranda F
FIR - Mizutani, Wesley
IR  - Mizutani W
FIR - Modiano, Manuel
IR  - Modiano M
FIR - Modugu, Sathish
IR  - Modugu S
FIR - Moidel, Robert
IR  - Moidel R
FIR - Mollen, Arthur
IR  - Mollen A
FIR - Molter, Darron
IR  - Molter D
FIR - Morcos, Chadia
IR  - Morcos C
FIR - Morelli, Joseph
IR  - Morelli J
FIR - Moretti, James
IR  - Moretti J
FIR - Morgan, Athol
IR  - Morgan A
FIR - Morgan, Cynthia
IR  - Morgan C
FIR - Morin, David
IR  - Morin D
FIR - Miller, Jerry
IR  - Miller J
FIR - Morris, David
IR  - Morris D
FIR - Surbeck, William
IR  - Surbeck W
FIR - Morris, Walter
IR  - Morris W
FIR - Davis, Keith
IR  - Davis K
FIR - Morrison, Bruce
IR  - Morrison B
FIR - Mortensen, Steen
IR  - Mortensen S
FIR - Lies, Richard
IR  - Lies R
FIR - Mossberg, Jane
IR  - Mossberg J
FIR - Moya-Hechevarria, Jaynier
IR  - Moya-Hechevarria J
FIR - Mugmon, Marc
IR  - Mugmon M
FIR - Meilman, Henry
IR  - Meilman H
FIR - Murillo, Abel
IR  - Murillo A
FIR - Myerson, Gary
IR  - Myerson G
FIR - Naini, Gnanasumathi
IR  - Naini G
FIR - Nalamachu, Srinivas
IR  - Nalamachu S
FIR - Neal, Jeffrey
IR  - Neal J
FIR - Neal, Nathaniel
IR  - Neal N
FIR - Neidorf, David
IR  - Neidorf D
FIR - Neutel, Joel
IR  - Neutel J
FIR - Neuwelt, Clark
IR  - Neuwelt C
FIR - Nguyen, Thach
IR  - Nguyen T
FIR - Nielsen, Richard
IR  - Nielsen R
FIR - Norwood, Paul
IR  - Norwood P
FIR - Novak, Holly
IR  - Novak H
FIR - Nualart, Maria
IR  - Nualart M
FIR - Ares-Romero, Patricia
IR  - Ares-Romero P
FIR - Columbie, Arsenio
IR  - Columbie A
FIR - Nwabara, Okechi
IR  - Nwabara O
FIR - Nwaneri, Uchenna
IR  - Nwaneri U
FIR - O'Barr, Thomas
IR  - O'Barr T
FIR - Oberoi, Mandeep
IR  - Oberoi M
FIR - Ocampo, Alvaro
IR  - Ocampo A
FIR - Oftadeh, Lydia
IR  - Oftadeh L
FIR - Azurin, Eleanor
IR  - Azurin E
FIR - Ogden, Paul
IR  - Ogden P
FIR - Old, Wayne
IR  - Old W
FIR - Olds, Shelby
IR  - Olds S
FIR - Martin, Frederick
IR  - Martin F
FIR - Ong, Stephen
IR  - Ong S
FIR - Oppy, J
IR  - Oppy J
FIR - Otah, Kenneth
IR  - Otah K
FIR - Uzoaga, Enyibuaku
IR  - Uzoaga E
FIR - Pace, Michael
IR  - Pace M
FIR - Paez, Henry
IR  - Paez H
FIR - Rousseau, Roger
IR  - Rousseau R
FIR - Palmer, William
IR  - Palmer W
FIR - Pamfilis, Stanley
IR  - Pamfilis S
FIR - Pando, Jose
IR  - Pando J
FIR - Gomez, John
IR  - Gomez J
FIR - Paraboschi, Charles
IR  - Paraboschi C
FIR - Pasya, Suresh Kumar
IR  - Pasya SK
FIR - Shamim, Talha
IR  - Shamim T
FIR - Patron, Andres
IR  - Patron A
FIR - Patton, Charles
IR  - Patton C
FIR - Colvin, David
IR  - Colvin D
FIR - Pavon, Humberto
IR  - Pavon H
FIR - Payne, Dayton
IR  - Payne D
FIR - Pearlstein, Philip
IR  - Pearlstein P
FIR - Peck, Brian
IR  - Peck B
FIR - Peller, Jeffrey
IR  - Peller J
FIR - Peniston, John
IR  - Peniston J
FIR - Pepine, Carl
IR  - Pepine C
FIR - Perez, Jorge
IR  - Perez J
FIR - Perry, Robert
IR  - Perry R
FIR - Peters, Lenin
IR  - Peters L
FIR - Peterson, Daniel
IR  - Peterson D
FIR - Pharr, Walter
IR  - Pharr W
FIR - Anderson, Anthony
IR  - Anderson A
FIR - Philander, Peter
IR  - Philander P
FIR - Pish, Richard
IR  - Pish R
FIR - Plancher, Kevin
IR  - Plancher K
FIR - Plasner, Samantha
IR  - Plasner S
FIR - Pattanayak, Minati
IR  - Pattanayak M
FIR - Poludniak, Julie
IR  - Poludniak J
FIR - Pomposini, Daniel
IR  - Pomposini D
FIR - Popeil, Larry
IR  - Popeil L
FIR - Porges, Andrew
IR  - Porges A
FIR - Porter, Clarence
IR  - Porter C
FIR - Porter, Annette
IR  - Porter A
FIR - Porterfield, James
IR  - Porterfield J
FIR - Poss, Geri
IR  - Poss G
FIR - Post, Gary
IR  - Post G
FIR - Potts, Jeffrey
IR  - Potts J
FIR - Pounds, Kevin
IR  - Pounds K
FIR - Prelutsky, David
IR  - Prelutsky D
FIR - Prentiss, Adrienne
IR  - Prentiss A
FIR - Prieto, Blas
IR  - Prieto B
FIR - Pritchett, Kevin
IR  - Pritchett K
FIR - Promin, Richard
IR  - Promin R
FIR - Pruitt, Ronald
IR  - Pruitt R
FIR - Prupas, Henry
IR  - Prupas H
FIR - Quartner, Jeffrey
IR  - Quartner J
FIR - Raad, George
IR  - Raad G
FIR - Radin, David
IR  - Radin D
FIR - Raja, Naveen
IR  - Raja N
FIR - Ramstad, David
IR  - Ramstad D
FIR - Ranasinghe, Elizabeth
IR  - Ranasinghe E
FIR - Randall, William
IR  - Randall W
FIR - Rapo, Seppo
IR  - Rapo S
FIR - Rapoport, Ronald
IR  - Rapoport R
FIR - Raupp, Mark
IR  - Raupp M
FIR - Recknor, Christopher
IR  - Recknor C
FIR - Reddy, Rajneesh
IR  - Reddy R
FIR - McNeff, John
IR  - McNeff J
FIR - Renzi, Michael
IR  - Renzi M
FIR - Reynolds, Albert
IR  - Reynolds A
FIR - Rhodes, Robert
IR  - Rhodes R
FIR - Riaz, Mohammad
IR  - Riaz M
FIR - Ricca, Anthony
IR  - Ricca A
FIR - Riccardi, Patrick
IR  - Riccardi P
FIR - Ricci, Donato
IR  - Ricci D
FIR - Rice, Doris
IR  - Rice D
FIR - Richwine, Randall
IR  - Richwine R
FIR - Rico, Angel
IR  - Rico A
FIR - Rictor, Kenneth
IR  - Rictor K
FIR - Riegel, Brian
IR  - Riegel B
FIR - Corbelli, John
IR  - Corbelli J
FIR - Riley, Steven
IR  - Riley S
FIR - Reilly, William
IR  - Reilly W
FIR - Rivas, Dency
IR  - Rivas D
FIR - Rizzo, Warren
IR  - Rizzo W
FIR - Roberts, Douglas
IR  - Roberts D
FIR - Robins, Guy
IR  - Robins G
FIR - McDavid, Richard
IR  - McDavid R
FIR - Robinson, Jerry
IR  - Robinson J
FIR - Jones, Conigliaro
IR  - Jones C
FIR - Rodriguez, Hector
IR  - Rodriguez H
FIR - Rodriguez, Ignacio
IR  - Rodriguez I
FIR - Rogers, Brenda
IR  - Rogers B
FIR - Rogusky, Edwin
IR  - Rogusky E
FIR - Rohr, Christine
IR  - Rohr C
FIR - Baumbach, Rebecca
IR  - Baumbach R
FIR - Rosen, Robert
IR  - Rosen R
FIR - Rosenblum, Gary
IR  - Rosenblum G
FIR - Rosenfeld, Jack
IR  - Rosenfeld J
FIR - Seidner, Michael
IR  - Seidner M
FIR - Rosenthal, Ann
IR  - Rosenthal A
FIR - Almassi, Gholam
IR  - Almassi G
FIR - Ross, Steven
IR  - Ross S
FIR - Ryan, William
IR  - Ryan W
FIR - Saifi, Ali
IR  - Saifi A
FIR - Saikali, Wassim
IR  - Saikali W
FIR - Sakiewicz, Andrew
IR  - Sakiewicz A
FIR - Sakornbut, Ellen
IR  - Sakornbut E
FIR - Salazar, Jorge
IR  - Salazar J
FIR - Salmon, James
IR  - Salmon J
FIR - Sandberg, Jay
IR  - Sandberg J
FIR - Saniuk, Robert
IR  - Saniuk R
FIR - Santhanam, Shankar
IR  - Santhanam S
FIR - Tengco, Romulo
IR  - Tengco R
FIR - Santoscoy, Raul
IR  - Santoscoy R
FIR - Nikas, Aris
IR  - Nikas A
FIR - Saponaro, Joseph
IR  - Saponaro J
FIR - Sauter, Michael
IR  - Sauter M
FIR - Berger, Malcolm
IR  - Berger M
FIR - Sayeed, Sifatur
IR  - Sayeed S
FIR - Schechtman, Joy
IR  - Schechtman J
FIR - Schenk, Alan
IR  - Schenk A
FIR - Scherbarth, Kenneth
IR  - Scherbarth K
FIR - Schiffman, Lawrence
IR  - Schiffman L
FIR - Schmedtje, John
IR  - Schmedtje J
FIR - Schneider, Robert
IR  - Schneider R
FIR - Schock, Joel
IR  - Schock J
FIR - Schramm, Erich
IR  - Schramm E
FIR - Schwartz, Kerry
IR  - Schwartz K
FIR - Schwartz, Stuart
IR  - Schwartz S
FIR - Schwartzenberg, Janet
IR  - Schwartzenberg J
FIR - Schwarz, Edward
IR  - Schwarz E
FIR - Scott, David
IR  - Scott D
FIR - Seals, Albert
IR  - Seals A
FIR - Meiners, Rebecca
IR  - Meiners R
FIR - Seaton, Bruce
IR  - Seaton B
FIR - Sebai, Mohamed
IR  - Sebai M
FIR - Boling, Eugene
IR  - Boling E
FIR - Sebba, Anthony
IR  - Sebba A
FIR - Seco, Gilberto
IR  - Seco G
FIR - Segal, Stewart
IR  - Segal S
FIR - Seidmeyer, Vicki
IR  - Seidmeyer V
FIR - Selsky, Evan
IR  - Selsky E
FIR - Jerome, Scott
IR  - Jerome S
FIR - Sensenbrenner, John
IR  - Sensenbrenner J
FIR - Shah, Shaukat
IR  - Shah S
FIR - Shah, Ahmed
IR  - Shah A
FIR - James, Erskine
IR  - James E
FIR - Shah, Dhiren
IR  - Shah D
FIR - Shah, Mahesh
IR  - Shah M
FIR - Shah, Gaurang
IR  - Shah G
FIR - Shammas, Nicolas
IR  - Shammas N
FIR - Duke, Shawna
IR  - Duke S
FIR - Shams, Fariborz
IR  - Shams F
FIR - Shandilya, Loknath
IR  - Shandilya L
FIR - Shemonsky, Natalie
IR  - Shemonsky N
FIR - Shergy, William
IR  - Shergy W
FIR - Sherman, Howard
IR  - Sherman H
FIR - Khan, Richard
IR  - Khan R
FIR - Shockey, Gerald
IR  - Shockey G
FIR - Shusman, Robert
IR  - Shusman R
FIR - Siegel, Evan
IR  - Siegel E
FIR - Sikes, David
IR  - Sikes D
FIR - Silverfield, Joel
IR  - Silverfield J
FIR - Simon, Robert
IR  - Simon R
FIR - Singhal, Atul
IR  - Singhal A
FIR - Sklaver, Neal
IR  - Sklaver N
FIR - Skyhar, Michael
IR  - Skyhar M
FIR - Slabic, Stan
IR  - Slabic S
FIR - Sligh, Teresa
IR  - Sligh T
FIR - Smith, Lynn
IR  - Smith L
FIR - Smith, Stephen
IR  - Smith S
FIR - Snyder, Brian
IR  - Snyder B
FIR - Solano, Royce
IR  - Solano R
FIR - Solinsky, Kenneth
IR  - Solinsky K
FIR - Solomon, Sheldon
IR  - Solomon S
FIR - Som, Deborah
IR  - Som D
FIR - Sonel, Elif
IR  - Sonel E
FIR - Sonel, Ali
IR  - Sonel A
FIR - Sosenko, Maria
IR  - Sosenko M
FIR - Sotolongo, Rodolfo
IR  - Sotolongo R
FIR - Sousa, Daniel
IR  - Sousa D
FIR - Ali, Moustafa
IR  - Ali M
FIR - Spivack, Eric
IR  - Spivack E
FIR - Sprague, Amy
IR  - Sprague A
FIR - Srivastava, Sunny
IR  - Srivastava S
FIR - Bilazarian, Seth
IR  - Bilazarian S
FIR - Livson, Anna
IR  - Livson A
FIR - Portnay, Gary
IR  - Portnay G
FIR - Stack, Michael
IR  - Stack M
FIR - Staub, Jonathan
IR  - Staub J
FIR - Stearns, Pamela
IR  - Stearns P
FIR - Stedman, Mary
IR  - Stedman M
FIR - Steffens, Rebecca
IR  - Steffens R
FIR - Stegemoller, Ronald
IR  - Stegemoller R
FIR - Steinberg, Paul
IR  - Steinberg P
FIR - Stephens, Michael
IR  - Stephens M
FIR - Stephens, Louis
IR  - Stephens L
FIR - Stern, Richard
IR  - Stern R
FIR - Stevens, Johnnie
IR  - Stevens J
FIR - Collins, Barry
IR  - Collins B
FIR - Stoltz, Steven
IR  - Stoltz S
FIR - Trevino, John
IR  - Trevino J
FIR - Stone, William
IR  - Stone W
FIR - Lesh, Kurt
IR  - Lesh K
FIR - Stout, Rodney
IR  - Stout R
FIR - Rasheed, Mehmoodur
IR  - Rasheed M
FIR - Strain, Richard
IR  - Strain R
FIR - Straniero, Nicholas
IR  - Straniero N
FIR - Studeny, Mark
IR  - Studeny M
FIR - Stupi, Angela
IR  - Stupi A
FIR - Shook, Betsy
IR  - Shook B
FIR - Tyma, Thomas
IR  - Tyma T
FIR - Subich, David
IR  - Subich D
FIR - Suiter, Daniel
IR  - Suiter D
FIR - Suley, Elhan
IR  - Suley E
FIR - Corst, Irine
IR  - Corst I
FIR - Sulich, Andrew
IR  - Sulich A
FIR - Sullivan, Neil
IR  - Sullivan N
FIR - Sutherland, John
IR  - Sutherland J
FIR - Ulven, Matthew
IR  - Ulven M
FIR - Swift, David
IR  - Swift D
FIR - Szewczak, Suzann
IR  - Szewczak S
FIR - Bock, Brain
IR  - Bock B
FIR - Tamayo, Raul
IR  - Tamayo R
FIR - Tan, Edison
IR  - Tan E
FIR - Taunton, Oscar
IR  - Taunton O
FIR - Tavel, Edward
IR  - Tavel E
FIR - Tawney, Kathryn
IR  - Tawney K
FIR - Silverblatt, James
IR  - Silverblatt J
FIR - Taylor, Philip
IR  - Taylor P
FIR - Tidmore, William
IR  - Tidmore W
FIR - Titus, John
IR  - Titus J
FIR - Woodruff, Mark
IR  - Woodruff M
FIR - Trapp, Robert
IR  - Trapp R
FIR - Trevino, Miguel
IR  - Trevino M
FIR - Trivedi, Ketan
IR  - Trivedi K
FIR - Alexander, Arnold
IR  - Alexander A
FIR - Troum, Orrin
IR  - Troum O
FIR - Tsai, Yong
IR  - Tsai Y
FIR - Turner, Mark
IR  - Turner M
FIR - Turner, Merle
IR  - Turner M
FIR - Tyndall, William
IR  - Tyndall W
FIR - Underwood, Paul
IR  - Underwood P
FIR - Valerio, Donald
IR  - Valerio D
FIR - van Cleeff, Martin
IR  - van Cleeff M
FIR - Vanderlaan, Ronald
IR  - Vanderlaan R
FIR - Vargo, Jill
IR  - Vargo J
FIR - Varma, Shalendra
IR  - Varma S
FIR - Vaughn, Michael
IR  - Vaughn M
FIR - Victoria, Rafaelito
IR  - Victoria R
FIR - Wadsworth, Larkin
IR  - Wadsworth L
FIR - Wagner, Stephen
IR  - Wagner S
FIR - Wallner, Harry
IR  - Wallner H
FIR - Walter, Norman
IR  - Walter N
FIR - Ward, Samuel
IR  - Ward S
FIR - Warfield, David
IR  - Warfield D
FIR - Waxman, Jack
IR  - Waxman J
FIR - Wayne, Jeffrey
IR  - Wayne J
FIR - Weaver, Cynthia
IR  - Weaver C
FIR - Moore, Charles
IR  - Moore C
FIR - Wei, Nathan
IR  - Wei N
FIR - Weinstein, Debra
IR  - Weinstein D
FIR - Weiss, Robert
IR  - Weiss R
FIR - Weitz, Michael
IR  - Weitz M
FIR - Wenocur, Howard
IR  - Wenocur H
FIR - Wentworth, Rance
IR  - Wentworth R
FIR - Weprin, Stuart
IR  - Weprin S
FIR - Wiesenhutter, Craig
IR  - Wiesenhutter C
FIR - Wieskopf, Bram
IR  - Wieskopf B
FIR - Wild, James
IR  - Wild J
FIR - Williams, David
IR  - Williams D
FIR - Williams, Tearani
IR  - Williams T
FIR - Conard, Scott
IR  - Conard S
FIR - Wilmer, Charles
IR  - Wilmer C
FIR - Wilson, Jonathan
IR  - Wilson J
FIR - Wilson, Scott
IR  - Wilson S
FIR - Winkler, Anne
IR  - Winkler A
FIR - Wood, John
IR  - Wood J
FIR - Woods, Bronwyn
IR  - Woods B
FIR - Yakubov, Steven
IR  - Yakubov S
FIR - Yamada, Hugo
IR  - Yamada H
FIR - Yang, Marcos
IR  - Yang M
FIR - Yataco, Alberto
IR  - Yataco A
FIR - Yates, Scott
IR  - Yates S
FIR - Yazdani, Shahbaz
IR  - Yazdani S
FIR - Ylisastigui, Pedro
IR  - Ylisastigui P
FIR - Yoachim, Robert
IR  - Yoachim R
FIR - Smith, Dirk
IR  - Smith D
FIR - Yood, Robert
IR  - Yood R
FIR - Young, Carol
IR  - Young C
FIR - Young, Douglas
IR  - Young D
FIR - Yuen, John
IR  - Yuen J
FIR - Zaheer, Amer
IR  - Zaheer A
FIR - Zaidi, Farrukh
IR  - Zaidi F
FIR - Zakko, Salam
IR  - Zakko S
EDAT- 2016/12/14 06:00
MHDA- 2017/01/11 06:00
CRDT- 2016/12/14 06:00
PHST- 2016/12/14 06:00 [pubmed]
PHST- 2017/01/11 06:00 [medline]
PHST- 2016/12/14 06:00 [entrez]
AID - 10.1056/NEJMoa1611593 [doi]
PST - ppublish
SO  - N Engl J Med. 2016 Dec 29;375(26):2519-29. doi: 10.1056/NEJMoa1611593. Epub 2016 
      Nov 13.

PMID- 27928943
OWN - NLM
STAT- MEDLINE
DCOM- 20180510
LR  - 20180510
IS  - 1875-5453 (Electronic)
IS  - 1389-2002 (Linking)
VI  - 18
IP  - 3
DP  - 2017
TI  - The Physiological/Pathophysiological Significance of Vitamin D in Cancer, 
      Cardiovascular Disorders and Beyond.
PG  - 207-224
LID - 10.2174/1389200217666161207161212 [doi]
AB  - BACKGROUND: Vitamin D, a molecular precursor of the potent steroid hormone 
      calcitriol, has crucial functions and roles in physiology and pathophysiology. 
      Tellingly, calcitriol has been shown to regulate various cellular signalling 
      networks and cascades that have crucial role in cancer biology and diagnostics. 
      Mounting lines of evidences from previous clinical and preclinical investigations 
      indicate that the deficiency of vitamin D may contribute to the carcinogenesis 
      risk. Concomitantly, recent reports suggested that significant reduction in the 
      cancer occurrence and progression is more likely to appear after vitamin D 
      supplementation. Furthermore, a pivotal role functioned by vitamin D in 
      cardiovascular physiology indicates that the deficiency of vitamin D is 
      significantly correlated with enhanced prevalence of stroke, hypertension and 
      myocardial infarction. Notably, vitamin D status is more likely to be used as a 
      lifestyle biomarker, since poor and unhealthy lifestyles are correlated with the 
      deficiency of vitamin D, a feature which may result in cardiovascular 
      complications. Moreover, recent reports revealed that the effect of vitamin D is 
      to cover not only cardiovascular system but also skeletal system. OBJECTIVE: 
      Herein, we are highlighting the recent knowledge of vitamin D roles and functions 
      with respect to pathophysiological disorders such as cancer, cardiovascular 
      diseases, rheumatoid arthritis (RA) and debate the potential avails of vitamin D 
      on slowing cancer, cardiovascular disease and RA progression. CONCLUSION: The 
      findings of this review confirm that the importance of vitamin D metabolites or 
      analogues which can provide a helpful platform to target some kinds of cancer, 
      particularly when used in combination with existing therapies. Moreover, the 
      correlation between vitamin D deficiencies with cardiovascular diseases and 
      rheumatoid arthritis (RA) progression might suggest a pivotal role of vitamin D 
      in either initiation or progression of these diseases.
CI  - Copyright© Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.org.
FAU - AlMatar, Manaf
AU  - AlMatar M
AD  - Department of Biotechnology, Institute of Natural and Applied Sciences (Fen 
      Bilimleri Enstitüsü), Cukurova University, 01330, Adana. Turkey.
FAU - AlMandeal, Husam
AU  - AlMandeal H
AD  - Universitatsklinikum des Saarlandes, Gebaude 90, Kirrberger Straβe D-66421 
      Homburg. Germany.
FAU - Makky, Essam A
AU  - Makky EA
AD  - University Malaysia Pahang, Faculty of Industrial Sciences & Technology, 26300 
      Kuantan, Pahang. Malaysia.
FAU - Kayar, Begum
AU  - Kayar B
AD  - Department of Medical Microbiology, Faculty of Medicine, Cukurova University, 
      TR-01100 Adana. Turkey.
FAU - Yarar, Emel
AU  - Yarar E
AD  - Department of Medical Microbiology, Faculty of Medicine, Cukurova University, 
      TR-01100 Adana. Turkey.
FAU - Var, Isıl
AU  - Var I
AD  - Department of Food Engineering, Agricultural Faculty, Cukurova University, 
      TR-01100 Adana. Turkey.
FAU - Koksal, Fatih
AU  - Koksal F
AD  - Department of Medical Microbiology, Faculty of Medicine, Cukurova University, 
      TR-01100 Adana. Turkey.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Netherlands
TA  - Curr Drug Metab
JT  - Current drug metabolism
JID - 100960533
RN  - 0 (Vitamins)
RN  - 1406-16-2 (Vitamin D)
SB  - IM
MH  - Animals
MH  - Cardiovascular Diseases/physiopathology
MH  - Humans
MH  - Neoplasms/physiopathology
MH  - Vitamin D/immunology/metabolism/*physiology
MH  - Vitamins/immunology/metabolism/*physiology
OTO - NOTNLM
OT  - Vitamin D
OT  - cancer
OT  - cardiovascular diseases
OT  - clinical trials
OT  - rheumatoid arthritis (RA)
OT  - therapeutic agent.
EDAT- 2016/12/09 06:00
MHDA- 2018/05/11 06:00
CRDT- 2016/12/09 06:00
PHST- 2016/08/07 00:00 [received]
PHST- 2016/11/20 00:00 [revised]
PHST- 2016/11/26 00:00 [accepted]
PHST- 2016/12/09 06:00 [pubmed]
PHST- 2018/05/11 06:00 [medline]
PHST- 2016/12/09 06:00 [entrez]
AID - CDM-EPUB-80202 [pii]
AID - 10.2174/1389200217666161207161212 [doi]
PST - ppublish
SO  - Curr Drug Metab. 2017;18(3):207-224. doi: 10.2174/1389200217666161207161212.

PMID- 27881629
OWN - NLM
STAT- MEDLINE
DCOM- 20170518
LR  - 20230808
IS  - 1526-632X (Electronic)
IS  - 0028-3878 (Print)
IS  - 0028-3878 (Linking)
VI  - 88
IP  - 1
DP  - 2017 Jan 3
TI  - Risk of fractures after stroke: Results from the Ontario Stroke Registry.
PG  - 57-64
LID - 10.1212/WNL.0000000000003457 [doi]
AB  - OBJECTIVE: To determine the risk of fractures after stroke. METHODS: Using the 
      Ontario Stroke Registry, we identified a population-based sample of consecutive 
      patients seen in the emergency department or hospitalized with stroke (n = 
      23,751) or TIA (n = 11,240) at any of 11 stroke centers in Ontario, Canada, and 
      discharged alive between July 1, 2003, and March 31, 2012. We compared the risk 
      of low-trauma fractures in patients with stroke vs those with TIA using 
      propensity score methods to adjust for differences in baseline factors. Secondary 
      analyses compared fracture risk poststroke with that in age-/sex-matched controls 
      without stroke or TIA (n = 23,751) identified from the Ontario Registered Persons 
      Database. RESULTS: The 2-year rate of fracture was 5.7% in those with stroke 
      compared to 4.8% in those with TIA (adjusted cause-specific hazard ratio [aHR] 
      for those with stroke vs TIA 1.32; 95% confidence interval [CI] 1.19-1.46) and 
      4.1% in age-/sex-matched controls (aHR for those with stroke vs controls 1.47; 
      95% CI 1.35-1.60). In the cohort with stroke, factors associated with fractures 
      were older age, female sex, moderate stroke severity, prior fractures or falls, 
      and preexisting osteoporosis, rheumatoid arthritis, hyperparathyroidism, and 
      atrial fibrillation. CONCLUSIONS: Stroke is associated with an increased risk of 
      low-trauma fractures. Individuals with stroke and additional risk factors for 
      fractures may benefit from targeted screening for low bone mineral density and 
      initiation of treatment for fracture prevention.
CI  - © 2016 American Academy of Neurology.
FAU - Kapral, Moira K
AU  - Kapral MK
AD  - From the Institute for Clinical Evaluative Sciences (M.K.K., J.F., P.C., M.S., 
      P.C.A.), Toronto; Department of Medicine, Division of General Internal Medicine 
      (M.K.K., S.M.H.A., P.C., A.M.C., M.P.), Institute of Health Policy, Management 
      and Evaluation (M.K.K., S.M.H.A., P.C., A.M.C., P.C.A.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University of Toronto; Division of 
      General Internal Medicine and Geriatrics and Toronto General Research Institute 
      (M.K.K., S.M.H.A., P.C., A.M.C.), Osteoporosis Program and Centre for Excellence 
      in Skeletal Health Assessment (M.K.K., S.M.H.A., A.M.C.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University Health Network, Toronto; and 
      Schulich School of Medicine and Dentistry (B.R.), University of Western Ontario, 
      London, Canada. moira.kapral@uhn.ca.
FAU - Fang, Jiming
AU  - Fang J
AD  - From the Institute for Clinical Evaluative Sciences (M.K.K., J.F., P.C., M.S., 
      P.C.A.), Toronto; Department of Medicine, Division of General Internal Medicine 
      (M.K.K., S.M.H.A., P.C., A.M.C., M.P.), Institute of Health Policy, Management 
      and Evaluation (M.K.K., S.M.H.A., P.C., A.M.C., P.C.A.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University of Toronto; Division of 
      General Internal Medicine and Geriatrics and Toronto General Research Institute 
      (M.K.K., S.M.H.A., P.C., A.M.C.), Osteoporosis Program and Centre for Excellence 
      in Skeletal Health Assessment (M.K.K., S.M.H.A., A.M.C.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University Health Network, Toronto; and 
      Schulich School of Medicine and Dentistry (B.R.), University of Western Ontario, 
      London, Canada.
FAU - Alibhai, Shabbir M H
AU  - Alibhai SM
AD  - From the Institute for Clinical Evaluative Sciences (M.K.K., J.F., P.C., M.S., 
      P.C.A.), Toronto; Department of Medicine, Division of General Internal Medicine 
      (M.K.K., S.M.H.A., P.C., A.M.C., M.P.), Institute of Health Policy, Management 
      and Evaluation (M.K.K., S.M.H.A., P.C., A.M.C., P.C.A.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University of Toronto; Division of 
      General Internal Medicine and Geriatrics and Toronto General Research Institute 
      (M.K.K., S.M.H.A., P.C., A.M.C.), Osteoporosis Program and Centre for Excellence 
      in Skeletal Health Assessment (M.K.K., S.M.H.A., A.M.C.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University Health Network, Toronto; and 
      Schulich School of Medicine and Dentistry (B.R.), University of Western Ontario, 
      London, Canada.
FAU - Cram, Peter
AU  - Cram P
AD  - From the Institute for Clinical Evaluative Sciences (M.K.K., J.F., P.C., M.S., 
      P.C.A.), Toronto; Department of Medicine, Division of General Internal Medicine 
      (M.K.K., S.M.H.A., P.C., A.M.C., M.P.), Institute of Health Policy, Management 
      and Evaluation (M.K.K., S.M.H.A., P.C., A.M.C., P.C.A.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University of Toronto; Division of 
      General Internal Medicine and Geriatrics and Toronto General Research Institute 
      (M.K.K., S.M.H.A., P.C., A.M.C.), Osteoporosis Program and Centre for Excellence 
      in Skeletal Health Assessment (M.K.K., S.M.H.A., A.M.C.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University Health Network, Toronto; and 
      Schulich School of Medicine and Dentistry (B.R.), University of Western Ontario, 
      London, Canada.
FAU - Cheung, Angela M
AU  - Cheung AM
AD  - From the Institute for Clinical Evaluative Sciences (M.K.K., J.F., P.C., M.S., 
      P.C.A.), Toronto; Department of Medicine, Division of General Internal Medicine 
      (M.K.K., S.M.H.A., P.C., A.M.C., M.P.), Institute of Health Policy, Management 
      and Evaluation (M.K.K., S.M.H.A., P.C., A.M.C., P.C.A.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University of Toronto; Division of 
      General Internal Medicine and Geriatrics and Toronto General Research Institute 
      (M.K.K., S.M.H.A., P.C., A.M.C.), Osteoporosis Program and Centre for Excellence 
      in Skeletal Health Assessment (M.K.K., S.M.H.A., A.M.C.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University Health Network, Toronto; and 
      Schulich School of Medicine and Dentistry (B.R.), University of Western Ontario, 
      London, Canada.
FAU - Casaubon, Leanne K
AU  - Casaubon LK
AD  - From the Institute for Clinical Evaluative Sciences (M.K.K., J.F., P.C., M.S., 
      P.C.A.), Toronto; Department of Medicine, Division of General Internal Medicine 
      (M.K.K., S.M.H.A., P.C., A.M.C., M.P.), Institute of Health Policy, Management 
      and Evaluation (M.K.K., S.M.H.A., P.C., A.M.C., P.C.A.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University of Toronto; Division of 
      General Internal Medicine and Geriatrics and Toronto General Research Institute 
      (M.K.K., S.M.H.A., P.C., A.M.C.), Osteoporosis Program and Centre for Excellence 
      in Skeletal Health Assessment (M.K.K., S.M.H.A., A.M.C.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University Health Network, Toronto; and 
      Schulich School of Medicine and Dentistry (B.R.), University of Western Ontario, 
      London, Canada.
FAU - Prager, Marla
AU  - Prager M
AD  - From the Institute for Clinical Evaluative Sciences (M.K.K., J.F., P.C., M.S., 
      P.C.A.), Toronto; Department of Medicine, Division of General Internal Medicine 
      (M.K.K., S.M.H.A., P.C., A.M.C., M.P.), Institute of Health Policy, Management 
      and Evaluation (M.K.K., S.M.H.A., P.C., A.M.C., P.C.A.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University of Toronto; Division of 
      General Internal Medicine and Geriatrics and Toronto General Research Institute 
      (M.K.K., S.M.H.A., P.C., A.M.C.), Osteoporosis Program and Centre for Excellence 
      in Skeletal Health Assessment (M.K.K., S.M.H.A., A.M.C.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University Health Network, Toronto; and 
      Schulich School of Medicine and Dentistry (B.R.), University of Western Ontario, 
      London, Canada.
FAU - Stamplecoski, Melissa
AU  - Stamplecoski M
AD  - From the Institute for Clinical Evaluative Sciences (M.K.K., J.F., P.C., M.S., 
      P.C.A.), Toronto; Department of Medicine, Division of General Internal Medicine 
      (M.K.K., S.M.H.A., P.C., A.M.C., M.P.), Institute of Health Policy, Management 
      and Evaluation (M.K.K., S.M.H.A., P.C., A.M.C., P.C.A.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University of Toronto; Division of 
      General Internal Medicine and Geriatrics and Toronto General Research Institute 
      (M.K.K., S.M.H.A., P.C., A.M.C.), Osteoporosis Program and Centre for Excellence 
      in Skeletal Health Assessment (M.K.K., S.M.H.A., A.M.C.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University Health Network, Toronto; and 
      Schulich School of Medicine and Dentistry (B.R.), University of Western Ontario, 
      London, Canada.
FAU - Rashkovan, Brennan
AU  - Rashkovan B
AD  - From the Institute for Clinical Evaluative Sciences (M.K.K., J.F., P.C., M.S., 
      P.C.A.), Toronto; Department of Medicine, Division of General Internal Medicine 
      (M.K.K., S.M.H.A., P.C., A.M.C., M.P.), Institute of Health Policy, Management 
      and Evaluation (M.K.K., S.M.H.A., P.C., A.M.C., P.C.A.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University of Toronto; Division of 
      General Internal Medicine and Geriatrics and Toronto General Research Institute 
      (M.K.K., S.M.H.A., P.C., A.M.C.), Osteoporosis Program and Centre for Excellence 
      in Skeletal Health Assessment (M.K.K., S.M.H.A., A.M.C.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University Health Network, Toronto; and 
      Schulich School of Medicine and Dentistry (B.R.), University of Western Ontario, 
      London, Canada.
FAU - Austin, Peter C
AU  - Austin PC
AD  - From the Institute for Clinical Evaluative Sciences (M.K.K., J.F., P.C., M.S., 
      P.C.A.), Toronto; Department of Medicine, Division of General Internal Medicine 
      (M.K.K., S.M.H.A., P.C., A.M.C., M.P.), Institute of Health Policy, Management 
      and Evaluation (M.K.K., S.M.H.A., P.C., A.M.C., P.C.A.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University of Toronto; Division of 
      General Internal Medicine and Geriatrics and Toronto General Research Institute 
      (M.K.K., S.M.H.A., P.C., A.M.C.), Osteoporosis Program and Centre for Excellence 
      in Skeletal Health Assessment (M.K.K., S.M.H.A., A.M.C.), and Department of 
      Medicine, Division of Neurology (L.K.C.), University Health Network, Toronto; and 
      Schulich School of Medicine and Dentistry (B.R.), University of Western Ontario, 
      London, Canada.
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
DEP - 20161123
PL  - United States
TA  - Neurology
JT  - Neurology
JID - 0401060
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Community Health Planning
MH  - Female
MH  - Fractures, Bone/*epidemiology
MH  - Humans
MH  - Ischemic Attack, Transient/epidemiology
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Ontario/epidemiology
MH  - Outcome Assessment, Health Care
MH  - Proportional Hazards Models
MH  - *Registries/statistics & numerical data
MH  - Retrospective Studies
MH  - *Risk
MH  - Stroke/*epidemiology
PMC - PMC5200858
EDAT- 2016/11/25 06:00
MHDA- 2017/05/19 06:00
PMCR- 2018/01/03
CRDT- 2016/11/25 06:00
PHST- 2016/05/06 00:00 [received]
PHST- 2016/09/22 00:00 [accepted]
PHST- 2016/11/25 06:00 [pubmed]
PHST- 2017/05/19 06:00 [medline]
PHST- 2016/11/25 06:00 [entrez]
PHST- 2018/01/03 00:00 [pmc-release]
AID - WNL.0000000000003457 [pii]
AID - NEUROLOGY2016743302 [pii]
AID - 10.1212/WNL.0000000000003457 [doi]
PST - ppublish
SO  - Neurology. 2017 Jan 3;88(1):57-64. doi: 10.1212/WNL.0000000000003457. Epub 2016 
      Nov 23.

PMID- 27854095
OWN - NLM
STAT- MEDLINE
DCOM- 20170606
LR  - 20170606
IS  - 1028-768X (Print)
IS  - 1028-768X (Linking)
VI  - 25
IP  - 2
DP  - 2016 Jun 15
TI  - Cerebral Venous Sinus Thrombosis in A Patient with Sjögren's Syndrome with 
      Atypical Antibodies: A Case Report.
PG  - 65-69
AB  - BACKGROUND: Although Sjögren's syndrome has been known to complicate with white 
      matter lesions, encephalopathy, or stroke, reports of cerebral venous sinus 
      thrombosis due to Sjögren's syndrome with atypical antibodies are rare. CASE 
      REPORT: A 50-year-old woman was admitted to our neurological ward with nausea and 
      vomiting following acute onset of severe headache in the left occipital region. 
      Brain computed tomography revealed no abnormalities. The patient was fully 
      conscious, with normal cognitive functioning, but exhibited unsteady tandem gait. 
      Both magnetic resonance venography and computed tomography venography suggested 
      left transverse sinus blockage. Intravenous enoxaparin, followed by oral 
      warfarin, was initiated as treatment for cerebral venous sinus thrombosis. After 
      investigation, Sjögren's syndrome was diagnosed and lupus anticoagulant antibody 
      test was positive. The patient was treated with hydroxychloroquine, and appeared 
      fully recovered at the 6-month follow-up, with no clinical or radiological signs 
      of relapse. CONCLUSION: This case reports the relationship between cerebral 
      venous sinus thrombosis and Sjögren's syndrome. It is necessary to screen 
      autoimmune disorders in patients with cerebral venous sinus thrombosis that 
      present with no common risk factors of venous thrombosis in order to prevent 
      inappropriate management, and potentially adverse outcomes.
FAU - Ho, Tsung-Han
AU  - Ho TH
AD  - Department of Neurology, Tri-Service General Hospital, National Defense Medical 
      Center, Taipei, Taiwan.
FAU - Hsu, Yu-Wei
AU  - Hsu YW
AD  - Department of Neurology, Tri-Service General Hospital, National Defense Medical 
      Center, Taipei, Taiwan.
FAU - Wang, Chih-Wei
AU  - Wang CW
AD  - Department of Radiology, Tri-Service General Hospital, National Defense Medical 
      Center.
FAU - Lee, Jiunn-Tay
AU  - Lee JT
AD  - Department of Neurology, Tri-Service General Hospital, National Defense Medical 
      Center, Taipei, Taiwan.
FAU - Ting, Chi-Hsin
AU  - Ting CH
AD  - Department of Neurology, Tri-Service General Hospital, National Defense Medical 
      Center, Taipei, Taiwan.
FAU - Yang, Fu-Chi
AU  - Yang FC
AD  - Department of Neurology, Tri-Service General Hospital, National Defense Medical 
      Center, Taipei, Taiwan.
LA  - eng
PT  - Case Reports
PT  - Journal Article
PL  - China (Republic : 1949- )
TA  - Acta Neurol Taiwan
JT  - Acta neurologica Taiwanica
JID - 9815355
RN  - 0 (Lupus Coagulation Inhibitor)
SB  - IM
MH  - Female
MH  - Humans
MH  - Lupus Coagulation Inhibitor/*immunology
MH  - Middle Aged
MH  - *Sinus Thrombosis, Intracranial/diagnosis/etiology/immunology
MH  - *Sjogren's Syndrome/complications/diagnosis/immunology
EDAT- 2016/11/18 06:00
MHDA- 2017/06/07 06:00
CRDT- 2016/11/18 06:00
PHST- 2016/11/18 06:00 [entrez]
PHST- 2016/11/18 06:00 [pubmed]
PHST- 2017/06/07 06:00 [medline]
AID - 10196099/252065 [pii]
PST - ppublish
SO  - Acta Neurol Taiwan. 2016 Jun 15;25(2):65-69.

PMID- 27841110
OWN - NLM
STAT- MEDLINE
DCOM- 20170203
LR  - 20220408
IS  - 1748-5460 (Electronic)
IS  - 0022-2151 (Print)
IS  - 0022-2151 (Linking)
VI  - 130
IP  - S2
DP  - 2016 May
TI  - Pre-treatment clinical assessment in head and neck cancer: United Kingdom 
      National Multidisciplinary Guidelines.
PG  - S13-S22
AB  - This is the official guideline endorsed by the specialty associations involved in 
      the care of head and neck cancer patients in the UK. This paper provides 
      recommendations on the pre-treatment clinical assessment of patients presenting 
      with head and neck cancer. Recommendations • Comorbidity data should be collected 
      as it is important in the analysis of survival, quality of life and functional 
      outcomes after treatment as well as for comparing results of different treatment 
      regimens and different centres. (R) • Patients with hypertension of over 180/110 
      or associated target organ damage, should have antihypertensive medication 
      started pre-operatively as per British Hypertension Society guidelines. (R) • 
      Rapidly correcting pre-operative hypertension with beta blockade appears to cause 
      higher mortality due to stroke and hypotension and should not be used. (R) • 
      Patients with poorly controlled or unstable ischaemic heart disease should be 
      referred for cardiology assessment pre-operatively. (G) • Patients within one 
      year of drug eluting stents should be discussed with the cardiologist who was 
      responsible for their percutaneous coronary intervention pre-operatively with 
      regard to cessation of antiplatelet medication due to risk of stent thrombosis. 
      (G) • Patients with multiple recent stents should be managed in a centre with 
      access to interventional cardiology. (G) • Surgery after myocardial infarction 
      should be delayed if possible to reduce mortality risk. (R) • Patients with 
      critical aortic stenosis (AS) should be considered for pre-operative 
      intervention. (G) • Clopidogrel should be discontinued 7 days pre-operatively; 
      warfarin should be discontinued 5 days pre-operatively. (R) • Patients with 
      thromboembolic disease or artificial heart valves require heparin therapy to 
      bridge peri-operative warfarin cessation, this should start 2 days after last 
      warfarin dose. (R) • Cardiac drugs other than angotensin-converting enzyme 
      inhibitors and angiotensin II antagonists should be continued including on the 
      day of surgery. (R) • Angotensin-converting enzyme inhibitors and angiotensin II 
      antagonists should be withheld on the day of surgery unless they are for the 
      treatment of heart failure. (R) • Post-operative care in a critical care area 
      should be considered for patients with heart failure or significant diastolic 
      dysfunction. (R) • Patients with respiratory disease should have their 
      peri-operative respiratory failure risk assessed and critical care booked 
      accordingly. (G) • Patients with severe lung disease should be assessed for right 
      heart disease pre-operatively. (G) • Patients with pulmonary hypertension and 
      right heart failure will be at extraordinarily high risk and should have the need 
      for surgery re-evaluated. (G) • Perioperative glucose readings should be kept 
      within 4-12 mmol/l. (R) • Patients with a high HbA1C facing urgent surgery should 
      have their diabetes management assessed by a diabetes specialist. (G) • 
      Insulin-dependent diabetic patients must not omit insulin for more than one 
      missed meal and will therefore require an insulin replacement regime. (R) • 
      Patients taking more than 5 mg of prednisolone daily should have steroid 
      replacement in the peri-operative period. (R) • Consider proton pump therapy for 
      patients taking steroids in the peri-operative phase if they fit higher risk 
      criteria. (R) • Surgery within three months of stroke carries high risk of 
      further stroke and should be delayed if possible. (R) • Patients with rheumatoid 
      arthritis should have flexion/extension views assessed by a senior radiologist 
      pre-operatively. (R) • Patients at risk of post-operative cognitive dysfunction 
      and delirium should be highlighted at pre-operative assessment. (G) • Patients 
      with Parkinson's disease (PD) must have enteral access so drugs can be given 
      intra-operatively. Liaison with a specialist in PD is essential. (R) • 
      Intravenous iron should be considered for anaemia in the urgent head and neck 
      cancer patient. (G) • Preoperative blood transfusion should be avoided where 
      possible. (R) • Where pre-operative transfusion is essential it should be 
      completed 24-48 hours pre-operatively. (R) • An accurate alcohol intake 
      assessment should be completed for all patients. (G) • Patients considered to 
      have a high level of alcohol dependency should be considered for active 
      in-patient withdrawal at least 48 hours pre-operatively in liaison with relevant 
      specialists. (R) • Parenteral B vitamins should be given routinely on admission 
      to alcohol-dependent patients. (R) • Smoking cessation, commenced preferably six 
      weeks before surgery, decreases the incidence of post-operative complications. 
      (R) • Antibiotics are necessary for clean-contaminated head and neck surgery, but 
      unnecessary for clean surgery. (R) • Antibiotics should be administered up to 60 
      minutes before skin incision, as close to the time of incision as possible. (R) • 
      Antibiotic regimes longer than 24 hours have no additional benefit in 
      clean-contaminated head and neck surgery. (R) • Repeat intra-operative antibiotic 
      dosing should be considered for longer surgeries or where there is major blood 
      loss. (R) • Local antibiotic policies should be developed and adhered to due to 
      local resistance patterns. (G) • Individual assessment for venous thromboembolism 
      (VTE) risk and bleeding risk should occur on admission and be reassessed 
      throughout the patients' stay. (G) • Mechanical prophylaxis for VTE is 
      recommended for all patients with one or more risk factors for VTE. (R) • 
      Patients with additional risk factors of VTE and low bleeding risk should have 
      low molecular weight heparin at prophylactic dose or unfractionated heparin if 
      they have severe renal impairment. (R).
FAU - Robson, A
AU  - Robson A
AD  - North Cumbria University Hospitals NHS Trust,Cumberland infirmary,Carlisle,UK.
FAU - Sturman, J
AU  - Sturman J
AD  - Department of Anaesthesia,Cumberland Infirmary,Carlisle,UK.
FAU - Williamson, P
AU  - Williamson P
AD  - Department of ENT Surgery,St George's Hospital NHS Trust,London,UK.
FAU - Conboy, P
AU  - Conboy P
AD  - Department of Otolaryngology-Head and Neck Surgery,University Hospitals of 
      Leicester,Leicester Royal Infirmary,Leicester,UK.
FAU - Penney, S
AU  - Penney S
AD  - Department of Otolaryngology-Head and Neck Surgery,Manchester Royal 
      Infirmary,Manchester,UK.
FAU - Wood, H
AU  - Wood H
AD  - Department of Anaesthesia,Freeman Hospital,Newcastle upon Tyne NHS Foundation 
      Trust,Newcastle upon Tyne,UK.
LA  - eng
PT  - Journal Article
PT  - Practice Guideline
PL  - England
TA  - J Laryngol Otol
JT  - The Journal of laryngology and otology
JID - 8706896
SB  - IM
MH  - Antibiotic Prophylaxis/standards
MH  - Head and Neck Neoplasms/complications/*diagnosis/surgery
MH  - Humans
MH  - Interdisciplinary Communication
MH  - Thromboembolism/prevention & control
MH  - United Kingdom
PMC - PMC4873895
EDAT- 2016/11/15 06:00
MHDA- 2017/02/06 06:00
PMCR- 2016/05/20
CRDT- 2016/11/15 06:00
PHST- 2016/11/15 06:00 [entrez]
PHST- 2016/11/15 06:00 [pubmed]
PHST- 2017/02/06 06:00 [medline]
PHST- 2016/05/20 00:00 [pmc-release]
AID - S0022215116000372 [pii]
AID - 00037 [pii]
AID - 10.1017/S0022215116000372 [doi]
PST - ppublish
SO  - J Laryngol Otol. 2016 May;130(S2):S13-S22. doi: 10.1017/S0022215116000372.

PMID- 27682808
OWN - NLM
STAT- MEDLINE
DCOM- 20171019
LR  - 20171019
IS  - 2184-8777 (Electronic)
IS  - 0303-464X (Linking)
VI  - 41
IP  - 3
DP  - 2016 Jul-Sep
TI  - Incidence and predictors of cardiovascular events in a cohort of patients with 
      rheumatoid arthritis.
PG  - 213-219
AB  - INTRODUCTION: An excess in cardiovascular (CV) morbidity and mortality has been 
      recognized in Rheumatoid Arthritis (RA) patients when compared to the general 
      population. Given the paucity of prospective data, our aim was to estimate the 
      incidence of CV events and the contribution of traditional CVD risk factors and 
      RA-related parameters to future events. METHODS: Incident fatal and non-fatal CV 
      events (hospitalizations due to unstable angina, myocardial infarction, coronary 
      artery revascularization procedures, stroke, or CV death) were assessed in a 
      prospective cohort of RA women followed since 2007 and without CV events at 
      cohort entry. The presence of traditional CV risk factors, disease 
      characteristics, medication, carotid ultrasound, and biomarkers of inflammation 
      and endothelial activation were evaluated at baseline. Univariate Cox 
      proportional hazard models were used to identify risk factors for CV events. 
      RESULTS: Among 106 women followed over 565 patient-years we identified 4 CV 
      events (1 fatal stroke, 2 myocardial infarction and 1 unstable angina), which 
      contributed to an incidence rate of 7 per 1000 person-years (95%CI 2.0- 13.9). 
      Patients who developed CV events were older, but the distribution of other 
      traditional CV risk factors was otherwise similar in both groups. Also, 
      corticosteroid dosage and proportion of patients with carotid atherosclerotic 
      plaques was higher in those with CV events. Erythrocyte sedimentation rate (ESR) 
      (HR 1.036; 95%CI 1.005-1.067) and soluble intercellular adhesion molecule-1 
      (sICAM-1) serum levels (HR 1.002; 95%CI 1.000-1.003) significantly contributed to 
      CV events. These results remained significant after adjusting for patients' age. 
      CONCLUSION: We found an incidence of cardiovascular events in women with RA of 7 
      per 1000 patent-years. This value is similar to that found in other Portuguese 
      cohort of RA patients1 and much higher than the incidence reported for the 
      general Portuguese population. Markers of inflammation and endothelial activation 
      contributed significantly to CV events, but the limited number of events prevents 
      further analysis.
FAU - Castro, A M
AU  - Castro AM
FAU - Carmona-Fernandes, D
AU  - Carmona-Fernandes D
FAU - Rodrigues, A M
AU  - Rodrigues AM
FAU - Pedro, L M
AU  - Pedro LM
FAU - Santos, M J
AU  - Santos MJ
FAU - Canhão, H
AU  - Canhão H
FAU - Fonseca, J E
AU  - Fonseca JE
LA  - eng
PT  - Journal Article
TT  - Incidence and predictors of cardiovascular events in a cohort of patients with 
      rheumatoid arthritis.
PL  - Portugal
TA  - Acta Reumatol Port
JT  - Acta reumatologica portuguesa
JID - 0431702
SB  - IM
MH  - Arthritis, Rheumatoid/*complications
MH  - Cardiovascular Diseases/*epidemiology/*etiology
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Middle Aged
MH  - Prospective Studies
MH  - Risk Assessment
MH  - Risk Factors
EDAT- 2016/10/26 06:00
MHDA- 2017/10/20 06:00
CRDT- 2016/09/30 06:00
PHST- 2016/10/26 06:00 [pubmed]
PHST- 2017/10/20 06:00 [medline]
PHST- 2016/09/30 06:00 [entrez]
AID - AO150151 [pii]
PST - ppublish
SO  - Acta Reumatol Port. 2016 Jul-Sep;41(3):213-219.

PMID- 27761055
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220408
IS  - 0098-6283 (Print)
IS  - 1532-8023 (Electronic)
IS  - 0098-6283 (Linking)
VI  - 43
IP  - 4
DP  - 2016 Oct
TI  - Life Stress and Health: A Review of Conceptual Issues and Recent Findings.
PG  - 346-355
AB  - Life stress is a central construct in many models of human health and disease. 
      The present article reviews research on stress and health, with a focus on (a) 
      how life stress has been conceptualized and measured over time, (b) recent 
      evidence linking stress and disease, and (c) mechanisms that might underlie these 
      effects. Emerging from this body of work is evidence that stress is involved in 
      the development, maintenance, or exacerbation of several mental and physical 
      health conditions, including asthma, rheumatoid arthritis, anxiety disorders, 
      depression, cardiovascular disease, chronic pain, human immunodeficiency 
      virus/AIDS, stroke, and certain types of cancer. Stress has also been implicated 
      in accelerated biological aging and premature mortality. These effects have been 
      studied most commonly using self-report checklist measures of life stress 
      exposure, although interview-based approaches provide a more comprehensive 
      assessment of individuals' exposure to stress. Most recently, online systems like 
      the Stress and Adversity Inventory (STRAIN) have been developed for assessing 
      lifetime stress exposure, and such systems may provide important new information 
      to help advance our understanding of how stressors occurring over the life course 
      get embedded in the brain and body to affect lifespan health.
FAU - Slavich, George M
AU  - Slavich GM
AD  - Cousins Center for Psychoneuroimmunology and Department of Psychiatry and 
      Biobehavioral Sciences, University of California, Los Angeles, CA, USA.
LA  - eng
GR  - K08 MH103443/MH/NIMH NIH HHS/United States
PT  - Journal Article
DEP - 20160816
PL  - United States
TA  - Teach Psychol
JT  - Teaching of psychology (Columbia, Mo.)
JID - 9881255
PMC - PMC5066570
MID - NIHMS811282
OTO - NOTNLM
OT  - STRAIN
OT  - classroom instruction
OT  - cytokines
OT  - disease
OT  - health
OT  - inflammation
OT  - interventions
OT  - measurement
OT  - mechanisms
OT  - risk
OT  - stress
OT  - transformational teaching
COIS- Declaration of Conflicting Interests The author declared no potential conflicts 
      of interest with respect to the research, authorship, and/or publication of this 
      article.
EDAT- 2016/10/21 06:00
MHDA- 2016/10/21 06:01
PMCR- 2016/10/17
CRDT- 2016/10/21 06:00
PHST- 2016/10/21 06:00 [pubmed]
PHST- 2016/10/21 06:01 [medline]
PHST- 2016/10/21 06:00 [entrez]
PHST- 2016/10/17 00:00 [pmc-release]
AID - 10.1177/0098628316662768 [doi]
PST - ppublish
SO  - Teach Psychol. 2016 Oct;43(4):346-355. doi: 10.1177/0098628316662768. Epub 2016 
      Aug 16.

PMID- 27705888
OWN - NLM
STAT- MEDLINE
DCOM- 20180529
LR  - 20240316
IS  - 1522-9645 (Electronic)
IS  - 0195-668X (Print)
IS  - 0195-668X (Linking)
VI  - 38
IP  - 23
DP  - 2017 Jun 14
TI  - Randomized trial of switching from prescribed non-selective non-steroidal 
      anti-inflammatory drugs to prescribed celecoxib: the Standard care vs. Celecoxib 
      Outcome Trial (SCOT).
PG  - 1843-1850
LID - 10.1093/eurheartj/ehw387 [doi]
AB  - BACKGROUND: Selective cyclooxygenase-2 inhibitors and conventional non-selective 
      non-steroidal anti-inflammatory drugs (nsNSAIDs) have been associated with 
      adverse cardiovascular (CV) effects. We compared the CV safety of switching to 
      celecoxib vs. continuing nsNSAID therapy in a European setting. METHOD: Patients 
      aged 60 years and over with osteoarthritis or rheumatoid arthritis, free from 
      established CV disease and taking chronic prescribed nsNSAIDs, were randomized to 
      switch to celecoxib or to continue their previous nsNSAID. The primary endpoint 
      was hospitalization for non-fatal myocardial infarction or other biomarker 
      positive acute coronary syndrome, non-fatal stroke or CV death analysed using a 
      Cox model with a pre-specified non-inferiority limit of 1.4 for the hazard ratio 
      (HR). RESULTS: In total, 7297 participants were randomized. During a median 
      3-year follow-up, fewer subjects than expected developed an on-treatment (OT) 
      primary CV event and the rate was similar for celecoxib, 0.95 per 100 
      patient-years, and nsNSAIDs, 0.86 per 100 patient-years (HR = 1.12, 95% 
      confidence interval, 0.81-1.55; P = 0.50). Comparable intention-to-treat (ITT) 
      rates were 1.14 per 100 patient-years with celecoxib and 1.10 per 100 
      patient-years with nsNSAIDs (HR = 1.04; 95% confidence interval, 0.81-1.33; 
      P = 0.75). Pre-specified non-inferiority was achieved in the ITT analysis. The 
      upper bound of the 95% confidence limit for the absolute increase in OT risk 
      associated with celecoxib treatment was two primary events per 1000 patient-years 
      exposure. There were only 15 adjudicated secondary upper gastrointestinal 
      complication endpoints (0.078/100 patient-years on celecoxib vs. 0.053 on 
      nsNSAIDs OT, 0.078 vs. 0.053 ITT). More gastrointestinal serious adverse 
      reactions and haematological adverse reactions were reported on nsNSAIDs than 
      celecoxib, but more patients withdrew from celecoxib than nsNSAIDs (50.9% 
      patients vs. 30.2%; P < 0.0001). INTERPRETATION: In subjects 60 years and over, 
      free from CV disease and taking prescribed chronic nsNSAIDs, CV events were 
      infrequent and similar on celecoxib and nsNSAIDs. There was no advantage of a 
      strategy of switching prescribed nsNSAIDs to prescribed celecoxib. This study 
      excluded an increased risk of the primary endpoint of more than two events per 
      1000 patient-years associated with switching to prescribed celecoxib. CLINICAL 
      TRIAL REGISTRATION: https://clinicaltrials.gov/show/NCT00447759; Unique 
      identifier: NCT00447759.
CI  - © The Author 2016. Published by Oxford University Press on behalf of the European 
      Society of Cardiology
FAU - MacDonald, Thomas M
AU  - MacDonald TM
AD  - Medicines Monitoring Unit (MEMO), Division of Molecular & Clinical Medicine, 
      University of Dundee, Ninewells Hospital & Medical School Dundee, Dundee DD1 9SY, 
      UK.
FAU - Hawkey, Chris J
AU  - Hawkey CJ
AD  - Faculty of Medicine & Health Sciences, University of Nottingham, Queen's Medical 
      Centre Nottingham, Nottingham NG7 2UH, UK.
FAU - Ford, Ian
AU  - Ford I
AD  - Robertson Centre for Biostatistics, University of Glasgow, Glasgow G12 8QQ, UK.
FAU - McMurray, John J V
AU  - McMurray JJV
AD  - British Heart Foundation Cardiovascular Research Centre, University of 
      Glasgow,126 University Place, GlasgowG12 8TA, UK.
FAU - Scheiman, James M
AU  - Scheiman JM
AD  - Division of Gastroenterology, University of Michigan Medical School, 1500 E 
      Medical Center Drive, Ann Arbor, MI 48109, USA.
FAU - Hallas, Jesper
AU  - Hallas J
AD  - Department of Public Health, Clinical Pharmacology, University of Southern 
      Denmark, J. B. Winsløws Vej 19, 2.5000 Odense, Denmark.
FAU - Findlay, Evelyn
AU  - Findlay E
AD  - Medicines Monitoring Unit (MEMO), Division of Molecular & Clinical Medicine, 
      University of Dundee, Ninewells Hospital & Medical School Dundee, Dundee DD1 9SY, 
      UK.
FAU - Grobbee, Diederick E
AU  - Grobbee DE
AD  - Julius Center for Health Sciences and Primary Care and Julius Clinical Academic 
      Research Organization, Utrecht, The Netherlands.
FAU - Hobbs, F D Richard
AU  - Hobbs FDR
AD  - Nuffield Department of Primary Care Health Sciences, University of Oxford, 
      Radcliffe Primary Care Building, Radcliffe Observatory Quarter, Woodstock Road, 
      Oxford OX2 6GG, UK.
FAU - Ralston, Stuart H
AU  - Ralston SH
AD  - Centre for Genomic and Experimental Medicine, Institute of Genetics and Molecular 
      Medicine, University of Edinburgh, Western General Hospital Edinburgh, Edinburgh 
      EH4 2XU, UK.
FAU - Reid, David M
AU  - Reid DM
AD  - School of Medicine & Dentistry, University of Aberdeen, Aberdeen AB25 2ZD, UK.
FAU - Walters, Matthew R
AU  - Walters MR
AD  - British Heart Foundation Cardiovascular Research Centre, University of 
      Glasgow,126 University Place, GlasgowG12 8TA, UK.
FAU - Webster, John
AU  - Webster J
AD  - School of Medicine & Dentistry, University of Aberdeen, Aberdeen AB25 2ZD, UK.
FAU - Ruschitzka, Frank
AU  - Ruschitzka F
AD  - Department of Cardiology, University Heart Center, Rämistrasse 100, 8091Zürich, 
      Switzerland.
FAU - Ritchie, Lewis D
AU  - Ritchie LD
AD  - Centre of Academic Primary Care, School of Medicine and Dentistry, University of 
      Aberdeen, AberdeenAB25 2ZD, UK.
FAU - Perez-Gutthann, Susana
AU  - Perez-Gutthann S
AD  - RTI Health Solutions, Trav. Gracia 56, Atico 1, Barcelona 08006, Spain.
FAU - Connolly, Eugene
AU  - Connolly E
AD  - British Heart Foundation Cardiovascular Research Centre, University of 
      Glasgow,126 University Place, GlasgowG12 8TA, UK.
FAU - Greenlaw, Nicola
AU  - Greenlaw N
AD  - Robertson Centre for Biostatistics, University of Glasgow, Glasgow G12 8QQ, UK.
FAU - Wilson, Adam
AU  - Wilson A
AD  - Medicines Monitoring Unit (MEMO), Division of Molecular & Clinical Medicine, 
      University of Dundee, Ninewells Hospital & Medical School Dundee, Dundee DD1 9SY, 
      UK.
FAU - Wei, Li
AU  - Wei L
AD  - Department of Practice and Policy, University College London, London WC1H 9JP, 
      UK.
FAU - Mackenzie, Isla S
AU  - Mackenzie IS
AD  - Medicines Monitoring Unit (MEMO), Division of Molecular & Clinical Medicine, 
      University of Dundee, Ninewells Hospital & Medical School Dundee, Dundee DD1 9SY, 
      UK.
LA  - eng
SI  - ClinicalTrials.gov/NCT00447759
GR  - G106/1249/MRC_/Medical Research Council/United Kingdom
PT  - Comparative Study
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
PL  - England
TA  - Eur Heart J
JT  - European heart journal
JID - 8006263
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
RN  - JCX84Q7J1L (Celecoxib)
SB  - IM
EIN - Eur Heart J. 2018 Mar 21;39(12):998. doi: 10.1093/eurheartj/ehw625. PMID: 
      28025195
CIN - Eur Heart J. 2017 Jun 14;38(23):1851-1852. doi: 10.1093/eurheartj/ehw507. PMID: 
      28329068
MH  - Acute Coronary Syndrome/chemically induced/epidemiology
MH  - Aged
MH  - Anti-Inflammatory Agents, Non-Steroidal/*adverse effects
MH  - Arthritis, Rheumatoid/drug therapy/epidemiology
MH  - Celecoxib/*adverse effects
MH  - Cyclooxygenase 2 Inhibitors/*adverse effects
MH  - Denmark/epidemiology
MH  - Drug Substitution
MH  - Female
MH  - Hospitalization/statistics & numerical data
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/chemically induced/epidemiology
MH  - Netherlands/epidemiology
MH  - Osteoarthritis/drug therapy/epidemiology
MH  - Patient Safety
MH  - Peptic Ulcer Hemorrhage/chemically induced
MH  - Prospective Studies
MH  - Stroke/chemically induced/epidemiology
MH  - United Kingdom/epidemiology
PMC - PMC5837371
OTO - NOTNLM
OT  - Arthritis
OT  - Cardiovascular
OT  - Celecoxib
OT  - NSAIDs
EDAT- 2016/10/06 06:00
MHDA- 2018/05/31 06:00
PMCR- 2016/10/04
CRDT- 2016/10/06 06:00
PHST- 2016/05/18 00:00 [received]
PHST- 2016/08/10 00:00 [accepted]
PHST- 2016/10/06 06:00 [pubmed]
PHST- 2018/05/31 06:00 [medline]
PHST- 2016/10/06 06:00 [entrez]
PHST- 2016/10/04 00:00 [pmc-release]
AID - ehw387 [pii]
AID - 10.1093/eurheartj/ehw387 [doi]
PST - ppublish
SO  - Eur Heart J. 2017 Jun 14;38(23):1843-1850. doi: 10.1093/eurheartj/ehw387.

PMID- 27625227
OWN - NLM
STAT- MEDLINE
DCOM- 20181105
LR  - 20181202
IS  - 0028-3886 (Print)
IS  - 0028-3886 (Linking)
VI  - 64
IP  - 5
DP  - 2016 Sep-Oct
TI  - Polymyalgia rheumatica and risk of cerebrovascular accident: A systematic review 
      and meta-analysis.
PG  - 906-11
LID - 10.4103/0028-3886.190273 [doi]
AB  - BACKGROUND: Several chronic inflammatory disorders, such as rheumatoid arthritis 
      and systemic lupus erythematosus, have been linked to an increased risk of 
      cerebrovascular accident (CVA), but the data on polymyalgia rheumatica (PMR) 
      remains unclear. MATERIALS AND METHODS: We conducted a systematic review and 
      meta-analysis of observational studies that reported odds ratio, relative risk, 
      hazard ratio, or standardized incidence ratio comparing the risk of CVA in 
      patients with PMR versus non-PMR controls. Pooled risk ratio and 95% confidence 
      interval (CI) were calculated using a random-effect, generic inverse variance 
      method of DerSimonian and Laird. RESULTS: Three retrospective cohort studies and 
      one cross-sectional study were identified and included in the data analysis. We 
      found a significantly elevated CVA risk in patients with PMR, with the pooled 
      risk ratio of 1.87 (95% CI, 1.43-2.43). The statistical heterogeneity was high, 
      with an I2 of 91%. CONCLUSIONS: Our study demonstrated a statistically 
      significantly increased CVA risk among patients with PMR.
FAU - Ungprasert, Patompong
AU  - Ungprasert P
AD  - Department of Internal Medicine, Division of Rheumatology, Mayo Clinic, 
      Rochester, Minnesota, USA; Department of Medicine, Division of Rheumatology, 
      Siriraj Hospital, Mahidol University, Bangkok, Thailand, .
FAU - Srivali, Narat
AU  - Srivali N
AD  - Division of Pulmonology and Critical Care Medicine, Mayo Clinic, Rochester, 
      Minnesota, USA.
FAU - Thongprayoon, Charat
AU  - Thongprayoon C
AD  - Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Review
PT  - Systematic Review
PL  - India
TA  - Neurol India
JT  - Neurology India
JID - 0042005
SB  - IM
MH  - Humans
MH  - Observational Studies as Topic
MH  - Polymyalgia Rheumatica/*complications
MH  - Risk Factors
MH  - Stroke/*complications
EDAT- 2016/09/15 06:00
MHDA- 2018/11/06 06:00
CRDT- 2016/09/15 06:00
PHST- 2016/09/15 06:00 [entrez]
PHST- 2016/09/15 06:00 [pubmed]
PHST- 2018/11/06 06:00 [medline]
AID - ni_2016_64_5_906_190273 [pii]
AID - 10.4103/0028-3886.190273 [doi]
PST - ppublish
SO  - Neurol India. 2016 Sep-Oct;64(5):906-11. doi: 10.4103/0028-3886.190273.

PMID- 27564390
OWN - NLM
STAT- MEDLINE
DCOM- 20170719
LR  - 20180524
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Linking)
VI  - 69
IP  - 1
DP  - 2017 Jan
TI  - Comorbidities in Patients With Primary Sjögren's Syndrome and Systemic Lupus 
      Erythematosus: A Comparative Registries-Based Study.
PG  - 38-45
LID - 10.1002/acr.23015 [doi]
AB  - OBJECTIVE: To compare the prevalence of the main comorbidities in 2 large cohorts 
      of patients with primary Sjögren's syndrome (SS) and systemic lupus erythematosus 
      (SLE), with a focus on cardiovascular (CV) diseases. METHODS: This was a 
      cross-sectional multicenter study where the prevalence of more relevant 
      comorbidities in 2 cohorts was compared. Patients under followup from SJOGRENSER 
      (Spanish Rheumatology Society Registry of Primary SS) and RELESSER (Spanish 
      Rheumatology Society Registry of SLE), and who fulfilled the 2002 
      American-European Consensus Group and 1997 American College of Rheumatology 
      classification criteria, respectively, were included. A binomial logistic 
      regression analysis was carried out to explore potential differences, making 
      general adjustments for age, sex, and disease duration and specific adjustments 
      for each variable, including CV risk factors and treatments, when appropriate. 
      RESULTS: A total of 437 primary SS patients (95% female) and 2,926 SLE patients 
      (89% female) were included. The mean age was 58.6 years (interquartile range 
      [IQR] 50.0-69.9 years) for primary SS patients and 45.1 years (IQR 36.4-56.3 
      years) for SLE patients (P < 0.001), and disease duration was 10.4 years (IQR 
      6.0-16.7 years) and 13.0 years (IQR 7.45-19.76 years), respectively (P < 0.001). 
      Smoking, dyslipidemia, and arterial hypertension were associated less frequently 
      with primary SS (odds ratio [OR] 0.36 [95% confidence interval (95% CI) 
      0.28-0.48], 0.74 [95% CI 0.58-0.94], and 0.50 [95% CI 0.38-0.66], respectively) 
      as were life-threatening CV events (i.e., stroke or myocardial infarction; OR 
      0.57 [95% CI 0.35-0.92]). Conversely, lymphoma was associated more frequently 
      with primary SS (OR 4.41 [95% CI 1.35-14.43]). The prevalence of severe infection 
      was lower in primary SS than in SLE (10.1% versus 16.9%; OR 0.54 [95% CI 
      0.39-0.76]; P < 0.001). CONCLUSION: Primary SS patients have a consistently less 
      serious CV comorbidity burden and a lower prevalence of severe infection than 
      those with SLE. In contrast, their risk of lymphoma is greater.
CI  - © 2016, American College of Rheumatology.
FAU - Rúa-Figueroa, Iñigo
AU  - Rúa-Figueroa I
AD  - Doctor Negrín Hospital of Gran Canaria, Spain.
FAU - Fernández Castro, Mónica
AU  - Fernández Castro M
AD  - Infanta Sofía Hospital, Madrid, Spain.
FAU - Andreu, José L
AU  - Andreu JL
AD  - Puerta de Hierro-Majadahonda Hospital, Madrid, Spain.
FAU - Sanchez-Piedra, Carlos
AU  - Sanchez-Piedra C
AD  - Spanish Society of Rheumatology, Madrid, Spain.
FAU - Martínez-Taboada, Víctor
AU  - Martínez-Taboada V
AD  - Marqués de Valdecilla Hospital, Santander, Spain.
FAU - Olivé, Alejandro
AU  - Olivé A
AD  - Germans Trias i Pujol Hospital, Barcelona, Spain.
FAU - López-Longo, Javier
AU  - López-Longo J
AD  - Gregorio Marañón Hospital, Madrid, Spain.
FAU - Rosas, José
AU  - Rosas J
AD  - Marina Baixa Hospital, Villajoyosa, Alicante, Spain.
FAU - Galindo, María
AU  - Galindo M
AD  - 12 Octubre Hospital, Madrid, Spain.
FAU - Calvo-Alén, Jaime
AU  - Calvo-Alén J
AD  - Araba Hospital, Vitoria, Spain.
FAU - Fernández-Nebro, Antonio
AU  - Fernández-Nebro A
AD  - Carlos Haya Hospital, Málaga, Spain.
FAU - Alonso, Fernando
AU  - Alonso F
AD  - Spanish Society of Rheumatology, Madrid, Spain.
FAU - Rodríguez-Lozano, Beatriz
AU  - Rodríguez-Lozano B
AD  - University Hospital of Canarias, Tenerife, Spain.
FAU - Alberto García Vadillo, Jesús
AU  - Alberto García Vadillo J
AD  - La Princesa Hospital, Madrid, Spain.
FAU - Menor, Raúl
AU  - Menor R
AD  - Jerez de la Frontera General Hospital, Cádiz, Spain.
FAU - Narváez, Francisco Javier
AU  - Narváez FJ
AD  - Bellvitge Hospital, Barcelona, Spain.
FAU - Erausquin, Celia
AU  - Erausquin C
AD  - Doctor Negrín Hospital of Gran Canaria, Spain.
FAU - García-Aparicio, Ángel
AU  - García-Aparicio Á
AD  - Virgen de la Salud Hospital, Toledo, Spain.
FAU - Tomero, Eva
AU  - Tomero E
AD  - La Princesa Hospital, Madrid, Spain.
FAU - Manrique-Arija, Sara
AU  - Manrique-Arija S
AD  - Carlos Haya Hospital, Málaga, Spain.
FAU - Horcada, Loreto
AU  - Horcada L
AD  - Navarra Hospital, Pamplona, Spain.
FAU - Uriarte, Esther
AU  - Uriarte E
AD  - Donosti Hospital, San Sebastián, Spain.
FAU - Gil, Susana
AU  - Gil S
AD  - Alicante General Hospital, Spain.
FAU - Blanco, Ricardo
AU  - Blanco R
AD  - Marqués de Valdecilla Hospital, Santander, Spain.
FAU - López-González, Ruth
AU  - López-González R
AD  - Virgen de la Concha Hospital, Zamora, Spain.
FAU - Boteanu, Alina
AU  - Boteanu A
AD  - Ramón y Cajal Hospital, Madrid, Spain.
FAU - Freire, Mercedes
AU  - Freire M
AD  - Juan Canalejo Hospital, A Coruña, Spain.
FAU - Galisteo, Carlos
AU  - Galisteo C
AD  - Parc-Taulí Hospital, Barcelona, Spain.
FAU - Rodríguez-Gómez, Manuel
AU  - Rodríguez-Gómez M
AD  - Hospital Complex of Orense, Spain.
FAU - Díez-Álvarez, Elvira
AU  - Díez-Álvarez E
AD  - León Hospital, León, Spain.
FAU - Pego-Reigosa, José M
AU  - Pego-Reigosa JM
AD  - Hospital Complex of Vigo and Instituto de Investigación Sanitaria Galicia Sur, 
      Vigo, Spain.
CN  - Sjogrenser and Relesser Researchers and EAS-SER Group
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20161121
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
SB  - IM
MH  - Adult
MH  - Aged
MH  - Cardiovascular Diseases/epidemiology
MH  - Cohort Studies
MH  - Comorbidity
MH  - Cross-Sectional Studies
MH  - Female
MH  - Humans
MH  - Lupus Erythematosus, Systemic/*epidemiology
MH  - Male
MH  - Middle Aged
MH  - Prevalence
MH  - Registries
MH  - Sjogren's Syndrome/*epidemiology
EDAT- 2016/08/27 06:00
MHDA- 2017/07/20 06:00
CRDT- 2016/08/27 06:00
PHST- 2016/03/31 00:00 [received]
PHST- 2016/07/06 00:00 [revised]
PHST- 2016/08/09 00:00 [accepted]
PHST- 2016/08/27 06:00 [pubmed]
PHST- 2017/07/20 06:00 [medline]
PHST- 2016/08/27 06:00 [entrez]
AID - 10.1002/acr.23015 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2017 Jan;69(1):38-45. doi: 10.1002/acr.23015. Epub 
      2016 Nov 21.

PMID- 27526101
OWN - NLM
STAT- MEDLINE
DCOM- 20170925
LR  - 20220129
IS  - 1868-601X (Electronic)
IS  - 1868-4483 (Print)
IS  - 1868-4483 (Linking)
VI  - 7
IP  - 5
DP  - 2016 Oct
TI  - Systematic Review and Meta-Analysis of the Efficacy of Interleukin-1 Receptor 
      Antagonist in Animal Models of Stroke: an Update.
PG  - 395-406
LID - 10.1007/s12975-016-0489-z [doi]
AB  - Interleukin-1 receptor antagonist (IL-1 RA) is an anti-inflammatory protein used 
      clinically to treat rheumatoid arthritis and is considered a promising candidate 
      therapy for stroke. Here, we sought to update the existing systematic review and 
      meta-analysis of IL-1 RA in models of ischaemic stroke, published in 2009, to 
      assess efficacy, the range of circumstances in which efficacy has been tested and 
      whether the data appear to be confounded due to reported study quality and 
      publication bias. We included 25 sources of data, 11 of which were additional to 
      the original review. Overall, IL-1 RA reduced infarct volume by 36.2 % (95 % 
      confidence interval 31.6-40.7, n = 76 comparisons from 1283 animals). Assessments 
      for publication bias suggest 30 theoretically missing studies which reduce 
      efficacy to 21.9 % (17.3-26.4). Efficacy was higher where IL-1 RA was 
      administered directly into the ventricles rather than peripherally, and studies 
      not reporting allocation concealment during the induction of ischaemia reported 
      larger treatment effects. The preclinical data supporting IL-1 RA as a candidate 
      therapy for ischaemic stroke have improved. The reporting of measures to reduce 
      the risk of bias has improved substantially in this update, and studies now 
      include the use of animals with relevant co-morbidities.
FAU - McCann, Sarah K
AU  - McCann SK
AD  - Centre for Clinical Brain Sciences, University of Edinburgh, Chancellor's 
      Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
FAU - Cramond, Fala
AU  - Cramond F
AD  - Centre for Clinical Brain Sciences, University of Edinburgh, Chancellor's 
      Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
FAU - Macleod, Malcolm R
AU  - Macleod MR
AD  - Centre for Clinical Brain Sciences, University of Edinburgh, Chancellor's 
      Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK.
FAU - Sena, Emily S
AU  - Sena ES
AD  - Centre for Clinical Brain Sciences, University of Edinburgh, Chancellor's 
      Building, 49 Little France Crescent, Edinburgh, EH16 4SB, UK. 
      emily.sena@ed.ac.uk.
LA  - eng
GR  - NC/L000970/1/NC3RS_/National Centre for the Replacement, Refinement and Reduction 
      of Animals in Research/United Kingdom
PT  - Journal Article
PT  - Meta-Analysis
PT  - Review
PT  - Systematic Review
DEP - 20160815
PL  - United States
TA  - Transl Stroke Res
JT  - Translational stroke research
JID - 101517297
RN  - 0 (Interleukin 1 Receptor Antagonist Protein)
RN  - 0 (Receptors, Interleukin-1)
SB  - IM
MH  - Animals
MH  - *Disease Models, Animal
MH  - Humans
MH  - Interleukin 1 Receptor Antagonist Protein/*therapeutic use
MH  - Receptors, Interleukin-1/*antagonists & inhibitors/metabolism
MH  - Stroke/*drug therapy
PMC - PMC5014900
OTO - NOTNLM
OT  - Experimental validity
OT  - Focal cerebral ischaemia
OT  - Interleukin-1 receptor antagonist
OT  - Meta-analysis
OT  - Neuroprotection
OT  - Systematic review
COIS- Compliance with Ethical Standards Funding This study was supported by the UK 
      National Centre for the Replacement, Refinement and Reduction of Animals in 
      Research (NC3Rs) infrastructure award: ivSyRMAF—the CAMARADES—NC3Rs in vivo 
      systematic review and meta-analysis facility (NC/L000970/1). The study sponsors 
      had no role in the design, collection, analysis or interpretation of data, 
      writing of the report or decision to submit the manuscript for publication. 
      Conflict of Interest The authors declare that they have no conflict of interest. 
      Ethics Approval This article does not contain any studies with human participants 
      or animals performed by any of the authors.
EDAT- 2016/08/16 06:00
MHDA- 2017/09/26 06:00
PMCR- 2016/08/15
CRDT- 2016/08/16 06:00
PHST- 2016/06/02 00:00 [received]
PHST- 2016/07/28 00:00 [accepted]
PHST- 2016/07/25 00:00 [revised]
PHST- 2016/08/16 06:00 [entrez]
PHST- 2016/08/16 06:00 [pubmed]
PHST- 2017/09/26 06:00 [medline]
PHST- 2016/08/15 00:00 [pmc-release]
AID - 10.1007/s12975-016-0489-z [pii]
AID - 489 [pii]
AID - 10.1007/s12975-016-0489-z [doi]
PST - ppublish
SO  - Transl Stroke Res. 2016 Oct;7(5):395-406. doi: 10.1007/s12975-016-0489-z. Epub 
      2016 Aug 15.

PMID- 27478728
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20160801
LR  - 20200930
IS  - 2193-1801 (Print)
IS  - 2193-1801 (Electronic)
IS  - 2193-1801 (Linking)
VI  - 5
IP  - 1
DP  - 2016
TI  - Risk for cardiovascular disease in Japanese patients with rheumatoid arthritis: a 
      large-scale epidemiological study using a healthcare database.
PG  - 1111
LID - 10.1186/s40064-016-2800-6 [doi]
LID - 1111
AB  - OBJECTIVES: To study risk for cardiovascular disease (CVD) in Japanese patients 
      with rheumatoid arthritis (RA). METHODS: We used a Medical Data Vision database 
      mainly composed of health insurance claim data and diagnosis-procedure 
      combination data from Japan. Patients with RA diagnosed from April 2011 to March 
      2014 at 71 hospitals were identified with the International Classification of 
      Diseases 10th revision (ICD-10) and history of anti-RA drug prescription. 
      Hospitalizations for CVD including ischemic heart disease, heart failure, and 
      stroke were identified by a combination of diagnosis (ICD-10) and diagnostic 
      procedures. CVD incidence rate ratio (IRR) for RA versus osteoarthritis was 
      calculated. Risk factors were analyzed using univariate and multivariate Cox 
      proportional hazard models with baseline C-reactive protein (CRP) and traditional 
      risk factors as covariates. RESULTS: We identified 8658 patients with RA. The 
      age-sex adjusted IRR for RA versus osteoarthritis was high for total CVD [2.12; 
      95 % confidence interval (CI) 1.93-2.32], ischemic heart disease (2.16; 95 % CI 
      1.86-2.50), heart failure (2.34; 95 % CI 2.07-2.65), and stroke (1.68; 95 % CI 
      1.41-2.00). Risk factor analysis showed a tendency for cardiovascular risk to 
      increase with higher baseline CRP, although the difference was not statistically 
      significant (hazard ratio 1.43; 95 % CI 0.99-2.07). CONCLUSION: Our study 
      indicates an increased risk for CVD and an association between systemic 
      inflammation and CVD in Japanese RA patients.
FAU - Tanaka, Kunihiko
AU  - Tanaka K
AD  - Drug Safety Division, Chugai Pharmaceutical Co. Ltd., 1-1 Nihonbashi-Muromachi 
      2-Chome, Chuo-ku, Tokyo, 103-8324 Japan.
FAU - Hamada, Kenji
AU  - Hamada K
AD  - Drug Safety Division, Chugai Pharmaceutical Co. Ltd., 1-1 Nihonbashi-Muromachi 
      2-Chome, Chuo-ku, Tokyo, 103-8324 Japan.
FAU - Nakayama, Terumi
AU  - Nakayama T
AD  - Drug Safety Division, Chugai Pharmaceutical Co. Ltd., 1-1 Nihonbashi-Muromachi 
      2-Chome, Chuo-ku, Tokyo, 103-8324 Japan.
FAU - Matsuda, Shinichi
AU  - Matsuda S
AD  - Drug Safety Division, Chugai Pharmaceutical Co. Ltd., 1-1 Nihonbashi-Muromachi 
      2-Chome, Chuo-ku, Tokyo, 103-8324 Japan.
FAU - Atsumi, Akihide
AU  - Atsumi A
AD  - Drug Safety Division, Chugai Pharmaceutical Co. Ltd., 1-1 Nihonbashi-Muromachi 
      2-Chome, Chuo-ku, Tokyo, 103-8324 Japan.
FAU - Shimura, Tomomi
AU  - Shimura T
AD  - Clinical Development Division, Chugai Pharmaceutical Co. Ltd., 1-1 
      Nihonbashi-Muromachi 2-Chome, Chuo-ku, Tokyo, 103-8324 Japan.
FAU - Nemoto, Masatomi
AU  - Nemoto M
AD  - Drug Safety Division, Chugai Pharmaceutical Co. Ltd., 1-1 Nihonbashi-Muromachi 
      2-Chome, Chuo-ku, Tokyo, 103-8324 Japan.
LA  - eng
PT  - Journal Article
DEP - 20160719
PL  - Switzerland
TA  - Springerplus
JT  - SpringerPlus
JID - 101597967
PMC - PMC4949177
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - Epidemiology
OT  - Healthcare database
OT  - Japanese
OT  - Rheumatoid arthritis
EDAT- 2016/08/02 06:00
MHDA- 2016/08/02 06:01
PMCR- 2016/07/19
CRDT- 2016/08/02 06:00
PHST- 2016/01/11 00:00 [received]
PHST- 2016/07/08 00:00 [accepted]
PHST- 2016/08/02 06:00 [entrez]
PHST- 2016/08/02 06:00 [pubmed]
PHST- 2016/08/02 06:01 [medline]
PHST- 2016/07/19 00:00 [pmc-release]
AID - 2800 [pii]
AID - 10.1186/s40064-016-2800-6 [doi]
PST - epublish
SO  - Springerplus. 2016 Jul 19;5(1):1111. doi: 10.1186/s40064-016-2800-6. eCollection 
      2016.

PMID- 27426420
OWN - NLM
STAT- MEDLINE
DCOM- 20171218
LR  - 20180605
IS  - 1873-5150 (Electronic)
IS  - 0887-8994 (Linking)
VI  - 62
DP  - 2016 Sep
TI  - The Unique Coexistence of Anti-SS-A/Ro Antibodies in a Neonate with Symptomatic 
      Ischemic Stroke.
PG  - 47-50
LID - S0887-8994(16)30142-4 [pii]
LID - 10.1016/j.pediatrneurol.2016.06.005 [doi]
AB  - BACKGROUND: Neonatal cerebral infarction is a relatively common cause of neonatal 
      seizures, with an incidence of at least 1:4000 live births and is associated with 
      a high incidence of neurological sequelae. However, the pathophysiological 
      mechanisms and predisposing factors responsible for neonatal infarction are not 
      fully established. PATIENT DESCRIPTION: A full-term baby boy was transferred at 
      two days of age for the treatment of a cluster of seizures. Cranial magnetic 
      resonance imaging revealed multiple lesions compatible with acute cerebral 
      infarction. The results of the blood tests performed to screen for thrombophilic 
      diseases were normal for his age, and his perinatal history was unremarkable. A 
      diagnosis of idiopathic cerebral infarction was made. Additional examination for 
      autoimmune diseases showed that both the mother and the patient had the 
      anti-SS-A/Ro antibody. The patient was treated with phenobarbital and has no 
      neurological sequelae. CONCLUSIONS: This is the first report demonstrating the 
      coexistence of neonatal cerebral infarction and neonatal lupus syndrome. Thus 
      neonatal lupus syndrome may be an additional risk factor for neonatal stroke.
CI  - Copyright © 2016 Elsevier Inc. All rights reserved.
FAU - Kanda, Kenji
AU  - Kanda K
AD  - Department of Pediatrics, Hikone Municipal Hospital, Hikone, Shiga, Japan. 
      Electronic address: kandak@municipal-hp.hikone.shiga.jp.
FAU - Sato, Aya
AU  - Sato A
AD  - Department of Pediatrics, Hikone Municipal Hospital, Hikone, Shiga, Japan.
FAU - Abe, Daisuke
AU  - Abe D
AD  - Department of Pediatrics, Hikone Municipal Hospital, Hikone, Shiga, Japan.
FAU - Nishijima, Setsuko
AU  - Nishijima S
AD  - Department of Pediatrics, Hikone Municipal Hospital, Hikone, Shiga, Japan.
FAU - Ishigami, Tsuyoshi
AU  - Ishigami T
AD  - Department of Pediatrics, Hikone Municipal Hospital, Hikone, Shiga, Japan.
LA  - eng
PT  - Case Reports
PT  - Journal Article
DEP - 20160615
PL  - United States
TA  - Pediatr Neurol
JT  - Pediatric neurology
JID - 8508183
RN  - 0 (Antibodies, Antinuclear)
RN  - 0 (SS-A antibodies)
RN  - Neonatal Systemic lupus erythematosus
SB  - IM
MH  - Antibodies, Antinuclear/*immunology
MH  - Brain/diagnostic imaging
MH  - Cerebral Infarction/complications/*diagnosis/drug therapy/*immunology
MH  - Diagnosis, Differential
MH  - Female
MH  - Humans
MH  - Infant, Newborn
MH  - Lupus Erythematosus, Systemic/complications/*congenital/diagnostic imaging
MH  - Male
MH  - Pregnancy
MH  - Pregnancy Complications/diagnosis
MH  - Sjogren's Syndrome/diagnosis
OTO - NOTNLM
OT  - cerebral infarction
OT  - maternal autoantibodies
OT  - neonatal lupus syndrome
OT  - neonate
EDAT- 2016/07/19 06:00
MHDA- 2017/12/19 06:00
CRDT- 2016/07/19 06:00
PHST- 2016/03/12 00:00 [received]
PHST- 2016/06/08 00:00 [accepted]
PHST- 2016/07/19 06:00 [entrez]
PHST- 2016/07/19 06:00 [pubmed]
PHST- 2017/12/19 06:00 [medline]
AID - S0887-8994(16)30142-4 [pii]
AID - 10.1016/j.pediatrneurol.2016.06.005 [doi]
PST - ppublish
SO  - Pediatr Neurol. 2016 Sep;62:47-50. doi: 10.1016/j.pediatrneurol.2016.06.005. Epub 
      2016 Jun 15.

PMID- 27310259
OWN - NLM
STAT- MEDLINE
DCOM- 20170712
LR  - 20190213
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 11
IP  - 6
DP  - 2016
TI  - Rheumatoid Arthritis Disadvantages Younger Patients for Cardiovascular Diseases: 
      A Meta-Analysis.
PG  - e0157360
LID - 10.1371/journal.pone.0157360 [doi]
LID - e0157360
AB  - INTRODUCTION: The incidence of cardiovascular diseases (CVD) is increased in 
      rheumatoid arthritis (RA) patients. It remains unclear whether the load of RA 
      increases cardiovascular (CV) risk especially in female and in younger RA 
      patients. In the present study we aim to analyse the influence of age and gender 
      on CV risk in RA relative to the general population, using meta-analysis of 
      direct comparative studies. METHOD: Systematic literature search was performed in 
      MEDLINE for studies reporting on occurrence of CV events in RA as compared to the 
      general population, stratified for gender and/or age. Quality was appraised using 
      the Newcastle-Ottawa scale. Meta-analysis was performed on rate ratios using 
      inverse variance methods. RESULTS: There were 1372 records screened and 13 
      studies included. RA females and males have a similar higher risk (95%CI) to 
      develop stroke with RR 1.35 (1.30-1.40) and RR 1.31 (1.21-1.43); coronary artery 
      disease with RR 1.65 (1.54-1.76) versus RR 1.55 ((1.41-1.69) in men; 
      cardiovascular disease with RR 1.56 (1.49-1.62) versus 1.50 (1.41-1.60). The 
      highest incidence of CV events was observed in the youngest patients, RR 2.59 
      (1.77-3.79), whereas older patients had the lowest relative risk when compared to 
      the general population, RR 1.27 (1.16-1.38). CONCLUSION: The relative risk of RA 
      patients for CVD is age dependent, but does not depend on gender: the relative 
      risk on CVD appears to be equally raised for males and females, while relatively 
      young RA patients (<50 years) have the highest, and older patients the lowest 
      relative risk.
FAU - Fransen, Jaap
AU  - Fransen J
AD  - Department of Rheumatology Radboud University Nijmegen Medical Centre, Nijmegen, 
      The Netherlands.
FAU - Kazemi-Bajestani, Seyyed M R
AU  - Kazemi-Bajestani SM
AD  - Department of Oncology, Faculty of Medicine, University of Alberta, Edmonton, 
      Canada.
FAU - Bredie, Sebastian J H
AU  - Bredie SJ
AD  - Department of Internal Medicine, Radboud University Nijmegen Medical Centre, 
      Nijmegen, The Netherlands.
FAU - Popa, Calin D
AU  - Popa CD
AD  - Department of Rheumatology Radboud University Nijmegen Medical Centre, Nijmegen, 
      The Netherlands.
AD  - Department of Rheumatology, Bernhoven Hospital, Uden, The Netherlands.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
DEP - 20160616
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Age Factors
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/complications/*diagnosis/epidemiology/physiopathology
MH  - Coronary Artery Disease/*diagnosis/epidemiology/etiology/physiopathology
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Netherlands/epidemiology
MH  - Risk Factors
MH  - Stroke/*diagnosis/epidemiology/etiology/physiopathology
PMC - PMC4911000
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2016/06/17 06:00
MHDA- 2017/07/14 06:00
PMCR- 2016/06/16
CRDT- 2016/06/17 06:00
PHST- 2015/12/03 00:00 [received]
PHST- 2016/05/27 00:00 [accepted]
PHST- 2016/06/17 06:00 [entrez]
PHST- 2016/06/17 06:00 [pubmed]
PHST- 2017/07/14 06:00 [medline]
PHST- 2016/06/16 00:00 [pmc-release]
AID - PONE-D-15-52443 [pii]
AID - 10.1371/journal.pone.0157360 [doi]
PST - epublish
SO  - PLoS One. 2016 Jun 16;11(6):e0157360. doi: 10.1371/journal.pone.0157360. 
      eCollection 2016.

PMID- 27303306
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20160615
LR  - 20240527
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 7
DP  - 2016
TI  - Electrophysiological Mechanisms of Bayés Syndrome: Insights from Clinical and 
      Mouse Studies.
PG  - 188
LID - 10.3389/fphys.2016.00188 [doi]
LID - 188
AB  - Bayés syndrome is an under-recognized clinical condition characterized by 
      inter-atrial block (IAB). This is defined electrocardiographically as P-wave 
      duration > 120 ms and can be categorized into first, second and third degree IAB. 
      It can be caused by inflammatory conditions such as systemic sclerosis and 
      rheumatoid arthritis, abnormal protein deposition in cardiac amyloidosis, or 
      neoplastic processes invading the inter-atrial conduction system, such as primary 
      cardiac lymphoma. It may arise transiently during volume overload, autonomic 
      dysfunction or electrolyte disturbances from vomiting. In other patients without 
      an obvious cause, the predisposing factors are diabetes mellitus, hypertensive 
      heart disease, and hypercholesterolemia. IAB has a strong association with atrial 
      arrhythmogenesis, left atrial enlargement (LAE), and electro-mechanical 
      discordance, increasing the risk of cerebrovascular accidents as well as 
      myocardial and mesenteric ischemia. The aim of this review article is to 
      synthesize experimental evidence on the pathogenesis of IAB and its underlying 
      molecular mechanisms. Current medical therapies include anti-fibrotic, 
      anti-arrhythmic and anti-coagulation agents, whereas interventional options 
      include atrial resynchronization therapy by single or multisite pacing. Future 
      studies will be needed to elucidate the significance of the link between IAB and 
      atrial tachyarrhythmias in patients with different underlying etiologies and 
      optimize the management options in these populations.
FAU - Tse, Gary
AU  - Tse G
AD  - Li Ka Shing Faculty of Medicine, School of Biomedical Sciences, University of 
      Hong Kong Hong Kong, China.
FAU - Lai, Eric Tsz Him
AU  - Lai ET
AD  - Li Ka Shing Faculty of Medicine, School of Biomedical Sciences, University of 
      Hong Kong Hong Kong, China.
FAU - Yeo, Jie Ming
AU  - Yeo JM
AD  - School of Medicine, Imperial College London London, UK.
FAU - Yan, Bryan P
AU  - Yan BP
AD  - Department of Medicine and Therapeutics, The Chinese University of Hong KongHong 
      Kong, China; Department of Epidemiology and Preventive Medicine, Monash 
      UniversityMelbourne, VIC, Australia.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20160531
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC4886053
OTO - NOTNLM
OT  - Bayés syndrome
OT  - conduction
OT  - electrophysiological remodeling
OT  - inter-atrial block
OT  - intra-atrial block
OT  - structural remodeling
EDAT- 2016/06/16 06:00
MHDA- 2016/06/16 06:01
PMCR- 2016/05/31
CRDT- 2016/06/16 06:00
PHST- 2016/03/31 00:00 [received]
PHST- 2016/05/10 00:00 [accepted]
PHST- 2016/06/16 06:00 [entrez]
PHST- 2016/06/16 06:00 [pubmed]
PHST- 2016/06/16 06:01 [medline]
PHST- 2016/05/31 00:00 [pmc-release]
AID - 10.3389/fphys.2016.00188 [doi]
PST - epublish
SO  - Front Physiol. 2016 May 31;7:188. doi: 10.3389/fphys.2016.00188. eCollection 
      2016.

PMID- 27283333
OWN - NLM
STAT- MEDLINE
DCOM- 20170531
LR  - 20170531
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 76
IP  - 2
DP  - 2017 Feb
TI  - Is ankylosing spondylitis a risk factor for cardiovascular disease, and how do 
      these risks compare with those in rheumatoid arthritis?
PG  - 364-370
LID - 10.1136/annrheumdis-2016-209315 [doi]
AB  - AIMS: To assess and compare the incidence of cardiovascular (CV) events, by CV 
      phenotype, between patients with ankylosing spondylitis (AS), rheumatoid 
      arthritis (RA) and the general population. METHODS: Using linkages of national 
      and population-based registers, we identified one cohort of prevalent patients 
      with AS (n=5358), one with RA (n=37 245) and one with matched general population 
      subjects (n=25 006). These cohorts were identified in 2006 through 2011 and were 
      followed in 31 December 2012, for first ever occurrence of acute coronary 
      syndromes (ACS), deep venous thromboembolism, pulmonary embolism and stroke, 
      respectively. For each outcome, we calculated incidence rates standardised to the 
      age and sex distribution of the AS cohort, as well as relative risks using Cox 
      proportional hazards models. RESULTS: Based on 69 ACS events during 20 251 
      person-years of follow-up of the patients with AS, and 966 events during 127 014 
      person-years in the RA cohort, the age/sex-adjusted relative risks for ACS 
      compared with the general population was 1.3 (95% CI 1.0 to 1.7) for AS and 1.7 
      (1.4 to 2.0) for RA. For thromboembolic events, the corresponding risks were 1.4 
      (1.1 to 1.9) in AS and 1.8 (1.5 to 2.1) in RA. Finally, for stroke, the relative 
      risks were 1.5 (1.1 to 2.0) in AS and 1.5 (1.2 to 1.8) in RA, compared with the 
      general population. CONCLUSIONS: Prevalent patients with AS are at a 30%-50% 
      increased risk of incident CV events. When compared with patients with RA, this 
      level of increase was similar for stroke, but only half as high for ACS and 
      thrombotic events.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://www.bmj.com/company/products-services/rights-and-licensing/.
FAU - Eriksson, Jonas K
AU  - Eriksson JK
AD  - Clinical Epidemiology Unit and Department of Medicine Solna, Karolinska 
      Institutet, Stockholm, Sweden.
FAU - Jacobsson, Lennart
AU  - Jacobsson L
AD  - Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at 
      University of Gothenburg, Gothenburg, Sweden.
FAU - Bengtsson, Karin
AU  - Bengtsson K
AD  - Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at 
      University of Gothenburg, Gothenburg, Sweden.
FAU - Askling, Johan
AU  - Askling J
AD  - Clinical Epidemiology Unit and Department of Medicine Solna, Karolinska 
      Institutet, Stockholm, Sweden.
AD  - Rheumatology Unit, Department of Medicine Solna, Karolinska Institutet, 
      Stockholm, Sweden.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20160609
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
MH  - Acute Coronary Syndrome/epidemiology
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Cardiovascular Diseases/*epidemiology
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Prevalence
MH  - Proportional Hazards Models
MH  - Pulmonary Embolism/epidemiology
MH  - *Registries
MH  - Risk Factors
MH  - Spondylitis, Ankylosing/*epidemiology
MH  - Stroke/epidemiology
MH  - Sweden/epidemiology
MH  - Venous Thrombosis/epidemiology
MH  - Young Adult
OTO - NOTNLM
OT  - Ankylosing Spondylitis
OT  - Cardiovascular Disease
OT  - Epidemiology
OT  - Psoriatic Arthritis
EDAT- 2016/06/11 06:00
MHDA- 2017/06/01 06:00
CRDT- 2016/06/11 06:00
PHST- 2016/02/02 00:00 [received]
PHST- 2016/05/03 00:00 [revised]
PHST- 2016/05/17 00:00 [accepted]
PHST- 2016/06/11 06:00 [pubmed]
PHST- 2017/06/01 06:00 [medline]
PHST- 2016/06/11 06:00 [entrez]
AID - annrheumdis-2016-209315 [pii]
AID - 10.1136/annrheumdis-2016-209315 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2017 Feb;76(2):364-370. doi: 10.1136/annrheumdis-2016-209315. Epub 
      2016 Jun 9.

PMID- 27159164
OWN - NLM
STAT- MEDLINE
DCOM- 20170719
LR  - 20221207
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Linking)
VI  - 69
IP  - 2
DP  - 2017 Feb
TI  - Association of Rheumatoid Factors With Subclinical and Clinical Atherosclerosis 
      in African American Women: The Multiethnic Study of Atherosclerosis.
PG  - 166-174
LID - 10.1002/acr.22930 [doi]
AB  - OBJECTIVE: Although the association between rheumatoid arthritis (RA) and 
      cardiovascular disease (CVD) is established, the exact mechanism is unknown. We 
      tested the hypothesis that RA-related autoantibodies are independent risk factors 
      for subclinical atherosclerosis and subsequent clinical CVD events. METHODS: The 
      Multi-Ethnic Study of Atherosclerosis (MESA) is a community-based cohort study 
      prospectively collecting CVD outcome and risk factor data in middle-aged to 
      elderly multiethnic participants since 2000. Rheumatoid factor (RF) and 
      anti-cyclic citrullinated peptide antibodies (anti-CCP2) by enzyme-linked 
      immunosorbent assay, and coronary artery calcium (CAC) by computed tomography, 
      were measured at MESA baseline in 6,532 participants who were followed for 10.3 
      years for coronary heart disease (CHD) end points (myocardial infarction, cardiac 
      arrest, CHD death) and CVD end points (included CHD end points, stroke, stroke 
      death). Multivariable logistic regression and Cox regression assessed 
      associations between RF/anti-CCP and CAC or CVD end points. RESULTS: IgM RF, IgA 
      RF, anti-CCP, and either RF isotype predictors were positive in 15.8%, 8.7%, 
      2.0%, and 20.6%, respectively. A total of 12.2% had CAC ≥300, 7.1% had CHD end 
      points, and 10.2% had CVD end points. IgA RF and anti-CCP were associated with 
      CAC ≥300 in African American women (odds ratio [OR] 2.4 [95% confidence interval 
      (95% CI) 1.2-5.1] and OR 4.1 [95% CI 1.3-12.7], respectively). RA-related 
      autoantibodies were also associated with clinical CVD events in African American 
      women (anti-CCP: OR 5.3 [95% CI 2.4-12.0]; either RF isotype: OR 2.4 [95% CI 
      1.4-4.0]). There was a trend for association between autoantibodies and CAC in 
      white women. No associations were found in men. CONCLUSION: RA-related 
      autoantibodies are associated with subclinical and clinical atherosclerosis in 
      African American women from a community-based non-RA cohort, indicating 
      autoimmune factors may play a role in the pathogenesis of atherosclerosis.
CI  - © 2016, American College of Rheumatology.
FAU - Majka, Darcy S
AU  - Majka DS
AD  - Northwestern University Feinberg School of Medicine, Chicago, Illinois.
FAU - Vu, Thanh-Huyen T
AU  - Vu TT
AD  - Northwestern University Feinberg School of Medicine, Chicago, Illinois.
FAU - Pope, Richard M
AU  - Pope RM
AD  - Northwestern University Feinberg School of Medicine, Chicago, Illinois.
FAU - Teodorescu, Marius
AU  - Teodorescu M
AD  - TheraTest Laboratories, University of Illinois College of Medicine, Chicago.
FAU - Karlson, Elizabeth W
AU  - Karlson EW
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Liu, Kiang
AU  - Liu K
AD  - Northwestern University Feinberg School of Medicine, Chicago, Illinois.
FAU - Chang, Rowland W
AU  - Chang RW
AD  - Northwestern University Feinberg School of Medicine, Chicago, Illinois.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 9009-79-4 (Rheumatoid Factor)
SB  - IM
MH  - Black or African American
MH  - Aged
MH  - Aged, 80 and over
MH  - Atherosclerosis/*epidemiology/*immunology
MH  - Cohort Studies
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Humans
MH  - Middle Aged
MH  - Prevalence
MH  - Rheumatoid Factor/*blood/*immunology
MH  - Risk Factors
EDAT- 2016/05/10 06:00
MHDA- 2017/07/20 06:00
CRDT- 2016/05/10 06:00
PHST- 2015/07/27 00:00 [received]
PHST- 2016/04/06 00:00 [revised]
PHST- 2016/04/26 00:00 [accepted]
PHST- 2016/05/10 06:00 [pubmed]
PHST- 2017/07/20 06:00 [medline]
PHST- 2016/05/10 06:00 [entrez]
AID - 10.1002/acr.22930 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2017 Feb;69(2):166-174. doi: 10.1002/acr.22930.

PMID- 27098820
OWN - NLM
STAT- MEDLINE
DCOM- 20161229
LR  - 20221207
IS  - 2044-6055 (Electronic)
IS  - 2044-6055 (Linking)
VI  - 6
IP  - 4
DP  - 2016 Apr 20
TI  - Multifactorial intervention to prevent cardiovascular disease in patients with 
      early rheumatoid arthritis: protocol for a multicentre randomised controlled 
      trial.
PG  - e009134
LID - 10.1136/bmjopen-2015-009134 [doi]
LID - e009134
AB  - INTRODUCTION: Cardiovascular morbidity is a major burden in patients with 
      rheumatoid arthritis (RA). In this study, we compare the effect of a targeted, 
      intensified, multifactorial intervention with that of conventional treatment of 
      modifiable risk factors for cardiovascular disease (CVD) in patients with early 
      RA fulfilling the 2010 American College of Rheumatology European League Against 
      Rheumatism (ACR/EULAR) criteria. METHODS AND ANALYSIS: The study is a 
      prospective, randomised, open label trial with blinded end point assessment and 
      balanced randomisation (1:1) conducted in 10 outpatient clinics in Denmark. The 
      primary end point after 5 years of follow-up is a composite of death from 
      cardiovascular causes, non-fatal myocardial infarction, non-fatal stroke and 
      cardiac revascularisation. Secondary outcomes are: the proportion of patients 
      achieving low-density lipoprotein cholesterol <2.5 mmol/L, glycated haemoglobin 
      <48 mmol/mol, blood pressure <140/90 mm  Hg for patients without diabetes and 
      <130/80 mm Hg for patients with diabetes and normoalbuminuria (urinary albumin 
      creatinine ratio <30 mg/g) after 1 year of follow-up and the proportion of 
      patients in each treatment group achieving low RA disease activity after 1 year, 
      defined as a disease activity score C-reactive protein (DAS28-CRP) <3.2 and a 
      DAS28-CRP score <2.6 after 12, 24 and 60 months. Furthermore, all 
      hospitalisations for acute and elective reasons will be adjudicated by the event 
      committee after 12, 24 and 60 months. Three hundred treatment-naive patients with 
      early RA will be randomly assigned (1:1) to receive either conventional treatment 
      administered and monitored by their general practitioner according to national 
      guidelines (control group) or a stepwise implementation administered and 
      monitored in a quarterly rheumatological nurse-administered set-up of behaviour 
      modification and pharmacological therapy targeting (1) hyperlipidaemia, (2) 
      hypertension, (3) hyperglycaemia and (4) microalbuminuria (intervention group). 
      ETHICS AND DISSEMINATION: This protocol is approved by the local ethics committee 
      (DK-S-2014007) and The Danish Health and Medicines Authority. Dissemination will 
      occur through presentations at National and International conferences and 
      publications in international peer-reviewed journals. TRIAL REGISTRATION NUMBER: 
      NCT02246257.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://www.bmj.com/company/products-services/rights-and-licensing/
FAU - Svensson, Annemarie Lyng
AU  - Svensson AL
AD  - Department of Rheumatology, Copenhagen University Hospital, Bispebjerg and 
      Frederiksberg, Denmark.
FAU - Christensen, Robin
AU  - Christensen R
AUID- ORCID: 0000-0002-6600-0631
AD  - Musculoskeletal Statistics Unit, Department of Rheumatology, The Parker 
      Institute, Copenhagen University Hospital, Bispebjerg and Frederiksberg, Denmark.
FAU - Persson, Frederik
AU  - Persson F
AUID- ORCID: 0000-0001-6242-6638
AD  - Steno Diabetes Center, Gentofte, Denmark.
FAU - Løgstrup, Brian Bridal
AU  - Løgstrup BB
AD  - Department of Cardiology, Aarhus University Hospital, Skejby, Denmark.
FAU - Giraldi, Annamaria
AU  - Giraldi A
AD  - Psychiatric Center, Sexological Clinic, Copenhagen University Hospital, Denmark.
FAU - Graugaard, Christian
AU  - Graugaard C
AD  - Department of Clinical Medicine, Center for Sexology Research, Aalborg 
      University, Aalborg, Denmark.
FAU - Fredberg, Ulrich
AU  - Fredberg U
AUID- ORCID: 0000-0002-7181-1113
AD  - Department of Rheumatology, Diagnostic Centre, Regional Hospital Silkeborg, 
      Denmark.
FAU - Blegvad, Jesper
AU  - Blegvad J
AD  - Department of Rheumatology, Diagnostic Centre, Regional Hospital Silkeborg, 
      Denmark.
FAU - Thygesen, Tina
AU  - Thygesen T
AD  - Department of Rheumatology, Diagnostic Centre, Regional Hospital Silkeborg, 
      Denmark.
FAU - Hansen, Inger Marie Jensen
AU  - Hansen IM
AUID- ORCID: 0000-0001-7283-9786
AD  - Department of Rheumatology, Svendborg Hospital, Svendborg, Denmark.
FAU - Colic, Ada
AU  - Colic A
AUID- ORCID: 0000-0001-9873-4528
AD  - Department of Rheumatology Sydvestjysk Sygehus, Esbjerg/Varde, Denmark.
FAU - Bagdat, Döne
AU  - Bagdat D
AUID- ORCID: 0000-0002-1347-0576
AD  - Department of Rheumatology Sydvestjysk Sygehus, Esbjerg/Varde, Denmark.
FAU - Ahlquist, Palle
AU  - Ahlquist P
AUID- ORCID: 0000-0003-2442-5014
AD  - Reumaklinik Fyn, Odense, Denmark.
FAU - Jensen, Hanne Slott
AU  - Jensen HS
AUID- ORCID: 0000-0002-7550-9894
AD  - Department of Rheumatology, Copenhagen University Hospital, Bispebjerg and 
      Frederiksberg, Denmark.
FAU - Hørslev-Petersen, Kim
AU  - Hørslev-Petersen K
AUID- ORCID: 0000-0002-5475-7610
AD  - Kong Christian X's Gigthospital i Gråsten, Denmark.
FAU - Sheetal, Ekta
AU  - Sheetal E
AD  - Department of Rheumatology, Odense University Hospital, Odense, Denmark.
FAU - Christensen, Torben Grube
AU  - Christensen TG
AUID- ORCID: 0000-0002-6600-0631
AD  - Reumaklinik, Roskilde, Denmark.
FAU - Svendsen, Lone
AU  - Svendsen L
AD  - Reumaklinik, Skanderborg, Denmark.
FAU - Emmertsen, Henrik
AU  - Emmertsen H
AD  - Reumaklinik, Aabenraa, Denmark.
FAU - Ellingsen, Torkell
AU  - Ellingsen T
AUID- ORCID: 0000-0003-0426-4962
AD  - Department of Rheumatology, Odense University Hospital, Odense, Denmark Danbio 
      National Registry, Glostrup University Hospital, Denmark.
LA  - eng
SI  - ClinicalTrials.gov/NCT02246257
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
DEP - 20160420
PL  - England
TA  - BMJ Open
JT  - BMJ open
JID - 101552874
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (Hypolipidemic Agents)
RN  - 0 (Lipoproteins, LDL)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - AGG2FN16EV (Simvastatin)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Albuminuria/prevention & control
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/*complications/drug therapy
MH  - C-Reactive Protein/analysis
MH  - Cardiovascular Diseases/*prevention & control
MH  - Denmark
MH  - Female
MH  - Glycated Hemoglobin/analysis
MH  - Humans
MH  - Hyperglycemia/prevention & control
MH  - Hyperlipidemias/prevention & control
MH  - Hypertension/prevention & control
MH  - Hypolipidemic Agents/*administration & dosage
MH  - Lipoproteins, LDL
MH  - Male
MH  - Middle Aged
MH  - Prospective Studies
MH  - *Research Design
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Simvastatin/*administration & dosage
MH  - Young Adult
PMC - PMC4838680
OTO - NOTNLM
OT  - RHEUMATOLOGY
EDAT- 2016/04/22 06:00
MHDA- 2016/12/31 06:00
PMCR- 2016/04/20
CRDT- 2016/04/22 06:00
PHST- 2016/04/22 06:00 [entrez]
PHST- 2016/04/22 06:00 [pubmed]
PHST- 2016/12/31 06:00 [medline]
PHST- 2016/04/20 00:00 [pmc-release]
AID - bmjopen-2015-009134 [pii]
AID - 10.1136/bmjopen-2015-009134 [doi]
PST - epublish
SO  - BMJ Open. 2016 Apr 20;6(4):e009134. doi: 10.1136/bmjopen-2015-009134.

PMID- 27028914
OWN - NLM
STAT- MEDLINE
DCOM- 20160409
LR  - 20220408
IS  - 1533-4406 (Electronic)
IS  - 0028-4793 (Linking)
VI  - 374
IP  - 13
DP  - 2016 Mar 31
TI  - Baricitinib in Patients with Refractory Rheumatoid Arthritis.
PG  - 1243-52
LID - 10.1056/NEJMoa1507247 [doi]
AB  - BACKGROUND: In phase 2 studies, baricitinib, an oral Janus kinase 1 and 2 
      inhibitor, reduced disease activity in patients with rheumatoid arthritis who had 
      not previously received treatment with biologic disease-modifying antirheumatic 
      drugs (DMARDs). METHODS: In this phase 3 study involving 527 patients with an 
      inadequate response to or unacceptable side effects associated with one or more 
      tumor necrosis factor inhibitors, other biologic DMARDs, or both, we randomly 
      assigned the patients in a 1:1:1 ratio to baricitinib at a dose of 2 or 4 mg 
      daily or placebo for 24 weeks. End points, tested hierarchically at week 12 to 
      control type 1 error, were the American College of Rheumatology 20% (ACR20) 
      response (primary end point), the Health Assessment Questionnaire-Disability 
      Index (HAQ-DI) score, the 28-joint Disease Activity Score based on C-reactive 
      protein level (DAS28-CRP), and a Simplified Disease Activity Index (SDAI) score 
      of 3.3 or less (on a scale of 0.1 to 86.0, with a score of 3.3 or less indicating 
      remission). Comparisons with placebo were made first with the 4-mg dose of 
      baricitinib and then with the 2-mg dose. RESULTS: Significantly more patients 
      receiving baricitinib at the 4-mg dose than those receiving placebo had an ACR20 
      response at week 12 (55% vs. 27%, P<0.001). Differences between the higher-dose 
      baricitinib group and the placebo group were also significant for the HAQ-DI 
      score and the DAS28-CRP but not for an SDAI score of 3.3 or less. Adverse-event 
      rates through 24 weeks were higher for patients receiving the 2-mg dose of 
      baricitinib and those receiving the 4-mg dose than for patients receiving placebo 
      (71% and 77%, respectively, vs. 64%), including infections (44% and 40%, vs. 
      31%). The rates of serious adverse events were 4%, 10%, and 7% in the three 
      groups, respectively. Two nonmelanoma skin cancers and two major adverse 
      cardiovascular events, including a fatal stroke, occurred in the higher-dose 
      group. Baricitinib was associated with a small reduction in neutrophil levels and 
      increases in serum creatinine and low-density lipoprotein cholesterol levels. 
      CONCLUSIONS: In patients with rheumatoid arthritis and an inadequate response to 
      biologic DMARDs, baricitinib at a daily dose of 4 mg was associated with clinical 
      improvement at 12 weeks. (Funded by Eli Lilly and Incyte; ClinicalTrials.gov 
      number, NCT01721044.).
FAU - Genovese, Mark C
AU  - Genovese MC
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Kremer, Joel
AU  - Kremer J
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Zamani, Omid
AU  - Zamani O
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Ludivico, Charles
AU  - Ludivico C
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Krogulec, Marek
AU  - Krogulec M
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Xie, Li
AU  - Xie L
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Beattie, Scott D
AU  - Beattie SD
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Koch, Alisa E
AU  - Koch AE
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Cardillo, Tracy E
AU  - Cardillo TE
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Rooney, Terence P
AU  - Rooney TP
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Macias, William L
AU  - Macias WL
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - de Bono, Stephanie
AU  - de Bono S
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Schlichting, Douglas E
AU  - Schlichting DE
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
FAU - Smolen, Josef S
AU  - Smolen JS
AD  - From the Stanford University Medical Center, Palo Alto, CA (M.C.G.); Albany 
      Medical College, Albany, NY ( J.K.); Rheumazentrum Favoriten (O.Z.) and the 
      Medical University of Vienna ( J.S.S.) - both in Vienna; East Penn Rheumatology, 
      Bethlehem, PA (C.L.); Rheumatology Clinic, MAK-MED, Nadarzyn, Poland (M.K.); and 
      Eli Lilly, Indianapolis (L.X., S.D.B., A.E.K., T.E.C., T.P.R., W.L.M., S.B., 
      D.E.S.).
LA  - eng
SI  - ClinicalTrials.gov/NCT01721044
PT  - Clinical Trial, Phase III
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - N Engl J Med
JT  - The New England journal of medicine
JID - 0255562
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Azetidines)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Purines)
RN  - 0 (Pyrazoles)
RN  - 0 (Sulfonamides)
RN  - EC 2.7.10.2 (Janus Kinase 1)
RN  - EC 2.7.10.2 (Janus Kinase 2)
RN  - ISP4442I3Y (baricitinib)
SB  - IM
CIN - Nat Rev Rheumatol. 2016 Jun;12(6):313. doi: 10.1038/nrrheum.2016.62. PMID: 
      27080693
MH  - Aged
MH  - Antirheumatic Agents/adverse effects/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Azetidines/adverse effects/*therapeutic use
MH  - Female
MH  - Humans
MH  - Janus Kinase 1/antagonists & inhibitors
MH  - Janus Kinase 2/antagonists & inhibitors
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Protein Kinase Inhibitors/adverse effects/*therapeutic use
MH  - Purines
MH  - Pyrazoles
MH  - Severity of Illness Index
MH  - Sulfonamides/adverse effects/*therapeutic use
EDAT- 2016/03/31 06:00
MHDA- 2016/04/10 06:00
CRDT- 2016/03/31 06:00
PHST- 2016/03/31 06:00 [entrez]
PHST- 2016/03/31 06:00 [pubmed]
PHST- 2016/04/10 06:00 [medline]
AID - 10.1056/NEJMoa1507247 [doi]
PST - ppublish
SO  - N Engl J Med. 2016 Mar 31;374(13):1243-52. doi: 10.1056/NEJMoa1507247.

PMID- 27002226
OWN - NLM
STAT- MEDLINE
DCOM- 20170531
LR  - 20170922
IS  - 1471-6348 (Electronic)
IS  - 0266-4623 (Linking)
VI  - 32
IP  - 1-2
DP  - 2016 Jan
TI  - THE EARLY BIRD CATCHES THE WORM: EARLY COST-EFFECTIVENESS ANALYSIS OF NEW MEDICAL 
      TESTS.
PG  - 46-53
LID - 10.1017/S0266462316000064 [doi]
AB  - OBJECTIVES: There is little specific guidance on performing an early 
      cost-effectiveness analysis (CEA) of medical tests. We developed a framework with 
      general steps and applied it to two cases. METHODS: Step 1 is to narrow down the 
      scope of analysis by defining the test's application, target population, outcome 
      measures, and investigating current test strategies and test strategies if the 
      new test were available. Step 2 is to collect evidence on the current test 
      strategy. Step 3 is to develop a conceptual model of the current and new test 
      strategies. Step 4 is to conduct the early-CEA by evaluating the potential 
      (cost-)effectiveness of the new test in clinical practice. Step 5 involves a 
      decision about the further development of the test. RESULTS: The first case 
      illustrated the impact of varying the test performance on the headroom (maximum 
      possible price) of an add-on test for patients with an intermediate-risk of 
      having rheumatoid arthritis. Analyses showed that the headroom is particularly 
      dependent on test performance. The second case estimated the minimum performance 
      of a confirmatory imaging test to predict individual stroke risk. Different 
      combinations of sensitivity and specificity were found to be cost-effective; if 
      these combinations are attainable, the medical test developer can feel more 
      confident about the value of further development of the test. CONCLUSIONS: A 
      well-designed early-CEA methodology can improve the ability to develop 
      (cost-)effective medical tests in an efficient manner. Early-CEAs should 
      continuously integrate insights and evidence that arise through feedback, which 
      may convince developers to return to earlier steps.
FAU - Buisman, Leander R
AU  - Buisman LR
AD  - Institute of Health Policy and Management,Erasmus University Rotterdam;Institute 
      for Medical Technology Assessment,Erasmus University Rotterdambuisman@bmg.eur.nl.
FAU - Rutten-van Mölken, Maureen P M H
AU  - Rutten-van Mölken MP
AD  - Institute of Health Policy and Management,Erasmus University Rotterdam;Institute 
      for Medical Technology Assessment,Erasmus University Rotterdam.
FAU - Postmus, Douwe
AU  - Postmus D
AD  - Department of Epidemiology,University of Groningen,University Medical Center 
      Groningen.
FAU - Luime, Jolanda J
AU  - Luime JJ
AD  - Department of Rheumatology,Erasmus MC,University Medical Center Rotterdam.
FAU - Uyl-de Groot, Carin A
AU  - Uyl-de Groot CA
AD  - Institute of Health Policy and Management,Erasmus University Rotterdam;Institute 
      for Medical Technology Assessment,Erasmus University Rotterdam.
FAU - Redekop, William K
AU  - Redekop WK
AD  - Institute of Health Policy and Management,Erasmus University Rotterdam;Institute 
      for Medical Technology Assessment,Erasmus University Rotterdam.
LA  - eng
PT  - Journal Article
DEP - 20160322
PL  - England
TA  - Int J Technol Assess Health Care
JT  - International journal of technology assessment in health care
JID - 8508113
SB  - IM
CIN - Int J Technol Assess Health Care. 2016 Jan;32(4):324-325. doi: 
      10.1017/S026646231600043X. PMID: 27691992
MH  - Arthritis, Rheumatoid/diagnosis
MH  - Cost-Benefit Analysis/*organization & administration
MH  - Decision Making
MH  - Diagnostic Techniques and Procedures/*economics
MH  - Humans
MH  - Models, Econometric
MH  - Recurrence
MH  - Sensitivity and Specificity
MH  - Stroke/physiopathology
MH  - Technology Assessment, Biomedical/*organization & administration
MH  - Time Factors
OTO - NOTNLM
OT  - Decision support
OT  - Early cost-effectiveness analysis
OT  - Manufacturer
OT  - Medical test
OT  - Research and development
OT  - Test developer
EDAT- 2016/03/24 06:00
MHDA- 2017/06/01 06:00
CRDT- 2016/03/23 06:00
PHST- 2016/03/23 06:00 [entrez]
PHST- 2016/03/24 06:00 [pubmed]
PHST- 2017/06/01 06:00 [medline]
AID - S0266462316000064 [pii]
AID - 10.1017/S0266462316000064 [doi]
PST - ppublish
SO  - Int J Technol Assess Health Care. 2016 Jan;32(1-2):46-53. doi: 
      10.1017/S0266462316000064. Epub 2016 Mar 22.

PMID- 26917565
OWN - NLM
STAT- MEDLINE
DCOM- 20160909
LR  - 20220409
IS  - 1524-4628 (Electronic)
IS  - 0039-2499 (Linking)
VI  - 47
IP  - 4
DP  - 2016 Apr
TI  - Cerebrovascular Disease in Rheumatic Diseases: A Systematic Review and 
      Meta-Analysis.
PG  - 943-50
LID - 10.1161/STROKEAHA.115.012052 [doi]
AB  - BACKGROUND AND PURPOSE: Some rheumatic diseases are associated with stroke. Less 
      is known about associations with stroke subtypes or stroke risk by age. We 
      quantified the association between stroke, its subtypes, and rheumatic diseases 
      and identified when stroke risk is greatest. METHODS: Searches of EMBASE (from 
      1980) and MEDLINE (from inception) to end 2014 and manual search of reference 
      lists for studies of stroke and stroke subtypes in rheumatic diseases as well as 
      studies measuring cerebrovascular disease from magnetic resonance imaging. 
      RESULTS: Prior published meta-analyses and new pooled analyses of any stroke in 
      rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, gout, 
      and psoriasis show an excess risk of stroke over the general population with odds 
      ratio (OR) ranging from 1.51 (95% confidence interval: 1.39-1.62) to 2.13 
      (1.53-2.98). New meta-analyses of stroke subtypes in rheumatoid arthritis 
      [ischemic: OR, 1.64 (1.32-2.05); hemorrhagic: OR, 1.68 (1.11-2.53)] and systemic 
      lupus erythematosus [ischemic: OR, 2.11 (1.66-2.67); hemorrhagic: OR, 1.82 
      (1.07-3.09)] show an excess risk of stroke over the general population. Stroke 
      risk across rheumatic diseases is highest in those aged <50 years [OR, 1.79 
      (1.46-2.20)] and reduces relatively with ageing [>65 years: OR, 1.14 (0.94-1.38); 
      difference P<0.007]. Inflammatory arthropathies conveyed higher stroke risk than 
      noninflammatory diseases (OR, 1.3, 1.2-1.3). It was not possible to adjust ORs 
      for risk factors or treatments. CONCLUSIONS: Risk of any stroke is higher in most 
      rheumatic diseases than in the general population, particularly <50 years. 
      Rheumatoid arthritis and systemic lupus erythematosus increase ischemic and 
      hemorrhagic stroke risk by 60% to 100% relative to the general population.
CI  - © 2016 American Heart Association, Inc.
FAU - Wiseman, Stewart J
AU  - Wiseman SJ
AD  - From the Centre for Clinical Brain Sciences, University of Edinburgh (S.J.W., 
      J.M.W.), Centre for Genomic and Experimental Medicine (S.H.R.), University of 
      Edinburgh, Edinburgh, United Kingdom.
FAU - Ralston, Stuart H
AU  - Ralston SH
AD  - From the Centre for Clinical Brain Sciences, University of Edinburgh (S.J.W., 
      J.M.W.), Centre for Genomic and Experimental Medicine (S.H.R.), University of 
      Edinburgh, Edinburgh, United Kingdom.
FAU - Wardlaw, Joanna M
AU  - Wardlaw JM
AD  - From the Centre for Clinical Brain Sciences, University of Edinburgh (S.J.W., 
      J.M.W.), Centre for Genomic and Experimental Medicine (S.H.R.), University of 
      Edinburgh, Edinburgh, United Kingdom. Joanna.Wardlaw@ed.ac.uk.
LA  - eng
GR  - MR/K026992/1/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PT  - Systematic Review
DEP - 20160225
PL  - United States
TA  - Stroke
JT  - Stroke
JID - 0235266
SB  - IM
MH  - Age Factors
MH  - Aged
MH  - Aged, 80 and over
MH  - Cerebrovascular Disorders/*epidemiology
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Registries
MH  - Rheumatic Diseases/*epidemiology
MH  - Risk
OTO - NOTNLM
OT  - arthritis
OT  - atrophy
OT  - inflammation
OT  - rheumatology
OT  - stroke
EDAT- 2016/02/27 06:00
MHDA- 2016/09/10 06:00
CRDT- 2016/02/27 06:00
PHST- 2015/11/04 00:00 [received]
PHST- 2016/02/03 00:00 [accepted]
PHST- 2016/02/27 06:00 [entrez]
PHST- 2016/02/27 06:00 [pubmed]
PHST- 2016/09/10 06:00 [medline]
AID - STROKEAHA.115.012052 [pii]
AID - 10.1161/STROKEAHA.115.012052 [doi]
PST - ppublish
SO  - Stroke. 2016 Apr;47(4):943-50. doi: 10.1161/STROKEAHA.115.012052. Epub 2016 Feb 
      25.

PMID- 26889323
OWN - NLM
STAT- MEDLINE
DCOM- 20160916
LR  - 20181113
IS  - 1937-8688 (Electronic)
VI  - 22
DP  - 2015
TI  - [Ischemic stroke in young patients: about 6 cases].
PG  - 142
LID - 10.11604/pamj.2015.22.142.7609 [doi]
LID - 142
FAU - Khammassi, Naziha
AU  - Khammassi N
AD  - Service de Médecine Interne, Hôpital Razi, La Manouba, Tunisie.
FAU - Sassi, Yosra Ben
AU  - Sassi YB
AD  - Service de Médecine Interne, Hôpital Razi, La Manouba, Tunisie.
FAU - Aloui, Asma
AU  - Aloui A
AD  - Service de Médecine Interne, Hôpital Razi, La Manouba, Tunisie.
FAU - Kort, Youssef
AU  - Kort Y
AD  - Service de Médecine Interne, Hôpital Razi, La Manouba, Tunisie.
FAU - Abdelhedi, Haykel
AU  - Abdelhedi H
AD  - Service de Médecine Interne, Hôpital Razi, La Manouba, Tunisie.
FAU - Cherif, Ouahida
AU  - Cherif O
AD  - Service de Médecine Interne, Hôpital Razi, La Manouba, Tunisie.
LA  - fre
PT  - Case Reports
PT  - Journal Article
TT  - L'accident ischémique cérébral chez le sujet jeune: à propos de 6 cas.
DEP - 20151014
PL  - Uganda
TA  - Pan Afr Med J
JT  - The Pan African medical journal
JID - 101517926
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - 12001-79-5 (Vitamin K)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Age Factors
MH  - Brain Ischemia/drug therapy/etiology/*pathology
MH  - Female
MH  - Humans
MH  - Male
MH  - Platelet Aggregation Inhibitors/*therapeutic use
MH  - Protein S Deficiency/complications
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Sjogren's Syndrome/complications
MH  - Sneddon Syndrome/complications
MH  - Stroke/drug therapy/etiology/*pathology
MH  - Vitamin K/*antagonists & inhibitors
PMC - PMC4742037
OTO - NOTNLM
OT  - Transient ischemic attack
OT  - diagnosis
OT  - etiology
OT  - treatment
OT  - young adult
EDAT- 2016/02/19 06:00
MHDA- 2016/09/17 06:00
PMCR- 2015/10/14
CRDT- 2016/02/19 06:00
PHST- 2015/07/26 00:00 [received]
PHST- 2015/08/19 00:00 [accepted]
PHST- 2016/02/19 06:00 [entrez]
PHST- 2016/02/19 06:00 [pubmed]
PHST- 2016/09/17 06:00 [medline]
PHST- 2015/10/14 00:00 [pmc-release]
AID - PAMJ-22-142 [pii]
AID - 10.11604/pamj.2015.22.142.7609 [doi]
PST - epublish
SO  - Pan Afr Med J. 2015 Oct 14;22:142. doi: 10.11604/pamj.2015.22.142.7609. 
      eCollection 2015.

PMID- 26835182
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2167-7921 (Print)
IS  - 2167-7921 (Electronic)
IS  - 2167-7921 (Linking)
VI  - 4
IP  - 4
DP  - 2015 Dec
TI  - The Risk for Cardiovascular Events Associated with Hyperlipdemia among Patients 
      with and Without Rheumatoid Arthritis.
LID - 178 [pii]
AB  - OBJECTIVES: To determine, using data from a real-world setting, the overall and 
      sex-specific risk of cardiovascular (CV) events in patients with rheumatoid 
      arthritis (RA), with or without comorbid hyperlipidemia, relative to those in a 
      non-RA cohort. METHODS: This retrospective cohort study using claims data from a 
      US commercial health plan (2005-2011) included patients with RA and a matched 
      non-RA cohort. Cox proportional hazards regression model determined the hazard 
      ratio (HR) for CV events (myocardial infarction, stroke, revascularization 
      procedures), using the presence of RA and hyperlipidemia as the independent 
      variables, controlling for other covariates (age, sex, diabetes, and 
      hypertension). RESULTS: The incidence of CV events per 1000 person-years was 
      10.19 for the RA cohort and 6.41 for the non-RA cohort (crude rate ratio [RR] 
      =1.59). Within the RA cohort, incidence was 15.54 for patients with 
      hyperlipidemia and 7.05 for patients without hyperlipidemia (crude RR=2.21); in 
      the non-RA cohort, incidence was 10.55 and 3.82 for those with and without 
      hyperlipidemia, respectively (crude RR=2.76). After controlling for covariates, 
      the HR of CV events among RA patients was 1.68 (95% CI: 1.50, 1.87) relative to 
      non-RA patients. After multivariable adjustment, hyperlipidemia conferred a 
      significant risk of CV events in both RA and non-RA patients; the interaction 
      between RA and hyperlipidemia was not significant (p=0.13). CONCLUSION: This 
      real-world analysis demonstrates that patients with RA have an increased risk of 
      CV events. Similar to a non-RA cohort, CV event rates were incrementally higher 
      for those patients with hyperlipidemia. SIGNIFICANCE: Cardiovascular disease is 
      an increasingly visible topic of concern in the rheumatoid arthritis community. 
      However, there are only limited data that informs both the absolute and relative 
      rates of CVD events, and the contribution of various risk factors such as 
      hyperlipidemia, compared to non-RA populationsThe 'lipid paradox' hypothesis in 
      RA suggests that elevated LDL cholesterol has a negligible effect on CVD risk in 
      RA, unlikely in the general population where it is a well-accepted CVD risk 
      factorThe incidence of CVD events in RA patients was 10/1000 patient years, a 1.6 
      fold greater risk compared to non-RA patientsThe contribution of hyperlipidemia 
      to CVD risk was associated with comparable or greater absolute increases in the 
      rate of CV events compared to non RA patients, a finding that does not support 
      the lipid paradox.
FAU - Nadkarni, Anagha
AU  - Nadkarni A
AD  - Bristol-Myers Squibb, Princeton, NJ, USA.
FAU - You, Min
AU  - You M
AD  - Bristol-Myers Squibb, Princeton, NJ, USA.
FAU - Resuehr, Holly
AU  - Resuehr H
AD  - University of Alabama at Birmingham, AL, USA.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AD  - University of Alabama at Birmingham, AL, USA.
LA  - eng
GR  - P60 AR064172/AR/NIAMS NIH HHS/United States
PT  - Journal Article
DEP - 20151205
PL  - United States
TA  - J Arthritis
JT  - Journal of arthritis
JID - 101674541
PMC - PMC4727537
MID - NIHMS748476
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - Hyperlipidemia
OT  - Inflammation
OT  - Rheumatoid arthritis
EDAT- 2016/02/03 06:00
MHDA- 2016/02/03 06:01
PMCR- 2016/12/01
CRDT- 2016/02/03 06:00
PHST- 2016/02/03 06:00 [entrez]
PHST- 2016/02/03 06:00 [pubmed]
PHST- 2016/02/03 06:01 [medline]
PHST- 2016/12/01 00:00 [pmc-release]
AID - 178 [pii]
AID - 10.4172/2167-7921.1000178 [doi]
PST - ppublish
SO  - J Arthritis. 2015 Dec;4(4):178. doi: 10.4172/2167-7921.1000178. Epub 2015 Dec 5.

PMID- 26818851
OWN - NLM
STAT- MEDLINE
DCOM- 20161006
LR  - 20220409
IS  - 1478-6362 (Electronic)
IS  - 1478-6354 (Print)
IS  - 1478-6354 (Linking)
VI  - 18
DP  - 2016 Jan 28
TI  - Co-morbidity in patients with early rheumatoid arthritis - inflammation matters.
PG  - 33
LID - 10.1186/s13075-016-0928-y [doi]
LID - 33
AB  - BACKGROUND: Patients with rheumatoid arthritis (RA) suffer from co-morbidities 
      that contribute to a shortened lifespan. Inflammation is important for the 
      development of cardiovascular disease, but little is known on its relationship 
      with other co-morbidities. We investigated the role of inflammation for the 
      development of new comorbidities in early RA. METHODS: Since 1995, all patients 
      with early RA in Northern Sweden are included in a prospective study on 
      co-morbidities, with a total of 950 patients being included. At the time for this 
      study, 726 had been ill for ≥5 years. Data on co-morbidities, clinical and 
      laboratory disease activity and pharmacological therapy were collected from 
      patient records and further validated using a questionnaire at RA onset (T0) and 
      after 5 years (T5). RESULTS: Of the patients, 53.2 % of the patients had one or 
      more co-morbidity at onset, the commonest being: hypertension (27.3 %), 
      obstructive pulmonary disease (13.9 %), diabetes (8.0 %), hypothyroidism (6.3 %) 
      and malignancy (5.0 %). After 5 years, 41.0 % had developed at least one new 
      co-morbidity, the most common being: hypertension (15.1 %), malignancy (7.6 %), 
      stroke/transient ischemic accident (5.1 %), myocardial infarction (4.3 %) and 
      osteoporosis (3.7 %). Age at disease onset, a raised erythrocyte sedimentation 
      rate (ESR) at inclusion, previous treatment with glucocorticoids (GC; p < 0.001 
      for all), extra-articular RA (Ex-RA; p < 0.01), DAS28 (area under the curve) at 
      24 months (p < 0.05), previous smoking at inclusion (p = 0.058) and male gender 
      (p < 0.01) were associated with a new co-morbidity overall at T5. Treatment with 
      biologics (p < 0.05) reduced the risk. In multiple logistic regression modelling, 
      ESR (p = 0.036) at inclusion was associated with a new co-morbidity after 
      5 years, adjusted for age, sex, smoking and GC treatment. In a similar model, 
      Ex-RA (p < 0.05) was associated with a new co-morbidity at T5. In a third model, 
      adjusted for age and sex, a new pulmonary co-morbidity was associated with a 
      smoking history at inclusion (p < 0.01), but not with ESR. CONCLUSION: There was 
      substantial co-morbidity among early RA patients already at disease onset, with 
      considerable new co-morbidity being added during the first five years. Measures 
      of disease activity were associated with the occurrence of a new co-morbidity 
      indicating that the inflammation is of importance in this context.
FAU - Innala, Lena
AU  - Innala L
AD  - Department of Public Health and Clinical Medicine, Rheumatology University 
      Hospital, Umeå, 90185, Sweden. Lena.Innala@vll.se.
FAU - Sjöberg, Clara
AU  - Sjöberg C
AD  - Department of Public Health and Clinical Medicine, Rheumatology University 
      Hospital, Umeå, 90185, Sweden. clara.sjoberg86@hotmail.com.
FAU - Möller, Bozena
AU  - Möller B
AD  - Department of Rheumatology, Sunderby Hospital, Luleå, 97180, Sweden. 
      bozena.moller@gmail.com.
FAU - Ljung, Lotta
AU  - Ljung L
AD  - Department of Public Health and Clinical Medicine, Rheumatology University 
      Hospital, Umeå, 90185, Sweden. Lotta.Ljung@telia.com.
FAU - Smedby, Torgny
AU  - Smedby T
AD  - Department of Rheumatology, Östersund Hospital, Östersund, 83183, Sweden. 
      torgny.smedby@jll.se.
FAU - Södergren, Anna
AU  - Södergren A
AD  - Department of Public Health and Clinical Medicine, Rheumatology University 
      Hospital, Umeå, 90185, Sweden. anna.sodergren@umu.se.
FAU - Magnusson, Staffan
AU  - Magnusson S
AD  - Department of Rheumatology, Sundsvall Hospital, Sundsvall, 85186, Sweden. 
      staffan.magnusson@lvn.se.
FAU - Rantapää-Dahlqvist, Solbritt
AU  - Rantapää-Dahlqvist S
AD  - Department of Public Health and Clinical Medicine, Rheumatology University 
      Hospital, Umeå, 90185, Sweden. solbritt.rantapaa.dahlqvist@umu.se.
FAU - Wållberg-Jonsson, Solveig
AU  - Wållberg-Jonsson S
AD  - Department of Public Health and Clinical Medicine, Rheumatology University 
      Hospital, Umeå, 90185, Sweden. solveig.wallberg.jonsson@umu.se.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160128
PL  - England
TA  - Arthritis Res Ther
JT  - Arthritis research & therapy
JID - 101154438
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/*diagnosis/drug therapy/*epidemiology
MH  - Comorbidity
MH  - Early Diagnosis
MH  - Female
MH  - Humans
MH  - Inflammation/diagnosis/drug therapy/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Prospective Studies
MH  - Risk Factors
MH  - Sweden/epidemiology
MH  - Young Adult
PMC - PMC4730785
EDAT- 2016/01/29 06:00
MHDA- 2016/10/08 06:00
PMCR- 2016/01/28
CRDT- 2016/01/29 06:00
PHST- 2015/05/25 00:00 [received]
PHST- 2016/01/07 00:00 [accepted]
PHST- 2016/01/29 06:00 [entrez]
PHST- 2016/01/29 06:00 [pubmed]
PHST- 2016/10/08 06:00 [medline]
PHST- 2016/01/28 00:00 [pmc-release]
AID - 10.1186/s13075-016-0928-y [pii]
AID - 928 [pii]
AID - 10.1186/s13075-016-0928-y [doi]
PST - epublish
SO  - Arthritis Res Ther. 2016 Jan 28;18:33. doi: 10.1186/s13075-016-0928-y.

PMID- 26749043
OWN - NLM
STAT- MEDLINE
DCOM- 20170707
LR  - 20210109
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Print)
IS  - 2326-5191 (Linking)
VI  - 68
IP  - 6
DP  - 2016 Jun
TI  - Association Between Ischemic Stroke and Tumor Necrosis Factor Inhibitor Therapy 
      in Patients With Rheumatoid Arthritis.
PG  - 1337-45
LID - 10.1002/art.39582 [doi]
AB  - OBJECTIVE: Patients with rheumatoid arthritis (RA) are at an increased risk of 
      ischemic stroke. Tumor necrosis factor inhibitors (TNFi) may influence risk and 
      mortality after ischemic stroke by reducing inflammation. This study was 
      undertaken to examine the association of TNFi with the risk of incident ischemic 
      stroke and with 30-day and 1-year mortality after ischemic stroke. METHODS: 
      Patients with RA starting therapy with TNFi and a biologics-naive comparator 
      group treated with synthetic disease-modifying antirheumatic drugs (DMARDs) only 
      were recruited to the British Society for Rheumatology Biologics Register for 
      Rheumatoid Arthritis from 2001 to 2009. Patients were followed up via clinical 
      and patient questionnaires as well as the national death register. Incident 
      strokes were classified as ischemic if brain imaging reports suggested ischemia 
      or if ischemic stroke was reported as the underlying cause of death on a death 
      certificate. Patients with a previous stroke were excluded. Risk of ischemic 
      stroke was compared between patients receiving synthetic DMARDs only and those 
      ever-exposed to TNFi using a Cox proportional hazards regression model adjusted 
      for potential confounders. Mortality after ischemic stroke was compared between 
      synthetic DMARD-treated patients and TNFi-treated patients using logistic 
      regression, adjusted for age and sex. RESULTS: To April 2010, 127 verified 
      incident ischemic strokes (21 in 3,271 synthetic DMARD-treated patients and 106 
      in 11,642 TNFi-treated patients) occurred during 11,973 and 61,226 person-years 
      of observation, respectively (incidence rate 175 versus 173 per 100,000 
      person-years). After adjustment for confounders, there was no association between 
      ever-exposure to TNFi and ischemic stroke (hazard ratio 0.99 [95% confidence 
      interval (95% CI) 0.54-1.81]). Mortality 30 days or 1 year after ischemic stroke 
      was not associated with concurrent TNFi exposure (odds ratio 0.18 [95% CI 
      0.03-1.21] and 0.60 [95% CI 0.16-2.28], respectively). CONCLUSION: Exposure to 
      TNFi does not appear to influence the occurrence of ischemic stroke in the medium 
      term in patients with RA. The impact on mortality after ischemic stroke remains 
      inconclusive.
CI  - © 2016 The Authors. Arthritis & Rheumatology published by Wiley Periodicals, Inc. 
      on behalf of the American College of Rheumatology.
FAU - Low, Audrey S L
AU  - Low AS
AD  - Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal 
      Research, Institute of Inflammation and Repair, The University of Manchester and 
      Salford Royal Hospital NHS Foundation Trust.
FAU - Lunt, Mark
AU  - Lunt M
AD  - Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal 
      Research, Institute of Inflammation and Repair, The University of Manchester.
FAU - Mercer, Louise K
AU  - Mercer LK
AD  - Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal 
      Research, Institute of Inflammation and Repair, The University of Manchester.
FAU - Watson, Kath D
AU  - Watson KD
AD  - Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal 
      Research, Institute of Inflammation and Repair, The University of Manchester.
FAU - Dixon, William G
AU  - Dixon WG
AD  - Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal 
      Research, Institute of Inflammation and Repair, The University of Manchester and 
      NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester NHS 
      Foundation Trust, Manchester Academic Health Science Centre, and Salford Royal 
      Hospital NHS Foundation Trust.
FAU - Symmons, Deborah P M
AU  - Symmons DP
AD  - Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal 
      Research, Institute of Inflammation and Repair, The University of Manchester and 
      NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester NHS 
      Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK.
FAU - Hyrich, Kimme L
AU  - Hyrich KL
AD  - Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal 
      Research, Institute of Inflammation and Repair, The University of Manchester and 
      NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester NHS 
      Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK.
LA  - eng
GR  - G0701380/MRC_/Medical Research Council/United Kingdom
GR  - G0902272/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Brain Ischemia/*chemically induced/mortality
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Prospective Studies
MH  - Risk Assessment
MH  - Stroke/*chemically induced/mortality
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
PMC - PMC4982051
EDAT- 2016/01/11 06:00
MHDA- 2017/07/08 06:00
PMCR- 2016/08/12
CRDT- 2016/01/11 06:00
PHST- 2015/04/03 00:00 [received]
PHST- 2016/01/05 00:00 [accepted]
PHST- 2016/01/11 06:00 [entrez]
PHST- 2016/01/11 06:00 [pubmed]
PHST- 2017/07/08 06:00 [medline]
PHST- 2016/08/12 00:00 [pmc-release]
AID - ART39582 [pii]
AID - 10.1002/art.39582 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2016 Jun;68(6):1337-45. doi: 10.1002/art.39582.

PMID- 26727968
OWN - NLM
STAT- MEDLINE
DCOM- 20161213
LR  - 20231111
IS  - 2047-9980 (Electronic)
IS  - 2047-9980 (Linking)
VI  - 5
IP  - 1
DP  - 2016 Jan 4
TI  - Hydroxychloroquine Use Is Associated With Decreased Incident Cardiovascular 
      Events in Rheumatoid Arthritis Patients.
LID - 10.1161/JAHA.115.002867 [doi]
LID - e002867
AB  - BACKGROUND: Cardiovascular disease (CVD) is the leading cause of death in 
      rheumatoid arthritis (RA) patients. This study is the first to report the 
      association of hydroxychloroquine (an antirheumatic medication that has been 
      associated with decreased risk of diabetes, a less atherogenic lipid profile, and 
      antithrombotic properties) with CVD in RA. METHODS AND RESULTS: A retrospective 
      incident RA cohort from January 1, 2001, to October 31, 2013, excluding patients 
      with CVD prior to RA diagnosis, was constructed. Patients were categorized as 
      hydroxychloroquine users versus nonusers and were allowed to contribute time to 
      either group according to hydroxychloroquine exposure. The primary outcome was 
      adjudicated incident CVD defined as a composite of coronary artery disease, 
      stroke, transient ischemic attack, sudden cardiac death, and peripheral artery 
      disease with arterial revascularization procedure. The secondary outcome was a 
      composite of incident coronary artery disease, stroke, and transient ischemic 
      attack. Cox time-varying regression models were used to estimate the association 
      between hydroxychloroquine exposure and development of CVD, after adjusting for 
      propensity score and relevant confounders, including demographics, CVD-related 
      comorbidities, RA severity, and activity indicators and medications. We included 
      1266 RA patients, 547 hydroxychloroquine users, and 719 nonusers. During the 
      observation period, 102 CVD events occurred, 3 in hydroxychloroquine users and 99 
      in nonusers. The fully adjusted Cox model showed a hazard ratio of 0.28 (95% CI 
      0.12-0.63, P=0.002) for incident CVD and 0.30 (95% CI 0.13-0.68, P=0.004) for 
      incident composite coronary artery disease, stroke, and transient ischemic attack 
      for hydroxychloroquine users versus nonusers, respectively. CONCLUSION: In this 
      hypothesis-generating study, hydroxychloroquine use was associated with a 72% 
      decrease in the risk of incident CVD in RA patients. If these preliminary results 
      are confirmed in larger studies, our findings may be used as a rationale for a 
      randomized study of hydroxychloroquine use for primary prevention of CVD in RA or 
      nonrheumatic high-risk patients.
CI  - © 2016 The Authors. Published on behalf of the American Heart Association, Inc., 
      by Wiley Blackwell.
FAU - Sharma, Tarun S
AU  - Sharma TS
AD  - Rheumatology Department, Geisinger Medical Center, Danville, PA (T.S.S., A.B.) 
      Rheumatology Department, West Penn Allegheny Health System, Pittsburgh, PA 
      (T.S.S., M.C.M.W., X.T.).
FAU - Wasko, Mary Chester M
AU  - Wasko MC
AD  - Rheumatology Department, West Penn Allegheny Health System, Pittsburgh, PA 
      (T.S.S., M.C.M.W., X.T.).
FAU - Tang, Xiaoqin
AU  - Tang X
AD  - Rheumatology Department, West Penn Allegheny Health System, Pittsburgh, PA 
      (T.S.S., M.C.M.W., X.T.) Biostatistics Department, Center for Health Research, 
      Danville, PA (X.T., X.Y.).
FAU - Vedamurthy, Deepak
AU  - Vedamurthy D
AD  - Hospital Medicine Department, Geisinger Medical Center, Danville, PA (D.V.).
FAU - Yan, Xiaowei
AU  - Yan X
AD  - Biostatistics Department, Center for Health Research, Danville, PA (X.T., X.Y.) 
      Sutter Health, Sacramento, CA (X.Y.).
FAU - Cote, Jonida
AU  - Cote J
AD  - Rheumatology Department, Geisinger Wyoming Valley, Wilkes-Barre, PA (J.C.).
FAU - Bili, Androniki
AU  - Bili A
AD  - Rheumatology Department, Geisinger Medical Center, Danville, PA (T.S.S., A.B.).
LA  - eng
PT  - Journal Article
DEP - 20160104
PL  - England
TA  - J Am Heart Assoc
JT  - Journal of the American Heart Association
JID - 101580524
RN  - 0 (Antirheumatic Agents)
RN  - 4QWG6N8QKH (Hydroxychloroquine)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/diagnosis/*drug therapy/epidemiology
MH  - Cardiovascular Diseases/diagnosis/epidemiology/*prevention & control
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Hydroxychloroquine/*therapeutic use
MH  - Incidence
MH  - Kaplan-Meier Estimate
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Pennsylvania/epidemiology
MH  - Propensity Score
MH  - Proportional Hazards Models
MH  - Protective Factors
MH  - Retrospective Studies
MH  - Risk Assessment
MH  - Risk Factors
MH  - Time Factors
MH  - Treatment Outcome
PMC - PMC4859400
OTO - NOTNLM
OT  - cardiovascular diseases
OT  - hydroxychloroquine
OT  - primary prevention
OT  - rheumatoid arthritis
EDAT- 2016/01/06 06:00
MHDA- 2016/12/15 06:00
PMCR- 2016/01/01
CRDT- 2016/01/06 06:00
PHST- 2016/01/06 06:00 [entrez]
PHST- 2016/01/06 06:00 [pubmed]
PHST- 2016/12/15 06:00 [medline]
PHST- 2016/01/01 00:00 [pmc-release]
AID - JAHA.115.002867 [pii]
AID - JAH31270 [pii]
AID - 10.1161/JAHA.115.002867 [doi]
PST - epublish
SO  - J Am Heart Assoc. 2016 Jan 4;5(1):e002867. doi: 10.1161/JAHA.115.002867.

PMID- 28329095
OWN - NLM
STAT- Publisher
LR  - 20240227
IS  - 2055-6845 (Electronic)
DP  - 2016 Dec 20
TI  - Congestive heart failure: More common as well as an important cardiovascular 
      outcome.
LID - 10.1093/ecam/pvw046 [doi]
AB  - Hydroxychloroquine, due to its multifaceted pleiotropic benefits including 
      anti-inflammatory effects has great potential in reducing cardiovascular (CV) 
      morbidity and mortality. CV outcome data of hydroxychloroquine is available 
      through 2 retrospective studies in rheumatoid arthritis patients, both of which 
      have not considered congestive heart failure (CHF) as an outcome measure. CHF is 
      an important CV outcome and is more common than myocardial infarction and stroke; 
      and increased age is associated with increased risk of CHF. Hydroxychloroquine 
      has potential in exerting beneficial effects on CHF because of it's effect of 
      mild bradycardia. Hence, we request authors to include CHF as one of the outcome 
      measure in the event driven protocol of the OXI trial.
CI  - Published on behalf of the European Society of Cardiology. All rights reserved. © 
      The Author 2016. For permissions please email: journals.permissions@oup.com.
FAU - Pareek, Anil
AU  - Pareek A
LA  - eng
PT  - Journal Article
DEP - 20161220
PL  - England
TA  - Eur Heart J Cardiovasc Pharmacother
JT  - European heart journal. Cardiovascular pharmacotherapy
JID - 101669491
EDAT- 2016/01/01 00:00
MHDA- 2016/01/01 00:00
CRDT- 2017/03/23 06:00
PHST- 2016/12/08 00:00 [received]
PHST- 2017/03/23 06:00 [entrez]
PHST- 2016/01/01 00:00 [pubmed]
PHST- 2016/01/01 00:00 [medline]
AID - 2726383 [pii]
AID - 10.1093/ecam/pvw046 [doi]
PST - aheadofprint
SO  - Eur Heart J Cardiovasc Pharmacother. 2016 Dec 20. doi: 10.1093/ecam/pvw046.

PMID- 26666335
OWN - NLM
STAT- MEDLINE
DCOM- 20160922
LR  - 20181113
IS  - 1476-7120 (Electronic)
IS  - 1476-7120 (Linking)
VI  - 13
DP  - 2015 Dec 15
TI  - Causes of changes in carotid intima-media thickness: a literature review.
PG  - 46
LID - 10.1186/s12947-015-0041-4 [doi]
LID - 46
AB  - Atherosclerosis causes significant morbidity and mortality. Carotid intima-media 
      thickness (CIMT) predicts future cardiovascular and ischaemic stroke incidence. 
      CIMT, a measure of atherosclerotic disease, can be reliably determined in vivo by 
      carotid ultrasound. In this review, we determined that CIMT is associated with 
      traditional cardiovascular risk factors such as age, sex, race, smoking, alcohol 
      consumption, habitual endurance exercise, blood pressure, dyslipidemia, dietary 
      patterns, risk-lowering drug therapy, glycemia, hyperuricemia, obesity-related 
      anthropometric parameters, obesity and obesity-related diseases. We also found 
      that CIMT is associated with novel risk factors, including heredity, certain 
      genotypic indices, anthropometric cardiovascular parameters, rheumatoid 
      arthritis, immunological diseases, inflammatory cytokines, lipid peroxidation, 
      anthropometric hemocyte parameters, infectious diseases, vitamin D, matrix 
      metalloproteinases, and other novel factors and diseases. However, the 
      conclusions are inconsonant; the underlying causes of these associations remain 
      to be further explored.
FAU - Qu, Baoge
AU  - Qu B
AD  - Department of Gastroenterology, Taishan Hospital, Taian, Shandong, 271000, P. R. 
      China. qubaoge@sina.com.
FAU - Qu, Tao
AU  - Qu T
AD  - Zhuhai Campus of Zunyi Medical College, Zhuhai, Guangdong, 519041, P. R. China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20151215
PL  - England
TA  - Cardiovasc Ultrasound
JT  - Cardiovascular ultrasound
JID - 101159952
SB  - IM
MH  - *Cardiovascular Diseases/diagnostic imaging/epidemiology/physiopathology
MH  - *Carotid Intima-Media Thickness
MH  - Global Health
MH  - Humans
MH  - Morbidity/trends
MH  - Risk Factors
MH  - Vascular Resistance/*physiology
PMC - PMC4678459
EDAT- 2015/12/17 06:00
MHDA- 2016/09/23 06:00
PMCR- 2015/12/15
CRDT- 2015/12/16 06:00
PHST- 2015/11/24 00:00 [received]
PHST- 2015/12/09 00:00 [accepted]
PHST- 2015/12/16 06:00 [entrez]
PHST- 2015/12/17 06:00 [pubmed]
PHST- 2016/09/23 06:00 [medline]
PHST- 2015/12/15 00:00 [pmc-release]
AID - 10.1186/s12947-015-0041-4 [pii]
AID - 41 [pii]
AID - 10.1186/s12947-015-0041-4 [doi]
PST - epublish
SO  - Cardiovasc Ultrasound. 2015 Dec 15;13:46. doi: 10.1186/s12947-015-0041-4.

PMID- 26635805
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20151204
LR  - 20220316
IS  - 1664-3224 (Print)
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 6
DP  - 2015
TI  - High-Risk Cardiovascular Patients: Clinical Features, Comorbidities, and 
      Interconnecting Mechanisms.
PG  - 591
LID - 10.3389/fimmu.2015.00591 [doi]
LID - 591
AB  - Cardiovascular disease is the leading cause of death in the Western world with an 
      increase over the last few decades. Atherosclerosis with its different 
      manifestations in the coronary artery tree, the cerebral, as well as peripheral 
      arteries is the basis for cardiovascular events, such as myocardial infarction, 
      stroke, and cardiovascular death. The pathophysiological understanding of the 
      mechanisms that promote the development of vascular disease has changed over the 
      last few decades, leading to the recognition that inflammation and inflammatory 
      processes in the vessel wall are major contributors in atherogenesis. In 
      addition, a subclinical inflammatory status, e.g., in patients with diabetes or 
      the presence of a chronic inflammatory disease, such as rheumatoid arthritis, 
      have been recognized as strong risk factors for cardiovascular disease. The 
      present review will summarize the different inflammatory processes in the vessel 
      wall leading to atherosclerosis and highlight the role of inflammation in 
      diabetes and chronic inflammatory diseases for cardiovascular morbidity and 
      mortality.
FAU - Schuett, Katharina Andrea
AU  - Schuett KA
AD  - Department of Internal Medicine I, University Hospital RWTH Aachen , Aachen , 
      Germany.
FAU - Lehrke, Michael
AU  - Lehrke M
AD  - Department of Internal Medicine I, University Hospital RWTH Aachen , Aachen , 
      Germany.
FAU - Marx, Nikolaus
AU  - Marx N
AD  - Department of Internal Medicine I, University Hospital RWTH Aachen , Aachen , 
      Germany.
FAU - Burgmaier, Mathias
AU  - Burgmaier M
AD  - Department of Internal Medicine I, University Hospital RWTH Aachen , Aachen , 
      Germany.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20151123
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
PMC - PMC4655316
OTO - NOTNLM
OT  - atherosclerosis
OT  - cardiovascular disease
OT  - coagulation
OT  - inflammation
OT  - rheumatoid arthritis
OT  - systemic lupus erythematosus
OT  - type 2 diabetes mellitus
EDAT- 2015/12/05 06:00
MHDA- 2015/12/05 06:01
PMCR- 2015/01/01
CRDT- 2015/12/05 06:00
PHST- 2015/07/13 00:00 [received]
PHST- 2015/11/03 00:00 [accepted]
PHST- 2015/12/05 06:00 [entrez]
PHST- 2015/12/05 06:00 [pubmed]
PHST- 2015/12/05 06:01 [medline]
PHST- 2015/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2015.00591 [doi]
PST - epublish
SO  - Front Immunol. 2015 Nov 23;6:591. doi: 10.3389/fimmu.2015.00591. eCollection 
      2015.

PMID- 26486791
OWN - NLM
STAT- MEDLINE
DCOM- 20160314
LR  - 20181202
IS  - 1534-6293 (Electronic)
IS  - 1528-4042 (Linking)
VI  - 15
IP  - 12
DP  - 2015 Dec
TI  - Prevention of Stroke in Rheumatoid Arthritis.
PG  - 77
LID - 10.1007/s11910-015-0600-y [doi]
AB  - The risk of cerebrovascular disease is increased among rheumatoid arthritis (RA) 
      patients and remains an underserved area of medical need. Only a minor proportion 
      of RA patients achieve suitable stroke prevention. Classical cardiovascular risk 
      factors appear to be under-diagnosed and undertreated among patients with RA. 
      Reducing the inflammatory burden is also necessary to lower the cardiovascular 
      risk. An adequate control of disease activity and cerebrovascular risk assessment 
      using national guidelines should be recommended for all patients with RA. For 
      patients with a documented history of cerebrovascular or cardiovascular risk 
      factors, smoking cessation and corticosteroids and non-steroidal 
      anti-inflammatory drugs at the lowest dose possible are crucial. Risk score 
      models should be adapted for patients with RA by introducing a 1.5 multiplication 
      factor, and their results interpreted to appropriately direct clinical care. 
      Statins, angiotensin-converting enzyme inhibitors, and angiotensin-II receptor 
      blockers are preferred treatment options. Biologic and non-biologic 
      disease-modifying anti-rheumatic drugs should be initiated early to mitigate the 
      necessity of symptom control drugs and to achieve early alleviation of the 
      inflammatory state. Early control can improve vascular compliance, decrease 
      atherosclerosis, improve overall lipid and metabolic profiles, and reduce the 
      incidence of heart disease that may lead to atrial fibrillation. In patients with 
      significant cervical spine involvement, early intervention and improved disease 
      control are necessary and may prevent further mechanical vascular injury.
FAU - Zha, Alicia M
AU  - Zha AM
AD  - Department of Neurology, The Ohio State University College of Medicine, Columbus, 
      OH, USA.
FAU - Di Napoli, Mario
AU  - Di Napoli M
AD  - Neurological Service, San Camillo de' Lellis General Hospital, Rieti, Italy.
AD  - SMDN-Neurological Section, Centre for Cardiovascular Medicine and Cerebrovascular 
      Disease Prevention, Sulmona, L'Aquila, Italy.
FAU - Behrouz, Réza
AU  - Behrouz R
AD  - Department of Neurology, School of Medicine, University of Texas Health Science 
      Center San Antonio, Medical Arts and Research Center, 8300 Floyd Curl Drive, MC 
      7883, San Antonio, TX, 78229, USA. Behrouz@uthscsa.edu.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Curr Neurol Neurosci Rep
JT  - Current neurology and neuroscience reports
JID - 100931790
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/*complications
MH  - Humans
MH  - Risk Factors
MH  - Stroke/complications/*prevention & control
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
OTO - NOTNLM
OT  - Autoimmune disease
OT  - Cerebrovascular disease
OT  - Inflammation
OT  - Rheumatoid arthritis
OT  - Risk factors
OT  - Stroke
EDAT- 2015/10/22 06:00
MHDA- 2016/03/15 06:00
CRDT- 2015/10/22 06:00
PHST- 2015/10/22 06:00 [entrez]
PHST- 2015/10/22 06:00 [pubmed]
PHST- 2016/03/15 06:00 [medline]
AID - 10.1007/s11910-015-0600-y [pii]
AID - 10.1007/s11910-015-0600-y [doi]
PST - ppublish
SO  - Curr Neurol Neurosci Rep. 2015 Dec;15(12):77. doi: 10.1007/s11910-015-0600-y.

PMID- 26467356
OWN - NLM
STAT- MEDLINE
DCOM- 20161219
LR  - 20220408
IS  - 2149-2271 (Electronic)
IS  - 2149-2263 (Print)
IS  - 2149-2263 (Linking)
VI  - 16
IP  - 1
DP  - 2016 Jan
TI  - Protective effects of methotrexate against ischemic cardiovascular disorders in 
      patients treated for rheumatoid arthritis or psoriasis: novel therapeutic 
      insights coming from a meta-analysis of the literature data.
PG  - 2-9
LID - 10.5152/akd.2015.6136 [doi]
AB  - OBJECTIVE: The association between chronic use of methotrexate and decreased risk 
      of ischemic cardiovascular events (CVE) among patients with psoriatic or 
      rheumatoid arthritis (RA) was investigated using a systematic review and 
      meta-analysis. METHODS: The studies should have recruited adults receiving 
      methotrexate, followed up for at least one year. Moreover, studies should have 
      reported "hard" cardiovascular endpoints, by evaluating the cardiovascular 
      outcomes of the habitual users of the drug or of new users compared with patients 
      with the same disease who had never used methotrexate. The outcome of interest 
      was the overall pooled odds ratio (OR) of major adverse cardiovascular events, 
      i.e., a composite of new- onset angina, acute coronary syndrome, need for 
      percutaneous or surgical coronary revascularization, stroke, and cardiovascular 
      death. The study was performed according to the PRISMA statement. RESULTS: Seven 
      observational studies, mostly engaging patients with RA, were included in the 
      meta-analysis. The pooled odds ratio (OR) was 0.73 (95% CI=0.70- 0.77 p<0.001). 
      When stratified meta-analysis models were assessed, the pooled OR was 0.80 (95% 
      CI=0.66-0.97; p=0.022) for studies adjusting for clinical severity of RA. 
      Furthermore, the OR was even more significant after adjustment for concomitant 
      use of other drugs specific for RA(OR=0.71, 95% CI=0.67-0.75, p<0.001). 
      CONCLUSION: Methotrexate at low doses, such those used for maintenance therapy of 
      RA, predicted a decreased risk of CVE. Since methotrexate doesn't interfere with 
      blood lipids, platelet aggregation or insulin resistance, the protective 
      association may originate from mechanisms other than those exerted by 
      antiplatelet drugs or statins.
FAU - De Vecchis, Renato
AU  - De Vecchis R
AD  - Cardiology Unit, Presidio Sanitario Intermedio "Elena d'Aosta"; Napoli-Italy. 
      r.de.vecchis@alice.it.
FAU - Baldi, Cesare
AU  - Baldi C
FAU - Palmisani, Leonardo
AU  - Palmisani L
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Systematic Review
PL  - Turkey
TA  - Anatol J Cardiol
JT  - Anatolian journal of cardiology
JID - 101652981
RN  - 0 (Antirheumatic Agents)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Antirheumatic Agents/administration & dosage/*therapeutic use
MH  - *Arthritis, Rheumatoid
MH  - Cardiovascular Diseases/*prevention & control
MH  - Humans
MH  - Methotrexate/administration & dosage/*therapeutic use
MH  - *Psoriasis
PMC - PMC5336700
COIS- Conflict of interest: None declared.
EDAT- 2015/10/16 06:00
MHDA- 2016/12/20 06:00
PMCR- 2016/01/01
CRDT- 2015/10/16 06:00
PHST- 2015/10/16 06:00 [entrez]
PHST- 2015/10/16 06:00 [pubmed]
PHST- 2016/12/20 06:00 [medline]
PHST- 2016/01/01 00:00 [pmc-release]
AID - AJC-16-2 [pii]
AID - 10.5152/akd.2015.6136 [doi]
PST - ppublish
SO  - Anatol J Cardiol. 2016 Jan;16(1):2-9. doi: 10.5152/akd.2015.6136.

PMID- 26457127
OWN - NLM
STAT- MEDLINE
DCOM- 20160725
LR  - 20240325
IS  - 1942-0994 (Electronic)
IS  - 1942-0900 (Print)
IS  - 1942-0994 (Linking)
VI  - 2015
DP  - 2015
TI  - NSAIDs and Cardiovascular Diseases: Role of Reactive Oxygen Species.
PG  - 536962
LID - 10.1155/2015/536962 [doi]
LID - 536962
AB  - Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most commonly used drugs 
      worldwide. NSAIDs are used for a variety of conditions including pain, rheumatoid 
      arthritis, and musculoskeletal disorders. The beneficial effects of NSAIDs in 
      reducing or relieving pain are well established, and other benefits such as 
      reducing inflammation and anticancer effects are also documented. The undesirable 
      side effects of NSAIDs include ulcers, internal bleeding, kidney failure, and 
      increased risk of heart attack and stroke. Some of these side effects may be due 
      to the oxidative stress induced by NSAIDs in different tissues. NSAIDs have been 
      shown to induce reactive oxygen species (ROS) in different cell types including 
      cardiac and cardiovascular related cells. Increases in ROS result in increased 
      levels of oxidized proteins which alters key intracellular signaling pathways. 
      One of these key pathways is apoptosis which causes cell death when significantly 
      activated. This review discusses the relationship between NSAIDs and 
      cardiovascular diseases (CVD) and the role of NSAID-induced ROS in CVD.
FAU - Ghosh, Rajeshwary
AU  - Ghosh R
AD  - Department of Neurobiology, Physiology, and Behavior, University of California, 
      Davis, CA 95616, USA.
FAU - Alajbegovic, Azra
AU  - Alajbegovic A
AD  - Department of Neurobiology, Physiology, and Behavior, University of California, 
      Davis, CA 95616, USA.
FAU - Gomes, Aldrin V
AU  - Gomes AV
AD  - Department of Neurobiology, Physiology, and Behavior, University of California, 
      Davis, CA 95616, USA ; Department of Physiology and Membrane Biology, University 
      of California, Davis, CA 95616, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20150920
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Reactive Oxygen Species)
RN  - 9035-51-2 (Cytochrome P-450 Enzyme System)
RN  - EC 1.13.11.12 (Lipoxygenase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.17.3.2 (Xanthine Oxidase)
RN  - EC 1.6.3.- (NADPH Oxidases)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal/*adverse effects/pharmacology/therapeutic 
      use
MH  - Arthritis/drug therapy
MH  - Cardiovascular Diseases/epidemiology/*etiology
MH  - Cytochrome P-450 Enzyme System/metabolism
MH  - Humans
MH  - Incidence
MH  - Lipoxygenase/metabolism
MH  - Mitochondria/drug effects/metabolism
MH  - NADPH Oxidases/metabolism
MH  - Nitric Oxide Synthase/metabolism
MH  - Reactive Oxygen Species/*metabolism
MH  - Xanthine Oxidase/metabolism
PMC - PMC4592725
EDAT- 2015/10/13 06:00
MHDA- 2016/07/28 06:00
PMCR- 2015/09/20
CRDT- 2015/10/13 06:00
PHST- 2014/12/22 00:00 [received]
PHST- 2015/03/03 00:00 [revised]
PHST- 2015/03/03 00:00 [accepted]
PHST- 2015/10/13 06:00 [entrez]
PHST- 2015/10/13 06:00 [pubmed]
PHST- 2016/07/28 06:00 [medline]
PHST- 2015/09/20 00:00 [pmc-release]
AID - 10.1155/2015/536962 [doi]
PST - ppublish
SO  - Oxid Med Cell Longev. 2015;2015:536962. doi: 10.1155/2015/536962. Epub 2015 Sep 
      20.

PMID- 26406879
OWN - NLM
STAT- MEDLINE
DCOM- 20160601
LR  - 20220409
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 10
IP  - 9
DP  - 2015
TI  - Increased Risk of Chronic Kidney Disease in Rheumatoid Arthritis Associated with 
      Cardiovascular Complications - A National Population-Based Cohort Study.
PG  - e0136508
LID - 10.1371/journal.pone.0136508 [doi]
LID - e0136508
AB  - BACKGROUND AND OBJECTIVES: There have been few large population-based studies of 
      the association between rheumatoid arthritis (RA) and chronic kidney disease 
      (CKD) and glomerulonephritis. This nationwide cohort study investigated the risks 
      of developing CKD and glomerulonephritis in patients with RA, and the associated 
      risks for cardiovascular complications. METHODS: From the Taiwan National Health 
      Insurance Research Database, we identified a study cohort of 12,579 patients with 
      RA and randomly selected 37,737 subjects without RA as a control cohort. Each 
      subject was individually followed for up for 5 years, and the risk of CKD was 
      analyzed using Cox proportional hazards regression models. RESULTS: During the 
      follow-up period, after adjusting for traditional cardiovascular risk factors RA 
      was independently associated with a significantly increased risk of CKD (adjusted 
      hazard ratio [aHR] 1.31; 95% confidence interval [CI] 1.23-1.40) and 
      glomerulonephritis (aHR 1.55; 95% CI 1.37-1.76). Increased risk of CKD was also 
      associated with the use of non-steroidal anti-inflammatory drugs, cyclosporine, 
      glucocorticoids, mycophenolate mofetil, and cyclophosphamide. Patients with 
      comorbidities had even greater increased risk of CKD. Moreover, RA patients with 
      concurrent CKD had significantly higher likelihood of developing ischemic heart 
      disease and stroke. CONCLUSIONS: RA patients had higher risk of developing CKD 
      and glomerulonephritis, independent of traditional cardiovascular risk factors. 
      Their increased risk of CKD may be attributed to glomerulonephritis, chronic 
      inflammation, comorbidities, and renal toxicity of antirheumatic drugs. Careful 
      monitoring of renal function in RA patients and tight control of their comorbid 
      diseases and cardiovascular risk factors are warranted.
FAU - Chiu, Hsien-Yi
AU  - Chiu HY
AD  - Institute of Biomedical Engineering, College of Medicine and College of 
      Engineering, National Taiwan University, Taipei, Taiwan; Department of 
      Dermatology, National Taiwan University Hospital Hsin-Chu Branch, Hsinchu, 
      Taiwan; Department of Dermatology, National Taiwan University Hospital and 
      National Taiwan University College of Medicine, Taipei, Taiwan; School of 
      Medicine, Fu Jen Catholic University, New Taipei City, Taiwan.
FAU - Huang, Hui-Ling
AU  - Huang HL
AD  - Institute of Bioinformatics and Systems Biology, National Chiao Tung University, 
      Hsinchu, Taiwan; Department of Biological Science and Technology, National Chiao 
      Tung University, Hsinchu, Taiwan.
FAU - Li, Chien-Hsun
AU  - Li CH
AD  - Institute of Bioinformatics and Systems Biology, National Chiao Tung University, 
      Hsinchu, Taiwan; Division of Neurosurgery, Department of Surgery, National Taiwan 
      University Hospital Hsin-Chu Branch, Hsinchu, Taiwan.
FAU - Chen, Hung-An
AU  - Chen HA
AD  - Institute of Bioinformatics and Systems Biology, National Chiao Tung University, 
      Hsinchu, Taiwan.
FAU - Yeh, Chia-Lun
AU  - Yeh CL
AD  - Institute of Bioinformatics and Systems Biology, National Chiao Tung University, 
      Hsinchu, Taiwan.
FAU - Chiu, Shih-Hsiang
AU  - Chiu SH
AD  - Institute of Bioinformatics and Systems Biology, National Chiao Tung University, 
      Hsinchu, Taiwan.
FAU - Lin, Wei-Chun
AU  - Lin WC
AD  - Institute of Bioinformatics and Systems Biology, National Chiao Tung University, 
      Hsinchu, Taiwan.
FAU - Cheng, Yu-Pin
AU  - Cheng YP
AD  - Department of Dermatology, Cathay General Hospital, Taipei, Taiwan.
FAU - Tsai, Tsen-Fang
AU  - Tsai TF
AD  - Department of Dermatology, National Taiwan University Hospital and National 
      Taiwan University College of Medicine, Taipei, Taiwan.
FAU - Ho, Shinn-Ying
AU  - Ho SY
AD  - Institute of Bioinformatics and Systems Biology, National Chiao Tung University, 
      Hsinchu, Taiwan; Department of Biological Science and Technology, National Chiao 
      Tung University, Hsinchu, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150925
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Antirheumatic Agents/adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/*complications/drug therapy/epidemiology
MH  - Cardiovascular Diseases/*complications/epidemiology
MH  - Cohort Studies
MH  - Comorbidity
MH  - Databases, Factual
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Incidence
MH  - Kaplan-Meier Estimate
MH  - Male
MH  - Middle Aged
MH  - *Population Surveillance
MH  - Proportional Hazards Models
MH  - Renal Insufficiency, Chronic/*epidemiology/*etiology/mortality
MH  - Risk
MH  - Taiwan/epidemiology
MH  - Urbanization
MH  - Young Adult
PMC - PMC4583248
COIS- Competing Interests: Dr. Tsai has conducted clinical trials or received honoraria 
      for serving as a consultant for Pfizer Pharmaceuticals, Serono International SA 
      (now Merck Serono International), UniPharma/Biogen Idec, Novartis Pharmaceuticals 
      and Janssen-Cilag Pharmaceutical and has received speaking fees from AbbVie. 
      Other authors have no conflicts of interest to declare. This does not alter the 
      authors' adherence to PLOS ONE policies on sharing data and materials.
EDAT- 2015/09/26 06:00
MHDA- 2016/06/02 06:00
PMCR- 2015/09/25
CRDT- 2015/09/26 06:00
PHST- 2015/06/01 00:00 [received]
PHST- 2015/08/04 00:00 [accepted]
PHST- 2015/09/26 06:00 [entrez]
PHST- 2015/09/26 06:00 [pubmed]
PHST- 2016/06/02 06:00 [medline]
PHST- 2015/09/25 00:00 [pmc-release]
AID - PONE-D-15-23571 [pii]
AID - 10.1371/journal.pone.0136508 [doi]
PST - epublish
SO  - PLoS One. 2015 Sep 25;10(9):e0136508. doi: 10.1371/journal.pone.0136508. 
      eCollection 2015.

PMID- 26242470
OWN - NLM
STAT- MEDLINE
DCOM- 20160727
LR  - 20181113
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 34
IP  - 10
DP  - 2015 Oct
TI  - Subcutaneous nodules are associated with cardiovascular events in patients with 
      rheumatoid arthritis: results from a large US registry.
PG  - 1697-704
LID - 10.1007/s10067-015-3032-9 [doi]
AB  - Subcutaneous nodules are the most common conspicuous extra-articular 
      manifestation of rheumatoid arthritis (RA). Cardiovascular disease (CVD) is the 
      leading cause of death in patients with RA. The objective of this study is to 
      examine the possibility of a relationship between subcutaneous nodules and "first 
      ever" cardiovascular disease event, i.e., myocardial infarction (MI), stroke, or 
      cardiovascular death in a large registry-cohort of patients with RA. Patient 
      information was collected from the CORRONA registry from October 2001 to 
      September 2011. A total of 26,042 patients with RA were studied for the presence 
      or absence of subcutaneous nodules. Cox proportional hazards regression models 
      were constructed to estimate the hazard ratios (HR) for CVD events in relation to 
      subcutaneous nodules at baseline. Three statistical models were used to examine 
      the association between subcutaneous nodules and CVD: Model A adjusted for age 
      and sex associated risk, model B adjusted for traditional CV risk factors, and 
      model C adjusted for factors in models A and B plus underlying RA-specific 
      measures. The definition of primary exposure was "subcutaneous nodules at 
      baseline." A total of 3908 patients had subcutaneous nodules at baseline. Of the 
      566 total composite CVD events, 138 occurred in the group that had SCN at 
      baseline. Incidence rate-ratio values (patients with subcutaneous nodules at 
      baseline vs. no subcutaneous nodules at baseline) for composite CVD events, MI, 
      stroke, and cardiovascular death were 1.55, 1.65, 1.37, and 1.68, respectively. 
      Adjusted HR values (95 % CI) for composite CVD events based on "subcutaneous 
      nodules-status at baseline" (primary exposure) were as follows: 1.35 (1.11-1.63) 
      for model A, 1.25 (1.03-1.52) for model B, and 1.03 (0.831-1.277) for model C. 
      Subcutaneous nodules were associated with increased CVD events in RA. This 
      association persisted after adjusting for age, sex, and traditional CV risk 
      factors.
FAU - Kaushik, Prashant
AU  - Kaushik P
AD  - Division of Rheumatology Stratton VAMC, Albany, NY, USA. prashant.kaushik@va.gov.
AD  - Department of Internal Medicine Albany Medical College, Albany, NY, USA. 
      prashant.kaushik@va.gov.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - Divisions of Rheumatology & Pharmacoepidemiology, Brigham and Women's Hospital, 
      Harvard Medical School, Boston, MA, USA. dsolomon@partners.org.
FAU - Greenberg, Jeffrey D
AU  - Greenberg JD
AD  - New York University School of Medicine, New York, USA. jgreenberg@corrona.org.
FAU - Anderson, James T
AU  - Anderson JT
AD  - Albany Medical College, Albany, NY, USA. jta0210@gmail.com.
FAU - Reed, George
AU  - Reed G
AD  - University of Massachusetts Medical School, Worcester, MA, USA. 
      greed@corrona.org.
FAU - Pala, Ozlem
AU  - Pala O
AD  - University of Miami Miller School of Medicine, Miami, FL, USA. 
      dr_ozlem@hotmail.com.
FAU - Sumbul-Yuksel, Bahar
AU  - Sumbul-Yuksel B
AD  - Division of Rheumatology, University of Nevada School of Medicine, Reno, NV, USA. 
      dr.sumbulyuksel@gmail.com.
FAU - Kadam, Pooja
AU  - Kadam P
AD  - Medical Registrar, Sydney, Australia. Pooja.libra27@gmail.com.
FAU - Kremer, Joel M
AU  - Kremer JM
AD  - Albany Medical College and Director of Research, The Center for Rheumatology, 
      Albany, NY, USA. jkremer@joint-docs.com.
CN  - CORRONA investigators
LA  - eng
PT  - Journal Article
DEP - 20150805
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications/epidemiology
MH  - Cardiovascular Diseases/*complications/epidemiology
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/complications/epidemiology
MH  - Proportional Hazards Models
MH  - Registries
MH  - Risk Factors
MH  - Stroke/complications/epidemiology
MH  - United States
OTO - NOTNLM
OT  - Cardiovascular disease events
OT  - Rheumatoid arthritis
OT  - Subcutaneous nodules
EDAT- 2015/08/06 06:00
MHDA- 2016/07/28 06:00
CRDT- 2015/08/06 06:00
PHST- 2015/05/05 00:00 [received]
PHST- 2015/07/20 00:00 [accepted]
PHST- 2015/06/24 00:00 [revised]
PHST- 2015/08/06 06:00 [entrez]
PHST- 2015/08/06 06:00 [pubmed]
PHST- 2016/07/28 06:00 [medline]
AID - 10.1007/s10067-015-3032-9 [pii]
AID - 10.1007/s10067-015-3032-9 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2015 Oct;34(10):1697-704. doi: 10.1007/s10067-015-3032-9. Epub 
      2015 Aug 5.

PMID- 26178285
OWN - NLM
STAT- MEDLINE
DCOM- 20160714
LR  - 20220321
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
VI  - 42
IP  - 10
DP  - 2015 Oct
TI  - Genetic Variants of the NLRP3 Inflammasome Are Associated with Stroke in Patients 
      with Rheumatoid Arthritis.
PG  - 1740-5
LID - 10.3899/jrheum.141529 [doi]
AB  - OBJECTIVE: Inflammasomes are intracellular protein complexes important for the 
      production of pro-inflammatory cytokines. Studies have suggested that the NLRP3 
      inflammasome influences both the severity of rheumatoid arthritis (RA) and 
      development of atherosclerosis. Therefore, we investigated whether functional 
      genetic variants related to the NLRP3 inflammasome influence the risk of 
      cardiovascular (CV) disease (CVD) in patients with RA. METHODS: The incidence of 
      CVD was assessed in 522 patients with established RA by a retrospective survey of 
      medical records in combination with a 6-year prospective followup. NLRP3-Q705K 
      and CARD8-C10X genotypes were analyzed in relation to CVD by logistic regression, 
      adjusting for traditional risk factors, antirheumatic treatment, and age at the 
      onset of RA. RESULTS: Carriage of the NLRP3-Q705K minor allele was associated 
      with an increased risk of stroke/transient ischemic attack (TIA; OR 2.01, 95% CI 
      1.0-4.1, p = 0.05), while CARD8-C10X was not associated with any type of CV 
      event. Patients with ≥ 1 variant allele in both polymorphisms had an increased 
      risk of CVD when compared with patients without variant alleles present in both 
      polymorphisms (adjusted OR 3.05, 95% CI 1.42-6.54, p = 0.004). Stratification 
      showed that this risk was confined to stroke/TIA (adjusted OR 5.09, 95% CI 
      2.27-11.44, p < 0.0001) and not to myocardial infarction (MI)/angina pectoris 
      (adjusted OR 1.58, 95% CI 0.67-3.73). Risk estimates were consistently higher 
      among female patients. CONCLUSION: Genetic variants of the NLRP3 inflammasome 
      influence the risk of stroke/TIA, but not of MI/angina pectoris in Swedish 
      patients with established RA.
FAU - Kastbom, Alf
AU  - Kastbom A
AD  - From the Department of Rheumatology, and Department of Clinical and Experimental 
      Medicine, Linköping University, Linköping; the Department of Public Health and 
      Clinical Medicine/Rheumatology, Umeå University, Umeå, Sweden.A. Kastbom, MD, 
      PhD, Department of Rheumatology, and Department of Clinical and Experimental 
      Medicine, Linköping University; L. Ärlestig, PhD; S. Rantapää-Dahlqvist, 
      Department of Public Health and Clinical Medicine/Rheumatology, Umeå University. 
      alf.kastbom@liu.se.
FAU - Ärlestig, Lisbeth
AU  - Ärlestig L
AD  - From the Department of Rheumatology, and Department of Clinical and Experimental 
      Medicine, Linköping University, Linköping; the Department of Public Health and 
      Clinical Medicine/Rheumatology, Umeå University, Umeå, Sweden.A. Kastbom, MD, 
      PhD, Department of Rheumatology, and Department of Clinical and Experimental 
      Medicine, Linköping University; L. Ärlestig, PhD; S. Rantapää-Dahlqvist, 
      Department of Public Health and Clinical Medicine/Rheumatology, Umeå University.
FAU - Rantapää-Dahlqvist, Solbritt
AU  - Rantapää-Dahlqvist S
AD  - From the Department of Rheumatology, and Department of Clinical and Experimental 
      Medicine, Linköping University, Linköping; the Department of Public Health and 
      Clinical Medicine/Rheumatology, Umeå University, Umeå, Sweden.A. Kastbom, MD, 
      PhD, Department of Rheumatology, and Department of Clinical and Experimental 
      Medicine, Linköping University; L. Ärlestig, PhD; S. Rantapää-Dahlqvist, 
      Department of Public Health and Clinical Medicine/Rheumatology, Umeå University.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150715
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Carrier Proteins)
RN  - 0 (Inflammasomes)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - 0 (NLRP3 protein, human)
SB  - IM
MH  - Age Distribution
MH  - Aged
MH  - Arthritis, Rheumatoid/diagnosis/drug therapy/*epidemiology
MH  - Cardiovascular Diseases/diagnosis/*epidemiology/genetics
MH  - Carrier Proteins/*genetics
MH  - Comorbidity
MH  - Confidence Intervals
MH  - Cross-Sectional Studies
MH  - Female
MH  - *Genetic Variation
MH  - Genotype
MH  - Humans
MH  - Incidence
MH  - Inflammasomes/genetics
MH  - Ischemic Attack, Transient/epidemiology/genetics/therapy
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - NLR Family, Pyrin Domain-Containing 3 Protein
MH  - Polymorphism, Single Nucleotide
MH  - Retrospective Studies
MH  - Sex Distribution
MH  - Stroke/*epidemiology/*genetics/therapy
MH  - Sweden/epidemiology
OTO - NOTNLM
OT  - CARDIOVASCULAR DISEASE
OT  - GENETICS
OT  - INFLAMMASOMES
OT  - RHEUMATOID ARTHRITIS
EDAT- 2015/07/17 06:00
MHDA- 2016/07/15 06:00
CRDT- 2015/07/17 06:00
PHST- 2015/06/03 00:00 [accepted]
PHST- 2015/07/17 06:00 [entrez]
PHST- 2015/07/17 06:00 [pubmed]
PHST- 2016/07/15 06:00 [medline]
AID - jrheum.141529 [pii]
AID - 10.3899/jrheum.141529 [doi]
PST - ppublish
SO  - J Rheumatol. 2015 Oct;42(10):1740-5. doi: 10.3899/jrheum.141529. Epub 2015 Jul 
      15.

PMID- 26169048
OWN - NLM
STAT- MEDLINE
DCOM- 20151105
LR  - 20220330
IS  - 1524-4563 (Electronic)
IS  - 0194-911X (Linking)
VI  - 66
IP  - 3
DP  - 2015 Sep
TI  - Use of Nonsteroidal Anti-Inflammatory Drugs and Risk of Chronic Kidney Disease in 
      Subjects With Hypertension: Nationwide Longitudinal Cohort Study.
PG  - 524-33
LID - 10.1161/HYPERTENSIONAHA.114.05105 [doi]
AB  - Limited studies have examined the effects of nonsteroidal anti-inflammatory drug 
      (NSAID) use on the risk of chronic kidney disease (CKD), especially in subjects 
      with hypertension. Using National Health Insurance claims data in Taiwan, we 
      conducted a propensity score-matched cohort study to investigate the relationship 
      between NSAID use and CKD in subjects with hypertension. A total of 31976 
      subjects were included in this study: subjects not taking any NSAIDs in 2007 
      (n=10782); subjects taking NSAIDs for 1 to 89 days in 2007 (n=10605); and 
      subjects taking NSAIDs for ≥90 days in 2007 (n=10589). We performed multivariable 
      proportional hazard models to determine the relationship between NSAID use and 
      CKD. The results showed that NSAID use was associated with a 1.18-fold increased 
      risk of CKD in subjects taking NSAIDs for 1 to 89 days; and a 1.32-fold increased 
      risk of CKD in hypertension subjects taking NSAIDs for ≥90 days, compared with 
      subjects not taking any NSAIDs, after controlling for the confounding factors. In 
      subgroup analyses, subjects taking NSAIDs for ≥90 days, >1 defined daily dose per 
      day or taking NSAIDs >15 cumulative defined daily doses had a greater risk of CKD 
      than subjects not taking any NSAID, but not for congestive heart failure, stroke, 
      cancer, osteoarthritis, or rheumatoid arthritis. These results provide supportive 
      evidence that NSAID use is associated with increased risk of CKD in subjects with 
      hypertension. It is important to closely monitor the effects of NSAID use, 
      particularly in patients with hypertension, a susceptible population for CKD.
CI  - © 2015 American Heart Association, Inc.
FAU - Hsu, Chih-Cheng
AU  - Hsu CC
AD  - From the Institute of Population Health Sciences, National Health Research 
      Institutes, Zhunan, Taiwan (C.-C.H., S.-Y.C., Y.-W.H., Y.-K.C., J.-S.L., C.A.H., 
      H.-J.T.); Departments of Health Services Administration (C.-C.H., Y.-H.H.) and 
      Public Health (H.-J.T.), China Medical University, Taichuang City, Taiwan; 
      Department of Cardiovascular Internal Medicine, State Key Laboratory of 
      Cardiovascular Disease, Fuwai Hospital, Beijing, China (H.W.); National Center 
      for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing, China (H.W.); Division of Nephrology, Department of 
      Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, 
      Chia-Yi City, Taiwan (Y.-H.H.); Department of Nursing, Min-Hwei College of Health 
      Care Management, Tainan City, Taiwan (Y.-H.H.); and Department of Pediatrics, 
      Feinberg School of Medicine, Northwestern University, Chicago, IL (H.-J.T.).
FAU - Wang, Hongjian
AU  - Wang H
AD  - From the Institute of Population Health Sciences, National Health Research 
      Institutes, Zhunan, Taiwan (C.-C.H., S.-Y.C., Y.-W.H., Y.-K.C., J.-S.L., C.A.H., 
      H.-J.T.); Departments of Health Services Administration (C.-C.H., Y.-H.H.) and 
      Public Health (H.-J.T.), China Medical University, Taichuang City, Taiwan; 
      Department of Cardiovascular Internal Medicine, State Key Laboratory of 
      Cardiovascular Disease, Fuwai Hospital, Beijing, China (H.W.); National Center 
      for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing, China (H.W.); Division of Nephrology, Department of 
      Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, 
      Chia-Yi City, Taiwan (Y.-H.H.); Department of Nursing, Min-Hwei College of Health 
      Care Management, Tainan City, Taiwan (Y.-H.H.); and Department of Pediatrics, 
      Feinberg School of Medicine, Northwestern University, Chicago, IL (H.-J.T.).
FAU - Hsu, Yueh-Han
AU  - Hsu YH
AD  - From the Institute of Population Health Sciences, National Health Research 
      Institutes, Zhunan, Taiwan (C.-C.H., S.-Y.C., Y.-W.H., Y.-K.C., J.-S.L., C.A.H., 
      H.-J.T.); Departments of Health Services Administration (C.-C.H., Y.-H.H.) and 
      Public Health (H.-J.T.), China Medical University, Taichuang City, Taiwan; 
      Department of Cardiovascular Internal Medicine, State Key Laboratory of 
      Cardiovascular Disease, Fuwai Hospital, Beijing, China (H.W.); National Center 
      for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing, China (H.W.); Division of Nephrology, Department of 
      Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, 
      Chia-Yi City, Taiwan (Y.-H.H.); Department of Nursing, Min-Hwei College of Health 
      Care Management, Tainan City, Taiwan (Y.-H.H.); and Department of Pediatrics, 
      Feinberg School of Medicine, Northwestern University, Chicago, IL (H.-J.T.).
FAU - Chuang, Shao-Yuan
AU  - Chuang SY
AD  - From the Institute of Population Health Sciences, National Health Research 
      Institutes, Zhunan, Taiwan (C.-C.H., S.-Y.C., Y.-W.H., Y.-K.C., J.-S.L., C.A.H., 
      H.-J.T.); Departments of Health Services Administration (C.-C.H., Y.-H.H.) and 
      Public Health (H.-J.T.), China Medical University, Taichuang City, Taiwan; 
      Department of Cardiovascular Internal Medicine, State Key Laboratory of 
      Cardiovascular Disease, Fuwai Hospital, Beijing, China (H.W.); National Center 
      for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing, China (H.W.); Division of Nephrology, Department of 
      Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, 
      Chia-Yi City, Taiwan (Y.-H.H.); Department of Nursing, Min-Hwei College of Health 
      Care Management, Tainan City, Taiwan (Y.-H.H.); and Department of Pediatrics, 
      Feinberg School of Medicine, Northwestern University, Chicago, IL (H.-J.T.).
FAU - Huang, Ya-Wen
AU  - Huang YW
AD  - From the Institute of Population Health Sciences, National Health Research 
      Institutes, Zhunan, Taiwan (C.-C.H., S.-Y.C., Y.-W.H., Y.-K.C., J.-S.L., C.A.H., 
      H.-J.T.); Departments of Health Services Administration (C.-C.H., Y.-H.H.) and 
      Public Health (H.-J.T.), China Medical University, Taichuang City, Taiwan; 
      Department of Cardiovascular Internal Medicine, State Key Laboratory of 
      Cardiovascular Disease, Fuwai Hospital, Beijing, China (H.W.); National Center 
      for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing, China (H.W.); Division of Nephrology, Department of 
      Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, 
      Chia-Yi City, Taiwan (Y.-H.H.); Department of Nursing, Min-Hwei College of Health 
      Care Management, Tainan City, Taiwan (Y.-H.H.); and Department of Pediatrics, 
      Feinberg School of Medicine, Northwestern University, Chicago, IL (H.-J.T.).
FAU - Chang, Yu-Kang
AU  - Chang YK
AD  - From the Institute of Population Health Sciences, National Health Research 
      Institutes, Zhunan, Taiwan (C.-C.H., S.-Y.C., Y.-W.H., Y.-K.C., J.-S.L., C.A.H., 
      H.-J.T.); Departments of Health Services Administration (C.-C.H., Y.-H.H.) and 
      Public Health (H.-J.T.), China Medical University, Taichuang City, Taiwan; 
      Department of Cardiovascular Internal Medicine, State Key Laboratory of 
      Cardiovascular Disease, Fuwai Hospital, Beijing, China (H.W.); National Center 
      for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing, China (H.W.); Division of Nephrology, Department of 
      Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, 
      Chia-Yi City, Taiwan (Y.-H.H.); Department of Nursing, Min-Hwei College of Health 
      Care Management, Tainan City, Taiwan (Y.-H.H.); and Department of Pediatrics, 
      Feinberg School of Medicine, Northwestern University, Chicago, IL (H.-J.T.).
FAU - Liu, Jia-Sin
AU  - Liu JS
AD  - From the Institute of Population Health Sciences, National Health Research 
      Institutes, Zhunan, Taiwan (C.-C.H., S.-Y.C., Y.-W.H., Y.-K.C., J.-S.L., C.A.H., 
      H.-J.T.); Departments of Health Services Administration (C.-C.H., Y.-H.H.) and 
      Public Health (H.-J.T.), China Medical University, Taichuang City, Taiwan; 
      Department of Cardiovascular Internal Medicine, State Key Laboratory of 
      Cardiovascular Disease, Fuwai Hospital, Beijing, China (H.W.); National Center 
      for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing, China (H.W.); Division of Nephrology, Department of 
      Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, 
      Chia-Yi City, Taiwan (Y.-H.H.); Department of Nursing, Min-Hwei College of Health 
      Care Management, Tainan City, Taiwan (Y.-H.H.); and Department of Pediatrics, 
      Feinberg School of Medicine, Northwestern University, Chicago, IL (H.-J.T.).
FAU - Hsiung, Chao A
AU  - Hsiung CA
AD  - From the Institute of Population Health Sciences, National Health Research 
      Institutes, Zhunan, Taiwan (C.-C.H., S.-Y.C., Y.-W.H., Y.-K.C., J.-S.L., C.A.H., 
      H.-J.T.); Departments of Health Services Administration (C.-C.H., Y.-H.H.) and 
      Public Health (H.-J.T.), China Medical University, Taichuang City, Taiwan; 
      Department of Cardiovascular Internal Medicine, State Key Laboratory of 
      Cardiovascular Disease, Fuwai Hospital, Beijing, China (H.W.); National Center 
      for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing, China (H.W.); Division of Nephrology, Department of 
      Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, 
      Chia-Yi City, Taiwan (Y.-H.H.); Department of Nursing, Min-Hwei College of Health 
      Care Management, Tainan City, Taiwan (Y.-H.H.); and Department of Pediatrics, 
      Feinberg School of Medicine, Northwestern University, Chicago, IL (H.-J.T.).
FAU - Tsai, Hui-Ju
AU  - Tsai HJ
AD  - From the Institute of Population Health Sciences, National Health Research 
      Institutes, Zhunan, Taiwan (C.-C.H., S.-Y.C., Y.-W.H., Y.-K.C., J.-S.L., C.A.H., 
      H.-J.T.); Departments of Health Services Administration (C.-C.H., Y.-H.H.) and 
      Public Health (H.-J.T.), China Medical University, Taichuang City, Taiwan; 
      Department of Cardiovascular Internal Medicine, State Key Laboratory of 
      Cardiovascular Disease, Fuwai Hospital, Beijing, China (H.W.); National Center 
      for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing, China (H.W.); Division of Nephrology, Department of 
      Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, 
      Chia-Yi City, Taiwan (Y.-H.H.); Department of Nursing, Min-Hwei College of Health 
      Care Management, Tainan City, Taiwan (Y.-H.H.); and Department of Pediatrics, 
      Feinberg School of Medicine, Northwestern University, Chicago, IL (H.-J.T.). 
      tsaihj@nhri.org.tw.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150713
PL  - United States
TA  - Hypertension
JT  - Hypertension (Dallas, Tex. : 1979)
JID - 7906255
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Anti-Inflammatory Agents, Non-Steroidal/*adverse effects/therapeutic use
MH  - Databases, Factual
MH  - Female
MH  - Humans
MH  - Hypertension/*complications
MH  - Incidence
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Renal Insufficiency, Chronic/chemically induced/*epidemiology/*etiology
MH  - Risk Factors
MH  - Young Adult
OTO - NOTNLM
OT  - chronic kidney disease
OT  - epidemiology
OT  - hypertension
OT  - nonsteroidal anti-inflammatory agent
EDAT- 2015/07/15 06:00
MHDA- 2015/11/06 06:00
CRDT- 2015/07/15 06:00
PHST- 2015/03/09 00:00 [received]
PHST- 2015/06/15 00:00 [accepted]
PHST- 2015/07/15 06:00 [entrez]
PHST- 2015/07/15 06:00 [pubmed]
PHST- 2015/11/06 06:00 [medline]
AID - HYPERTENSIONAHA.114.05105 [pii]
AID - 10.1161/HYPERTENSIONAHA.114.05105 [doi]
PST - ppublish
SO  - Hypertension. 2015 Sep;66(3):524-33. doi: 10.1161/HYPERTENSIONAHA.114.05105. Epub 
      2015 Jul 13.

PMID- 26025436
OWN - NLM
STAT- MEDLINE
DCOM- 20160818
LR  - 20181202
IS  - 1439-7609 (Electronic)
IS  - 1439-7595 (Linking)
VI  - 26
IP  - 1
DP  - 2016
TI  - Risk of ischemic stroke in patients with systemic sclerosis: A systematic review 
      and meta-analysis.
PG  - 128-31
LID - 10.3109/14397595.2015.1056931 [doi]
AB  - BACKGROUND: Several chronic inflammatory disorders, such as rheumatoid arthritis 
      and idiopathic inflammatory myositis, have been shown to increase risk of 
      ischemic stroke but the data on systemic sclerosis (SSc) remains unclear. 
      METHODS: We conducted a systematic review and meta-analysis of observational 
      studies that reported odds ratio, relative risk, hazard ratio, or standardized 
      incidence ratio comparing risk of ischemic stroke in patients with SSc versus 
      non-SSc participants. Pooled risk ratio and 95% confidence intervals (CIs) were 
      calculated using a random-effect, generic inverse variance method of DerSimonian 
      and Laird. RESULTS: Four retrospective cohort studies were identified and 
      included in our data analysis. We found a statistically significant elevated 
      ischemic stroke risk in patients with SSc with a pooled risk ratio of 1.68 (95% 
      CI, 1.26-2.24). The statistical heterogeneity was moderate with an I(2) of 69%. 
      CONCLUSIONS: Our study demonstrated a statistically significant increased 
      ischemic stroke risk among patients with SSc.
FAU - Ungprasert, Patompong
AU  - Ungprasert P
AD  - a Division of Rheumatology, Department of Internal Medicine , Mayo Clinic , 
      Rochester , MN , USA.
AD  - b Department of Medicine , Faculty of Medicine Siriraj hospital, Mahidol 
      University , Bangkok , Thailand.
FAU - Sanguankeo, Anawin
AU  - Sanguankeo A
AD  - c Department of Preventive and Social Medicine , Faculty of medicine Siriraj 
      hospital, Mahidol University , Bangkok , Thailand.
FAU - Upala, Sikarin
AU  - Upala S
AD  - c Department of Preventive and Social Medicine , Faculty of medicine Siriraj 
      hospital, Mahidol University , Bangkok , Thailand.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Review
PT  - Systematic Review
DEP - 20150916
PL  - England
TA  - Mod Rheumatol
JT  - Modern rheumatology
JID - 100959226
SB  - IM
MH  - Brain Ischemia/*epidemiology/etiology
MH  - Humans
MH  - Incidence
MH  - Myositis/complications
MH  - Risk
MH  - Scleroderma, Systemic/*complications
MH  - Stroke/*epidemiology/etiology
OTO - NOTNLM
OT  - Epidemiology
OT  - Inflammation
OT  - Meta-analysis
OT  - Stroke
OT  - Systemic sclerosis
EDAT- 2015/05/31 06:00
MHDA- 2016/08/19 06:00
CRDT- 2015/05/31 06:00
PHST- 2015/05/31 06:00 [entrez]
PHST- 2015/05/31 06:00 [pubmed]
PHST- 2016/08/19 06:00 [medline]
AID - 10.3109/14397595.2015.1056931 [doi]
PST - ppublish
SO  - Mod Rheumatol. 2016;26(1):128-31. doi: 10.3109/14397595.2015.1056931. Epub 2015 
      Sep 16.

PMID- 25989470
OWN - NLM
STAT- MEDLINE
DCOM- 20151013
LR  - 20220331
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Linking)
VI  - 67
IP  - 8
DP  - 2015 May
TI  - Derivation and internal validation of an expanded cardiovascular risk prediction 
      score for rheumatoid arthritis: a Consortium of Rheumatology Researchers of North 
      America Registry Study.
PG  - 1995-2003
LID - 10.1002/art.39195 [doi]
AB  - OBJECTIVE: Cardiovascular disease (CVD) is the leading cause of mortality in 
      rheumatoid arthritis (RA), but CV risk prediction scores derived from the general 
      population do not accurately predict CV risk in RA patients. The goal of these 
      analyses was to develop and internally validate an expanded CV risk prediction 
      score for RA. METHODS: Study participants were patients with RA and no known CVD 
      from the Consortium of Rheumatology Researchers of North America registry. 
      Two-thirds of the cohort were used to derive the CV risk prediction score, and 
      one-third for internal validation. Traditional CV risk factors were included in 
      the base Cox regression model, and RA-related variables were assessed in an 
      expanded model predicting confirmed CV events. Fit and utility of the expanded 
      model were evaluated. RESULTS: The study cohort included 23,605 RA patients with 
      437 CV events over a median followup of 2.2 years. The RA variables found to be 
      significant in the regression models and included in the expanded risk model were 
      disease activity (Clinical Disease Activity Index >10 versus ≤10), disability 
      (modified Health Assessment Questionnaire disability index >0.5 versus ≤0.5), 
      daily prednisone use (any versus none), and disease duration (≥10 years versus 
      <10 years). The expanded model had good fit (Hosmer-Lemeshow goodness of fit 
      P = 0.94) and a lower Akaike's information criterion than the base model. In the 
      internal validation cohort, the c-statistic for model discrimination was 
      significantly improved from the base model to the expanded model (from 0.7261 to 
      0.7609; P = 0.0104). The net reclassification index of CV risk in models using a 
      4-category CV risk prediction tool was 40% (95% confidence interval 37-44%). 
      CONCLUSION: This newly developed, expanded risk score for CV outcomes in RA 
      performs well and improves the classification of CV risk in comparison to a risk 
      prediction score in which only traditional risk factors were included.
CI  - © 2015, American College of Rheumatology.
FAU - Solomon, D H
AU  - Solomon DH
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Greenberg, J
AU  - Greenberg J
AD  - New York University School of Medicine and New York University Hospital for Joint 
      Diseases, New York, New York, and CORRONA, Southborough, Massachusetts.
FAU - Curtis, J R
AU  - Curtis JR
AD  - University of Alabama at Birmingham.
FAU - Liu, M
AU  - Liu M
AD  - CORRONA, Southborough, Massachusetts.
FAU - Farkouh, M E
AU  - Farkouh ME
AD  - Mount Sinai School of Medicine, New York, New York, and University of Toronto, 
      Toronto, Ontario, Canada.
FAU - Tsao, P
AU  - Tsao P
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Kremer, J M
AU  - Kremer JM
AD  - Albany Medical College and Center for Rheumatology, Albany, New York, and 
      CORRONA, Southborough, Massachusetts.
FAU - Etzel, C J
AU  - Etzel CJ
AD  - University of Texas MD Anderson Cancer Center, Houston, and CORRONA, 
      Southborough, Massachusetts.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Validation Study
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Glucocorticoids)
RN  - VB0R961HZT (Prednisone)
SB  - IM
CIN - Arthritis Rheumatol. 2015 Dec;67(12):3327-8. doi: 10.1002/art.39413. PMID: 
      26315328
CIN - Arthritis Rheumatol. 2015 Dec;67(12):3327. doi: 10.1002/art.39404. PMID: 26316319
EIN - Arthritis Rheumatol. 2016 Feb;68(2):515. doi: 10.1002/art.39597. PMID: 26808829
MH  - Adult
MH  - Age Factors
MH  - Aged
MH  - Arthritis, Rheumatoid/drug therapy/*epidemiology/physiopathology
MH  - Cardiovascular Diseases/*epidemiology/mortality
MH  - Cohort Studies
MH  - Comorbidity
MH  - Diabetes Mellitus/epidemiology
MH  - Female
MH  - Glucocorticoids/therapeutic use
MH  - Humans
MH  - Hyperlipidemias/epidemiology
MH  - Hypertension/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology/mortality
MH  - Prednisone/therapeutic use
MH  - Proportional Hazards Models
MH  - *Registries
MH  - Risk Assessment/methods
MH  - Severity of Illness Index
MH  - Sex Factors
MH  - Smoking/epidemiology
MH  - Stroke/epidemiology/mortality
MH  - Time Factors
EDAT- 2015/05/20 06:00
MHDA- 2015/10/16 06:00
CRDT- 2015/05/20 06:00
PHST- 2014/12/02 00:00 [received]
PHST- 2015/05/12 00:00 [accepted]
PHST- 2015/05/20 06:00 [entrez]
PHST- 2015/05/20 06:00 [pubmed]
PHST- 2015/10/16 06:00 [medline]
AID - 10.1002/art.39195 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2015 May;67(8):1995-2003. doi: 10.1002/art.39195.

PMID- 25988241
OWN - NLM
STAT- MEDLINE
DCOM- 20151116
LR  - 20240615
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Print)
IS  - 2326-5191 (Linking)
VI  - 67
IP  - 9
DP  - 2015 Sep
TI  - Rheumatoid Arthritis, Anti-Cyclic Citrullinated Peptide Positivity, and 
      Cardiovascular Disease Risk in the Women's Health Initiative.
PG  - 2311-22
LID - 10.1002/art.39198 [doi]
AB  - OBJECTIVE: To evaluate the incidence of cardiovascular disease (CVD) morbidity 
      and mortality over the course of 10 years among the more than 160,000 
      postmenopausal women in the Women's Health Initiative (WHI) in relation to 
      self-reported rheumatoid arthritis (RA), taking disease-modifying antirheumatic 
      drugs (DMARDs), anti-cyclic citrullinated peptide (anti-CCP) positivity, 
      rheumatoid factor (RF) positivity, CVD risk factors, joint pain, and inflammation 
      (white blood cell count and interleukin-6 levels). METHODS: Anti-CCP and RF were 
      measured in a sample of WHI participants with self-reported RA (n = 9,988). RA 
      was classified as self-reported RA plus anti-CCP positivity and/or taking DMARDs. 
      Anti-CCP-negative women with self-reported RA and not taking DMARDs were 
      classified as having "unverified RA." RESULTS: Age-adjusted rates of coronary 
      heart disease (CHD), stroke, CVD, fatal CVD, and total mortality were higher in 
      women with RA than in women with no reported RA, with multivariable-adjusted 
      hazard ratios of 1.46 (95% confidence interval [95% CI] 1.17-1.83) for CHD and 
      2.55 (95% CI 1.86-3.51) for fatal CVD. Among women with RA, anti-CCP positivity 
      and RF positivity were not significantly associated with higher risk of any 
      outcomes, despite slightly higher risk of death for those who were anti-CCP 
      positive than for those who were anti-CCP negative. Joint pain severity and CVD 
      risk factors were strongly associated with CVD risk, even in women with no 
      reported RA. CVD incidence was increased in women with RA versus women with no 
      reported RA at almost all risk factor levels, except for low levels of joint pain 
      or inflammation. Among women with RA, inflammation was more strongly associated 
      with fatal CVD and total mortality than with CHD or CVD. CONCLUSION: Among 
      postmenopausal women, RA was associated with 1.5-2.5-fold higher CVD risk. CVD 
      risk was strongly associated with CVD risk factors, joint pain severity, and 
      inflammation, but not with anti-CCP positivity or RF positivity.
CI  - © 2015, American College of Rheumatology.
FAU - Mackey, Rachel H
AU  - Mackey RH
AD  - University of Pittsburgh, Pittsburgh, Pennsylvania.
FAU - Kuller, Lewis H
AU  - Kuller LH
AD  - University of Pittsburgh, Pittsburgh, Pennsylvania.
FAU - Deane, Kevin D
AU  - Deane KD
AD  - University of Colorado, Denver.
FAU - Walitt, Brian T
AU  - Walitt BT
AD  - Washington Hospital Center, Washington, DC.
FAU - Chang, Yue-Fang
AU  - Chang YF
AD  - University of Pittsburgh, Pittsburgh, Pennsylvania.
FAU - Holers, V Michael
AU  - Holers VM
AD  - University of Colorado, Denver.
FAU - Robinson, William H
AU  - Robinson WH
AD  - Stanford University, Stanford, California, and VA Palo Alto Health Care System, 
      Palo Alto, California.
FAU - Tracy, Russell P
AU  - Tracy RP
AD  - University of Vermont, Burlington.
FAU - Hlatky, Mark A
AU  - Hlatky MA
AD  - Stanford University, Stanford, California.
FAU - Eaton, Charles B
AU  - Eaton CB
AD  - Brown University, Providence, Rhode Island.
FAU - Liu, Simin
AU  - Liu S
AD  - Brown University, Providence, Rhode Island.
FAU - Freiberg, Matthew S
AU  - Freiberg MS
AD  - Vanderbilt University and Nashville VA Medical Center, Nashville, Tennessee.
FAU - Talabi, Mehret Birru
AU  - Talabi MB
AD  - University of Pittsburgh, Pittsburgh, Pennsylvania.
FAU - Schelbert, Erik B
AU  - Schelbert EB
AD  - University of Pittsburgh, Pittsburgh, Pennsylvania.
FAU - Moreland, Larry W
AU  - Moreland LW
AD  - University of Pittsburgh, Pittsburgh, Pennsylvania.
LA  - eng
GR  - N01-WH-32118/WH/WHI NIH HHS/United States
GR  - N01-WH-42129-32/WH/WHI NIH HHS/United States
GR  - N01-WH-32115/WH/WHI NIH HHS/United States
GR  - N01-WH-32108-9/WH/WHI NIH HHS/United States
GR  - HHSN268201100003C/WH/WHI NIH HHS/United States
GR  - N01-WH-42107-26/WH/WHI NIH HHS/United States
GR  - HHSN268201100002C/WH/WHI NIH HHS/United States
GR  - N01-WH-44221/WH/WHI NIH HHS/United States
GR  - N01-WH-32122/WH/WHI NIH HHS/United States
GR  - N01-WH-24152/WH/WHI NIH HHS/United States
GR  - HHSN268200900006C/HL/NHLBI NIH HHS/United States
GR  - HHSN268201100046C/HL/NHLBI NIH HHS/United States
GR  - N01-WH-32105-6/WH/WHI NIH HHS/United States
GR  - HHSN271201100004C/AG/NIA NIH HHS/United States
GR  - HHSN268200960006C/PHS HHS/United States
GR  - N01-WH-22110/WH/WHI NIH HHS/United States
GR  - N01-WH-32119/WH/WHI NIH HHS/United States
GR  - N01-WH-32111-13/WH/WHI NIH HHS/United States
GR  - N01-WH-32100-2/WH/WHI NIH HHS/United States
GR  - HHSN268201100001C/WH/WHI NIH HHS/United States
GR  - N01WH22110/WH/WHI NIH HHS/United States
GR  - HHSN268201100004C/WH/WHI NIH HHS/United States
PT  - Journal Article
PT  - Observational Study
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Autoantibodies)
RN  - 0 (IL6 protein, human)
RN  - 0 (Interleukin-6)
RN  - 0 (Peptides, Cyclic)
RN  - 0 (cyclic citrullinated peptide)
RN  - 9009-79-4 (Rheumatoid Factor)
SB  - IM
CIN - Arthritis Rheumatol. 2016 Feb;68(2):555-6. doi: 10.1002/art.39471. PMID: 26473508
CIN - Arthritis Rheumatol. 2016 Feb;68(2):554-5. doi: 10.1002/art.39467. PMID: 26474273
MH  - Aged
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/drug therapy/*epidemiology/immunology
MH  - Autoantibodies/*immunology
MH  - Cardiovascular Diseases/epidemiology/immunology
MH  - Cohort Studies
MH  - Coronary Disease/*epidemiology/immunology
MH  - Diabetes Mellitus/epidemiology
MH  - Female
MH  - Humans
MH  - Hypercholesterolemia/epidemiology
MH  - Hypertension/epidemiology
MH  - Incidence
MH  - Interleukin-6/immunology
MH  - Leukocyte Count
MH  - Middle Aged
MH  - Peptides, Cyclic/*immunology
MH  - Postmenopause
MH  - Prospective Studies
MH  - Rheumatoid Factor/immunology
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Smoking/epidemiology
MH  - Stroke/*epidemiology/immunology
MH  - United States/epidemiology
PMC - PMC4551571
MID - NIHMS694172
EDAT- 2015/05/20 06:00
MHDA- 2015/11/17 06:00
PMCR- 2016/09/01
CRDT- 2015/05/20 06:00
PHST- 2014/09/11 00:00 [received]
PHST- 2015/05/05 00:00 [accepted]
PHST- 2015/05/20 06:00 [entrez]
PHST- 2015/05/20 06:00 [pubmed]
PHST- 2015/11/17 06:00 [medline]
PHST- 2016/09/01 00:00 [pmc-release]
AID - 10.1002/art.39198 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2015 Sep;67(9):2311-22. doi: 10.1002/art.39198.

PMID- 25981388
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150518
LR  - 20200930
IS  - 1092-8480 (Print)
IS  - 1092-8480 (Linking)
VI  - 17
IP  - 7
DP  - 2015 Jul
TI  - Prevention of stroke in rheumatoid arthritis.
PG  - 356
LID - 10.1007/s11940-015-0356-3 [doi]
AB  - Recognizing that systemic inflammation is a major contributor to the increased 
      risk of cardiovascular disease (CVD), including stroke, in rheumatoid arthritis 
      (RA) serves as the basis for prevention strategies for cerebrovascular disease in 
      RA. In addition to traditional cardiovascular risk factors, recognize that RA may 
      be an independent risk factor for cerebrovascular accident (CVA). The risk of CVD 
      should be assessed in each patient with RA, utilizing modified risk score 
      calculators. Careful monitoring and control of systemic inflammation should be 
      undertaken in conjunction with assessing each patient's CVD risk, acknowledging 
      the benefits and risks of specific RA-directed therapies. Emphasis should be 
      given to early and aggressive control of inflammation in RA patients, 
      particularly those with seropositivity, increased inflammatory markers, long 
      disease duration (>10 years), and/or extra-articular manifestations. In RA 
      patients requiring glucocorticoid therapy, attempts should be made to use or wean 
      to the minimal effective dose (preferably less than 7.5 mg/day). It should be 
      recognized that both disease-modifying antirheumatic drugs (DMARDs), particularly 
      methotrexate, and tumor necrosis factor (TNF)-alpha inhibitors partially mitigate 
      the risk of CVD. In patients with inadequate control of inflammation with DMARDs, 
      consideration should be given to switch to anti-TNF agents earlier in the disease 
      process. Modifiable risk factors should be addressed as per guidelines for the 
      general population. Active RA may be considered as a risk equivalent to diabetes 
      mellitus when applying these guidelines. With regard to lipid management and use 
      of statin therapy, further studies are required given the apparent "lipid 
      paradox" in RA. Use of aspirin for primary prevention in RA has not been well 
      studied; however, when aspirin is used for secondary prevention, one should 
      recognize that concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs) 
      may decrease the antiplatelet effect. Given the cardiovascular risk associated 
      with NSAIDs, the lowest possible dose for the shortest time should be used.
FAU - Dhillon, Namrata
AU  - Dhillon N
AD  - Division of Rheumatology and Clinical Immunology, University of Pittsburgh 
      Medical Center, 3500 Terrace St. BST South, S723, Pittsburgh, PA, 15261, USA, 
      dhillonn@upmc.edu.
FAU - Liang, Kimberly
AU  - Liang K
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Curr Treat Options Neurol
JT  - Current treatment options in neurology
JID - 9815940
EDAT- 2015/05/20 06:00
MHDA- 2015/05/20 06:01
CRDT- 2015/05/19 06:00
PHST- 2015/05/19 06:00 [entrez]
PHST- 2015/05/20 06:00 [pubmed]
PHST- 2015/05/20 06:01 [medline]
AID - 10.1007/s11940-015-0356-3 [doi]
PST - ppublish
SO  - Curr Treat Options Neurol. 2015 Jul;17(7):356. doi: 10.1007/s11940-015-0356-3.

PMID- 25962765
OWN - NLM
STAT- MEDLINE
DCOM- 20151002
LR  - 20170112
IS  - 0392-856X (Print)
IS  - 0392-856X (Linking)
VI  - 33
IP  - 4
DP  - 2015 Jul-Aug
TI  - TNF-related apoptosis-inducing ligand and cardiovascular disease in rheumatoid 
      arthritis.
PG  - 491-7
AB  - OBJECTIVES: We examined the association of TNF-related apoptosis-inducing ligand 
      (TRAIL) concentrations with cardiovascular disease (CVD) in rheumatoid arthritis 
      (RA) and, since osteoprotegerin (OPG) can act as a decoy receptor for TRAIL, 
      whether TRAIL concentrations impact on the OPG level-atherosclerotic CVD relation 
      that was recently documented in the present cohort. METHODS: TRAIL concentrations 
      were assessed by ELISA in 151 RA patients of which 75 (49.7%) had CVD comprising 
      ischaemic heart disease (n=27), cerebrovascular accident (n=26), peripheral 
      artery disease (n=9) or/and heart failure (HF) (n=27), and 62 controls. RESULTS: 
      Mean RA duration was 12 years. In RA patients, C-reactive protein (CRP) levels 
      and cholesterol-HDL cholesterol ratio related to TRAIL concentrations [partial 
      R=-0.222 (p=0.006) and 0.174 (p=0.04), respectively]. TRAIL concentrations were 
      smaller in RA patients compared to controls (median (interquartile range) = 80.2 
      (60.9-120.4) versus 130.4 (89.4-167.7) pg/ml, p<0.0001)). TRAIL levels were 
      larger in RA patients with compared to those without HF (105.5 (66.5-143.4) 
      versus 79.9 (57.8-110.6), p=0.02); this difference was independent of demographic 
      characteristics and traditional cardiovascular risk factors (p=0.04) but not CRP 
      concentrations (p=0.1). TRAIL levels were consistently unrelated to 
      atherosclerotic CVD. Our previously reported OPG-atherosclerotic CVD relation in 
      RA survived adjustment for TRAIL concentrations in a mixed regression model 
      (p=0.04). CONCLUSIONS: TRAIL concentrations are markedly reduced and associated 
      with HF in established RA, this relationship being explained by CRP levels. OPG 
      may directly enhance CVD risk in RA.
FAU - Dessein, Patrick H
AU  - Dessein PH
AD  - Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, 
      Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South 
      Africa.
FAU - Lopez-Mejias, Raquel
AU  - Lopez-Mejias R
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de 
      Valdecilla, IDIVAL, Santander, Spain.
FAU - Ubilla, Begona
AU  - Ubilla B
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de 
      Valdecilla, IDIVAL, Santander, Spain.
FAU - Genre, Fernanda
AU  - Genre F
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de 
      Valdecilla, IDIVAL, Santander, Spain.
FAU - Corrales, Alfonso
AU  - Corrales A
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de 
      Valdecilla, IDIVAL, Santander, Spain.
FAU - Hernandez, Jose L
AU  - Hernandez JL
AD  - Department of Internal Medicine, Hospital Universitario Marques de Valdecilla, 
      University of Cantabria, RETICEF, IDIVAL, Santander, Spain.
FAU - Ferraz-Amaro, Ivan
AU  - Ferraz-Amaro I
AD  - Rheumatology Division, Hospital Universitario de Canarias, Tenerife, Spain.
FAU - Tsang, Linda
AU  - Tsang L
AD  - Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, 
      Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South 
      Africa.
FAU - Pina, Trinitario
AU  - Pina T
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de 
      Valdecilla, IDIVAL, Santander, Spain.
FAU - Llorca, Javier
AU  - Llorca J
AD  - Department of Epidemiology and Computational Biology, School of Medicine, 
      University of Cantabria, and CIBER Epidemiología y Salud Pública (CIBERESP), 
      IDIVAL, Santander, Spain.
FAU - Blanco, Ricardo
AU  - Blanco R
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marques de 
      Valdecilla, IDIVAL, Santander, Spain.
FAU - Gonzalez-Juanatey, Carlos
AU  - Gonzalez-Juanatey C
AD  - Cardiology Division, Hospital Lucus Augusti, Lugo, Spain.
FAU - Gonzalez-Gay, Miguel A
AU  - Gonzalez-Gay MA
AD  - Cardiovascular Pathophysiology and Genomics Research Unit, University of the 
      Witwatersrand, Johannesburg, South Africa; and Epidemiology, Genetics and 
      Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology, 
      IDIVAL, Santander, Spain.
LA  - eng
PT  - Journal Article
DEP - 20150511
PL  - Italy
TA  - Clin Exp Rheumatol
JT  - Clinical and experimental rheumatology
JID - 8308521
RN  - 0 (Cholesterol, HDL)
RN  - 0 (Osteoprotegerin)
RN  - 0 (TNF-Related Apoptosis-Inducing Ligand)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/*metabolism
MH  - Atherosclerosis/metabolism
MH  - C-Reactive Protein/analysis
MH  - Cholesterol, HDL/blood
MH  - Female
MH  - *Heart Failure/epidemiology/metabolism
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Myocardial Ischemia/epidemiology/metabolism
MH  - Osteoprotegerin/*blood
MH  - *Peripheral Arterial Disease/epidemiology/metabolism
MH  - Regression Analysis
MH  - Risk Factors
MH  - Spain
MH  - *Stroke/epidemiology/metabolism
MH  - TNF-Related Apoptosis-Inducing Ligand/*blood
EDAT- 2015/05/13 06:00
MHDA- 2015/10/03 06:00
CRDT- 2015/05/13 06:00
PHST- 2014/12/22 00:00 [received]
PHST- 2015/02/19 00:00 [accepted]
PHST- 2015/05/13 06:00 [entrez]
PHST- 2015/05/13 06:00 [pubmed]
PHST- 2015/10/03 06:00 [medline]
AID - 8997 [pii]
PST - ppublish
SO  - Clin Exp Rheumatol. 2015 Jul-Aug;33(4):491-7. Epub 2015 May 11.

PMID- 25940579
OWN - NLM
STAT- MEDLINE
DCOM- 20151221
LR  - 20220318
IS  - 1875-9114 (Electronic)
IS  - 0277-0008 (Linking)
VI  - 35
IP  - 5
DP  - 2015 May
TI  - Safety of nonsteroidal antiinflammatory drugs in patients with cardiovascular 
      disease.
PG  - 520-35
LID - 10.1002/phar.1584 [doi]
AB  - Nonsteroidal antiinflammatory drugs (NSAIDs) are used in the management of a 
      variety of conditions, but their prevalence is likely underreported as a result 
      of widespread availability and the perception that nonprescription therapies are 
      unnecessary to report during medication history taking. However, NSAIDs are 
      associated with a number of adverse effects, especially in patients with 
      cardiovascular disease (CVD). Patients with CVD and comorbidities for which 
      NSAIDs may provide symptomatic relief (e.g., osteoarthritis, rheumatoid 
      arthritis) tend to be older, which places them at greater risk of harm. For these 
      reasons, the use of NSAIDs in patients with CVD is a significant public health 
      concern. An understanding of the risks associated with NSAIDs is critical for 
      clinicians across practice settings. In this review, we detail the safety of 
      NSAIDs in patients with CVD, provide recommendations on their use in specific 
      disease states, and discuss therapeutic alternatives.
CI  - © 2015 Pharmacotherapy Publications, Inc.
FAU - Danelich, Ilya M
AU  - Danelich IM
AD  - Department of Pharmacy, Mayo Clinic, Rochester, Minnesota.
FAU - Wright, Sampaguita S
AU  - Wright SS
AD  - Department of Pharmacy, Mayo Clinic, Rochester, Minnesota.
FAU - Lose, Jennifer M
AU  - Lose JM
AD  - Department of Pharmacy, Mayo Clinic, Rochester, Minnesota.
FAU - Tefft, Brittany J
AU  - Tefft BJ
AD  - Department of Pharmacy, Mayo Clinic, Rochester, Minnesota.
FAU - Cicci, Jonathan D
AU  - Cicci JD
AD  - Department of Pharmacy, University of North Carolina Hospitals, Chapel Hill, 
      North Carolina.
FAU - Reed, Brent N
AU  - Reed BN
AD  - Department of Pharmacy Practice and Science, University of Maryland School of 
      Pharmacy, Baltimore, Maryland.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20150504
PL  - United States
TA  - Pharmacotherapy
JT  - Pharmacotherapy
JID - 8111305
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Anticoagulants)
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal/*adverse effects/pharmacology
MH  - Anticoagulants/adverse effects
MH  - Aspirin/adverse effects
MH  - Atrial Fibrillation/etiology/physiopathology
MH  - Blood Pressure/drug effects
MH  - Cardiovascular Diseases/*etiology/physiopathology
MH  - Coronary Artery Disease/etiology/physiopathology
MH  - Cyclooxygenase Inhibitors/adverse effects
MH  - Drug Interactions
MH  - Heart Failure/etiology/physiopathology
MH  - Hemorrhage/chemically induced
MH  - Humans
MH  - Platelet Aggregation Inhibitors/adverse effects
MH  - Risk
MH  - Stroke/etiology/physiopathology
MH  - Surgical Procedures, Operative
OTO - NOTNLM
OT  - bleeding
OT  - cardiac surgery
OT  - cardiovascular disease
OT  - noncardiac surgery
OT  - nonsteroidal antiinflammatory drugs
EDAT- 2015/05/06 06:00
MHDA- 2015/12/22 06:00
CRDT- 2015/05/06 06:00
PHST- 2015/05/06 06:00 [entrez]
PHST- 2015/05/06 06:00 [pubmed]
PHST- 2015/12/22 06:00 [medline]
AID - 10.1002/phar.1584 [doi]
PST - ppublish
SO  - Pharmacotherapy. 2015 May;35(5):520-35. doi: 10.1002/phar.1584. Epub 2015 May 4.

PMID- 25917955
OWN - NLM
STAT- MEDLINE
DCOM- 20151013
LR  - 20181113
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Print)
IS  - 2326-5191 (Linking)
VI  - 67
IP  - 8
DP  - 2015 May
TI  - Association between lipid levels and major adverse cardiovascular events in 
      rheumatoid arthritis compared to non-rheumatoid arthritis patients.
PG  - 2004-10
LID - 10.1002/art.39165 [doi]
AB  - OBJECTIVE: Lower levels of low-density lipoprotein (LDL) cholesterol may be 
      associated with increased cardiovascular (CV) risk in rheumatoid arthritis (RA). 
      This study was undertaken to determine whether the complex relationship between 
      levels of LDL and high-density lipoprotein (HDL) cholesterol and CV risk is 
      different in RA patients as compared to non-RA controls. METHODS: Using data from 
      a US health insurance plan (2003-2012), we conducted a cohort study that included 
      patients with RA and non-RA control subjects matched with regard to age, sex, and 
      index date. The nonlinearity of associations between lipid levels and incidence 
      of major adverse CV events (MACE) was tested. We used multivariable Cox 
      proportional hazards regression models to examine for an interaction between 
      lipid levels and RA status in relation to the risk of MACE, after adjustment for 
      CV risk factors. RESULTS: In total, 16,085 RA patients and 48,499 non-RA controls 
      were studied. The mean age was 52.6 years and 78.6% were women. The relationship 
      between LDL cholesterol levels and incidence of MACE was nonlinear and similar 
      between RA patients and non-RA controls (P for interaction = 0.72). No 
      significant increase in CV risk was observed between the lowest quintile of LDL 
      cholesterol levels (≤91.0 mg/dl) and the second, third, or fourth quintiles, 
      whereas the highest quintile (>190.0 mg/dl) conveyed a 40% increase in risk of 
      MACE (hazard ratio [HR] 1.40, 95% confidence interval [95% CI] 1.17-1.68). The 
      relationship between HDL cholesterol levels and incidence of MACE was also 
      nonlinear and similar between RA patients and non-RA controls (P for 
      interaction = 0.39). Compared to the lowest quintile of HDL cholesterol levels, 
      each successive quintile was associated with a reduced risk of MACE (HR 0.45, 95% 
      CI 0.48-0.72 for lowest quintile [≤43.0 mg/dl] versus highest quintile [>71.0 
      mg/dl]). CONCLUSION: The complex relationship between LDL cholesterol levels, HDL 
      cholesterol levels, and risk of MACE was nonlinear in RA patients and also not 
      statistically significantly different from that in an age- and sex-matched non-RA 
      cohort.
CI  - © 2015, American College of Rheumatology.
FAU - Liao, Katherine P
AU  - Liao KP
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Liu, Jun
AU  - Liu J
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Lu, Bing
AU  - Lu B
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Kim, Seoyoung C
AU  - Kim SC
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
LA  - eng
GR  - K08 AR060257/AR/NIAMS NIH HHS/United States
GR  - K23-AR-059677/AR/NIAMS NIH HHS/United States
GR  - K24-AR-055989/AR/NIAMS NIH HHS/United States
GR  - K24 AR055989/AR/NIAMS NIH HHS/United States
GR  - K23 AR059677/AR/NIAMS NIH HHS/United States
GR  - K08-AR-060257/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Cholesterol, HDL)
RN  - 0 (Cholesterol, LDL)
RN  - 0 (Triglycerides)
SB  - IM
MH  - Adult
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Cardiovascular Diseases/*epidemiology/surgery
MH  - Case-Control Studies
MH  - Cholesterol, HDL/*blood
MH  - Cholesterol, LDL/*blood
MH  - Comorbidity
MH  - Coronary Artery Bypass/statistics & numerical data
MH  - Coronary Artery Disease/epidemiology/surgery
MH  - Dyslipidemias/blood/*epidemiology
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology/surgery
MH  - Percutaneous Coronary Intervention/statistics & numerical data
MH  - Proportional Hazards Models
MH  - Stroke/epidemiology
MH  - Triglycerides/blood
PMC - PMC4418211
MID - NIHMS684134
EDAT- 2015/04/29 06:00
MHDA- 2015/10/16 06:00
PMCR- 2016/05/01
CRDT- 2015/04/29 06:00
PHST- 2015/01/02 00:00 [received]
PHST- 2015/04/21 00:00 [accepted]
PHST- 2015/04/29 06:00 [entrez]
PHST- 2015/04/29 06:00 [pubmed]
PHST- 2015/10/16 06:00 [medline]
PHST- 2016/05/01 00:00 [pmc-release]
AID - 10.1002/art.39165 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2015 May;67(8):2004-10. doi: 10.1002/art.39165.

PMID- 25876749
OWN - NLM
STAT- MEDLINE
DCOM- 20160606
LR  - 20190823
IS  - 1875-533X (Electronic)
IS  - 0929-8673 (Linking)
VI  - 22
IP  - 16
DP  - 2015
TI  - Cardiovascular effects of methotrexate in rheumatoid arthritis revisited.
PG  - 1903-10
AB  - Cardiovascular events such as myocardial infarction (MI) and stroke due to 
      enhanced inflammatory atherosclerosis account for increased premature mortality 
      in rheumatoid arthritis (RA). Accumulated evidence suggests that accelerated 
      atherosclerosis and related cardiovascular comorbidities in RA are confounded not 
      only by traditional risk factors (TRF) but also by a number of immune and 
      inflammatory pathways. Since chronic inflammation and autoimmune disorders play a 
      key role in atherosclerosis and related cardiovascular complications in RA, 
      effective suppression of systemic inflammation can be viewed as a strategy for 
      cardiovascular therapy and prevention in this disease. This article overviews 
      some mechanisms of action of methotrexate on TRF, clinical and subclinical 
      manifestations of RA-induced atherosclerosis, and related cardiovascular 
      morbidity and mortality.
FAU - Popkova, Tatyana V
AU  - Popkova TV
AD  - Department of Vascular Pathology of Rheumatic Diseases, V.A. Nasonova Research 
      Institute of Rheumatology, Russian Academy Sciences, Kashirskoe Shosse, 34A, 
      Moscow, 115522, Russian Federation. popkovatv@mail.ru.
FAU - Novikova, Diana S
AU  - Novikova DS
FAU - Gasparyan, Armen Yuri
AU  - Gasparyan AY
FAU - Nasonov, Evgeny L
AU  - Nasonov EL
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United Arab Emirates
TA  - Curr Med Chem
JT  - Current medicinal chemistry
JID - 9440157
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Arthritis, Rheumatoid/*complications/*drug therapy
MH  - Cardiovascular Diseases/*complications/*drug therapy
MH  - Humans
MH  - Methotrexate/*therapeutic use
EDAT- 2015/04/17 06:00
MHDA- 2016/06/09 06:00
CRDT- 2015/04/17 06:00
PHST- 2015/01/26 00:00 [received]
PHST- 2015/01/25 00:00 [revised]
PHST- 2015/04/13 00:00 [accepted]
PHST- 2015/04/17 06:00 [entrez]
PHST- 2015/04/17 06:00 [pubmed]
PHST- 2016/06/09 06:00 [medline]
AID - CMC-EPUB-66546 [pii]
AID - 10.2174/0929867322666150415122039 [doi]
PST - ppublish
SO  - Curr Med Chem. 2015;22(16):1903-10. doi: 10.2174/0929867322666150415122039.

PMID- 25862150
OWN - NLM
STAT- MEDLINE
DCOM- 20160208
LR  - 20150507
IS  - 1873-569X (Electronic)
IS  - 0923-1811 (Linking)
VI  - 78
IP  - 3
DP  - 2015 Jun
TI  - Risk of incident chronic kidney disease and end-stage renal disease in patients 
      with psoriasis: A nationwide population-based cohort study.
PG  - 232-8
LID - S0923-1811(15)00112-7 [pii]
LID - 10.1016/j.jdermsci.2015.03.012 [doi]
AB  - BACKGROUND: Psoriasis is a chronic inflammatory dermatosis that has been 
      associated with various cardiovascular and metabolic comorbidities, including 
      myocardial infarction, stroke, and diabetes mellitus. Recently, there are studies 
      reporting the association of psoriasis with renal diseases. OBJECTIVE: To 
      evaluate the risk of incident chronic kidney disease (CKD) and end-stage renal 
      disease (ESRD) in people with psoriasis. METHODS: We used the Taiwan's National 
      Health Insurance Research Database to conduct a nationwide population-based 
      cohort study to assess the risk of incident CKD and ESRD in people with psoriasis 
      and to further evaluate the respective risk estimates in those with mild and 
      severe psoriasis based on treatment patterns. RESULTS: A total of 4633 psoriatic 
      patients and 922,534 nonpsoriatic controls were included. Severe psoriasis, but 
      not mild psoriasis, was an independent risk factor of incident CKD and ESRD 
      (adjusted hazard ratio being 1.90 (95% confidence interval 1.33-2.70) and 2.97 
      (95% confidence interval 1.72-5.11), respectively) after adjustment for potential 
      confounders including age, gender, comorbidities, and used of nonsteroidal 
      anti-inflammatory drugs (NSAIDs). Severe psoriasis remained an independent risk 
      factor of incident CKD and ESRD after various sensitivity analyses after 
      adjusting for the presence of osteoarthritis and/or rheumatoid arthritis, use of 
      methotrexate and/or cyclosporine, and chronic use of NSAIDs for at least 2 
      months. Psoriatic arthritis was an effect modifier for CKD and ESRD. CONCLUSIONS: 
      The associations of severe psoriasis with CKD and ESRD should be recognized. 
      Assessment of renal function and avoidance of long-term use of nephrotoxic drugs 
      shall be implemented in the integrative care for patients with severe psoriasis.
CI  - Copyright © 2015. Published by Elsevier Ireland Ltd.
FAU - Chi, Ching-Chi
AU  - Chi CC
AD  - Department of Dermatology and Centre for Evidence-Based Medicine, Chang Gung 
      Memorial Hospital, Chiayi, Taiwan; College of Medicine, Chang Gung University, 
      Taoyuan, Taiwan.
FAU - Wang, Jui
AU  - Wang J
AD  - Faculty of Public Health, College of Medicine, Fu Jen Catholic University, New 
      Taipei, Taiwan; School of Public Health, College of Public Health and Nutrition, 
      Taipei Medical University, Taipei, Taiwan; Institute of Epidemiology and 
      Preventive Medicine, College of Public Health, National Taiwan University, 
      Taipei, Taiwan.
FAU - Chen, Yu-Fen
AU  - Chen YF
AD  - Division for Disease Control and Prevention, Department of Health, Taipei City 
      Government, Taipei, Taiwan; Institute of Health and Welfare Policy, National 
      Yang-Ming University, Taipei, Taiwan; Department of Nursing, Kang-Ning Junior 
      College of Medical Care and Management, Taipei, Taiwan.
FAU - Wang, Shu-Hui
AU  - Wang SH
AD  - Department of Dermatology, Far Eastern Memorial Hospital, New Taipei, Taiwan.
FAU - Chen, Fu-Li
AU  - Chen FL
AD  - Faculty of Public Health, College of Medicine, Fu Jen Catholic University, New 
      Taipei, Taiwan.
FAU - Tung, Tao-Hsin
AU  - Tung TH
AD  - Faculty of Public Health, College of Medicine, Fu Jen Catholic University, New 
      Taipei, Taiwan; Department of Medical Research and Education, Cheng Hsin General 
      Hospital, Taipei, Taiwan. Electronic address: ch2876@chgh.org.tw.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150330
PL  - Netherlands
TA  - J Dermatol Sci
JT  - Journal of dermatological science
JID - 9011485
SB  - IM
MH  - Adult
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Kidney Failure, Chronic/*etiology
MH  - Male
MH  - Middle Aged
MH  - Psoriasis/*complications
MH  - Risk Factors
OTO - NOTNLM
OT  - Chronic kidney disease
OT  - End-stage renal disease
OT  - Psoriasis
OT  - Psoriatic arthritis
EDAT- 2015/04/12 06:00
MHDA- 2016/02/09 06:00
CRDT- 2015/04/12 06:00
PHST- 2014/12/31 00:00 [received]
PHST- 2015/03/16 00:00 [revised]
PHST- 2015/03/21 00:00 [accepted]
PHST- 2015/04/12 06:00 [entrez]
PHST- 2015/04/12 06:00 [pubmed]
PHST- 2016/02/09 06:00 [medline]
AID - S0923-1811(15)00112-7 [pii]
AID - 10.1016/j.jdermsci.2015.03.012 [doi]
PST - ppublish
SO  - J Dermatol Sci. 2015 Jun;78(3):232-8. doi: 10.1016/j.jdermsci.2015.03.012. Epub 
      2015 Mar 30.

PMID- 25825628
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150331
LR  - 20231111
IS  - 1941-5893 (Print)
IS  - 1944-141X (Electronic)
IS  - 1941-5893 (Linking)
VI  - 8
IP  - 1
DP  - 2015 Feb
TI  - Antithrombotic Utilization Trends after Noncardioembolic Ischemic Stroke or TIA 
      in the Setting of Large Antithrombotic Trials (2002-2009).
PG  - 20-6
AB  - BACKGROUND AND PURPOSE: Several large trials published over the last decade have 
      significantly altered recommended guidelines for therapy following a 
      noncardioembolic ischemic stroke or transient ischemic attack (TIA). The impact 
      of these studies on patient usage of alternative antithrombotic agents has 
      hitherto not been evaluated. We examined the usage of these agents in the United 
      States over the last decade, with regard to the publication of the Management of 
      Atherothrombosis with Clopidogrel in High-Risk Patients (MATCH), 
      European/Australasian Stroke Prevention in Reversible Ischaemia Trial (ESPRIT), 
      and Prevention Regimen for Effectively Avoiding Second Strokes (PRoFESS) clinical 
      trials, in order to test the hypothesis that resulting recommendations are 
      reflected in usage trends. METHODS: Antithrombotic utilization was prospectively 
      collected as part of the National Ambulatory Medical Care Survey (NAMCS) on a 
      total of 53,608,351 patients in the United States between 2002 and 2009. Patients 
      with a history of ischemic stroke or TIA were included. Patients were excluded if 
      there was a prior history of subarachnoid or intracerebral hemorrhage, or if 
      other indications for antithrombotic treatment were present, including deep 
      venous thrombosis, pulmonary embolism, atrial fibrillation or flutter, mechanical 
      cardiac valve replacement, congestive heart failure, coronary artery disease, 
      peripheral arterial disease, and rheumatoid arthritis. Annual utilization of the 
      following antithrombotic strategies was compared in 53,608,351 patients: 1) 
      aspirin monotherapy, 2) clopidogrel monotherapy, 3) combined clopidogrel and 
      aspirin, 4) combined extended-release dipyridamole (ERDP) and aspirin, and 5) 
      warfarin. Annual utilization was compared before and after publication of MATCH, 
      ESPRIT, and PRoFESS in 2004, 2006, and 2008, respectively. Trend analysis was 
      performed with the Mantel-Haenszel test for trends. Sensitivity analysis of 
      demographic and clinical characteristics stratified by antithrombotic-usage group 
      was performed using the Wald Chi-square test. RESULTS: Utilization of combined 
      clopidogrel and aspirin increased from 3.3% to 6.7% after the MATCH trial 
      (p<0.0001). Following the results of the ESPRIT trial, utilization of combination 
      ERDP and aspirin decreased from 4% to 3% (p<0.0001), utilization of clopidogrel 
      declined from 6.8% to 6% (p<0.0001), and utilization of aspirin remained 
      essentially unchanged. After the PRoFESS trial, utilization of clopidogrel 
      increased from 5% to 9% (p<0.0001), utilization of ERDP-aspirin increased from 3 
      % to 4.6% (p<0.0001), and utilization of aspirin increased from 15.6% to 17.8% 
      (p<0.0001). The proportion of patients on none of the five antithrombotic 
      secondary prevention strategies steadily declined from a peak of 74% in 2003 to 
      57% by 2009. CONCLUSIONS: The impact of the MATCH, ESPRIT, and PRoFESS trials on 
      antithrombotic utilization has been variable. These findings highlight the 
      importance of addressing factors that affect the implementation of findings from 
      major clinical trials.
FAU - Khan, Amir S
AU  - Khan AS
AD  - Zeenat Qureshi Stroke Institute.
FAU - Chaudhry, Saqib
AU  - Chaudhry S
AD  - Zeenat Qureshi Stroke Institute.
FAU - Qureshi, Adnan I
AU  - Qureshi AI
AD  - Zeenat Qureshi Stroke Institute.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Vasc Interv Neurol
JT  - Journal of vascular and interventional neurology
JID - 101511381
PMC - PMC4367803
EDAT- 2015/04/01 06:00
MHDA- 2015/04/01 06:01
PMCR- 2015/02/01
CRDT- 2015/04/01 06:00
PHST- 2015/04/01 06:00 [entrez]
PHST- 2015/04/01 06:00 [pubmed]
PHST- 2015/04/01 06:01 [medline]
PHST- 2015/02/01 00:00 [pmc-release]
AID - jvin-8-1.4 [pii]
PST - ppublish
SO  - J Vasc Interv Neurol. 2015 Feb;8(1):20-6.

PMID- 25789516
OWN - NLM
STAT- MEDLINE
DCOM- 20150721
LR  - 20220629
IS  - 1980-5322 (Electronic)
IS  - 1807-5932 (Print)
IS  - 1807-5932 (Linking)
VI  - 70
IP  - 2
DP  - 2015 Feb
TI  - Increased risk of depression in patients with rheumatoid arthritis: a seven-year 
      population-based cohort study.
PG  - 91-6
LID - 10.6061/clinics/2015(02)04 [doi]
AB  - OBJECTIVE: Rheumatoid arthritis (RA) is a costly and crippling autoimmune disease 
      that can lead to the development of depression, contributing to suboptimal 
      clinical outcomes. However, no longitudinal studies have identified an 
      association between rheumatoid arthritis and subsequent depression. This study 
      aimed to investigate the incidence and risk factors of depression among RA 
      patients in Taiwan. METHODS: Using Taiwan's National Health Insurance Research 
      Database, we identified 3,698 newly diagnosed RA patients aged 18 years or older, 
      together with 7,396 subjects without RA matched by sex, age and index date, 
      between 2000 and 2004. The incidence of depression and the risk factors among RA 
      cases were evaluated using Cox proportional-hazard regression. RESULTS: The 
      incidence of depression was 1.74-fold greater in the RA cohort than in the non-RA 
      cohort (11.80 versus 6.89 per 1,000 person-years; p<0.01). Multivariate analysis 
      showed that RA subjects who were female, were older, or had comorbidities such as 
      stroke, chronic kidney disease, or cancer had a significantly greater risk of 
      depression compared with those without these conditions. CONCLUSION: This 
      population-based cohort study showed a strong relationship between RA and a 
      subsequent risk of depression. The findings could be beneficial to healthcare 
      providers for identifying individuals with a higher predisposition for 
      depression, thereby possibly facilitating the provision of an appropriate 
      rehabilitation intervention after RA onset to support the patient's adaptation.
FAU - Lin, Miao-Chiu
AU  - Lin MC
AD  - Department of Nursing, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical 
      Foundation, Chiayi, Taiwan.
FAU - Guo, How-Ran
AU  - Guo HR
AD  - Department of Environmental and Occupational Health, College of Medicine, 
      National Cheng Kung University, Tainan, Taiwan.
FAU - Lu, Ming-Chi
AU  - Lu MC
AD  - Division of Allergy, Immunology and Rheumatology, Dalin Tzu Chi Hospital, 
      Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan.
FAU - Livneh, Hanoch
AU  - Livneh H
AD  - Rehabilitation Counseling Program, Portland State University, Portland, OR, USA.
FAU - Lai, Ning-Sheng
AU  - Lai NS
AD  - Division of Allergy, Immunology and Rheumatology, Dalin Tzu Chi Hospital, 
      Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan.
FAU - Tsai, Tzung-Yi
AU  - Tsai TY
AD  - Department of Environmental and Occupational Health, College of Medicine, 
      National Cheng Kung University, Tainan, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Clinics (Sao Paulo)
JT  - Clinics (Sao Paulo, Brazil)
JID - 101244734
SB  - IM
MH  - Adult
MH  - Age Distribution
MH  - Aged
MH  - Arthritis, Rheumatoid/epidemiology/*psychology
MH  - Cohort Studies
MH  - Comorbidity
MH  - Databases, Factual
MH  - Depression/epidemiology/*psychology
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - Sex Distribution
MH  - Taiwan/epidemiology
MH  - Young Adult
PMC - PMC4351304
COIS- No potential conflict of interest was reported.
EDAT- 2015/03/20 06:00
MHDA- 2015/07/22 06:00
PMCR- 2015/02/01
CRDT- 2015/03/20 06:00
PHST- 2014/08/20 00:00 [received]
PHST- 2014/12/05 00:00 [accepted]
PHST- 2015/03/20 06:00 [entrez]
PHST- 2015/03/20 06:00 [pubmed]
PHST- 2015/07/22 06:00 [medline]
PHST- 2015/02/01 00:00 [pmc-release]
AID - S1807-5932(22)00800-6 [pii]
AID - cln_70p91 [pii]
AID - 10.6061/clinics/2015(02)04 [doi]
PST - ppublish
SO  - Clinics (Sao Paulo). 2015 Feb;70(2):91-6. doi: 10.6061/clinics/2015(02)04.

PMID- 25777147
OWN - NLM
STAT- MEDLINE
DCOM- 20160425
LR  - 20181113
IS  - 1613-7671 (Electronic)
IS  - 0043-5325 (Linking)
VI  - 127
IP  - 13-14
DP  - 2015 Jul
TI  - Can the ankle brachial pressure index (ABPI) and carotis intima media thickness 
      (CIMT) be new early stage markers of subclinical atherosclerosis in patients with 
      rheumatoid arthritis?
PG  - 529-34
LID - 10.1007/s00508-015-0767-x [doi]
AB  - BACKGROUND: It takes years for atherosclerosis to manifest symptoms. However, it 
      needs to be identified earlier because of the premature cardiovascular risk 
      factors in patients with rheumatoid arthritis (RA). In this study, we aimed to 
      investigate the effect of atherosclerosis on the ankle brachial pressure index 
      (ABPI) and carotis intima media thickness (CIMT) in patients with RA. METHODS: RA 
      patients attending the rheumatology clinic were examined retrospectively; then we 
      called them for the measurements of ABPI and CIMT prospectively. Subjects were 
      divided into four groups, as follows (Table 1): group 1 comprised RA patients 
      with an ABPI less than 0.9; group 2 included RA patients with an ABPI between 0.9 
      and 1.2; group 3 was made up of RA patients with an ABPI greater than 1.2; and 
      group 4 included patients without RA with an ABPI between 0.9 and 1.2 as a 
      control group. Patients' demographic data were recorded. Hypertension (HT), 
      diabetes mellitus, ABPI and CIMT measurements were taken by specialists. Duration 
      of RA and disease scores (disease activity score-28, health assessment 
      questionnaire score and visual assessment score) were recorded. RESULTS: The 
      prevalence of peripheral vascular disease in patients with RA was twice as high 
      as that in the normal population of equivalent age. Patients in group 2, with RA 
      and normal ABPI, exhibited a significant higher mean in CIMT (mm) compared with 
      the control group (p < 0.01), despite having normal ABPI. This confirms that 
      these patients have a higher risk of stroke compared with the control group. 
      Group 1's newly diagnosed HT (p < 0.01) and systolic blood pressure (SBP) values 
      (p < 0.01) were higher and statistically significant when compared with the group 
      4 (control group); in addition, significant plaque levels were observed in the 
      carotid arteries (p < 0.01). Group 3 patients had a similar history of HT and 
      increased SBP compared with patients in group 4 (p < 0.01), and had similar 
      characteristics to with group 1. No statistically significant differences were 
      found between the groups in terms of inflammatory markers such as C-reactive 
      protein and rheumatoid factor, anti-cyclic citrullinated peptide and white blood 
      cell counts. CONCLUSION: Based on the present findings, patients with RA need to 
      be evaluated in the early stage of the disease for subclinical peripheral artery 
      disease using the ABPI, as well as CIMT, which is also a non-invasive technique, 
      in terms of cerebrovascular events. Inflammatory markers exhibited no 
      statistically significant difference. We think that the atherosclerotic process 
      stems not only from the inflammatory effects of RA, but also perhaps from its 
      immunological nature.
FAU - Kurt, Tolga
AU  - Kurt T
AD  - Faculty of Medicine, Department of Cardiovascular Surgery, School of Medicine, 
      Canakkale Onsekiz Mart University, Terzioglu Yerleskesi dekanlık binası kat: 2 
      Kepez, Canakkale, Turkey, drtolgakurt17@gmail.com.
FAU - Temiz, Ahmet
AU  - Temiz A
FAU - Gokmen, Ferhat
AU  - Gokmen F
FAU - Adam, Gurhan
AU  - Adam G
FAU - Ozcan, Sedat
AU  - Ozcan S
FAU - Ozbudak, Ersan
AU  - Ozbudak E
FAU - Sacar, Mustafa
AU  - Sacar M
LA  - eng
PT  - Journal Article
DEP - 20150317
PL  - Austria
TA  - Wien Klin Wochenschr
JT  - Wiener klinische Wochenschrift
JID - 21620870R
SB  - IM
MH  - Ankle Brachial Index/*statistics & numerical data
MH  - Arthritis, Rheumatoid/*diagnosis/*epidemiology
MH  - Asymptomatic Diseases
MH  - Atherosclerosis/*diagnosis/*epidemiology
MH  - Carotid Intima-Media Thickness/*statistics & numerical data
MH  - Causality
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Reproducibility of Results
MH  - Risk Factors
MH  - Sensitivity and Specificity
MH  - Turkey/epidemiology
EDAT- 2015/03/18 06:00
MHDA- 2016/04/26 06:00
CRDT- 2015/03/18 06:00
PHST- 2014/09/09 00:00 [received]
PHST- 2015/02/09 00:00 [accepted]
PHST- 2015/03/18 06:00 [entrez]
PHST- 2015/03/18 06:00 [pubmed]
PHST- 2016/04/26 06:00 [medline]
AID - 10.1007/s00508-015-0767-x [doi]
PST - ppublish
SO  - Wien Klin Wochenschr. 2015 Jul;127(13-14):529-34. doi: 10.1007/s00508-015-0767-x. 
      Epub 2015 Mar 17.

PMID- 25776112
OWN - NLM
STAT- MEDLINE
DCOM- 20150807
LR  - 20220330
IS  - 2326-5205 (Electronic)
IS  - 2326-5191 (Print)
IS  - 2326-5191 (Linking)
VI  - 67
IP  - 6
DP  - 2015 Jun
TI  - Disease activity in rheumatoid arthritis and the risk of cardiovascular events.
PG  - 1449-55
LID - 10.1002/art.39098 [doi]
AB  - OBJECTIVE: Use of several immunomodulatory agents has been associated with 
      reduced numbers of cardiovascular (CV) events in epidemiologic studies of 
      rheumatoid arthritis (RA). However, it is unknown whether time-averaged disease 
      activity in RA correlates with CV events. METHODS: We studied patients with RA 
      whose cases were followed in a longitudinal US-based registry. Time-averaged 
      disease activity was assessed during followup using the area under the curve of 
      the Clinical Disease Activity Index (CDAI), a validated measure of RA disease 
      activity. Age, sex, presence of diabetes mellitus, hypertension, or 
      hyperlipidemia, body mass index, family history of myocardial infarction (MI), 
      use of aspirin or nonsteroidal antiinflammatory drugs (NSAIDs), presence of CV 
      disease, and baseline use of an immunomodulator were assessed at baseline. Cox 
      proportional hazards regression models were examined to determine the risk of a 
      composite CV end point that included MI, stroke, and death from CV causes. 
      RESULTS: A total of 24,989 patients who had been followed up for a median of 2.7 
      years were included in these analyses. During followup, we observed 534 confirmed 
      CV end points, for an incidence rate of 7.8 per 1,000 person-years (95% 
      confidence interval [95% CI] 6.7-8.9). In models adjusted for variables noted 
      above, a 10-point reduction in the time-averaged CDAI was associated with a 21% 
      reduction in CV risk (95% CI 13-29). These results were robust in subgroup 
      analyses stratified by the presence of CV disease, use of corticosteroids, use of 
      NSAIDs or selective cyclooxygenase 2 inhibitors, and change in RA treatment, as 
      well as when restricted to events adjudicated as definite or probable. 
      CONCLUSION: Our findings showed that reduced time-averaged disease activity in RA 
      is associated with fewer CV events.
CI  - © 2015, American College of Rheumatology.
FAU - Solomon, D H
AU  - Solomon DH
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Reed, G W
AU  - Reed GW
AD  - University of Massachusetts Medical School, Worcester and the Consortium of 
      Rheumatology Researchers of North America (CORRONA), Southborough, Massachusetts.
FAU - Kremer, J M
AU  - Kremer JM
AD  - Albany Medical College and Center for Rheumatology, Albany, New York and CORRONA, 
      Southborough, Massachusetts.
FAU - Curtis, J R
AU  - Curtis JR
AD  - University of Alabama at Birmingham.
FAU - Farkouh, M E
AU  - Farkouh ME
AD  - Mount Sinai School of Medicine, New York, New York.
FAU - Harrold, L R
AU  - Harrold LR
AD  - University of Massachusetts Medical School, Worcester and the Consortium of 
      Rheumatology Researchers of North America (CORRONA), Southborough, Massachusetts.
FAU - Hochberg, M C
AU  - Hochberg MC
AD  - University of Maryland School of Medicine, Baltimore.
FAU - Tsao, P
AU  - Tsao P
AD  - Brigham and Women's Hospital, Boston, Massachusetts.
FAU - Greenberg, J D
AU  - Greenberg JD
AD  - New York University School of Medicine and New York University Hospital for Joint 
      Diseases, New York, New York, and CORRONA, Southborough, Massachusetts.
LA  - eng
GR  - R01-HS-018517/HS/AHRQ HHS/United States
GR  - K24 AR055989/AR/NIAMS NIH HHS/United States
GR  - P60 AR064172/AR/NIAMS NIH HHS/United States
GR  - R01 HS018517/HS/AHRQ HHS/United States
GR  - AR-064172/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Rheumatol
JT  - Arthritis & rheumatology (Hoboken, N.J.)
JID - 101623795
RN  - 0 (Adrenal Cortex Hormones)
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
SB  - IM
MH  - Adrenal Cortex Hormones/therapeutic use
MH  - Adult
MH  - Aged
MH  - Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/drug therapy/*epidemiology/physiopathology
MH  - Cardiovascular Diseases/epidemiology/mortality
MH  - Cohort Studies
MH  - Cyclooxygenase 2 Inhibitors/therapeutic use
MH  - Diabetes Mellitus/epidemiology
MH  - Female
MH  - Humans
MH  - Hyperlipidemias/epidemiology
MH  - Hypertension/epidemiology
MH  - Incidence
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*epidemiology/mortality
MH  - Proportional Hazards Models
MH  - Registries
MH  - Severity of Illness Index
MH  - Stroke/*epidemiology/mortality
MH  - United States/epidemiology
PMC - PMC4446181
MID - NIHMS668993
EDAT- 2015/03/18 06:00
MHDA- 2015/08/08 06:00
PMCR- 2016/06/01
CRDT- 2015/03/18 06:00
PHST- 2014/10/20 00:00 [received]
PHST- 2015/02/26 00:00 [accepted]
PHST- 2015/03/18 06:00 [entrez]
PHST- 2015/03/18 06:00 [pubmed]
PHST- 2015/08/08 06:00 [medline]
PHST- 2016/06/01 00:00 [pmc-release]
AID - 10.1002/art.39098 [doi]
PST - ppublish
SO  - Arthritis Rheumatol. 2015 Jun;67(6):1449-55. doi: 10.1002/art.39098.

PMID- 25766275
OWN - NLM
STAT- MEDLINE
DCOM- 20160125
LR  - 20150427
IS  - 1347-4820 (Electronic)
IS  - 1346-9843 (Linking)
VI  - 79
IP  - 5
DP  - 2015
TI  - Modulation of autoimmunity and atherosclerosis - common targets and promising 
      translational approaches against disease.
PG  - 924-33
LID - 10.1253/circj.CJ-15-0167 [doi]
AB  - Atherosclerosis is a chronic inflammatory disease of the arterial wall that is 
      influenced by several risk factors, including hyperlipidemia and hypertension. 
      Autoimmune diseases substantially increase the risk for cardiovascular disease 
      (CVD). Although atherosclerotic CVD, such as myocardial and stroke, is much more 
      prevalent than classical autoimmune conditions such as rheumatoid arthritis, 
      psoriasis, and systemic lupus erythematosus, these types of pathology have many 
      similarities, raising the possibility that therapies against autoimmune disease 
      can have beneficial effects on CVD. Substantial clinical and experimental data 
      support the potential for immunomodulatory approaches to combating both 
      autoimmune and cardiovascular diseases, including classical immunosuppressants, 
      anticytokine therapy, the targeting of T and B cells and their responses, and 
      vaccination. In this review, we discuss experimental and clinical studies that 
      have used immunomodulatory approaches to mitigate autoimmune reactions and 
      examine their potential to prevent and treat atherosclerotic CVD.
FAU - Ketelhuth, Daniel F J
AU  - Ketelhuth DF
AD  - Center for Molecular Medicine, Department of Medicine, Karolinska Institutet, 
      Karolinska University Hospital.
FAU - Hansson, Göran K
AU  - Hansson GK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20150311
PL  - Japan
TA  - Circ J
JT  - Circulation journal : official journal of the Japanese Circulation Society
JID - 101137683
RN  - 0 (Immunosuppressive Agents)
SB  - IM
MH  - Atherosclerosis/*drug therapy/immunology/pathology
MH  - Humans
MH  - Immunosuppressive Agents/*therapeutic use
MH  - Lupus Erythematosus, Systemic/*drug therapy/immunology/pathology
MH  - Myocardial Infarction/*drug therapy/immunology/pathology
MH  - Stroke/*drug therapy/immunology/pathology
EDAT- 2015/03/15 06:00
MHDA- 2016/01/26 06:00
CRDT- 2015/03/14 06:00
PHST- 2015/03/14 06:00 [entrez]
PHST- 2015/03/15 06:00 [pubmed]
PHST- 2016/01/26 06:00 [medline]
AID - 10.1253/circj.CJ-15-0167 [doi]
PST - ppublish
SO  - Circ J. 2015;79(5):924-33. doi: 10.1253/circj.CJ-15-0167. Epub 2015 Mar 11.

PMID- 25744772
OWN - NLM
STAT- MEDLINE
DCOM- 20161103
LR  - 20180614
IS  - 1648-9144 (Electronic)
IS  - 1010-660X (Linking)
VI  - 51
IP  - 1
DP  - 2015
TI  - Predictors of mortality in patients with rheumatoid arthritis in Lithuania: Data 
      from a cohort study over 10 years.
PG  - 25-31
LID - S1010-660X(14)00107-4 [pii]
LID - 10.1016/j.medici.2014.11.001 [doi]
AB  - BACKGROUND AND OBJECTIVE: Increased mortality and shorter survival among 
      rheumatoid arthritis (RA) patients are recognized but not fully explained. This 
      cohort study aimed to identify predictors of mortality among RA patients at a 
      tertiary clinical setting. MATERIALS AND METHODS: Patients with RA were recruited 
      during 1998-2003 and followed up until April 1, 2012, or death whichever happened 
      first. Baseline variables included sociodemographic and disease characteristics, 
      and comorbidities. Cox regression and hazard risk (HR) were computed to estimate 
      risks for mortality. RESULTS: One hundred ninety-one patients were included into 
      the study, 186 patients were eligible for the analysis and of these 131 patients 
      (70.4%) completed the entire period of followed-up while 55 patients (29.6%) 
      died. The average follow up period was equivalent to 9.24 year per person. A Cox 
      regression model identified four major factors having an impact on survival. 
      History of a stroke at baseline was identified as a major factor (HR=5.33; 95% 
      CI, 2.13-13.32). Statistically significant risk factors were also age over 50 
      years (HR=4.59; 95% CI, 2.04-10.30); education less than 11 years (HR=3.3; 95% 
      CI, 1.72-6.33) and angina pectoris (HR=1.98; 95% CI, 1.03-3.80). CONCLUSIONS: 
      Higher age, lower education and cardiovascular comorbidities were identified as 
      predictors of mortality in this prospective cohort study while disease-related 
      variables were not independent predictors of mortality.
CI  - Copyright © 2014 Lithuanian University of Health Sciences. Production and hosting 
      by Elsevier Urban & Partner Sp. z o.o. All rights reserved.
FAU - Dadonienė, Jolanta
AU  - Dadonienė J
AD  - Medical Faculty, Vilnius University, Vilnius, Lithuania; State Research Institute 
      for Innovative Medicine, Vilnius, Lithuania. Electronic address: 
      jolanta.dadoniene@mf.vu.lt.
FAU - Stropuvienė, Sigita
AU  - Stropuvienė S
AD  - Medical Faculty, Vilnius University, Vilnius, Lithuania; State Research Institute 
      for Innovative Medicine, Vilnius, Lithuania.
FAU - Stukas, Rimantas
AU  - Stukas R
AD  - Medical Faculty, Vilnius University, Vilnius, Lithuania.
FAU - Venalis, Algirdas
AU  - Venalis A
AD  - Medical Faculty, Vilnius University, Vilnius, Lithuania; State Research Institute 
      for Innovative Medicine, Vilnius, Lithuania.
FAU - Sokka-Isler, Tuulikki
AU  - Sokka-Isler T
AD  - Jyvaskyla Central Hospital, Jyvaskyla, Finland.
LA  - eng
PT  - Journal Article
DEP - 20141126
PL  - Switzerland
TA  - Medicina (Kaunas)
JT  - Medicina (Kaunas, Lithuania)
JID - 9425208
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Angina Pectoris/mortality
MH  - Arthritis, Rheumatoid/*mortality
MH  - Cohort Studies
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Lithuania/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Prospective Studies
MH  - Risk Factors
MH  - Stroke/mortality
MH  - Young Adult
OTO - NOTNLM
OT  - Cohort study
OT  - Comorbidities
OT  - Mortality
OT  - Predictors
OT  - Rheumatoid arthritis
EDAT- 2015/03/07 06:00
MHDA- 2016/11/04 06:00
CRDT- 2015/03/07 06:00
PHST- 2013/07/04 00:00 [received]
PHST- 2014/11/18 00:00 [accepted]
PHST- 2015/03/07 06:00 [entrez]
PHST- 2015/03/07 06:00 [pubmed]
PHST- 2016/11/04 06:00 [medline]
AID - S1010-660X(14)00107-4 [pii]
AID - 10.1016/j.medici.2014.11.001 [doi]
PST - ppublish
SO  - Medicina (Kaunas). 2015;51(1):25-31. doi: 10.1016/j.medici.2014.11.001. Epub 2014 
      Nov 26.

PMID- 25726631
OWN - NLM
STAT- MEDLINE
DCOM- 20150417
LR  - 20150302
IS  - 1220-4749 (Print)
IS  - 1220-4749 (Linking)
VI  - 52
IP  - 4
DP  - 2014 Oct-Dec
TI  - Rheumatoid arthritis and ischemic strokes in a young woman. Are these conditions 
      interrelated?
PG  - 273-8
AB  - Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease which is 
      associated with an increased risk of cardio and cerebrovascular pathology. A 
      48-year old Caucasian female was admitted for diffuse arthralgias. She was 
      diagnosed eight years before with seropositive RA and she received Methotrexate, 
      Prednisone and anti-inflammatory drugs. A week after the admission the patient 
      presented sudden onset of left hemiplegia. Cerebral CT scan was suggestive for 
      acute infarction in the right middle cerebral artery area and an old sequelar 
      infarction in the left posterior artery area. Laboratory tests revealed: 
      erythrocyte sedimentation rate of 40 mm/hour, fibrinogen 656 mg/dL, C-reactive 
      protein of 20 mg/dL, rheumatoid factor 66.83 U/mL, anti CCP3 IgG 213.54 U/mL, ANA 
      128.126 U/mL. Also, she had high LDL-cholesterol serum concentration (190 mg/dL). 
      The ECG revealed sinus rhythm, QRS axis-45 degrees, antero-lateral ischemia. 
      Ultrasound examination of cervico-cerebral arteries emphasized occlusion of the 
      left internal carotid artery, large atheromas in both carotid and vertebral 
      arteries. A treatment with anti-aggregant and statin was started, and the former 
      treatment for RA was continued with a raised Prednisone dose. The outcome was 
      favorable, the patient's motor deficit improved (3/5 BMRC at the upper limb and 
      4/5 at the inferior limb) and she was able to walk with a cane support. She also 
      presented an alleviation in the laboratory test status. Ischemic stroke is a 
      possible complication of RA, presenting as principal risk factor precocious 
      atherosclerosis. A better control of inflammation by new anti-rheumatic 
      treatments will protect the RA patients of deleterious effects of ischemic 
      stroke.
FAU - Cojocaru, Inimioara Mihaela
AU  - Cojocaru IM
FAU - Ştefănescu, V
AU  - Ştefănescu V
FAU - Cojocaru, M
AU  - Cojocaru M
FAU - Chicoş, B
AU  - Chicoş B
FAU - Traşcă, Daniela
AU  - Traşcă D
FAU - Şerban-Pereţeanu, Adelina
AU  - Şerban-Pereţeanu A
LA  - eng
PT  - Case Reports
PT  - Journal Article
PL  - Germany
TA  - Rom J Intern Med
JT  - Romanian journal of internal medicine = Revue roumaine de medecine interne
JID - 9304507
SB  - IM
MH  - Arthritis, Rheumatoid/*complications
MH  - Brain Infarction/*etiology
MH  - Female
MH  - Humans
MH  - Middle Aged
EDAT- 2015/03/03 06:00
MHDA- 2015/04/18 06:00
CRDT- 2015/03/03 06:00
PHST- 2015/03/03 06:00 [entrez]
PHST- 2015/03/03 06:00 [pubmed]
PHST- 2015/04/18 06:00 [medline]
PST - ppublish
SO  - Rom J Intern Med. 2014 Oct-Dec;52(4):273-8.

PMID- 25726324
OWN - NLM
STAT- MEDLINE
DCOM- 20160301
LR  - 20240526
IS  - 2213-8595 (Electronic)
IS  - 2213-8587 (Print)
IS  - 2213-8587 (Linking)
VI  - 3
IP  - 4
DP  - 2015 Apr
TI  - Cardiometabolic effects of genetic upregulation of the interleukin 1 receptor 
      antagonist: a Mendelian randomisation analysis.
PG  - 243-53
LID - S2213-8587(15)00034-0 [pii]
LID - 10.1016/S2213-8587(15)00034-0 [doi]
AB  - BACKGROUND: To investigate potential cardiovascular and other effects of 
      long-term pharmacological interleukin 1 (IL-1) inhibition, we studied genetic 
      variants that produce inhibition of IL-1, a master regulator of inflammation. 
      METHODS: We created a genetic score combining the effects of alleles of two 
      common variants (rs6743376 and rs1542176) that are located upstream of IL1RN, the 
      gene encoding the IL-1 receptor antagonist (IL-1Ra; an endogenous inhibitor of 
      both IL-1α and IL-1β); both alleles increase soluble IL-1Ra protein 
      concentration. We compared effects on inflammation biomarkers of this genetic 
      score with those of anakinra, the recombinant form of IL-1Ra, which has 
      previously been studied in randomised trials of rheumatoid arthritis and other 
      inflammatory disorders. In primary analyses, we investigated the score in 
      relation to rheumatoid arthritis and four cardiometabolic diseases (type 2 
      diabetes, coronary heart disease, ischaemic stroke, and abdominal aortic 
      aneurysm; 453,411 total participants). In exploratory analyses, we studied the 
      relation of the score to many disease traits and to 24 other disorders of 
      proposed relevance to IL-1 signalling (746,171 total participants). FINDINGS: For 
      each IL1RN minor allele inherited, serum concentrations of IL-1Ra increased by 
      0.22 SD (95% CI 0.18-0.25; 12.5%; p = 9.3 × 10(-33)), concentrations of 
      interleukin 6 decreased by 0.02 SD (-0.04 to -0.01; -1.7%; p = 3.5 × 10(-3)), and 
      concentrations of C-reactive protein decreased by 0.03 SD (-0.04 to -0.02; -3.4%; 
      p = 7.7 × 10(-14)). We noted the effects of the genetic score on these 
      inflammation biomarkers to be directionally concordant with those of anakinra. 
      The allele count of the genetic score had roughly log-linear, dose-dependent 
      associations with both IL-1Ra concentration and risk of coronary heart disease. 
      For people who carried four IL-1Ra-raising alleles, the odds ratio for coronary 
      heart disease was 1.15 (1.08-1.22; p = 1.8 × 10(-6)) compared with people who 
      carried no IL-1Ra-raising alleles; the per-allele odds ratio for coronary heart 
      disease was 1.03 (1.02-1.04; p = 3.9 × 10(-10)). Per-allele odds ratios were 0.97 
      (0.95-0.99; p = 9.9 × 10(-4)) for rheumatoid arthritis, 0.99 (0.97-1.01; p = 
      0.47) for type 2 diabetes, 1.00 (0.98-1.02; p = 0.92) for ischaemic stroke, and 
      1.08 (1.04-1.12; p = 1.8 × 10(-5)) for abdominal aortic aneurysm. In exploratory 
      analyses, we observed per-allele increases in concentrations of proatherogenic 
      lipids, including LDL-cholesterol, but no clear evidence of association for blood 
      pressure, glycaemic traits, or any of the 24 other disorders studied. Modelling 
      suggested that the observed increase in LDL-cholesterol could account for about a 
      third of the association observed between the genetic score and increased 
      coronary risk. INTERPRETATION: Human genetic data suggest that long-term dual 
      IL-1α/β inhibition could increase cardiovascular risk and, conversely, reduce the 
      risk of development of rheumatoid arthritis. The cardiovascular risk might, in 
      part, be mediated through an increase in proatherogenic lipid concentrations.
CI  - Copyright © 2015 The Interleukin 1 Genetics Consortium. Open Access article 
      distributed under the terms of CC-BY-NC-ND. Published by Elsevier Ltd.. All 
      rights reserved.
CN  - Interleukin 1 Genetics Consortium
LA  - eng
GR  - 12076/CRUK_/Cancer Research UK/United Kingdom
GR  - 10589/CRUK_/Cancer Research UK/United Kingdom
GR  - 19167/CRUK_/Cancer Research UK/United Kingdom
GR  - MC_U127527198/MRC_/Medical Research Council/United Kingdom
GR  - MC_UU_12013/1/MRC_/Medical Research Council/United Kingdom
GR  - SP/09/002/BHF_/British Heart Foundation/United Kingdom
GR  - 268834/ERC_/European Research Council/International
GR  - RG/08/014/24067/BHF_/British Heart Foundation/United Kingdom
GR  - WT_/Wellcome Trust/United Kingdom
GR  - G0800270/MRC_/Medical Research Council/United Kingdom
GR  - RC1 AR058587/AR/NIAMS NIH HHS/United States
GR  - G0502131/MRC_/Medical Research Council/United Kingdom
GR  - R01 HL120393/HL/NHLBI NIH HHS/United States
GR  - MR/L003120/1/MRC_/Medical Research Council/United Kingdom
GR  - UL1 TR000427/TR/NCATS NIH HHS/United States
GR  - R01 HL105756/HL/NHLBI NIH HHS/United States
GR  - U01 HG006389/HG/NHGRI NIH HHS/United States
GR  - 095198/WT_/Wellcome Trust/United Kingdom
GR  - MC_UU_12013/4/MRC_/Medical Research Council/United Kingdom
GR  - MC_UU_12013/3/MRC_/Medical Research Council/United Kingdom
GR  - P30 AR047363/AR/NIAMS NIH HHS/United States
GR  - MC_PC_U127527198/MRC_/Medical Research Council/United Kingdom
GR  - K23 HL114724/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150226
PL  - England
TA  - Lancet Diabetes Endocrinol
JT  - The lancet. Diabetes & endocrinology
JID - 101618821
RN  - 0 (Cholesterol, LDL)
RN  - 0 (IL1RN protein, human)
RN  - 0 (IL6 protein, human)
RN  - 0 (Interleukin 1 Receptor Antagonist Protein)
RN  - 0 (Interleukin-6)
RN  - 0 (RNA, Messenger)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
CIN - Lancet Diabetes Endocrinol. 2015 Apr;3(4):228-9. doi: 
      10.1016/S2213-8587(15)00035-2. PMID: 25726325
EIN - Lancet Diabetes Endocrinol. 2015 Jun;3(6):e4. doi: 10.1016/S2213-8587(15)00145-X. 
      PMID: 28823410
MH  - Alleles
MH  - Aortic Aneurysm, Abdominal/*genetics/metabolism
MH  - Arthritis, Rheumatoid/drug therapy/genetics/metabolism
MH  - C-Reactive Protein/metabolism
MH  - Cardiovascular Diseases/genetics/metabolism
MH  - Cholesterol, LDL/metabolism
MH  - Coronary Disease/*genetics/metabolism
MH  - Diabetes Mellitus, Type 2/*genetics/metabolism
MH  - Gene Dosage
MH  - Genotype
MH  - Humans
MH  - Interleukin 1 Receptor Antagonist Protein/*genetics/metabolism/therapeutic use
MH  - Interleukin-6/metabolism
MH  - Mendelian Randomization Analysis
MH  - Odds Ratio
MH  - RNA, Messenger/*metabolism
MH  - Stroke/*genetics/metabolism
MH  - Up-Regulation
PMC - PMC4648058
FIR - Freitag, Daniel F
IR  - Freitag DF
FIR - Butterworth, Adam S
IR  - Butterworth AS
FIR - Willeit, Peter
IR  - Willeit P
FIR - Howson, Joanna M M
IR  - Howson JM
FIR - Burgess, Stephen
IR  - Burgess S
FIR - Kaptoge, Stephen
IR  - Kaptoge S
FIR - Young, Robin
IR  - Young R
FIR - Ho, Weang Kee
IR  - Ho WK
FIR - Wood, Angela M
IR  - Wood AM
FIR - Sweeting, Michael
IR  - Sweeting M
FIR - Spackman, Sarah
IR  - Spackman S
FIR - Staley, James R
IR  - Staley JR
FIR - Ramond, Anna
IR  - Ramond A
FIR - Harshfield, Eric
IR  - Harshfield E
FIR - Nielsen, Sune F
IR  - Nielsen SF
FIR - Grande, Peer
IR  - Grande P
FIR - Lange, Leslie A
IR  - Lange LA
FIR - Bown, Matthew J
IR  - Bown MJ
FIR - Jones, Gregory T
IR  - Jones GT
FIR - Scott, Robert A
IR  - Scott RA
FIR - Bevan, Steve
IR  - Bevan S
FIR - Porcu, Eleonora
IR  - Porcu E
FIR - Thorleifsson, Gudmar
IR  - Thorleifsson G
FIR - Zeng, Lingyao
IR  - Zeng L
FIR - Kessler, Thorsten
IR  - Kessler T
FIR - Do, Ron
IR  - Do R
FIR - Nikpay, Majid
IR  - Nikpay M
FIR - Zhang, Weihua
IR  - Zhang W
FIR - Hopewell, Jemma C
IR  - Hopewell JC
FIR - Kleber, Marcus
IR  - Kleber M
FIR - Delgado, Graciela E
IR  - Delgado GE
FIR - Nelson, Christopher P
IR  - Nelson CP
FIR - Goel, Anuj
IR  - Goel A
FIR - Bis, Joshua C
IR  - Bis JC
FIR - Dehghan, Abbas
IR  - Dehghan A
FIR - Ligthart, Symen
IR  - Ligthart S
FIR - Smith, Albert V
IR  - Smith AV
FIR - Qu, Liming
IR  - Qu L
FIR - van 't Hof, Femke N G
IR  - van 't Hof FN
FIR - de Bakker, Paul I W
IR  - de Bakker PI
FIR - Baas, Annette F
IR  - Baas AF
FIR - van Rij, Andre
IR  - van Rij A
FIR - Tromp, Gerard
IR  - Tromp G
FIR - Kuivaniemi, Helena
IR  - Kuivaniemi H
FIR - Ritchie, Marylyn D
IR  - Ritchie MD
FIR - Verma, Shefali S
IR  - Verma SS
FIR - Crawford, Dana C
IR  - Crawford DC
FIR - Malinowski, Jennifer
IR  - Malinowski J
FIR - de Andrade, Mariza
IR  - de Andrade M
FIR - Kullo, Iftikhar J
IR  - Kullo IJ
FIR - Peissig, Peggy L
IR  - Peissig PL
FIR - McCarty, Catherine A
IR  - McCarty CA
FIR - Böttinger, Erwin P
IR  - Böttinger EP
FIR - Gottesman, Omri
IR  - Gottesman O
FIR - Crosslin, David R
IR  - Crosslin DR
FIR - Carrell, David S
IR  - Carrell DS
FIR - Rasmussen-Torvik, Laura J
IR  - Rasmussen-Torvik LJ
FIR - Pacheco, Jennifer A
IR  - Pacheco JA
FIR - Huang, Jie
IR  - Huang J
FIR - Timpson, Nicholas J
IR  - Timpson NJ
FIR - Kettunen, Johannes
IR  - Kettunen J
FIR - Ala-Korpela, Mika
IR  - Ala-Korpela M
FIR - Mitchell, Gary F
IR  - Mitchell GF
FIR - Parsa, Afshin
IR  - Parsa A
FIR - Wilkinson, Ian B
IR  - Wilkinson IB
FIR - Gorski, Mathias
IR  - Gorski M
FIR - Li, Yong
IR  - Li Y
FIR - Franceschini, Nora
IR  - Franceschini N
FIR - Keller, Margaux F
IR  - Keller MF
FIR - Ganesh, Santhi K
IR  - Ganesh SK
FIR - Langefeld, Carl D
IR  - Langefeld CD
FIR - Bruijn, Lucie
IR  - Bruijn L
FIR - Brown, Matthew A
IR  - Brown MA
FIR - Evans, David M
IR  - Evans DM
FIR - Baltic, Svetlana
IR  - Baltic S
FIR - Ferreira, Manuel A
IR  - Ferreira MA
FIR - Baurecht, Hansjörg
IR  - Baurecht H
FIR - Weidinger, Stephan
IR  - Weidinger S
FIR - Franke, Andre
IR  - Franke A
FIR - Lubitz, Steven A
IR  - Lubitz SA
FIR - Müller-Nurasyid, Martina
IR  - Müller-Nurasyid M
FIR - Felix, Janine F
IR  - Felix JF
FIR - Smith, Nicholas L
IR  - Smith NL
FIR - Sudman, Marc
IR  - Sudman M
FIR - Thompson, Susan D
IR  - Thompson SD
FIR - Zeggini, Eleftheria
IR  - Zeggini E
FIR - Panoutsopoulou, Kalliope
IR  - Panoutsopoulou K
FIR - Nalls, Mike A
IR  - Nalls MA
FIR - Singleton, Andrew
IR  - Singleton A
FIR - Polychronakos, Constantin
IR  - Polychronakos C
FIR - Bradfield, Jonathan P
IR  - Bradfield JP
FIR - Hakonarson, Hakon
IR  - Hakonarson H
FIR - Easton, Douglas F
IR  - Easton DF
FIR - Thompson, Deborah
IR  - Thompson D
FIR - Tomlinson, Ian P
IR  - Tomlinson IP
FIR - Dunlop, Malcolm
IR  - Dunlop M
FIR - Hemminki, Kari
IR  - Hemminki K
FIR - Morgan, Gareth
IR  - Morgan G
FIR - Eisen, Timothy
IR  - Eisen T
FIR - Goldschmidt, Hartmut
IR  - Goldschmidt H
FIR - Allan, James M
IR  - Allan JM
FIR - Henrion, Marc
IR  - Henrion M
FIR - Whiffin, Nicola
IR  - Whiffin N
FIR - Wang, Yufei
IR  - Wang Y
FIR - Chubb, Daniel
IR  - Chubb D
FIR - Houlston, Richard S
IR  - Houlston RS
FIR - Iles, Mark M
IR  - Iles MM
FIR - Bishop, D Timothy
IR  - Bishop DT
FIR - Law, Matthew H
IR  - Law MH
FIR - Hayward, Nicholas K
IR  - Hayward NK
FIR - Luo, Yang
IR  - Luo Y
FIR - Nejentsev, Sergey
IR  - Nejentsev S
FIR - Barbalic, Maja
IR  - Barbalic M
FIR - Crossman, David
IR  - Crossman D
FIR - Sanna, Serena
IR  - Sanna S
FIR - Soranzo, Nicole
IR  - Soranzo N
FIR - Markus, Hugh S
IR  - Markus HS
FIR - Wareham, Nicholas J
IR  - Wareham NJ
FIR - Rader, Daniel J
IR  - Rader DJ
FIR - Reilly, Muredach
IR  - Reilly M
FIR - Assimes, Themistocles
IR  - Assimes T
FIR - Harris, Tamara B
IR  - Harris TB
FIR - Hofman, Albert
IR  - Hofman A
FIR - Franco, Oscar H
IR  - Franco OH
FIR - Gudnason, Vilmundur
IR  - Gudnason V
FIR - Tracy, Russell
IR  - Tracy R
FIR - Psaty, Bruce M
IR  - Psaty BM
FIR - Farrall, Martin
IR  - Farrall M
FIR - Watkins, Hugh
IR  - Watkins H
FIR - Hall, Alistair S
IR  - Hall AS
FIR - Samani, Nilesh J
IR  - Samani NJ
FIR - März, Winfried
IR  - März W
FIR - Clarke, Robert
IR  - Clarke R
FIR - Collins, Rory
IR  - Collins R
FIR - Kooner, Jaspal S
IR  - Kooner JS
FIR - Chambers, John C
IR  - Chambers JC
FIR - Kathiresan, Sekar
IR  - Kathiresan S
FIR - McPherson, Ruth
IR  - McPherson R
FIR - Erdmann, Jeanette
IR  - Erdmann J
FIR - Kastrati, Adnan
IR  - Kastrati A
FIR - Schunkert, Heribert
IR  - Schunkert H
FIR - Stefánsson, Kári
IR  - Stefánsson K
FIR - Walston, Jeremy D
IR  - Walston JD
FIR - Tybjærg-Hansen, Anne
IR  - Tybjærg-Hansen A
FIR - Alam, Dewan S
IR  - Alam DS
FIR - Majumder, Abdullah Al Shafi
IR  - Majumder AA
FIR - Di Angelantonio, Emanuele
IR  - Di Angelantonio E
FIR - Chowdhury, Rajiv
IR  - Chowdhury R
FIR - Nordestgaard, Børge G
IR  - Nordestgaard BG
FIR - Saleheen, Danish
IR  - Saleheen D
FIR - Thompson, Simon G
IR  - Thompson SG
FIR - Danesh, John
IR  - Danesh J
EDAT- 2015/03/03 06:00
MHDA- 2016/03/02 06:00
PMCR- 2015/04/01
CRDT- 2015/03/02 06:00
PHST- 2015/03/02 06:00 [entrez]
PHST- 2015/03/03 06:00 [pubmed]
PHST- 2016/03/02 06:00 [medline]
PHST- 2015/04/01 00:00 [pmc-release]
AID - S2213-8587(15)00034-0 [pii]
AID - 10.1016/S2213-8587(15)00034-0 [doi]
PST - ppublish
SO  - Lancet Diabetes Endocrinol. 2015 Apr;3(4):243-53. doi: 
      10.1016/S2213-8587(15)00034-0. Epub 2015 Feb 26.

PMID- 25716179
OWN - NLM
STAT- MEDLINE
DCOM- 20160111
LR  - 20150414
IS  - 1432-0533 (Electronic)
IS  - 0001-6322 (Linking)
VI  - 129
IP  - 5
DP  - 2015 May
TI  - The role of IL-17 in CNS diseases.
PG  - 625-37
LID - 10.1007/s00401-015-1402-7 [doi]
AB  - Cytokines of the IL-17 family are uniquely placed on the border between immune 
      cells and tissue. Although IL-17 was originally found to induce the activation 
      and mobilization of neutrophils to sites of inflammation, its tissue-specific 
      function is not yet fully understood. The best-studied IL-17 family members, 
      IL-17A and IL-17F, are both typically produced by immune cells such as Th17, γδ T 
      cells and innate lymphoid cells group 3. However, the cells that respond to these 
      cytokines are mostly found in inflamed tissue. As seen in psoriatic skin lesions 
      or in joints of rheumatoid arthritis patients, high levels of IL-17 have been 
      detected in the central nervous system (CNS) during inflammatory responses. Here, 
      we provide a general review of the molecular function of IL-17 and its role in 
      the CNS in particular. Of the different inflammatory conditions of the CNS, we 
      found multiple sclerosis (MS) to be the one most associated with the presence of 
      Th17 cells and IL-17. In particular, many studies using the murine model for MS, 
      experimental autoimmune encephalomyelitis, found a clear association of Th17 and 
      IL-17 with disease severity and progression. We summarize the recent advances 
      made in correlating the presence of IL-17 with impaired blood-brain barrier 
      integrity as well as the activation of astrocytes and microglia and the 
      consequences for disease progression. There is also evidence that IL-17 plays a 
      pathogenic role in the post-ischemic phase of stroke as well as its experimental 
      model. We review the limited but promising data on the sources of post-stroke 
      IL-17 production and its effects on CNS-resident target cells. In addition to MS 
      and stroke, there is also evidence linking high levels of IL-17 to depression, as 
      a frequent comorbidity of several inflammatory diseases, as well as to different 
      types of infections of the CNS. The evidence we supply here suggests that 
      inhibiting the function of the IL-17 cytokine family could have a beneficial 
      effect on pathogenic conditions in the CNS.
FAU - Waisman, Ari
AU  - Waisman A
AD  - Institute for Molecular Medicine, University Medical Center of the Johannes 
      Gutenberg-University Mainz, Obere Zahlbacher Straße 67, 55131, Mainz, Germany, 
      waisman@uni-mainz.de.
FAU - Hauptmann, Judith
AU  - Hauptmann J
FAU - Regen, Tommy
AU  - Regen T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20150226
PL  - Germany
TA  - Acta Neuropathol
JT  - Acta neuropathologica
JID - 0412041
RN  - 0 (IL17A protein, human)
RN  - 0 (IL17F protein, human)
RN  - 0 (Interleukin-17)
SB  - IM
MH  - Animals
MH  - Astrocytes/cytology/immunology
MH  - Blood-Brain Barrier/immunology/pathology
MH  - Central Nervous System Diseases/*immunology/*pathology
MH  - Depression/immunology/pathology
MH  - Disease Progression
MH  - Encephalomyelitis, Autoimmune, Experimental/immunology/pathology
MH  - Humans
MH  - Inflammation/*immunology/pathology
MH  - Interleukin-17/classification/*immunology
MH  - Microglia/cytology/immunology
MH  - Multiple Sclerosis/immunology/pathology
MH  - Risk Factors
MH  - Stroke/immunology/pathology
MH  - Th17 Cells/*immunology
EDAT- 2015/02/27 06:00
MHDA- 2016/01/12 06:00
CRDT- 2015/02/27 06:00
PHST- 2014/12/19 00:00 [received]
PHST- 2015/02/19 00:00 [accepted]
PHST- 2015/02/18 00:00 [revised]
PHST- 2015/02/27 06:00 [entrez]
PHST- 2015/02/27 06:00 [pubmed]
PHST- 2016/01/12 06:00 [medline]
AID - 10.1007/s00401-015-1402-7 [doi]
PST - ppublish
SO  - Acta Neuropathol. 2015 May;129(5):625-37. doi: 10.1007/s00401-015-1402-7. Epub 
      2015 Feb 26.

PMID- 25689371
OWN - NLM
STAT- MEDLINE
DCOM- 20160112
LR  - 20220321
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 10
IP  - 2
DP  - 2015
TI  - The impact of traditional cardiovascular risk factors on cardiovascular outcomes 
      in patients with rheumatoid arthritis: a systematic review and meta-analysis.
PG  - e0117952
LID - 10.1371/journal.pone.0117952 [doi]
LID - e0117952
AB  - BACKGROUND: Rheumatoid arthritis (RA) is known to increase the risk of 
      cardiovascular (CV) disease. However, the individual impact of traditional CV 
      risk factors in RA is unknown. OBJECTIVE: To assess the strength of the 
      association between individual CV risk factors and rate of either myocardial 
      infarction (MI), combined CV morbidity (MI, angina pectoris, heart failure, 
      stroke, and peripheral arterial disease (PAD)) or CV mortality in RA patients. 
      METHODS: RA studies reporting traditional CV risk factors [hypertension, type 2 
      diabetes (T2D), smoking, hypercholesterolaemia, obesity, and physical inactivity] 
      as exposures and MI, CV morbidity (MI, angina, heart failure, stroke, and PAD 
      combined) or CV mortality alone as outcomes were searched until March 2013 using 
      MEDLINE, Scopus and Cochrane. Meta-analyses combined relative risk (RR) estimates 
      from each study where either the RR and 95% confidence intervals or where raw 
      counts were available. RESULTS: Ten studies reporting sufficient data for 
      inclusion into meta-analyses were identified. Relevant data was available for 
      each risk factor and MI and CV morbidity but no studies reported on CV mortality. 
      Risk of MI increased in RA patients with hypertension (RR 1.84, 95% CI 1.38, 
      2.46) and T2D (RR 1.89, 95% CI 1.36, 2.63). CV morbidity increased with 
      hypertension (RR 2.24, 95% CI 1.42, 3.06), T2D (RR 1.94, 95% CI 1.58, 2.30), 
      smoking (RR 1.50, 95% CI 1.15, 1.84), hypercholesterolaemia (RR 1.73, 95% CI 
      1.03, 2.44) and obesity (RR 1.16, 95% CI 1.03, 1.29) but not with physical 
      inactivity (RR 1.00, 95% CI 0.71, 1.29). CONCLUSION: Hypertension, T2D, smoking, 
      hypercholesterolaemia and obesity increased CV risk in patients with RA. These 
      results highlight the importance of managing CV risk factors in RA, similarly to 
      non-RA patients.
FAU - Baghdadi, Leena R
AU  - Baghdadi LR
AD  - Department of Family and Community Medicine, King Saud University, Riyadh, Saudi 
      Arabia, Department of Clinical Pharmacology, School of Medicine, Flinders 
      University, Adelaide, Australia; Flinders Centre for Epidemiology and 
      Biostatistics, School of Medicine, Flinders University, Adelaide, Australia; 
      Department of Clinical Pharmacology, School of Medicine, Flinders University, 
      Adelaide, Australia.
FAU - Woodman, Richard J
AU  - Woodman RJ
AD  - Flinders Centre for Epidemiology and Biostatistics, School of Medicine, Flinders 
      University, Adelaide, Australia.
FAU - Shanahan, E Michael
AU  - Shanahan EM
AD  - Department of Rheumatology, School of Medicine, Flinders University, Adelaide, 
      Australia.
FAU - Mangoni, Arduino A
AU  - Mangoni AA
AD  - Department of Clinical Pharmacology, School of Medicine, Flinders University, 
      Adelaide, Australia.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Review
PT  - Systematic Review
DEP - 20150217
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
SB  - IM
MH  - Arthritis, Rheumatoid/*complications
MH  - Cardiovascular Diseases/*etiology/*mortality
MH  - Diabetes Mellitus, Type 2/complications
MH  - Humans
MH  - Life Style
MH  - Obesity/complications
MH  - Risk Factors
MH  - Smoking/adverse effects
PMC - PMC4331556
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2015/02/18 06:00
MHDA- 2016/01/13 06:00
PMCR- 2015/02/17
CRDT- 2015/02/18 06:00
PHST- 2014/10/01 00:00 [received]
PHST- 2015/01/03 00:00 [accepted]
PHST- 2015/02/18 06:00 [entrez]
PHST- 2015/02/18 06:00 [pubmed]
PHST- 2016/01/13 06:00 [medline]
PHST- 2015/02/17 00:00 [pmc-release]
AID - PONE-D-14-43366 [pii]
AID - 10.1371/journal.pone.0117952 [doi]
PST - epublish
SO  - PLoS One. 2015 Feb 17;10(2):e0117952. doi: 10.1371/journal.pone.0117952. 
      eCollection 2015.

PMID- 25609412
OWN - NLM
STAT- MEDLINE
DCOM- 20160628
LR  - 20181113
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Print)
IS  - 0003-4967 (Linking)
VI  - 75
IP  - 2
DP  - 2016 Feb
TI  - Association of hyperlipidaemia, inflammation and serological status and coronary 
      heart disease among patients with rheumatoid arthritis: data from the National 
      Veterans Health Administration.
PG  - 341-7
LID - 10.1136/annrheumdis-2013-204987 [doi]
AB  - OBJECTIVE: To examine the association of serum lipids, inflammation and 
      seropositivity on coronary heart disease (CHD) and stroke in patients with 
      rheumatoid arthritis (RA). METHODS: The incidence of hospitalised myocardial 
      infarction (MI) or stroke was calculated in a cohort of patients with RA 
      receiving care within the national Veterans Health Administration from 1998 to 
      2011. Cox proportional hazard models were used to examine the association between 
      these outcomes and low-density lipoprotein cholesterol (LDL-C), high-density 
      lipoprotein cholesterol (HDL-C), C reactive protein (CRP) and erythrocyte 
      sedimentation rate (ESR) as time-varying variables, divided into quintiles. 
      RESULTS: There were 37,568 patients with RA in the cohort with mean age of 
      63 years (SD 12.1); 90% were men. There was a no clear association between LDL-C 
      and CHD/stroke. Compared with lower HDL-C (<34 mg/dL), higher HDL-C (≥54 mg/dL) 
      was inversely associated with MI (hazard ratio (HR)=0.68, 95% CI 0.55 to 0.85) 
      and stroke (HR=0.69, 95% CI 0.50 to 0.96). Higher CRP >2.17 mg/dL (vs CRP 
      <0.26 mg/dL) was associated with increased risk (HR=2.43, 95% CI 1.77 to 3.33) 
      for MI and 2.02 (95% CI 1.32 to 3.08) for stroke. ESR >47 mm/h compared with 
      <8 mm/h had an HR 1.87 (95% CI 1.39 to 2.52) for MI and 2.00 (95% CI 1.26 to 
      3.18) for stroke. The association between MI was significant for RA 
      seropositivity (HR=1.23, 95% CI 1.03 to 1.48). CONCLUSIONS: In this predominantly 
      older male RA cohort, there was no clear association between LDL-C and CHD, 
      whereas higher HDL-C was inversely associated with MI and stroke. CRP and ESR 
      were similarly associated with increase MI risk and stroke, reflecting the 
      prominent role of inflammation in CHD risk in RA.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://www.bmj.com/company/products-services/rights-and-licensing/
FAU - Navarro-Millán, Iris
AU  - Navarro-Millán I
AD  - Birmingham VA Medical Center, Birmingham, Alabama, USA University of Alabama at 
      Birmingham Division of Clinical Immunology and Rheumatology, Birmingham, Alabama, 
      USA.
FAU - Yang, Shuo
AU  - Yang S
AD  - Birmingham VA Medical Center, Birmingham, Alabama, USA University of Alabama at 
      Birmingham Division of Clinical Immunology and Rheumatology, Birmingham, Alabama, 
      USA.
FAU - DuVall, Scott L
AU  - DuVall SL
AD  - VA Salt Lake City Health Care System and University of Utah School of Medicine, 
      Salt Lake City, Utah, USA.
FAU - Chen, Lang
AU  - Chen L
AD  - Birmingham VA Medical Center, Birmingham, Alabama, USA University of Alabama at 
      Birmingham Division of Clinical Immunology and Rheumatology, Birmingham, Alabama, 
      USA.
FAU - Baddley, John
AU  - Baddley J
AD  - Birmingham VA Medical Center, Birmingham, Alabama, USA University of Alabama at 
      Birmingham Division of Clinical Immunology and Rheumatology, Birmingham, Alabama, 
      USA.
FAU - Cannon, Grant W
AU  - Cannon GW
AD  - VA Salt Lake City Health Care System and University of Utah School of Medicine, 
      Salt Lake City, Utah, USA.
FAU - Delzell, Elizabeth S
AU  - Delzell ES
AD  - University of Alabama at Birmingham Division of Clinical Immunology and 
      Rheumatology, Birmingham, Alabama, USA.
FAU - Zhang, Jie
AU  - Zhang J
AD  - University of Alabama at Birmingham Division of Clinical Immunology and 
      Rheumatology, Birmingham, Alabama, USA.
FAU - Safford, Monika M
AU  - Safford MM
AD  - University of Alabama at Birmingham Division of Clinical Immunology and 
      Rheumatology, Birmingham, Alabama, USA.
FAU - Patkar, Nivedita M
AU  - Patkar NM
AD  - University of Alabama at Birmingham Division of Clinical Immunology and 
      Rheumatology, Birmingham, Alabama, USA.
FAU - Mikuls, Ted R
AU  - Mikuls TR
AD  - Omaha VA and University of Nebraska Medical Center, Omaha, Nebraska, USA.
FAU - Singh, Jasvinder A
AU  - Singh JA
AD  - Birmingham VA Medical Center, Birmingham, Alabama, USA University of Alabama at 
      Birmingham Division of Clinical Immunology and Rheumatology, Birmingham, Alabama, 
      USA.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AD  - Birmingham VA Medical Center, Birmingham, Alabama, USA University of Alabama at 
      Birmingham Division of Clinical Immunology and Rheumatology, Birmingham, Alabama, 
      USA.
LA  - eng
GR  - K23 AR053351/AR/NIAMS NIH HHS/United States
GR  - R01 AR062376/AR/NIAMS NIH HHS/United States
GR  - R01 HS018517/HS/AHRQ HHS/United States
PT  - Journal Article
DEP - 20150121
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Cholesterol, HDL)
RN  - 0 (Cholesterol, LDL)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/blood/*complications
MH  - Blood Sedimentation
MH  - C-Reactive Protein/analysis
MH  - Cholesterol, HDL/blood
MH  - Cholesterol, LDL/blood
MH  - Coronary Disease/blood/*etiology
MH  - Female
MH  - Humans
MH  - Hyperlipidemias/*blood/complications
MH  - Incidence
MH  - Inflammation/blood/*complications
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/blood/epidemiology/*etiology
MH  - Proportional Hazards Models
MH  - Stroke/blood/etiology
MH  - United States/epidemiology
MH  - United States Department of Veterans Affairs/statistics & numerical data
PMC - PMC4752663
MID - NIHMS688421
OTO - NOTNLM
OT  - Cardiovascular Disease
OT  - Inflammation
OT  - Rheumatoid Arthritis
EDAT- 2015/01/23 06:00
MHDA- 2016/06/29 06:00
PMCR- 2016/02/13
CRDT- 2015/01/23 06:00
PHST- 2013/11/30 00:00 [received]
PHST- 2014/11/07 00:00 [accepted]
PHST- 2015/01/23 06:00 [entrez]
PHST- 2015/01/23 06:00 [pubmed]
PHST- 2016/06/29 06:00 [medline]
PHST- 2016/02/13 00:00 [pmc-release]
AID - annrheumdis-2013-204987 [pii]
AID - 10.1136/annrheumdis-2013-204987 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2016 Feb;75(2):341-7. doi: 10.1136/annrheumdis-2013-204987. Epub 
      2015 Jan 21.

PMID- 25550360
OWN - NLM
STAT- MEDLINE
DCOM- 20150309
LR  - 20240512
IS  - 1476-6256 (Electronic)
IS  - 0002-9262 (Print)
IS  - 0002-9262 (Linking)
VI  - 181
IP  - 2
DP  - 2015 Jan 15
TI  - Antioxidant vitamin intake and mortality: the Leisure World Cohort Study.
PG  - 120-6
LID - 10.1093/aje/kwu294 [doi]
AB  - To assess the relationship between antioxidant vitamin intake and all-cause 
      mortality in older adults, we examined these associations using data from the 
      Leisure World Cohort Study, a prospective study of residents of the Leisure World 
      retirement community in Laguna Hills, California. In the early 1980s, 
      participants (who were aged 44-101 years) completed a postal survey, which 
      included details on use of vitamin supplements and dietary intake of foods 
      containing vitamins A and C. Age-adjusted and multivariate-adjusted (for factors 
      related to mortality in this cohort—smoking, alcohol intake, caffeine 
      consumption, exercise, body mass index, and histories of hypertension, angina, 
      heart attack, stroke, diabetes, rheumatoid arthritis, and cancer) hazard ratios 
      for death were calculated using Cox regression for 8,640 women and 4,983 men 
      (median age at entry, 74 years). During follow-up (1981-2013), 13,104 
      participants died (median age at death, 88 years). Neither dietary nor 
      supplemental intake of vitamin A or vitamin C nor supplemental intake of vitamin 
      E was significantly associated with mortality after multivariate adjustment. A 
      compendium that summarizes previous findings of cohort studies evaluating vitamin 
      intake and mortality is provided. Attenuation in the observed associations 
      between mortality and antioxidant vitamin use after adjustment for confounders in 
      our study and in previous studies suggests that such consumption identifies 
      persons with other mortality-associated lifestyle and health risk factors.
CI  - © The Author 2014. Published by Oxford University Press on behalf of the Johns 
      Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, 
      please e-mail: journals.permissions@oup.com.
FAU - Paganini-Hill, Annlia
AU  - Paganini-Hill A
FAU - Kawas, Claudia H
AU  - Kawas CH
FAU - Corrada, María M
AU  - Corrada MM
LA  - eng
GR  - P50 AG016573/AG/NIA NIH HHS/United States
GR  - R01 AG021055/AG/NIA NIH HHS/United States
GR  - R01 CA032197/CA/NCI NIH HHS/United States
GR  - R01AG21055/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20141229
PL  - United States
TA  - Am J Epidemiol
JT  - American journal of epidemiology
JID - 7910653
RN  - 0 (Antioxidants)
RN  - 11103-57-4 (Vitamin A)
RN  - 1406-18-4 (Vitamin E)
RN  - PQ6CK8PD0R (Ascorbic Acid)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Antioxidants/*administration & dosage
MH  - Ascorbic Acid/*administration & dosage
MH  - California
MH  - Dietary Supplements/*statistics & numerical data
MH  - Female
MH  - Health Behavior
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Mortality
MH  - Prospective Studies
MH  - Vitamin A/*administration & dosage
MH  - Vitamin E/administration & dosage
PMC - PMC4351350
OTO - NOTNLM
OT  - adults
OT  - aging
OT  - antioxidants
OT  - cohort studies
OT  - longevity
OT  - mortality
OT  - risk factors
OT  - vitamins
EDAT- 2015/01/01 06:00
MHDA- 2015/03/10 06:00
PMCR- 2016/01/15
CRDT- 2015/01/01 06:00
PHST- 2015/01/01 06:00 [entrez]
PHST- 2015/01/01 06:00 [pubmed]
PHST- 2015/03/10 06:00 [medline]
PHST- 2016/01/15 00:00 [pmc-release]
AID - kwu294 [pii]
AID - 10.1093/aje/kwu294 [doi]
PST - ppublish
SO  - Am J Epidemiol. 2015 Jan 15;181(2):120-6. doi: 10.1093/aje/kwu294. Epub 2014 Dec 
      29.

PMID- 25527879
OWN - NLM
STAT- MEDLINE
DCOM- 20150619
LR  - 20160519
IS  - 1878-8769 (Electronic)
IS  - 1878-8750 (Linking)
VI  - 83
IP  - 4
DP  - 2015 Apr
TI  - Risks of in-hospital death and complications after fusion surgery in patients 
      with atlantoaxial subluxation: analysis of 1090 patients using the Japanese 
      Diagnosis Procedure Combination database.
PG  - 603-7
LID - S1878-8750(14)01390-4 [pii]
LID - 10.1016/j.wneu.2014.12.019 [doi]
AB  - OBJECTIVE: To examine in-hospital mortality and postoperative major complications 
      in patients undergoing fusion surgery for atlantoaxial subluxation (AAS) and to 
      examine whether the risk of perioperative complications varies between patients 
      with and without rheumatoid arthritis (RA). METHODS: A retrospective analysis of 
      data from the Diagnosis Procedure Combination database, a nationwide 
      administrative impatient database in Japan, identified 1090 patients who 
      underwent spinal fusion surgery for AAS during 2007-2012. Patients' clinical 
      characteristics were extracted, including age, sex, use of homologous blood 
      transfusion, length of stay, and type of hospital. Clinical outcomes included 
      in-hospital death and major complications, including surgical-site infection, 
      sepsis, cardiac events, respiratory disorders, acute renal failure, pulmonary 
      embolism, perioperative stroke, and vertebral injury. Massive blood transfusion 
      was defined as at least 6 units of red blood cells. RESULTS: Four hundred 
      sixty-five patients (42.7%) were classified as the RA group. In-hospital 
      mortality after fusion surgery for AAS was 0.5% (5/1090), and major complications 
      occurred in 5% (55/1090). Multivariate analyses showed that patients with RA were 
      more likely to have major complications after surgery than patients without RA 
      (odds ratio: 1.69; 95% confidence interval: 0.96-2.97; P = 0.07), and the rate of 
      massive blood transfusion was significantly greater in patients with RA than in 
      patients without RA (odds ratio: 2.29; 95% confidence interval: 1.12-4.68; P = 
      0.02). CONCLUSIONS: The in-hospital mortality after fusion surgery for AAS was 
      relatively low. However, patients with RA had an increased risk of postoperative 
      complications and massive blood transfusion compared with patients without RA.
CI  - Copyright © 2015 Elsevier Inc. All rights reserved.
FAU - Ohya, Junichi
AU  - Ohya J
AD  - Department of Orthopaedic Surgery, Faculty of Medicine, The University of Tokyo, 
      Tokyo, Japan. Electronic address: oyaj-ort@h.u-tokyo.ac.jp.
FAU - Chikuda, Hirotaka
AU  - Chikuda H
AD  - Department of Orthopaedic Surgery, Faculty of Medicine, The University of Tokyo, 
      Tokyo, Japan.
FAU - Kato, So
AU  - Kato S
AD  - Department of Orthopaedic Surgery, Faculty of Medicine, The University of Tokyo, 
      Tokyo, Japan.
FAU - Horiguchi, Hiromasa
AU  - Horiguchi H
AD  - Department of Clinical Epidemiology and Health Economics, School of Public 
      Health, The University of Tokyo, Tokyo, Japan.
FAU - Takeshita, Katsushi
AU  - Takeshita K
AD  - Department of Orthopaedic Surgery, Faculty of Medicine, The University of Tokyo, 
      Tokyo, Japan.
FAU - Tanaka, Sakae
AU  - Tanaka S
AD  - Department of Orthopaedic Surgery, Faculty of Medicine, The University of Tokyo, 
      Tokyo, Japan.
FAU - Yasunaga, Hideo
AU  - Yasunaga H
AD  - Department of Clinical Epidemiology and Health Economics, School of Public 
      Health, The University of Tokyo, Tokyo, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141218
PL  - United States
TA  - World Neurosurg
JT  - World neurosurgery
JID - 101528275
SB  - IM
CIN - World Neurosurg. 2015 Aug;84(2):226-7. doi: 10.1016/j.wneu.2015.04.026. PMID: 
      25896855
MH  - Aged
MH  - Aged, 80 and over
MH  - Atlanto-Axial Joint/*injuries
MH  - Databases, Factual
MH  - Female
MH  - Hospital Mortality
MH  - Humans
MH  - Japan/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Postoperative Complications/*mortality
MH  - Risk
MH  - Spinal Fusion/*mortality
MH  - Treatment Outcome
OTO - NOTNLM
OT  - Atlantoaxial subluxation
OT  - Complications
OT  - Database
OT  - Mortality
OT  - Rheumatoid arthritis
EDAT- 2014/12/22 06:00
MHDA- 2015/06/20 06:00
CRDT- 2014/12/22 06:00
PHST- 2014/07/03 00:00 [received]
PHST- 2014/09/06 00:00 [revised]
PHST- 2014/12/10 00:00 [accepted]
PHST- 2014/12/22 06:00 [entrez]
PHST- 2014/12/22 06:00 [pubmed]
PHST- 2015/06/20 06:00 [medline]
AID - S1878-8750(14)01390-4 [pii]
AID - 10.1016/j.wneu.2014.12.019 [doi]
PST - ppublish
SO  - World Neurosurg. 2015 Apr;83(4):603-7. doi: 10.1016/j.wneu.2014.12.019. Epub 2014 
      Dec 18.

PMID- 25455683
OWN - NLM
STAT- MEDLINE
DCOM- 20160406
LR  - 20220321
IS  - 1532-866X (Electronic)
IS  - 0049-0172 (Linking)
VI  - 44
IP  - 5
DP  - 2015 Apr
TI  - Cardiovascular events in ankylosing spondylitis: an updated meta-analysis.
PG  - 551-555
LID - S0049-0172(14)00248-0 [pii]
LID - 10.1016/j.semarthrit.2014.10.007 [doi]
AB  - OBJECTIVES: Rheumatoid arthritis is associated with increased cardiovascular 
      risk. In the guidelines, ankylosing spondylitis (AS) is considered to have an 
      equally high cardiovascular risk. The literature findings remain controversial. 
      This study aims to assess the risk of myocardial infarction (MI) and stroke in AS 
      patients. METHODS: An updated meta-analysis with a new systematic literature 
      review using PubMed was conducted up to January 2014. Incidence of MI or stroke 
      was calculated by metaproportion. RESULTS: In addition to the 11 previously 
      included studies, six new studies assessed the occurrence of MI or stroke in AS 
      patients. (1) MI. A total of 2131 MI were reported in AS patients (n = 27,532) 
      over a mean follow-up of 15 years: incidence 5.3% (1.6%-11.0%), i.e., 0.36/100 
      pyrs. Seven studies revealed 17,410 MI [2.5% (95% CI: 1.8%-3.4%)] in the control 
      group (n = 1,349,964). Meta-analysis of the seven longitudinal studies showed a 
      significant increase in MI [OR = 1.60 (95% CI: 1.32-1.93)] in AS patients. (2) 
      Stroke. In 11 longitudinal studies (n = 51,990), 1807 strokes were reported in AS 
      patients over 17.6 years of follow-up: incidence 3.6% (1.5%-6.5%), i.e., 0.24/100 
      pyrs. Three studies reported 22,899 strokes in controls (n = 1,239,041), giving 
      an incidence of 1.78% (1.75%-1.80%). A significant increase in stroke [OR = 1.50 
      (95% CI: 1.39-1.62)] in AS patients was found. CONCLUSION: AS patients appear to 
      have a higher risk of MI and stroke. Management of cardiovascular risk factors 
      and control of systemic inflammation should be taken into account in AS to 
      decrease this high cardiovascular risk.
CI  - Copyright © 2014 Elsevier Inc. All rights reserved.
FAU - Mathieu, Sylvain
AU  - Mathieu S
AD  - Rheumatology Department, Gabriel Montpied Teaching Hospital, 58 Rue Montalembert, 
      Clermont-Ferrand 63003, France; GenHotel-Auvergne, EA4679, Faculty of Medicine, 
      Clermont 1 University, Clermont-Ferrand, France. Electronic address: 
      smathieu@chu-clermontferrand.fr.
FAU - Pereira, Bruno
AU  - Pereira B
AD  - DRCI, Gabriel Montpied Teaching Hospital, Clermont-Ferrand, France.
FAU - Soubrier, Martin
AU  - Soubrier M
AD  - Rheumatology Department, Gabriel Montpied Teaching Hospital, 58 Rue Montalembert, 
      Clermont-Ferrand 63003, France.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Systematic Review
DEP - 20141018
PL  - United States
TA  - Semin Arthritis Rheum
JT  - Seminars in arthritis and rheumatism
JID - 1306053
SB  - IM
MH  - Cardiovascular Diseases/*epidemiology/*etiology
MH  - Humans
MH  - Incidence
MH  - Risk Factors
MH  - Spondylitis, Ankylosing/*complications
OTO - NOTNLM
OT  - Ankylosing spondylitis
OT  - Myocardial infarction
OT  - Stroke
EDAT- 2014/12/03 06:00
MHDA- 2016/04/07 06:00
CRDT- 2014/12/03 06:00
PHST- 2014/05/09 00:00 [received]
PHST- 2014/10/09 00:00 [revised]
PHST- 2014/10/10 00:00 [accepted]
PHST- 2014/12/03 06:00 [entrez]
PHST- 2014/12/03 06:00 [pubmed]
PHST- 2016/04/07 06:00 [medline]
AID - S0049-0172(14)00248-0 [pii]
AID - 10.1016/j.semarthrit.2014.10.007 [doi]
PST - ppublish
SO  - Semin Arthritis Rheum. 2015 Apr;44(5):551-555. doi: 
      10.1016/j.semarthrit.2014.10.007. Epub 2014 Oct 18.

PMID- 25446727
OWN - NLM
STAT- MEDLINE
DCOM- 20150720
LR  - 20220321
IS  - 1759-5053 (Electronic)
IS  - 1759-5045 (Linking)
VI  - 12
IP  - 1
DP  - 2015 Jan
TI  - Epidemiology, risk factors and management of cardiovascular diseases in IBD.
PG  - 26-35
LID - 10.1038/nrgastro.2014.202 [doi]
AB  - IBD is an established risk factor for venous thromboembolism. In the past few 
      years, studies have suggested that patients with IBD might also be at an 
      increased risk of coronary heart disease and stroke. The increased risk is 
      thought to be similar to the level of risk seen in patients with other chronic 
      systemic inflammatory diseases such as rheumatoid arthritis. The risk of 
      developing these conditions is particularly increased in young adults with IBD, 
      and more so in women than in men. Conventional cardiovascular risk factors are 
      not over-represented in patients with IBD, so the increased risk could be 
      attributable to inflammation-mediated atherosclerosis. Patients with IBD often 
      have premature atherosclerosis and have biochemical and genetic markers similar 
      to those seen in patients with atherosclerotic cardiovascular disease. The role 
      of chronic inflammation in IBD-associated cardiovascular disease merits further 
      evaluation. Particular attention should be given to the increased risk observed 
      during periods of increased disease activity and potential modification of the 
      risk by immunosuppressive and biologic therapies for IBD that can modify the 
      disease activity. In addition, preclinical studies suggest that cardiovascular 
      medications such as statins and angiotensin-converting enzyme inhibitors might 
      also favourably modify IBD disease activity, which warrants further evaluation.
FAU - Singh, Siddharth
AU  - Singh S
AD  - Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, 
      USA.
FAU - Kullo, Iftikhar J
AU  - Kullo IJ
AD  - Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA.
FAU - Pardi, Darrell S
AU  - Pardi DS
AD  - Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, 
      USA.
FAU - Loftus, Edward V Jr
AU  - Loftus EV Jr
AD  - Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, 
      USA.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20141202
PL  - England
TA  - Nat Rev Gastroenterol Hepatol
JT  - Nature reviews. Gastroenterology & hepatology
JID - 101500079
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - A74586SNO7 (Clopidogrel)
RN  - OM90ZUW7M1 (Ticlopidine)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
MH  - Aspirin/therapeutic use
MH  - Cardiovascular Diseases/epidemiology/genetics/prevention & control
MH  - Clopidogrel
MH  - Endothelium, Vascular/metabolism
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use
MH  - Inflammatory Bowel Diseases/*epidemiology/genetics
MH  - Platelet Aggregation Inhibitors/therapeutic use
MH  - Risk Factors
MH  - Ticlopidine/analogs & derivatives/therapeutic use
EDAT- 2014/12/03 06:00
MHDA- 2015/07/21 06:00
CRDT- 2014/12/03 06:00
PHST- 2014/12/03 06:00 [entrez]
PHST- 2014/12/03 06:00 [pubmed]
PHST- 2015/07/21 06:00 [medline]
AID - nrgastro.2014.202 [pii]
AID - 10.1038/nrgastro.2014.202 [doi]
PST - ppublish
SO  - Nat Rev Gastroenterol Hepatol. 2015 Jan;12(1):26-35. doi: 
      10.1038/nrgastro.2014.202. Epub 2014 Dec 2.

PMID- 25431465
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150831
LR  - 20161025
IS  - 1469-0756 (Electronic)
IS  - 0032-5473 (Linking)
VI  - 90
IP  - 1070
DP  - 2014 Dec
TI  - Republished: The association between inflammatory markers, serum lipids and the 
      risk of cardiovascular events in patients with rheumatoid arthritis.
PG  - 722-9
LID - 10.1136/postgradmedj-2013-204715rep [doi]
AB  - OBJECTIVE: To examine the association of serum inflammatory markers (erythrocyte 
      sedimentation rate (ESR) and C-reactive protein (CRP)) and serum lipid measures 
      (low-density lipoprotein (LDL)- and high-density lipoprotein (HDL)-cholesterol) 
      with risk of myocardial infarction (MI) and ischaemic stroke (IS) among 
      rheumatoid arthritis (RA) patients. METHODS: We conducted a retrospective cohort 
      study using 2005-2010 data from a US commercial health plan. Eligible patients 
      had two or more physician diagnoses of RA during a baseline period of at least 
      180 days with continuous medical and pharmacy coverage. We computed age-adjusted 
      incidence rates of MI and IS, and used spline regression to assess non-linear 
      associations and Cox-regression to quantify the independent association between 
      the laboratory values and the outcomes. RESULTS: We identified 44 418 eligible RA 
      patients (mean age 49 years; 76% women). CRP>10 mg/L compared with <1 mg/L was 
      associated with increased MI risk (HR 2.12; 95% CI 1.02 to 4.38). ESR>42 mm/h 
      compared with <14 mm/h was associated with increased risk of MI (HR 2.53; 95% CI 
      1.48 to 4.31) and IS (HR 2.51; 95% CI 1.33 to 4.75) risk. HDL-cholesterol 
      ≥60 mg/dL (1.6 mmol/L) compared with <40 mg/dL (1.0 mmol/L) was associated with 
      reduced MI risk (HR 0.37; 0.21 to 0.66). The association between LDL and MI was 
      not linear; the lowest risk was observed among patients with LDL between 70 mg/L 
      (1.8 mmol/L) and 100 mg/L (2.6 mmol/L). We did not observe a significant 
      association between LDL and IS. CONCLUSIONS: This study provides evidence 
      supporting the hypothesis that RA-related systemic inflammation plays a role in 
      determining cardiovascular risk and a complex relationship between LDL and 
      cardiovascular risk.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://group.bmj.com/group/rights-licensing/permissions.
FAU - Zhang, Jie
AU  - Zhang J
AD  - Division of Clinical Immunology and Rheumatology, University of Alabama at 
      Birmingham, Birmingham, Alabama, USA Department of Epidemiology, University of 
      Alabama at Birmingham, Birmingham, Alabama, USA.
FAU - Chen, Lang
AU  - Chen L
AD  - Division of Clinical Immunology and Rheumatology, University of Alabama at 
      Birmingham, Birmingham, Alabama, USA.
FAU - Delzell, Elizabeth
AU  - Delzell E
AD  - Department of Epidemiology, University of Alabama at Birmingham, Birmingham, 
      Alabama, USA.
FAU - Muntner, Paul
AU  - Muntner P
AD  - Department of Epidemiology, University of Alabama at Birmingham, Birmingham, 
      Alabama, USA.
FAU - Hillegass, William B
AU  - Hillegass WB
AD  - Division of Preventive Medicine, University of Alabama at Birmingham, Birmingham, 
      Alabama, USA.
FAU - Safford, Monika M
AU  - Safford MM
AD  - Division of Preventive Medicine, University of Alabama at Birmingham, Birmingham, 
      Alabama, USA.
FAU - Millan, Iris Yolanda Navarro
AU  - Millan IY
AD  - Division of Clinical Immunology and Rheumatology, University of Alabama at 
      Birmingham, Birmingham, Alabama, USA.
FAU - Crowson, Cynthia S
AU  - Crowson CS
AD  - Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AD  - Division of Clinical Immunology and Rheumatology, University of Alabama at 
      Birmingham, Birmingham, Alabama, USA Department of Epidemiology, University of 
      Alabama at Birmingham, Birmingham, Alabama, USA.
LA  - eng
GR  - R01 HS018517/HS/AHRQ HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Postgrad Med J
JT  - Postgraduate medical journal
JID - 0234135
RPF - Ann Rheum Dis. 2014 Jul;73(7):1301-8. doi: 10.1136/annrheumdis-2013-204715. PMID: 
      24796336
OTO - NOTNLM
OT  - Cardiovascular Disease
OT  - Epidemiology
OT  - Inflammation
OT  - Rheumatoid Arthritis
EDAT- 2014/11/29 06:00
MHDA- 2014/11/29 06:01
CRDT- 2014/11/29 06:00
PHST- 2014/11/29 06:00 [entrez]
PHST- 2014/11/29 06:00 [pubmed]
PHST- 2014/11/29 06:01 [medline]
AID - postgradmedj-2013-204715rep [pii]
AID - 10.1136/postgradmedj-2013-204715rep [doi]
PST - ppublish
SO  - Postgrad Med J. 2014 Dec;90(1070):722-9. doi: 
      10.1136/postgradmedj-2013-204715rep.

PMID- 25384055
OWN - NLM
STAT- MEDLINE
DCOM- 20160118
LR  - 20220310
IS  - 1528-1159 (Electronic)
IS  - 0362-2436 (Linking)
VI  - 40
IP  - 3
DP  - 2015 Feb 1
TI  - Rheumatoid arthritis-induced lateral atlantoaxial subluxation with multiple 
      vertebrobasilar infarctions.
PG  - E186-9
LID - 10.1097/BRS.0000000000000701 [doi]
AB  - STUDY DESIGN: Case report. OBJECTIVE: To highlight the probability that lateral 
      atlantoaxial subluxation (AAS) exists in patients with rheumatoid arthritis (RA) 
      and induces vertebrobasilar infarctions that are more foregrounded than 
      compressive myelopathy. SUMMARY OF BACKGROUND DATA: Although lateral subluxation 
      is a well-known subtype of AAS, a case of cerebral ischemia associated with 
      lateral AAS has not been reported before. METHODS: A 52-year-old male with a 
      6-year history of RA had a sudden onset of visual field defect and mild right 
      cerebellar ataxia. Head magnetic resonance imaging revealed acute multiple 
      infarctions in the vertebrobasilar area, and magnetic resonance angiography 
      revealed stenosis of the left vertebral artery (VA). Lateral radiograph of the 
      cervical spine in the neutral position revealed atlanto-occipital assimilation 
      and anterior AAS. T2-weighted sagittal images on cervical magnetic resonance 
      imaging revealed high signal intensity in the spinal cord at C1-C2. Cerebral 
      angiography revealed right VA occlusion and severe stenosis of the left V3 
      segment of VA. Three-dimensional computed tomography angiography of the 
      craniovertebral junction revealed lateral AAS, which was due to severe erosive 
      changes of the facet joints, and the left V3 portion was stenosed by a bony 
      component. During conservative therapy, the patient experienced left occulomotor 
      nerve palsy due to a second stroke. RESULTS: Two months later, the patient 
      underwent occipitocervical posterior fusion with an iliac bone graft. His 
      postoperative course was uneventful, and the left VA stenosis disappeared. At the 
      45-month follow-up, he had no further infarctions. Bony fusion was radiologically 
      confirmed, and 3-dimensional computed tomography angiography revealed good 
      patency of the affected left VA. CONCLUSION: In patients with RA, the potential 
      risk of AAS should be recognized. Lateral AAS in particular may induce cerebral 
      ischemia by positional VA occlusion in advanced stages of the disease. LEVEL OF 
      EVIDENCE: N/A.
FAU - Takeshima, Yasuhiro
AU  - Takeshima Y
AD  - From the Department of Neurosurgery, Nara Medical University School of Medicine, 
      Kashihara, Japan.
FAU - Matsuda, Ryosuke
AU  - Matsuda R
FAU - Hironaka, Yasuo
AU  - Hironaka Y
FAU - Motoyama, Yasushi
AU  - Motoyama Y
FAU - Nakase, Hiroyuki
AU  - Nakase H
LA  - eng
PT  - Case Reports
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Spine (Phila Pa 1976)
JT  - Spine
JID - 7610646
SB  - IM
MH  - Arthritis, Rheumatoid/*complications/surgery
MH  - Atlanto-Axial Joint/*injuries/surgery
MH  - Humans
MH  - Joint Dislocations/*etiology/surgery
MH  - Magnetic Resonance Angiography
MH  - Male
MH  - Middle Aged
MH  - Spinal Fusion
MH  - Treatment Outcome
MH  - Vertebrobasilar Insufficiency/*complications/surgery
MH  - Zygapophyseal Joint/surgery
EDAT- 2014/11/11 06:00
MHDA- 2016/01/19 06:00
CRDT- 2014/11/11 06:00
PHST- 2014/11/11 06:00 [entrez]
PHST- 2014/11/11 06:00 [pubmed]
PHST- 2016/01/19 06:00 [medline]
AID - 10.1097/BRS.0000000000000701 [doi]
PST - ppublish
SO  - Spine (Phila Pa 1976). 2015 Feb 1;40(3):E186-9. doi: 
      10.1097/BRS.0000000000000701.

PMID- 25354465
OWN - NLM
STAT- MEDLINE
DCOM- 20160329
LR  - 20181202
IS  - 1437-160X (Electronic)
IS  - 0172-8172 (Linking)
VI  - 35
IP  - 5
DP  - 2015 May
TI  - Risk of ischemic stroke in patients with polymyositis and dermatomyositis: a 
      systematic review and meta-analysis.
PG  - 905-9
LID - 10.1007/s00296-014-3166-0 [doi]
AB  - Several chronic inflammatory disorders, such as rheumatoid arthritis and systemic 
      lupus erythematosus, have been demonstrated to increase ischemic stroke risk, but 
      the data on polymyositis (PM) and dermatomyositis (DM) remain unclear. We 
      conducted a systematic review and meta-analysis of observational studies that 
      reported odds ratio, relative risk, hazard ratio or standardized incidence ratio 
      comparing ischemic risk in patients with PM/DM versus non-PM/DM participants. 
      Pooled risk ratio and 95 % confidence intervals were calculated using a 
      random-effect, generic inverse variance method of DerSimonian and Laird. Three 
      cohort studies were identified and included in our data analysis. The pooled risk 
      ratio of ischemic stroke in patients with PM/DM was 1.61 (95 % CI 1.28-2.02). The 
      statistical heterogeneity of this meta-analysis was insignificant with an I (2) 
      of 0 %. Our study demonstrated a statistically significant increased ischemic 
      stroke risk among patients with PM/DM.
FAU - Ungprasert, Patompong
AU  - Ungprasert P
AD  - Division of Rheumatology, Department of Medicine, Mayo Clinic, Rochester, MN, 
      USA, P.Ungprasert@gmail.com.
FAU - Cheungpasitporn, Wisit
AU  - Cheungpasitporn W
FAU - Wijarnpreecha, Karn
AU  - Wijarnpreecha K
FAU - Ahuja, Wasin
AU  - Ahuja W
FAU - Ratanasrimetha, Praveen
AU  - Ratanasrimetha P
FAU - Thongprayoon, Charat
AU  - Thongprayoon C
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Review
PT  - Systematic Review
DEP - 20141030
PL  - Germany
TA  - Rheumatol Int
JT  - Rheumatology international
JID - 8206885
SB  - IM
MH  - Brain Ischemia/complications/*epidemiology
MH  - Dermatomyositis/*epidemiology
MH  - Humans
MH  - Polymyositis/*epidemiology
MH  - Risk Factors
MH  - Stroke/*epidemiology/etiology
EDAT- 2014/10/31 06:00
MHDA- 2016/03/30 06:00
CRDT- 2014/10/31 06:00
PHST- 2014/07/21 00:00 [received]
PHST- 2014/10/24 00:00 [accepted]
PHST- 2014/10/31 06:00 [entrez]
PHST- 2014/10/31 06:00 [pubmed]
PHST- 2016/03/30 06:00 [medline]
AID - 10.1007/s00296-014-3166-0 [doi]
PST - ppublish
SO  - Rheumatol Int. 2015 May;35(5):905-9. doi: 10.1007/s00296-014-3166-0. Epub 2014 
      Oct 30.

PMID- 25351522
OWN - NLM
STAT- MEDLINE
DCOM- 20150316
LR  - 20220409
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Print)
IS  - 0003-4967 (Linking)
VI  - 74
IP  - 2
DP  - 2015 Feb
TI  - Risk of major cardiovascular events in patients with psoriatic arthritis, 
      psoriasis and rheumatoid arthritis: a population-based cohort study.
PG  - 326-32
LID - 10.1136/annrheumdis-2014-205675 [doi]
AB  - OBJECTIVES: We aimed to quantify the risk of major adverse cardiovascular events 
      (MACE) among patients with psoriatic arthritis (PsA), rheumatoid arthritis (RA) 
      and psoriasis without known PsA compared with the general population after 
      adjusting for traditional cardiovascular risk factors. METHODS: A 
      population-based longitudinal cohort study from 1994 to 2010 was performed in The 
      Health Improvement Network (THIN), a primary care medical record database in the 
      UK. Patients aged 18-89 years of age with PsA, RA or psoriasis were included. Up 
      to 10 unexposed controls matched on practice and index date were selected for 
      each patient with PsA. Outcomes included cardiovascular death, myocardial 
      infarction, cerebrovascular accidents and the composite outcome (MACE). Cox 
      proportional hazards models were used to calculate the HRs for each outcome 
      adjusted for traditional risk factors. A priori, we hypothesised an interaction 
      between disease status and disease-modifying antirheumatic drug (DMARD) use. 
      RESULTS: Patients with PsA (N=8706), RA (N=41 752), psoriasis (N=138 424) and 
      unexposed controls (N=81 573) were identified. After adjustment for traditional 
      risk factors, the risk of MACE was higher in patients with PsA not prescribed a 
      DMARD (HR 1.24, 95% CI 1.03 to 1.49), patients with RA (No DMARD: HR 1.39, 95% CI 
      1.28 to 1.50, DMARD: HR 1.58, 95% CI 1.46 to 1.70), patients with psoriasis not 
      prescribed a DMARD (HR 1.08, 95% CI 1.02 to 1.15) and patients with severe 
      psoriasis (DMARD users: HR 1.42, 95% CI 1.17 to 1.73). CONCLUSIONS: 
      Cardiovascular risk should be addressed with all patients affected by psoriasis, 
      PsA or RA.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://group.bmj.com/group/rights-licensing/permissions.
FAU - Ogdie, Alexis
AU  - Ogdie A
AD  - Division of Rheumatology, Center for Clinical Epidemiology and Biostatistics, 
      Center for Pharmacoepidemiology Research and Training, Perelman School of 
      Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA.
FAU - Yu, YiDing
AU  - Yu Y
AD  - Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA 
      Department of Population Medicine, Harvard Medical School, Boston, Massachusetts, 
      USA.
FAU - Haynes, Kevin
AU  - Haynes K
AD  - Center for Clinical Epidemiology and Biostatistics, Center for 
      Pharmacoepidemiology Research and Training, Department of Biostatistics and 
      Epidemiology, Perelman School of Medicine at the University of Pennsylvania, 
      Philadelphia, Pennsylvania, USA.
FAU - Love, Thorvardur Jon
AU  - Love TJ
AD  - University of Iceland, Reykjavik, Iceland.
FAU - Maliha, Samantha
AU  - Maliha S
AD  - New York University School of Medicine, New York, NY, USA.
FAU - Jiang, Yihui
AU  - Jiang Y
AD  - Division of Rheumatology, Perelman School of Medicine at the University of 
      Pennsylvania, Philadelphia, Pennsylvania, USA.
FAU - Troxel, Andrea B
AU  - Troxel AB
AD  - Center for Clinical Epidemiology and Biostatistics, Center for 
      Pharmacoepidemiology Research and Training, Department of Biostatistics and 
      Epidemiology, Perelman School of Medicine at the University of Pennsylvania, 
      Philadelphia, Pennsylvania, USA.
FAU - Hennessy, Sean
AU  - Hennessy S
AD  - Center for Clinical Epidemiology and Biostatistics, Center for 
      Pharmacoepidemiology Research and Training, Department of Biostatistics and 
      Epidemiology, Perelman School of Medicine at the University of Pennsylvania, 
      Philadelphia, Pennsylvania, USA.
FAU - Kimmel, Steven E
AU  - Kimmel SE
AD  - Department of Medicine, Center for Clinical Epidemiology and Biostatistics, 
      Center for Pharmacoepidemiology Research and Training, Center for Therapeutic 
      Effectiveness Research, Perelman School of Medicine at the University of 
      Pennsylvania, Philadelphia, Pennsylvania, USA.
FAU - Margolis, David J
AU  - Margolis DJ
AD  - Department of Dermatology, Center for Clinical Epidemiology and Biostatistics, 
      Center for Dermatoepidemiology and Translation, Perelman School of Medicine at 
      the University of Pennsylvania, Philadelphia, Pennsylvania, USA.
FAU - Choi, Hyon
AU  - Choi H
AD  - Section of Rheumatology and the Clinical Epidemiology Unit, Boston University 
      School of Medicine, Boston, Massachusetts, USA.
FAU - Mehta, Nehal N
AU  - Mehta NN
AD  - Section of Inflammation and Cardiometabolic Diseases, National Heart, Lung, and 
      Blood Institute, Bethesda, Maryland, USA.
FAU - Gelfand, Joel M
AU  - Gelfand JM
AD  - Department of Dermatology, Center for Clinical Epidemiology and Biostatistics, 
      Center for Dermatoepidemiology and Translation, Perelman School of Medicine at 
      the University of Pennsylvania, Philadelphia, Pennsylvania, USA Department of 
      Biostatistics and Epidemiology, Center for Clinical Epidemiology and 
      Biostatistics, Center for Pharmacoepidemiology Research and Training, Perelman 
      School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, 
      USA.
LA  - eng
GR  - K24AR064310/AR/NIAMS NIH HHS/United States
GR  - R01AG025152/AG/NIA NIH HHS/United States
GR  - K23AR063764/AR/NIAMS NIH HHS/United States
GR  - 8UL1TR000003/TR/NCATS NIH HHS/United States
GR  - UL1 TR000003/TR/NCATS NIH HHS/United States
GR  - K23 AR063764/AR/NIAMS NIH HHS/United States
GR  - K23HL097151-01/HL/NHLBI NIH HHS/United States
GR  - R01 AG025152/AG/NIA NIH HHS/United States
GR  - L30 AR060070/AR/NIAMS NIH HHS/United States
GR  - R01HL089744/HL/NHLBI NIH HHS/United States
GR  - R01 HL089744/HL/NHLBI NIH HHS/United States
GR  - K23 HL097151/HL/NHLBI NIH HHS/United States
GR  - K24 AR064310/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20141028
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Antirheumatic Agents)
SB  - IM
CIN - Ann Rheum Dis. 2015 Feb;74(2):321-2. doi: 10.1136/annrheumdis-2014-206617. PMID: 
      25429028
CIN - Cutis. 2019 Aug;104(2S):6. PMID: 31634383
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Psoriatic/*complications/drug therapy
MH  - Arthritis, Rheumatoid/complications/drug therapy
MH  - Cardiovascular Diseases/*epidemiology
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Proportional Hazards Models
MH  - Risk Factors
MH  - Young Adult
PMC - PMC4341911
MID - NIHMS665693
OTO - NOTNLM
OT  - Epidemiology
OT  - Outcomes research
OT  - Psoriatic Arthritis
OT  - Rheumatoid Arthritis
EDAT- 2014/10/30 06:00
MHDA- 2015/03/17 06:00
PMCR- 2015/06/01
CRDT- 2014/10/30 06:00
PHST- 2014/10/30 06:00 [entrez]
PHST- 2014/10/30 06:00 [pubmed]
PHST- 2015/03/17 06:00 [medline]
PHST- 2015/06/01 00:00 [pmc-release]
AID - annrheumdis-2014-205675 [pii]
AID - 10.1136/annrheumdis-2014-205675 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2015 Feb;74(2):326-32. doi: 10.1136/annrheumdis-2014-205675. Epub 
      2014 Oct 28.

PMID- 25342992
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20141024
LR  - 20211021
IS  - 1759-720X (Print)
IS  - 1759-7218 (Electronic)
IS  - 1759-720X (Linking)
VI  - 6
IP  - 4
DP  - 2014 Aug
TI  - Comparative evaluation of cardiovascular outcomes in patients with osteoarthritis 
      and rheumatoid arthritis on recommended doses of nonsteroidal anti-inflammatory 
      drugs.
PG  - 111-30
LID - 10.1177/1759720X14541668 [doi]
AB  - AIMS AND OBJECTIVES: We conducted an analysis to explore whether the 
      cardiovascular outcomes associated with nonsteroidal anti-inflammatory drugs 
      (NSAIDs), when used in licensed doses by patients with osteoarthritis or 
      rheumatoid arthritis, was class or compound dependent. METHODS: Using the Ovid 
      technology search engine, we conducted a search of the literature for relevant 
      studies published between 1995 and 2011. We also retrieved further studies 
      following manual searches. The primary endpoint was major vascular events and the 
      secondary endpoints were stroke, hypertension and congestive heart failure. A 
      total of 19 studies were analysed. Studies conducted in the osteoarthritis and 
      rheumatoid arthritis patients' population that reported on cardiovascular events 
      were included in the analysis. The analysis was conducted using the software 
      Review Manager 5.1 and Cochrane methodology. RESULTS: Using the primary endpoint 
      of major vascular events (MVE) and a prespecified cutoff point of 1.30, 
      diclofenac (versus 1 comparator) and rofecoxib (versus 2 comparators) had 
      increased risk for MVE [odds ratio (OR) >1.30]. Using the same criteria, 
      diclofenac (versus 1 comparator) had an increased risk of myocardial infarction 
      (MI). Although celecoxib had a slightly increased risk for MI (OR 1.33, versus 1 
      comparator), the confidence interval included 1 and was not significant. For the 
      secondary endpoints, etoricoxib and rofecoxib were significantly worse off for HT 
      (versus 1 comparator each) and naproxen was significantly worse off for stroke 
      (versus 1 comparator). Although ibuprofen was worse off for HT (versus 1 
      comparator) the increased risk was not significant. CONCLUSION: From the analysis 
      conducted, it appears that the risk for cardiovascular events in arthritis 
      patients on licensed doses of NSAIDs varies considerably and is likely to depend 
      on the individual compound.
FAU - Fabule, John
AU  - Fabule J
AD  - Astrazeneca - Global Medical Affairs, 2 Kingdom Street, London W2 6BD, UK.
FAU - Adebajo, Ade
AU  - Adebajo A
AD  - Academic Rheumatology Group, Faculty of Medicine, University of Sheffield and 
      Barnsley Hospital NHS Foundation Trust, Barnsley, UK.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Ther Adv Musculoskelet Dis
JT  - Therapeutic advances in musculoskeletal disease
JID - 101517322
PMC - PMC4206656
OTO - NOTNLM
OT  - NSAIDs
OT  - cardiovascular risk
OT  - nonsteroidal anti-inflammatory drugs
COIS- Conflict of interest statement: J.F. is an ex-employee of Pfizer Ltd and 
      currently works at Astrazeneca.
EDAT- 2014/10/25 06:00
MHDA- 2014/10/25 06:01
PMCR- 2014/08/01
CRDT- 2014/10/25 06:00
PHST- 2014/10/25 06:00 [entrez]
PHST- 2014/10/25 06:00 [pubmed]
PHST- 2014/10/25 06:01 [medline]
PHST- 2014/08/01 00:00 [pmc-release]
AID - 10.1177_1759720X14541668 [pii]
AID - 10.1177/1759720X14541668 [doi]
PST - ppublish
SO  - Ther Adv Musculoskelet Dis. 2014 Aug;6(4):111-30. doi: 10.1177/1759720X14541668.

PMID- 25336834
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20141022
LR  - 20211021
IS  - 0974-8237 (Print)
IS  - 0976-9285 (Electronic)
IS  - 0974-8237 (Linking)
VI  - 5
IP  - 3
DP  - 2014 Jul
TI  - Hemodynamic stroke: A rare pitfall in cranio cervical junction surgery.
PG  - 122-4
LID - 10.4103/0974-8237.142306 [doi]
AB  - Surgical C1C2-stabilization may be complicated by arterial-arterial embolism or 
      arterial injury. Another potential complication is hemodynamic stroke. The latter 
      might be induced in patients with poor posterior fossa collateralization (risk 
      factor 1) when the vertebral artery (VA) is compressed during reduction (risk 
      factor 2). We report a clinical case where this rare situation occurred: A 
      72-year old patient was undergoing C1C2-stabilization for subluxation due to 
      rheumatoid arthritis. Preoperative computed tomography angiography (CTA) had 
      shown poor collaterals in the posterior fossa. Furthermore, intraoperative 
      Doppler ultrasound (US) detected unilateral VA occlusion during reduction. It 
      appeared to be a high-risk situation for hemodynamic stroke. Surgical inspection 
      of the VA found osteofibrous compressing elements. Arterial decompression was 
      performed resulting in the normal flow as detected by US. Subsequently, 
      C1C2-stabilization could be realized. The clinical and radiological outcome was 
      very favorable. In C1C2-stabilization precise analysis of preoperative CTA and 
      intraoperative US are important to detect risk factors of hemodynamic stroke. 
      Using these data may prevent this rare, but potentially life-threatening 
      complication.
FAU - Cornelius, Jan Frederick
AU  - Cornelius JF
AD  - Department of Neurosurgery, University Hospital, Heinrich Heine University, 
      Düsseldorf, Germany.
FAU - Slotty, Philipp
AU  - Slotty P
AD  - Department of Neurosurgery, University Hospital, Heinrich Heine University, 
      Düsseldorf, Germany.
FAU - El Khatib, Mustafa
AU  - El Khatib M
AD  - Department of Neurosurgery, University Hospital, Heinrich Heine University, 
      Düsseldorf, Germany.
FAU - Bostelmann, Richard
AU  - Bostelmann R
AD  - Department of Neurosurgery, University Hospital, Heinrich Heine University, 
      Düsseldorf, Germany.
FAU - Hänggi, Daniel
AU  - Hänggi D
AD  - Department of Neurosurgery, University Hospital, Heinrich Heine University, 
      Düsseldorf, Germany.
FAU - Steiger, Hans Jakob
AU  - Steiger HJ
AD  - Department of Neurosurgery, University Hospital, Heinrich Heine University, 
      Düsseldorf, Germany.
LA  - eng
PT  - Journal Article
PL  - India
TA  - J Craniovertebr Junction Spine
JT  - Journal of craniovertebral junction & spine
JID - 101536746
PMC - PMC4201012
OTO - NOTNLM
OT  - Atlanto-axial instability
OT  - bow hunter's syndrome
OT  - cranio cervical junction
OT  - doppler ultrasound
OT  - skull base
OT  - vertebral artery
OT  - vertebro-basilar insufficiency
COIS- Conflict of Interest: None declared.
EDAT- 2014/10/23 06:00
MHDA- 2014/10/23 06:01
PMCR- 2014/07/01
CRDT- 2014/10/23 06:00
PHST- 2014/10/23 06:00 [entrez]
PHST- 2014/10/23 06:00 [pubmed]
PHST- 2014/10/23 06:01 [medline]
PHST- 2014/07/01 00:00 [pmc-release]
AID - JCVJS-5-122 [pii]
AID - 10.4103/0974-8237.142306 [doi]
PST - ppublish
SO  - J Craniovertebr Junction Spine. 2014 Jul;5(3):122-4. doi: 
      10.4103/0974-8237.142306.

PMID- 25266144
OWN - NLM
STAT- MEDLINE
DCOM- 20150217
LR  - 20141201
IS  - 1872-8421 (Electronic)
IS  - 0165-5728 (Linking)
VI  - 277
IP  - 1-2
DP  - 2014 Dec 15
TI  - The risk of ischemic stroke in major rheumatic disorders.
PG  - 1-5
LID - S0165-5728(14)00886-8 [pii]
LID - 10.1016/j.jneuroim.2014.09.009 [doi]
AB  - Rheumatic disorders (RD) are a range of conditions associated with inflammation 
      of joints and connective tissue. They can manifest beyond the musculoskeletal 
      system. Recent focus has been placed on the association of ischemic stroke with 
      these conditions. Traditional vascular risk factors seem to be more prevalent in 
      patients with certain types of RD than in the general population, but these 
      factors do not fully explain the enhanced vascular risk in this population. Four 
      major RD will be discussed in terms of their relationship with ischemic stroke: 
      rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, and 
      psoriatic arthritis.
CI  - Copyright © 2014 Elsevier B.V. All rights reserved.
FAU - Behrouz, Réza
AU  - Behrouz R
AD  - Division of Cerebrovascular Diseases and Neurosciences Critical Care, Department 
      of Neurology, The Ohio State University College of Medicine, Columbus, OH, USA. 
      Electronic address: Reza.Behrouz@osumc.edu.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20140922
PL  - Netherlands
TA  - J Neuroimmunol
JT  - Journal of neuroimmunology
JID - 8109498
SB  - IM
MH  - Animals
MH  - Humans
MH  - Ischemia/complications/epidemiology
MH  - Rheumatic Diseases/*epidemiology
MH  - Risk Factors
MH  - Stroke/*epidemiology/etiology
OTO - NOTNLM
OT  - Ankylosing spondylitis
OT  - Ischemic stroke
OT  - Psoriatic arthritis
OT  - Rheumatoid arthritis
OT  - Systemic lupus erythematosus
EDAT- 2014/10/01 06:00
MHDA- 2015/02/18 06:00
CRDT- 2014/10/01 06:00
PHST- 2014/07/16 00:00 [received]
PHST- 2014/09/12 00:00 [revised]
PHST- 2014/09/13 00:00 [accepted]
PHST- 2014/10/01 06:00 [entrez]
PHST- 2014/10/01 06:00 [pubmed]
PHST- 2015/02/18 06:00 [medline]
AID - S0165-5728(14)00886-8 [pii]
AID - 10.1016/j.jneuroim.2014.09.009 [doi]
PST - ppublish
SO  - J Neuroimmunol. 2014 Dec 15;277(1-2):1-5. doi: 10.1016/j.jneuroim.2014.09.009. 
      Epub 2014 Sep 22.

PMID- 25239880
OWN - NLM
STAT- MEDLINE
DCOM- 20150528
LR  - 20220408
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 54
IP  - 4
DP  - 2015 Apr
TI  - Red cell distribution width is associated with cardiovascular risk and disease 
      parameters in rheumatoid arthritis.
PG  - 641-6
LID - 10.1093/rheumatology/keu345 [doi]
AB  - OBJECTIVE: Since red cell distribution width (RDW) has been associated with 
      cardiovascular (CV) disease and inflammation in several conditions, the main aim 
      of this study was to evaluate its prognostic value in RA patients and its 
      potential associations with clinical features. METHODS: The history of CV events 
      was retrospectively reviewed in 160 RA patients and RDW was recorded at disease 
      onset and 6 and 12 months after diagnosis to calculate the accumulated value 
      [area under the curve (AUC) RDW] and change during the first year (ΔRDW). In 
      addition, RDW was analysed in 110 patients with established disease in relation 
      to clinical features. RESULTS: Increased RDW at diagnosis and AUC RDW were able 
      to predict the occurrence of CV events in RA patients [hazard ratio (HR) 1.247 
      (95% CI 1.079, 1.441), P = 0.003 and HR 1.038 (95% CI 1.018, 1.059), P = 0.0001, 
      respectively] after adjusting by potential confounding factors. Receiver 
      operating characteristic curve analyses revealed a better power of discrimination 
      for the AUC RDW (P = 3.394 × 10(-5)). In addition, an increase in RDW during the 
      first year was associated with poor CV outcome (P = 0.010). On the other hand, 
      RDW in patients with established RA was significantly associated with disease 
      activity, acute phase reactants and severity. CONCLUSION: RDW at disease onset 
      may be used as an early marker of CV risk in RA, whereas in patients with 
      established disease it was related to the activity of the disease. These findings 
      suggest that RDW can be considered as a surrogate marker of inflammation and, 
      consequently, CV risk in RA patients.
CI  - © The Author 2014. Published by Oxford University Press on behalf of the British 
      Society for Rheumatology. All rights reserved. For Permissions, please email: 
      journals.permissions@oup.com.
FAU - Rodríguez-Carrio, Javier
AU  - Rodríguez-Carrio J
AD  - Area of Immunology, Department of Functional Biology, University of Oviedo and 
      Department of Rheumatology, Hospital Universitario Central de Asturias, Oveido, 
      Spain.
FAU - Alperi-López, Mercedes
AU  - Alperi-López M
AD  - Area of Immunology, Department of Functional Biology, University of Oviedo and 
      Department of Rheumatology, Hospital Universitario Central de Asturias, Oveido, 
      Spain.
FAU - López, Patricia
AU  - López P
AD  - Area of Immunology, Department of Functional Biology, University of Oviedo and 
      Department of Rheumatology, Hospital Universitario Central de Asturias, Oveido, 
      Spain.
FAU - Alonso-Castro, Sara
AU  - Alonso-Castro S
AD  - Area of Immunology, Department of Functional Biology, University of Oviedo and 
      Department of Rheumatology, Hospital Universitario Central de Asturias, Oveido, 
      Spain.
FAU - Ballina-García, Francisco J
AU  - Ballina-García FJ
AD  - Area of Immunology, Department of Functional Biology, University of Oviedo and 
      Department of Rheumatology, Hospital Universitario Central de Asturias, Oveido, 
      Spain.
FAU - Suárez, Ana
AU  - Suárez A
AD  - Area of Immunology, Department of Functional Biology, University of Oviedo and 
      Department of Rheumatology, Hospital Universitario Central de Asturias, Oveido, 
      Spain. anasua@uniovi.es.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140918
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Area Under Curve
MH  - Arthritis, Rheumatoid/*blood/epidemiology
MH  - Cardiovascular Diseases/blood/epidemiology
MH  - *Erythrocyte Indices
MH  - Female
MH  - Heart Failure/*blood/epidemiology
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Ischemia/*blood/epidemiology
MH  - Proportional Hazards Models
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Stroke/*blood/epidemiology
MH  - Young Adult
OTO - NOTNLM
OT  - biomarker
OT  - cardiovascular disease
OT  - red cell distribution width
OT  - rheumatoid arthritis
EDAT- 2014/09/23 06:00
MHDA- 2015/05/29 06:00
CRDT- 2014/09/21 06:00
PHST- 2014/09/21 06:00 [entrez]
PHST- 2014/09/23 06:00 [pubmed]
PHST- 2015/05/29 06:00 [medline]
AID - keu345 [pii]
AID - 10.1093/rheumatology/keu345 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2015 Apr;54(4):641-6. doi: 10.1093/rheumatology/keu345. 
      Epub 2014 Sep 18.

PMID- 25220474
OWN - NLM
STAT- MEDLINE
DCOM- 20150528
LR  - 20140923
IS  - 1744-8344 (Electronic)
IS  - 1477-9072 (Linking)
VI  - 12
IP  - 10
DP  - 2014 Oct
TI  - Updates on NSAIDs in patients with and without coronary artery disease: pitfalls, 
      interactions and cardiovascular outcomes.
PG  - 1185-203
LID - 10.1586/14779072.2014.964687 [doi]
AB  - NSAIDs are used worldwide by more than 30 million people everyday, given their 
      anti-inflammatory, analgesic and antipyretic effects. NSAIDs are approved for 
      several common adult diseases, including acute and chronic musculoskeletal or 
      inflammatory disease, osteoarthritis, rheumatoid arthritis and other arthritic 
      conditions, as well as for children with juvenile idiopathic arthritis. 
      Importantly, the population commonly taking NSAIDs is that of older individuals 
      who also represent the population with the highest risk for cardiovascular (CV) 
      and gastrointestinal adverse effects. In recent years, a growing body of evidence 
      regarding potential risks from chronic use of NSAIDs has emerged. The aim of this 
      review is to update the available data concerning chronic use of NSAIDs in 
      patients with and without CV disease by analyzing the mechanisms of action, the 
      interference of specific NSAIDs with the established CV protective role of 
      low-dose aspirin, and the potential increased risk of myocardial infarction, 
      stroke, hypertension, heart failure and atrial fibrillation.
FAU - Gargiulo, Giuseppe
AU  - Gargiulo G
AD  - Division of Cardiology, Ferrarotto Hospital, University of Catania, Via Citelli 
      6, 95124 Catania, Italy.
FAU - Capodanno, Davide
AU  - Capodanno D
FAU - Longo, Giovanni
AU  - Longo G
FAU - Capranzano, Piera
AU  - Capranzano P
FAU - Tamburino, Corrado
AU  - Tamburino C
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20140915
PL  - England
TA  - Expert Rev Cardiovasc Ther
JT  - Expert review of cardiovascular therapy
JID - 101182328
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal/administration & dosage/*adverse effects
MH  - Aspirin/pharmacology/therapeutic use
MH  - Cardiovascular Diseases/*chemically induced/epidemiology/physiopathology
MH  - Coronary Artery Disease/*complications
MH  - Drug Interactions
MH  - Humans
MH  - Risk
OTO - NOTNLM
OT  - aspirin interaction
OT  - atrial fibrillation
OT  - cardiovascular disease
OT  - heart failure
OT  - hypertension
OT  - myocardial infarction
OT  - non-steroidal anti-inflammatory drugs
OT  - risk
OT  - stroke
EDAT- 2014/09/16 06:00
MHDA- 2015/05/29 06:00
CRDT- 2014/09/16 06:00
PHST- 2014/09/16 06:00 [entrez]
PHST- 2014/09/16 06:00 [pubmed]
PHST- 2015/05/29 06:00 [medline]
AID - 10.1586/14779072.2014.964687 [doi]
PST - ppublish
SO  - Expert Rev Cardiovasc Ther. 2014 Oct;12(10):1185-203. doi: 
      10.1586/14779072.2014.964687. Epub 2014 Sep 15.

PMID- 25213826
OWN - NLM
STAT- MEDLINE
DCOM- 20141231
LR  - 20221207
IS  - 1532-6500 (Electronic)
IS  - 1058-2746 (Linking)
VI  - 23
IP  - 11
DP  - 2014 Nov
TI  - Comparison of perioperative complications after total elbow arthroplasty in 
      patients with and without diabetes.
PG  - 1599-606
LID - S1058-2746(14)00347-4 [pii]
LID - 10.1016/j.jse.2014.06.045 [doi]
AB  - BACKGROUND: Few studies have analyzed the effect of diabetes on outcomes after 
      total elbow arthroplasty (TEA). We investigated the perioperative complications 
      after TEA in patients with and without diabetes. METHODS: We evaluated the 
      Nationwide Inpatient Sample (NIS) database from 2005 to 2010 for patients who 
      underwent a TEA. Our retrospective study included 3184 patients based on 
      International Classification of Diseases-Ninth Revision, Clinical Modification 
      codes. We compared outcomes in 488 patients with diabetes and in 2696 patients 
      without diabetes. RESULTS: Patients with diabetes had a significantly older mean 
      age (66.8 vs 58.5 years, P < .001). There was no statistically significant 
      difference when comparing length of stay (4.1 vs 3.7 days, P = .056) and cost of 
      surgery ($56,582 vs $56,092, P = .833). A significantly higher percentage of 
      diabetic patients underwent TEA for the indication of fracture (73.4% vs 65.3%), 
      but a lower percentage for rheumatoid arthritis (10.2% vs 19.2%). They also had 
      significantly increased rates of pneumonia (odds ratio [OR], 2.7), urinary tract 
      infection (OR, 2.2), blood transfusion (OR, 2.1), and nonroutine discharge (OR, 
      1.9). After adjusting for significantly increased rates of comorbidities in 
      diabetic patients, our multivariate analysis showed that having diabetes was 
      independently associated with an increased risk of pneumonia (relative risk [RR], 
      2.6), urinary tract infection (RR, 1.9), and cerebrovascular accident (RR, 9.1). 
      However, diabetes was not independently associated with hospital length of stay 
      (P = .75), after correction, hospital cost (P = .63), or proportion of routine 
      discharges (P = .12). CONCLUSION: Patients with diabetes have higher rates of 
      comorbidities and perioperative complications after TEA.
CI  - Copyright © 2014 Journal of Shoulder and Elbow Surgery Board of Trustees. 
      Published by Elsevier Inc. All rights reserved.
FAU - Toor, Aneet S
AU  - Toor AS
AD  - Department of Orthopaedic Surgery, University of Chicago Medical Center, Chicago, 
      IL, USA.
FAU - Jiang, Jimmy J
AU  - Jiang JJ
AD  - Department of Orthopaedic Surgery, University of Chicago Medical Center, Chicago, 
      IL, USA.
FAU - Shi, Lewis L
AU  - Shi LL
AD  - Department of Orthopaedic Surgery, University of Chicago Medical Center, Chicago, 
      IL, USA.
FAU - Koh, Jason L
AU  - Koh JL
AD  - Department of Orthopaedic Surgery, NorthShore University HealthSystem, Evanston, 
      IL, USA. Electronic address: kohj1@hotmail.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140909
PL  - United States
TA  - J Shoulder Elbow Surg
JT  - Journal of shoulder and elbow surgery
JID - 9206499
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthroplasty, Replacement, Elbow/*adverse effects/statistics & numerical data
MH  - Comorbidity
MH  - Databases, Factual
MH  - Diabetes Complications/epidemiology
MH  - Elbow Joint/*surgery
MH  - Female
MH  - Hospitalization/economics/statistics & numerical data
MH  - Humans
MH  - Joint Diseases/*surgery
MH  - Length of Stay/statistics & numerical data
MH  - Male
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Elbow Injuries
OTO - NOTNLM
OT  - Total elbow arthroplasty
OT  - complication
OT  - diabetes
OT  - perioperative outcome
EDAT- 2014/09/13 06:00
MHDA- 2015/01/01 06:00
CRDT- 2014/09/13 06:00
PHST- 2013/10/08 00:00 [received]
PHST- 2014/06/14 00:00 [revised]
PHST- 2014/06/19 00:00 [accepted]
PHST- 2014/09/13 06:00 [entrez]
PHST- 2014/09/13 06:00 [pubmed]
PHST- 2015/01/01 06:00 [medline]
AID - S1058-2746(14)00347-4 [pii]
AID - 10.1016/j.jse.2014.06.045 [doi]
PST - ppublish
SO  - J Shoulder Elbow Surg. 2014 Nov;23(11):1599-606. doi: 10.1016/j.jse.2014.06.045. 
      Epub 2014 Sep 9.

PMID- 25185440
OWN - NLM
STAT- MEDLINE
DCOM- 20150226
LR  - 20220331
IS  - 1468-2079 (Electronic)
IS  - 0007-1161 (Linking)
VI  - 98
IP  - 12
DP  - 2014 Dec
TI  - Prevalence and risk factors of dry eye disease in a British female cohort.
PG  - 1712-7
LID - 10.1136/bjophthalmol-2014-305201 [doi]
AB  - BACKGROUND/AIMS: To estimate the prevalence and risk factors of dry eye disease 
      (DED) in a female cohort in the UK. METHODS: Population-based cross-sectional 
      association study of 3824 women from the TwinsUK cohort aged 20-87 years. A 
      questionnaire was used to evaluate DED and several risk factors. Binary logistic 
      regression, corrected for age, was used to examine the association between DED 
      and risk factors. RESULTS: 9.6% of women had a DED diagnosis and concomitant use 
      of artificial tears, and 20.8% experienced DED symptoms in the past 3 months. 
      Risk factors that were significantly associated with DED were age, asthma, 
      eczema, the presence of any allergy, cataract surgery, rheumatoid arthritis, 
      osteoarthritis, migraine and stroke. The highest effect sizes were found with 
      depression, pelvic pain, irritable bowel syndrome and chronic widespread pain 
      syndrome (all p<0.0005). Subjects with DED symptoms scored significantly lower on 
      self-perceived health, compared with controls (p=0.001). CONCLUSIONS: DED is 
      common and increases with age within this cohort of female twins. We confirmed 
      established risk factors for the first time in a British population, and found 
      important risk factors that might relate to an underlying aetiology involving 
      chronic pain predisposition or somatisation.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://group.bmj.com/group/rights-licensing/permissions.
FAU - Vehof, Jelle
AU  - Vehof J
AD  - Department of Twin Research & Genetic Epidemiology, King's College London, St 
      Thomas' Hospital, London, UK Department of Ophthalmology & Epidemiology, 
      University Medical Center Groningen, Groningen, The Netherlands.
FAU - Kozareva, Diana
AU  - Kozareva D
AD  - Department of Twin Research & Genetic Epidemiology, King's College London, St 
      Thomas' Hospital, London, UK.
FAU - Hysi, Pirro G
AU  - Hysi PG
AD  - Department of Twin Research & Genetic Epidemiology, King's College London, St 
      Thomas' Hospital, London, UK.
FAU - Hammond, Christopher J
AU  - Hammond CJ
AD  - Department of Twin Research & Genetic Epidemiology, King's College London, St 
      Thomas' Hospital, London, UK Department of Ophthalmology, King's College London, 
      St Thomas' Hospital, London, UK.
LA  - eng
GR  - SRF/01/010/DH_/Department of Health/United Kingdom
GR  - WT_/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Twin Study
DEP - 20140903
PL  - England
TA  - Br J Ophthalmol
JT  - The British journal of ophthalmology
JID - 0421041
SB  - IM
CIN - BMJ. 2016 May 04;353:i2333. doi: 10.1136/bmj.i2333. PMID: 27146709
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Aging/physiology
MH  - Cohort Studies
MH  - Cross-Sectional Studies
MH  - Dry Eye Syndromes/diagnosis/*epidemiology
MH  - Female
MH  - Humans
MH  - Middle Aged
MH  - Prevalence
MH  - Registries
MH  - Risk Factors
MH  - Surveys and Questionnaires
MH  - United Kingdom/epidemiology
MH  - Women's Health/*statistics & numerical data
MH  - Young Adult
OTO - NOTNLM
OT  - Conjunctiva
OT  - Cornea
OT  - Epidemiology
OT  - Ocular surface
EDAT- 2014/09/05 06:00
MHDA- 2015/02/27 06:00
CRDT- 2014/09/05 06:00
PHST- 2014/09/05 06:00 [entrez]
PHST- 2014/09/05 06:00 [pubmed]
PHST- 2015/02/27 06:00 [medline]
AID - bjophthalmol-2014-305201 [pii]
AID - 10.1136/bjophthalmol-2014-305201 [doi]
PST - ppublish
SO  - Br J Ophthalmol. 2014 Dec;98(12):1712-7. doi: 10.1136/bjophthalmol-2014-305201. 
      Epub 2014 Sep 3.

PMID- 25184828
OWN - NLM
STAT- MEDLINE
DCOM- 20151130
LR  - 20220408
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 9
IP  - 9
DP  - 2014
TI  - Osteoprotegerin CGA haplotype protection against cerebrovascular complications in 
      anti-CCP negative patients with rheumatoid arthritis.
PG  - e106823
LID - 10.1371/journal.pone.0106823 [doi]
LID - e106823
AB  - INTRODUCTION: Rheumatoid arthritis is an inflammatory disease with high incidence 
      of cardiovascular disease due to accelerated atherosclerosis. Osteoprotegerin 
      (OPG) has been associated with increased risk of atherosclerotic disease in the 
      general population. Several polymorphisms in the OPG gene with functional effects 
      on cardiovascular disease in non-rheumatic individuals have been described. 
      Therefore, we aimed to analyze the effect of three of these functional OPG 
      polymorphisms on the risk of cardiovascular disease in a large and 
      well-characterized cohort of Spanish patients with rheumatoid arthritis. METHODS: 
      Three OPG gene variants (rs3134063, rs2073618 and rs3134069) were genotyped by 
      TaqMan assays in 2027 Spanish patients with rheumatoid arthritis. Anti-cyclic 
      citrullinated peptide (anti-CCP) antibody testing was positive in 997 of 1714 
      tested. Also, 18.3% of the whole series had experienced cardiovascular events, 
      including 5.4% with cerebrovascular accidents. The relationship between OPG 
      variants and cardiovascular events was assessed using Cox regression. RESULTS: No 
      association between OPG gene variants and cardiovascular disease was observed in 
      the whole group of rheumatoid arthritis patients or in anti-CCP positive 
      patients. Nevertheless, a protective effect of CGA haplotype on the risk of 
      cardiovascular disease in general, and specifically in the risk of 
      cerebrovascular complications after adjusting for sex, age at disease diagnosis 
      and traditional cardiovascular risk factors was disclosed in anti-CCP negative 
      patients (HR = 0.54; 95%CI: 0.31-0.95; p = 0.032 and HR = 0.17; 95%CI: 0.04-0.78; 
      p = 0.022, respectively). CONCLUSION: Our results indicate a protective effect of 
      the OPG CGA haplotype on cardiovascular risk, mainly due to a protective effect 
      against cerebrovascular events in anti-CCP negative rheumatoid arthritis 
      patients.
FAU - Genre, Fernanda
AU  - Genre F
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, IDIVAL, Santander, Spain.
FAU - López-Mejías, Raquel
AU  - López-Mejías R
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, IDIVAL, Santander, Spain.
FAU - García-Bermúdez, Mercedes
AU  - García-Bermúdez M
AD  - Instituto de Parasitología y Biomedicina López-Neyra, IPBLN-CSIC, Granada, Spain.
FAU - Castañeda, Santos
AU  - Castañeda S
AD  - Department of Rheumatology, Hospital Universitario la Princesa, IIS-Princesa, 
      Madrid, Spain.
FAU - González-Juanatey, Carlos
AU  - González-Juanatey C
AD  - Cardiology Division, Hospital Universitario Lucus Augusti, Lugo, Spain.
FAU - Llorca, Javier
AU  - Llorca J
AD  - Department of Epidemiology and Computational Biology, School of Medicine, 
      University of Cantabria, and CIBER Epidemiología y Salud Pública (CIBERESP), 
      IDIVAL, Santander, Spain.
FAU - Corrales, Alfonso
AU  - Corrales A
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, IDIVAL, Santander, Spain.
FAU - Ubilla, Begoña
AU  - Ubilla B
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, IDIVAL, Santander, Spain.
FAU - Miranda-Filloy, José A
AU  - Miranda-Filloy JA
AD  - Division of Rheumatology, Hospital Universitario Lucus Augusti, Lugo, Spain.
FAU - Pina, Trinitario
AU  - Pina T
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, IDIVAL, Santander, Spain.
FAU - Gómez-Vaquero, Carmen
AU  - Gómez-Vaquero C
AD  - Department of Rheumatology, Hospital Universitario Bellvitge, Barcelona, Spain.
FAU - Rodríguez-Rodríguez, Luis
AU  - Rodríguez-Rodríguez L
AD  - Department of Rheumatology, Hospital Clínico San Carlos, Madrid, Spain.
FAU - Fernández-Gutiérrez, Benjamín
AU  - Fernández-Gutiérrez B
AD  - Department of Rheumatology, Hospital Clínico San Carlos, Madrid, Spain.
FAU - Balsa, Alejandro
AU  - Balsa A
AD  - Department of Rheumatology, Hospital Universitario La Paz, Madrid, Spain.
FAU - Pascual-Salcedo, Dora
AU  - Pascual-Salcedo D
AD  - Department of Rheumatology, Hospital Universitario La Paz, Madrid, Spain.
FAU - López-Longo, Francisco J
AU  - López-Longo FJ
AD  - Department of Rheumatology, Hospital General Universitario Gregorio Marañón, 
      Madrid, Spain.
FAU - Carreira, Patricia
AU  - Carreira P
AD  - Department of Rheumatology, Hospital Universitario 12 de Octubre, Madrid, Spain.
FAU - Blanco, Ricardo
AU  - Blanco R
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, IDIVAL, Santander, Spain.
FAU - González-Álvaro, Isidoro
AU  - González-Álvaro I
AD  - Department of Rheumatology, Hospital Universitario la Princesa, IIS-Princesa, 
      Madrid, Spain.
FAU - Martín, Javier
AU  - Martín J
AD  - Instituto de Parasitología y Biomedicina López-Neyra, IPBLN-CSIC, Granada, Spain.
FAU - González-Gay, Miguel A
AU  - González-Gay MA
AD  - Epidemiology, Genetics and Atherosclerosis Research Group on Systemic 
      Inflammatory Diseases, Rheumatology Division, IDIVAL, Santander, Spain.
LA  - eng
PT  - Clinical Study
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20140903
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Autoantibodies)
RN  - 0 (Osteoprotegerin)
RN  - 0 (Peptides, Cyclic)
RN  - 0 (TNFRSF11B protein, human)
RN  - 0 (cyclic citrullinated peptide)
SB  - IM
MH  - Adult
MH  - Aged
MH  - *Arthritis, Rheumatoid/blood/complications/genetics
MH  - Autoantibodies/*blood
MH  - *Cerebrovascular Disorders/blood/etiology/genetics
MH  - Female
MH  - *Haplotypes
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Osteoprotegerin/*genetics
MH  - Peptides, Cyclic/blood
MH  - *Polymorphism, Single Nucleotide
MH  - Spain
PMC - PMC4153690
COIS- Competing Interests: This study was funded in part by grants from the European 
      IMI BTCure Program. This does not alter the authors’ adherence to PLOS ONE 
      policies on sharing data and materials.
EDAT- 2014/09/04 06:00
MHDA- 2015/12/15 06:00
PMCR- 2014/09/03
CRDT- 2014/09/04 06:00
PHST- 2014/05/23 00:00 [received]
PHST- 2014/08/01 00:00 [accepted]
PHST- 2014/09/04 06:00 [entrez]
PHST- 2014/09/04 06:00 [pubmed]
PHST- 2015/12/15 06:00 [medline]
PHST- 2014/09/03 00:00 [pmc-release]
AID - PONE-D-14-23093 [pii]
AID - 10.1371/journal.pone.0106823 [doi]
PST - epublish
SO  - PLoS One. 2014 Sep 3;9(9):e106823. doi: 10.1371/journal.pone.0106823. eCollection 
      2014.

PMID- 25180996
OWN - NLM
STAT- MEDLINE
DCOM- 20141030
LR  - 20140903
IS  - 1439-4413 (Electronic)
IS  - 0012-0472 (Linking)
VI  - 139
IP  - 37
DP  - 2014 Sep
TI  - [Safety of biologic therapy - results from the German biologics register RABBIT].
PG  - 1817-20
LID - 10.1055/s-0034-1370252 [doi]
FAU - Strangfeld, A
AU  - Strangfeld A
AD  - Programmbereich Epidemiologie, Deutsches Rheuma-Forschungszentrum Berlin.
FAU - Zink, A
AU  - Zink A
AD  - Programmbereich Epidemiologie, Deutsches Rheuma-Forschungszentrum Berlin.
LA  - ger
PT  - Journal Article
PT  - Review
TT  - Sicherheit unter Biologika - Ergebnisse aus dem deutschen Biologika-Register 
      RABBIT.
DEP - 20140902
PL  - Germany
TA  - Dtsch Med Wochenschr
JT  - Deutsche medizinische Wochenschrift (1946)
JID - 0006723
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Biological Products)
RN  - 0 (Glucocorticoids)
SB  - IM
MH  - Adverse Drug Reaction Reporting Systems
MH  - Antirheumatic Agents/adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy/mortality
MH  - Biological Products/*adverse effects/*therapeutic use
MH  - Comorbidity
MH  - Glucocorticoids/adverse effects/therapeutic use
MH  - Heart Failure/chemically induced/diagnosis
MH  - Humans
MH  - Myocardial Infarction/chemically induced/diagnosis
MH  - Neoplasms/chemically induced
MH  - Opportunistic Infections/etiology
MH  - *Registries
MH  - Risk
MH  - Stroke/chemically induced/diagnosis
MH  - Survival Analysis
EDAT- 2014/09/03 06:00
MHDA- 2014/10/31 06:00
CRDT- 2014/09/03 06:00
PHST- 2014/09/03 06:00 [entrez]
PHST- 2014/09/03 06:00 [pubmed]
PHST- 2014/10/31 06:00 [medline]
AID - 10.1055/s-0034-1370252 [doi]
PST - ppublish
SO  - Dtsch Med Wochenschr. 2014 Sep;139(37):1817-20. doi: 10.1055/s-0034-1370252. Epub 
      2014 Sep 2.

PMID- 25088171
OWN - NLM
STAT- MEDLINE
DCOM- 20151117
LR  - 20170908
IS  - 1532-8511 (Electronic)
IS  - 1052-3057 (Linking)
VI  - 23
IP  - 8
DP  - 2014 Sep
TI  - Efficacy of extracranial-intracranial bypass for progressive middle cerebral 
      artery occlusion associated with active Sjögren's syndrome: case report.
PG  - e399-e402
LID - S1052-3057(14)00111-6 [pii]
LID - 10.1016/j.jstrokecerebrovasdis.2014.02.022 [doi]
AB  - Sjögren syndrome affecting the major cerebral arteries is rare, and an optimal 
      therapeutic strategy to counteract such a lesion has not yet been established. We 
      herein report a case of a 39-year-old woman with a history of primary Sjögren 
      syndrome, which had previously been treated with immunosuppressive therapy, 
      manifesting with a crescendo transient ischemic attack because of left middle 
      cerebral artery stenosis. Despite the administration of high doses of 
      prednisolone and azathioprine for active Sjögren syndrome, the frequency of 
      crescendo transient ischemic attacks increased with the progression of stenosis 
      and magnetic resonance imaging showed the development of subacute cerebral 
      infarction. Single-photon emission computed tomography with 
      N-isopropyl[(123)I]-p-iodoamphetamine revealed apparent hemodynamic compromise in 
      the affected cerebral hemisphere. In light of the increased risk of further 
      progression of cerebral infarction, we decided to perform surgical 
      revascularization in spite of her active inflammatory condition. The patient 
      underwent extracranial-intracranial bypass without complications and was treated 
      with intensive immunosuppressive therapy during the perioperative period. Based 
      on our findings, we recommend surgical revascularization for occlusive 
      cerebrovascular disease with hemodynamic compromise in combination with intensive 
      immunosuppressive therapy, even in the active inflammatory state of autoimmune 
      diseases, if ischemic symptoms are medically uncontrollable.
CI  - Copyright © 2014 National Stroke Association. All rights reserved.
FAU - Sakata, Hiroyuki
AU  - Sakata H
AD  - Department of Neurosurgery, Tohoku University Graduate School of Medicine, 
      Sendai, Japan.
FAU - Fujimura, Miki
AU  - Fujimura M
AD  - Department of Neurosurgery, Tohoku University Graduate School of Medicine, 
      Sendai, Japan. Electronic address: fujimur@nsg.med.tohoku.ac.jp.
FAU - Sato, Kenichi
AU  - Sato K
AD  - Department of Neurosurgery, Tohoku University Graduate School of Medicine, 
      Sendai, Japan.
FAU - Shimizu, Hiroaki
AU  - Shimizu H
AD  - Department of Neurosurgery, Tohoku University Graduate School of Medicine, 
      Sendai, Japan.
FAU - Tominaga, Teiji
AU  - Tominaga T
AD  - Department of Neurosurgery, Tohoku University Graduate School of Medicine, 
      Sendai, Japan.
LA  - eng
PT  - Case Reports
PT  - Journal Article
DEP - 20140801
PL  - United States
TA  - J Stroke Cerebrovasc Dis
JT  - Journal of stroke and cerebrovascular diseases : the official journal of National 
      Stroke Association
JID - 9111633
RN  - 0 (Immunosuppressive Agents)
SB  - IM
MH  - Adult
MH  - Cerebral Infarction/*prevention & control
MH  - Cerebral Revascularization/*methods
MH  - Female
MH  - Humans
MH  - Immunosuppressive Agents/therapeutic use
MH  - Ischemic Attack, Transient/complications/diagnostic 
      imaging/etiology/pathology/*surgery
MH  - Magnetic Resonance Imaging
MH  - Middle Cerebral Artery/*pathology
MH  - Minimally Invasive Surgical Procedures
MH  - Neurosurgical Procedures/methods
MH  - Sjogren's Syndrome/*complications/drug therapy
MH  - Tomography, Emission-Computed, Single-Photon
MH  - Treatment Outcome
OTO - NOTNLM
OT  - Sjögren's syndrome
OT  - cerebral artery occlusion
OT  - cerebral infarction
OT  - immunosuppressive therapy
EDAT- 2014/08/05 06:00
MHDA- 2015/11/18 06:00
CRDT- 2014/08/05 06:00
PHST- 2013/12/25 00:00 [received]
PHST- 2014/02/20 00:00 [revised]
PHST- 2014/02/26 00:00 [accepted]
PHST- 2014/08/05 06:00 [entrez]
PHST- 2014/08/05 06:00 [pubmed]
PHST- 2015/11/18 06:00 [medline]
AID - S1052-3057(14)00111-6 [pii]
AID - 10.1016/j.jstrokecerebrovasdis.2014.02.022 [doi]
PST - ppublish
SO  - J Stroke Cerebrovasc Dis. 2014 Sep;23(8):e399-e402. doi: 
      10.1016/j.jstrokecerebrovasdis.2014.02.022. Epub 2014 Aug 1.

PMID- 25048420
OWN - NLM
STAT- MEDLINE
DCOM- 20170911
LR  - 20181202
IS  - 2041-1626 (Electronic)
IS  - 2041-1618 (Linking)
VI  - 7
IP  - 1
DP  - 2016 Feb
TI  - Association between indices of clinically-defined periodontitis and self-reported 
      history of systemic medical conditions.
PG  - 27-36
LID - 10.1111/jicd.12119 [doi]
AB  - AIM: The aim of the current research was to investigate whether possible 
      associations exist between indices of clinically-defined periodontitis and 
      several systemic medical conditions in outpatients referred to a special hospital 
      clinic. METHODS: The study sample consisted of 3360 outpatients aged 45-65 years. 
      Data were collected by means of an oral clinical examination and a 
      self-administered questionnaire. Statistical analysis of the questionnaire items 
      was done with Fisher's exact test and the logistic regression model to assess 
      possible associations between systemic medical conditions as independent 
      variables, and the relative frequency of periodontal pockets ≥5 mm and clinical 
      attachment loss (CAL) of ≥6 mm as dependent variables. RESULTS: The depth of 
      periodontal pockets was significantly associated with male sex, the presence of 
      vascular disease, hypertension, stroke, heart attack, diabetes mellitus, other 
      endocrine diseases, thyroid disease, respiratory allergies, and rheumatoid 
      arthritis. CAL was significantly associated with the mentioned conditions, and 
      also infective endocarditis and chronic obstructive pulmonary disease, but not 
      other endocrine and thyroid disease. CONCLUSIONS: The findings confirm the 
      results from previous investigations in which a number of systemic medical 
      conditions were significantly associated with probing pocket depth and/or CAL.
CI  - © 2014 Wiley Publishing Asia Pty Ltd.
FAU - Chrysanthakopoulos, Nikolaos A
AU  - Chrysanthakopoulos NA
AD  - Department of Pathological Anatomy, Medical School, University of Athens, Athens, 
      Greece.
FAU - Chrysanthakopoulos, Panagiotis A
AU  - Chrysanthakopoulos PA
AD  - Department of Neurosurgery, Military Hospital of Athens, Athens, Greece.
LA  - eng
PT  - Journal Article
DEP - 20140722
PL  - Australia
TA  - J Investig Clin Dent
JT  - Journal of investigative and clinical dentistry
JID - 101524471
SB  - IM
MH  - Aged
MH  - *Chronic Disease
MH  - Diabetes Mellitus
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Periodontal Pocket
MH  - Periodontitis/*complications
MH  - Self Report
OTO - NOTNLM
OT  - clinical attachment loss
OT  - periodontal disease
OT  - pocket depth
OT  - risk factor
OT  - systemic condition
EDAT- 2014/07/23 06:00
MHDA- 2017/09/12 06:00
CRDT- 2014/07/23 06:00
PHST- 2014/03/01 00:00 [received]
PHST- 2014/05/29 00:00 [accepted]
PHST- 2014/07/23 06:00 [entrez]
PHST- 2014/07/23 06:00 [pubmed]
PHST- 2017/09/12 06:00 [medline]
AID - 10.1111/jicd.12119 [doi]
PST - ppublish
SO  - J Investig Clin Dent. 2016 Feb;7(1):27-36. doi: 10.1111/jicd.12119. Epub 2014 Jul 
      22.

PMID- 24928341
OWN - NLM
STAT- MEDLINE
DCOM- 20161007
LR  - 20211021
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 35
IP  - 1
DP  - 2016 Jan
TI  - The impact of inflammatory rheumatic diseases on the presentation, severity, and 
      outcome of acute coronary syndrome.
PG  - 233-7
LID - 10.1007/s10067-014-2695-y [doi]
AB  - Patients with inflammatory rheumatic diseases (IRD) have a high burden of 
      cardiovascular disease (CVD), leading to increased mortality and morbidity. 
      However, it is not clear whether increased CVD mortality in IRD is due to a 
      higher incidence or worse outcome of cardiovascular events (higher case 
      fatality). In this observational case-control study, we assessed the outcome of 
      acute coronary syndrome (ACS) in patients with IRDs compared to matched controls 
      without IRD, using data from the Acute Coronary Syndrome Israeli Survey (ACSIS), 
      a large, national, real-life registry detailing the extent, severity, and outcome 
      of ACS. Of 2,193 subjects enrolled to the ACSIS, 20 (nine men) were identified 
      with IRD, including 11 patients with rheumatoid arthritis, five patients with 
      systemic lupus erythematosus (SLE), three patients with ankylosing spondylitis 
      (AS), and one patient with psoriatic arthritis (PsA). The study patients were 
      compared to 120 matched control patients (adjusted for age and risk factors for 
      CVD) without IRD. Compared to controls, IRD patients had similar clinical 
      presentation and similar type of ACS and received identical initial treatment at 
      the ER. The two groups had comparable rates of complications including major 
      adverse cardiovascular events (death, recurrent myocardial infarction, stroke, 
      major bleeding, and definite stent thrombosis) (10 vs. 11.7% in the study and 
      control group, respectively, p > 0.05), re-hospitalization (20 vs. 21.1%, 
      respectively, p > 0.05), and severe congestive heart failure (7.7 vs. 6.9%, 
      respectively, p > 0.05) within 30 days. The outcome and prognosis of ACS in 
      patients with IRD is not worse than that of control, supporting the higher 
      prevalence of CVD in this population as the cause for their excess mortality.
FAU - Ben-Zvi, Ilan
AU  - Ben-Zvi I
AD  - Department of Medicine F and the Rheumatology Unit, Sheba Medical Center, Tel 
      Hashomer, Israel. Ilan.BenZvi@sheba.health.gov.il.
AD  - Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. 
      Ilan.BenZvi@sheba.health.gov.il.
AD  - The Dr. Pinchas Borenstein Talpiot Medical Leadership Program 2012, Chaim Sheba 
      Medical Center, Tel Hashomer, Israel. Ilan.BenZvi@sheba.health.gov.il.
FAU - Goldenberg, Ilan
AU  - Goldenberg I
AD  - Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
AD  - The Leviev Heart Institute, Sheba Medical Center, Tel Hashomer, Israel.
AD  - Neufeld Cardiac Research Institute, Sackler School of Medicine, Tel Aviv 
      University, Tel Aviv, Israel.
FAU - Matetzky, Shlomi
AU  - Matetzky S
AD  - Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
AD  - The Leviev Heart Institute, Sheba Medical Center, Tel Hashomer, Israel.
AD  - Neufeld Cardiac Research Institute, Sackler School of Medicine, Tel Aviv 
      University, Tel Aviv, Israel.
FAU - Grossman, Chagai
AU  - Grossman C
AD  - Department of Medicine F and the Rheumatology Unit, Sheba Medical Center, Tel 
      Hashomer, Israel.
FAU - Elis, Avishay
AU  - Elis A
AD  - Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
AD  - Department of Medicine, Rabin Medical Center, Beilinson Campus, Petah-Tikva, 
      Israel.
FAU - Gavrielov-Yusim, Natalie
AU  - Gavrielov-Yusim N
AD  - Neufeld Cardiac Research Institute, Sackler School of Medicine, Tel Aviv 
      University, Tel Aviv, Israel.
FAU - Livneh, Avi
AU  - Livneh A
AD  - Department of Medicine F and the Rheumatology Unit, Sheba Medical Center, Tel 
      Hashomer, Israel.
AD  - Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
LA  - eng
PT  - Journal Article
PT  - Observational Study
DEP - 20140615
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
SB  - IM
MH  - Acute Coronary Syndrome/*epidemiology
MH  - Aged
MH  - Arthritis, Psoriatic/*complications
MH  - Arthritis, Rheumatoid/*complications
MH  - Case-Control Studies
MH  - Female
MH  - Heart Failure/epidemiology
MH  - Humans
MH  - Israel/epidemiology
MH  - Lupus Erythematosus, Systemic/*complications
MH  - Male
MH  - Middle Aged
MH  - Patient Readmission/statistics & numerical data
MH  - Prognosis
MH  - Registries
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Spondylitis, Ankylosing/*complications
OTO - NOTNLM
OT  - Cardiovascular
OT  - Coronary syndrome
OT  - Inflammation
OT  - Rheumatoid arthritis
EDAT- 2014/06/15 06:00
MHDA- 2016/10/08 06:00
CRDT- 2014/06/15 06:00
PHST- 2014/05/15 00:00 [received]
PHST- 2014/05/23 00:00 [accepted]
PHST- 2014/06/15 06:00 [entrez]
PHST- 2014/06/15 06:00 [pubmed]
PHST- 2016/10/08 06:00 [medline]
AID - 10.1007/s10067-014-2695-y [pii]
AID - 10.1007/s10067-014-2695-y [doi]
PST - ppublish
SO  - Clin Rheumatol. 2016 Jan;35(1):233-7. doi: 10.1007/s10067-014-2695-y. Epub 2014 
      Jun 15.

PMID- 24922069
OWN - NLM
STAT- MEDLINE
DCOM- 20150129
LR  - 20220408
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 9
IP  - 6
DP  - 2014
TI  - Platelet activation and anti-phospholipid antibodies collaborate in the 
      activation of the complement system on platelets in systemic lupus erythematosus.
PG  - e99386
LID - 10.1371/journal.pone.0099386 [doi]
LID - e99386
AB  - Anti-phospholipid (aPL) antibodies are important contributors to development of 
      thrombosis in patients with the autoimmune rheumatic disease systemic lupus 
      erythematosus (SLE). The underlying mechanism of aPL antibody-mediated thrombosis 
      is not fully understood but existing data suggest that platelets and the 
      complement system are key components. Complement activation on platelets is seen 
      in SLE patients, especially in patients with aPL antibodies, and has been related 
      to venous thrombosis and stroke. The aim of this study was to investigate if aPL 
      antibodies could support classical pathway activation on platelets in vitro as 
      well as in SLE patients. Furthermore, we investigated if complement deposition on 
      platelets was associated with vascular events, either arterial or venous, when 
      the data had been adjusted for traditional cardiovascular risk factors. Finally, 
      we analyzed if platelet complement deposition, both C1q and C4d, was specific for 
      SLE. We found that aPL antibodies supported C4d deposition on platelets in vitro 
      as well as in SLE patients (p = 0.001 and p<0.05, respectively). Complement 
      deposition on platelets was increased in SLE patients when compared with healthy 
      individuals (p<0.0001). However, high levels of C4d deposition and a pronounced 
      C1q deposition were also seen in patients with rheumatoid arthritis and systemic 
      sclerosis. In SLE, C4d deposition on platelets was associated with platelet 
      activation, complement consumption, disease activity and venous (OR = 5.3, 
      p = 0.02), but not arterial, thrombosis, observations which were independent of 
      traditional cardiovascular risk factors. In conclusion, several mechanisms 
      operate in SLE to amplify platelet complement deposition, of which aPL antibodies 
      and platelet activation were identified as important contributors in this 
      investigation. Complement deposition on platelets was identified as a marker of 
      venous, but not arterial thrombosis, in SLE patients independently of traditional 
      risk factors and aPL antibodies. Further studies are needed to elucidate the role 
      of complement deposition on platelets in development of venous thrombosis.
FAU - Lood, Christian
AU  - Lood C
AD  - Department of Clinical Sciences Lund, Section of Rheumatology, Lund University 
      and Skåne University Hospital, Lund, Sweden.
FAU - Tydén, Helena
AU  - Tydén H
AD  - Department of Clinical Sciences Lund, Section of Rheumatology, Lund University 
      and Skåne University Hospital, Lund, Sweden.
FAU - Gullstrand, Birgitta
AU  - Gullstrand B
AD  - Department of Laboratory Medicine Lund, Section of Microbiology, Immunology and 
      Glycobiology, Lund University, Lund, Sweden.
FAU - Sturfelt, Gunnar
AU  - Sturfelt G
AD  - Department of Clinical Sciences Lund, Section of Rheumatology, Lund University 
      and Skåne University Hospital, Lund, Sweden.
FAU - Jönsen, Andreas
AU  - Jönsen A
AD  - Department of Clinical Sciences Lund, Section of Rheumatology, Lund University 
      and Skåne University Hospital, Lund, Sweden.
FAU - Truedsson, Lennart
AU  - Truedsson L
AD  - Department of Laboratory Medicine Lund, Section of Microbiology, Immunology and 
      Glycobiology, Lund University, Lund, Sweden.
FAU - Bengtsson, Anders A
AU  - Bengtsson AA
AD  - Department of Clinical Sciences Lund, Section of Rheumatology, Lund University 
      and Skåne University Hospital, Lund, Sweden.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140612
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antibodies, Antiphospholipid)
RN  - 0 (Cardiolipins)
RN  - 0 (Peptide Fragments)
RN  - 80295-50-7 (Complement C4b)
RN  - 80295-52-9 (complement C4d)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Antibodies, Antiphospholipid/*immunology
MH  - Blood Platelets/*immunology
MH  - Cardiolipins/immunology
MH  - Complement Activation/*immunology
MH  - Complement C4b/immunology
MH  - Female
MH  - Humans
MH  - Lupus Erythematosus, Systemic/*blood/*immunology
MH  - Male
MH  - Middle Aged
MH  - Peptide Fragments/immunology
MH  - Platelet Activation/*immunology
MH  - Risk Factors
MH  - Thrombosis/blood/immunology
MH  - Young Adult
PMC - PMC4055750
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2014/06/13 06:00
MHDA- 2015/01/30 06:00
PMCR- 2014/06/12
CRDT- 2014/06/13 06:00
PHST- 2014/01/20 00:00 [received]
PHST- 2014/05/14 00:00 [accepted]
PHST- 2014/06/13 06:00 [entrez]
PHST- 2014/06/13 06:00 [pubmed]
PHST- 2015/01/30 06:00 [medline]
PHST- 2014/06/12 00:00 [pmc-release]
AID - PONE-D-14-02789 [pii]
AID - 10.1371/journal.pone.0099386 [doi]
PST - epublish
SO  - PLoS One. 2014 Jun 12;9(6):e99386. doi: 10.1371/journal.pone.0099386. eCollection 
      2014.

PMID- 24898360
OWN - NLM
STAT- MEDLINE
DCOM- 20151112
LR  - 20211021
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 4
DP  - 2014 Jun 5
TI  - Risk of stroke in patients with rheumatism: a nationwide longitudinal 
      population-based study.
PG  - 5110
LID - 10.1038/srep05110 [doi]
LID - 5110
AB  - The aim of this study was to investigate rheumatoid arthritis (RA), and systemic 
      lupus erythematous (SLE) as risk factors for stroke. The study was analyzed by 
      Using the Taiwan Longitudinal Health Insurance Database 2005 (LHID2005), this 
      cohort study investigated patients with a recorded diagnosis of RA (N = 6114), 
      and SLE (N = 621) between January 1, 2004, and December 31, 2007, with 
      age-matched controls (1:4) (for RA, N = 24456; SLE, N = 2484). We used Cox 
      proportional-hazard regressions to evaluate the hazard ratios (HRs) after 
      adjusting confounding factors. Our study found 383 of 6114 RA patients, 
      experienced stroke during the 20267 person-year follow-up period. The adjusted HR 
      of stroke for RA patients was 1.24 (95% CI, 1.11 to 1.39), and for SLE patients 
      was 1.88 (95% CI, 1.08 to 3.27). When steroid was added as additional confounding 
      factor, the adjusted HR of ischemic stroke for RA patients was 1.32 (95% CI, 1.15 
      to 1.50), and for SLE patients was 1.31 (95% CI, 0.51 to 3.34). In conclusion, 
      the rheumatic diseases of RA, and SLE are all risk factors for stroke. After 
      controlled the effect of steroid prescription, RA is risk factor for ischemic 
      stroke.
FAU - Liou, Tsan-Hon
AU  - Liou TH
AD  - 1] Department of Physical Medicine and Rehabilitation, Shuang Ho Hospital, Taipei 
      Medical University, Taipei, Taiwan [2] Graduate Institute of Injury Prevention 
      and Control, Taipei Medical University, Taipei, Taiwan [3].
FAU - Huang, Shih-Wei
AU  - Huang SW
AD  - 1] Department of Physical Medicine and Rehabilitation, Shuang Ho Hospital, Taipei 
      Medical University, Taipei, Taiwan [2].
FAU - Lin, Jia-Wei
AU  - Lin JW
AD  - 1] Department of Neurosurgery, Shuang Ho Hospital, Taipei Medical University, 
      Taipei, Taiwan [2] Graduate Institute of Clinical Medicine, Collage of Medicine, 
      Taipei Medical University, Taipei, Taiwan.
FAU - Chang, Yu-Sheng
AU  - Chang YS
AD  - Department of Rheumatology, Shuang Ho Hospital, Taipei Medical University, 
      Taipei, Taiwan.
FAU - Wu, Chin-Wen
AU  - Wu CW
AD  - Department of Physical Medicine and Rehabilitation, Shuang Ho Hospital, Taipei 
      Medical University, Taipei, Taiwan.
FAU - Lin, Hui-Wen
AU  - Lin HW
AD  - 1] Department of Mathematics, Soochow University, Taipei, Taiwan [2] 
      Evidence-Based Medicine Center, Wan Fang Hospital, Taipei Medical University, 
      Taipei, Taiwan.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140605
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
SB  - IM
MH  - Adult
MH  - Aged
MH  - Case-Control Studies
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Rheumatic Diseases/*complications/epidemiology
MH  - Risk Factors
MH  - Stroke/epidemiology/*etiology
MH  - Taiwan/epidemiology
PMC - PMC4046260
EDAT- 2014/06/06 06:00
MHDA- 2015/11/13 06:00
PMCR- 2014/06/05
CRDT- 2014/06/06 06:00
PHST- 2014/01/20 00:00 [received]
PHST- 2014/05/13 00:00 [accepted]
PHST- 2014/06/06 06:00 [entrez]
PHST- 2014/06/06 06:00 [pubmed]
PHST- 2015/11/13 06:00 [medline]
PHST- 2014/06/05 00:00 [pmc-release]
AID - srep05110 [pii]
AID - 10.1038/srep05110 [doi]
PST - epublish
SO  - Sci Rep. 2014 Jun 5;4:5110. doi: 10.1038/srep05110.

PMID- 24796336
OWN - NLM
STAT- MEDLINE
DCOM- 20140818
LR  - 20220408
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 73
IP  - 7
DP  - 2014 Jul
TI  - The association between inflammatory markers, serum lipids and the risk of 
      cardiovascular events in patients with rheumatoid arthritis.
PG  - 1301-8
LID - 10.1136/annrheumdis-2013-204715 [doi]
AB  - OBJECTIVE: To examine the association of serum inflammatory markers (erythrocyte 
      sedimentation rate (ESR) and C-reactive protein (CRP)) and serum lipid measures 
      (low-density lipoprotein (LDL)- and high-density lipoprotein (HDL)-cholesterol) 
      with risk of myocardial infarction (MI) and ischaemic stroke (IS) among 
      rheumatoid arthritis (RA) patients. METHODS: We conducted a retrospective cohort 
      study using 2005-2010 data from a US commercial health plan. Eligible patients 
      had two or more physician diagnoses of RA during a baseline period of at least 
      180 days with continuous medical and pharmacy coverage. We computed age-adjusted 
      incidence rates of MI and IS, and used spline regression to assess non-linear 
      associations and Cox-regression to quantify the independent association between 
      the laboratory values and the outcomes. RESULTS: We identified 44 418 eligible RA 
      patients (mean age 49 years; 76% women). CRP>10 mg/L compared with <1 mg/L was 
      associated with increased MI risk (HR 2.12; 95% CI 1.02 to 4.38). ESR>42 mm/h 
      compared with <14 mm/h was associated with increased risk of MI (HR 2.53; 95% CI 
      1.48 to 4.31) and IS (HR 2.51; 95% CI 1.33 to 4.75) risk. HDL-cholesterol ≥60 
      mg/dL (1.6 mmol/L) compared with <40 mg/dL (1.0 mmol/L) was associated with 
      reduced MI risk (HR 0.37; 0.21 to 0.66). The association between LDL and MI was 
      not linear; the lowest risk was observed among patients with LDL between 70 mg/L 
      (1.8 mmol/L) and 100 mg/L (2.6 mmol/L). We did not observe a significant 
      association between LDL and IS. CONCLUSIONS: This study provides evidence 
      supporting the hypothesis that RA-related systemic inflammation plays a role in 
      determining cardiovascular risk and a complex relationship between LDL and 
      cardiovascular risk.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://group.bmj.com/group/rights-licensing/permissions.
FAU - Zhang, Jie
AU  - Zhang J
AD  - Division of Clinical Immunology and Rheumatology, University of Alabama at 
      Birmingham, Birmingham, Alabama, USA Department of Epidemiology, University of 
      Alabama at Birmingham, Birmingham, Alabama, USA.
FAU - Chen, Lang
AU  - Chen L
AD  - Division of Clinical Immunology and Rheumatology, University of Alabama at 
      Birmingham, Birmingham, Alabama, USA.
FAU - Delzell, Elizabeth
AU  - Delzell E
AD  - Department of Epidemiology, University of Alabama at Birmingham, Birmingham, 
      Alabama, USA.
FAU - Muntner, Paul
AU  - Muntner P
AD  - Department of Epidemiology, University of Alabama at Birmingham, Birmingham, 
      Alabama, USA.
FAU - Hillegass, William B
AU  - Hillegass WB
AD  - Division of Preventive Medicine, University of Alabama at Birmingham, Birmingham, 
      Alabama, USA.
FAU - Safford, Monika M
AU  - Safford MM
AD  - Division of Preventive Medicine, University of Alabama at Birmingham, Birmingham, 
      Alabama, USA.
FAU - Millan, Iris Yolanda Navarro
AU  - Millan IY
AD  - Division of Clinical Immunology and Rheumatology, University of Alabama at 
      Birmingham, Birmingham, Alabama, USA.
FAU - Crowson, Cynthia S
AU  - Crowson CS
AD  - Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA.
FAU - Curtis, Jeffrey R
AU  - Curtis JR
AD  - Division of Clinical Immunology and Rheumatology, University of Alabama at 
      Birmingham, Birmingham, Alabama, USA Department of Epidemiology, University of 
      Alabama at Birmingham, Birmingham, Alabama, USA.
LA  - eng
GR  - R01 HS018517/HS/AHRQ HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20140505
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Biomarkers)
RN  - 0 (Cholesterol, HDL)
RN  - 0 (Cholesterol, LDL)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
RPI - Postgrad Med J. 2014 Dec;90(1070):722-9. doi: 
      10.1136/postgradmedj-2013-204715rep. PMID: 25431465
MH  - Adult
MH  - Arthritis, Rheumatoid/*blood/complications/metabolism
MH  - Biomarkers/blood/metabolism
MH  - Blood Sedimentation
MH  - Brain Ischemia/*blood/complications/metabolism
MH  - C-Reactive Protein/*metabolism
MH  - Cholesterol, HDL/*blood
MH  - Cholesterol, LDL/*blood
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Inflammation/blood/complications/metabolism
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Myocardial Infarction/*blood/complications/metabolism
MH  - Proportional Hazards Models
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Stroke/*blood/etiology/metabolism
OTO - NOTNLM
OT  - Cardiovascular Disease
OT  - Epidemiology
OT  - Inflammation
OT  - Rheumatoid Arthritis
EDAT- 2014/05/07 06:00
MHDA- 2014/08/19 06:00
CRDT- 2014/05/07 06:00
PHST- 2014/05/07 06:00 [entrez]
PHST- 2014/05/07 06:00 [pubmed]
PHST- 2014/08/19 06:00 [medline]
AID - annrheumdis-2013-204715 [pii]
AID - 10.1136/annrheumdis-2013-204715 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2014 Jul;73(7):1301-8. doi: 10.1136/annrheumdis-2013-204715. Epub 
      2014 May 5.

PMID- 24685688
OWN - NLM
STAT- MEDLINE
DCOM- 20150526
LR  - 20221207
IS  - 1876-4738 (Electronic)
IS  - 0914-5087 (Linking)
VI  - 64
IP  - 5
DP  - 2014 Nov
TI  - Disease duration and severity impacts on long-term cardiovascular events in 
      Japanese patients with rheumatoid arthritis.
PG  - 366-70
LID - S0914-5087(14)00073-2 [pii]
LID - 10.1016/j.jjcc.2014.02.018 [doi]
AB  - BACKGROUND: Rheumatoid arthritis (RA) increases the mortality and morbidity of 
      cardiovascular disease (CVD). However, the relationship between RA and the risk 
      of CVD in the Japanese population remains unclear. METHODS AND RESULTS: This 
      study comprised 571 RA patients who were admitted to Juntendo University Hospital 
      from January 1990 to December 2000. Cardiovascular events (CVEs) were defined as 
      cardiac death, acute coronary syndrome (ACS), symptomatic stroke, and congestive 
      heart failure. During follow-up (mean 11.7 ± 5.8 years), 7.5% of the patients 
      died from all causes and 11.0% experienced CVEs. The morbidity of stroke and ACS 
      was 3.6 and 2.5 per 1000 person-years, respectively. The mean RA disease duration 
      at enrolment was significantly longer in patients who experienced CVEs than in 
      those who did not experience CVEs (15.0 ± 12.7 years vs. 10. 8 ± 9.7 years; p = 
      0.01). Physical disabilities due to RA were more severe in patients who 
      experienced CVEs than in those who did not experience CVEs. Patients with a long 
      RA disease duration showed significantly higher event rates (p = 0.033). Cox 
      proportional hazards analysis identified a longer RA duration as an independent 
      risk factor for CVD (hazard ratio 1.57, 95% CI 1.09-2.30, p = 0.02). CONCLUSION: 
      Japanese RA patients showed a relatively high incidence of CVD, despite the fact 
      that they had few coronary risk factors. The RA disease duration was an 
      independent risk factor for CVEs.
CI  - Copyright © 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All 
      rights reserved.
FAU - Masuda, Hiroshi
AU  - Masuda H
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan.
FAU - Miyazaki, Tetsuro
AU  - Miyazaki T
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan. Electronic address: tetsuro@juntendo.ac.jp.
FAU - Shimada, Kazunori
AU  - Shimada K
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan.
FAU - Tamura, Naoto
AU  - Tamura N
AD  - Department of Internal Medicine and Rheumatology, Juntendo University, School of 
      Medicine, Tokyo, Japan.
FAU - Matsudaira, Ran
AU  - Matsudaira R
AD  - Department of Internal Medicine and Rheumatology, Juntendo University, School of 
      Medicine, Tokyo, Japan.
FAU - Yoshihara, Takuma
AU  - Yoshihara T
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan.
FAU - Ohsaka, Hiromichi
AU  - Ohsaka H
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan.
FAU - Sai, Eiryu
AU  - Sai E
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan.
FAU - Matsumori, Rie
AU  - Matsumori R
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan.
FAU - Fukao, Kosuke
AU  - Fukao K
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan.
FAU - Hiki, Makoto
AU  - Hiki M
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan.
FAU - Kume, Atsumi
AU  - Kume A
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan.
FAU - Kiyanagi, Takashi
AU  - Kiyanagi T
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan.
FAU - Takasaki, Yoshinari
AU  - Takasaki Y
AD  - Department of Internal Medicine and Rheumatology, Juntendo University, School of 
      Medicine, Tokyo, Japan.
FAU - Daida, Hiroyuki
AU  - Daida H
AD  - Department of Cardiovascular Medicine, Juntendo University, School of Medicine, 
      Tokyo, Japan.
LA  - eng
PT  - Journal Article
DEP - 20140328
PL  - Netherlands
TA  - J Cardiol
JT  - Journal of cardiology
JID - 8804703
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications
MH  - Asian People
MH  - Cardiovascular Diseases/epidemiology/*etiology/mortality
MH  - Disabled Persons
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Proportional Hazards Models
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Time Factors
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - Inflammation
OT  - Risk factors
EDAT- 2014/04/02 06:00
MHDA- 2015/05/27 06:00
CRDT- 2014/04/02 06:00
PHST- 2013/09/17 00:00 [received]
PHST- 2014/01/19 00:00 [revised]
PHST- 2014/02/19 00:00 [accepted]
PHST- 2014/04/02 06:00 [entrez]
PHST- 2014/04/02 06:00 [pubmed]
PHST- 2015/05/27 06:00 [medline]
AID - S0914-5087(14)00073-2 [pii]
AID - 10.1016/j.jjcc.2014.02.018 [doi]
PST - ppublish
SO  - J Cardiol. 2014 Nov;64(5):366-70. doi: 10.1016/j.jjcc.2014.02.018. Epub 2014 Mar 
      28.

PMID- 24651915
OWN - NLM
STAT- MEDLINE
DCOM- 20150224
LR  - 20211021
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 33
IP  - 7
DP  - 2014 Jul
TI  - Primary Sjögren's syndrome and risk of ischemic stroke: a nationwide study.
PG  - 931-7
LID - 10.1007/s10067-014-2573-7 [doi]
AB  - Few studies are available on the risk of ischemic stroke after a diagnosis of 
      primary Sjögren's syndrome (PSS). This study investigated whether PSS increased 
      the risk of ischemic stroke in a large, nationwide cohort. Data for 4,276 
      patients who were newly diagnosed with PSS from 2000 to 2006 and who did not have 
      a stroke prior to diagnosis of PSS were obtained from the Registry of 
      Catastrophic Illness in Taiwan. For each PSS patient, data for ten controls 
      (matched by age, gender, comorbidities, and enrollment date) without systemic 
      autoimmune disease or previous stroke were obtained from the Longitudinal Health 
      Insurance 2000 database. All study subjects were followed up from the date of 
      enrollment until they developed ischemic stroke, died, or until the end of 2006, 
      whichever was earliest. To investigate if PSS was an independent factor in 
      determining the risk of developing ischemic stroke, a Cox regression model was 
      used with adjustment for age, gender, and comorbid disorders. Among 4,276 PSS 
      patients and 42,760 controls, 669 subjects (51 PSS patients and 618 controls) 
      developed ischemic stroke during the mean 3.7-year follow-up period 
      (interquartile range 2.2-5.2 years). Patients with PSS and controls had a similar 
      incidence of ischemic stroke occurrence (3.17/1,000 vs. 3.90/1,000 person years). 
      Multivariate analysis adjusted for baseline covariates indicated that PSS did not 
      increase the risk of ischemic stroke (adjusted hazard ratio: 0.84, 95 % 
      confidence interval: 0.63-1.12, P = 0.244). PSS is not associated with an 
      increased risk of ischemic stroke subsequent to diagnosis.
FAU - Chiang, Chia-Hung
AU  - Chiang CH
AD  - Division of Cardiology, Department of Medicine, Da-Chien General Hospital, 
      Miaoli, Taiwan.
FAU - Liu, Chia-Jen
AU  - Liu CJ
FAU - Chen, Ping-Jen
AU  - Chen PJ
FAU - Huang, Chin-Chou
AU  - Huang CC
FAU - Hsu, Chien-Yi
AU  - Hsu CY
FAU - Chan, Wan-Leong
AU  - Chan WL
FAU - Huang, Po-Hsun
AU  - Huang PH
FAU - Chen, Tzeng-Ji
AU  - Chen TJ
FAU - Lin, Shing-Jong
AU  - Lin SJ
FAU - Chen, Jaw-Wen
AU  - Chen JW
FAU - Leu, Hsin-Bang
AU  - Leu HB
LA  - eng
PT  - Journal Article
DEP - 20140321
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
SB  - IM
MH  - Adult
MH  - Aged
MH  - Atherosclerosis/complications
MH  - Brain Ischemia/*complications/mortality
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Proportional Hazards Models
MH  - Registries
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Sjogren's Syndrome/*complications/mortality
MH  - Stroke/*complications/mortality
MH  - Taiwan/epidemiology
MH  - Treatment Outcome
EDAT- 2014/03/22 06:00
MHDA- 2015/02/25 06:00
CRDT- 2014/03/22 06:00
PHST- 2013/10/31 00:00 [received]
PHST- 2014/03/02 00:00 [accepted]
PHST- 2014/03/22 06:00 [entrez]
PHST- 2014/03/22 06:00 [pubmed]
PHST- 2015/02/25 06:00 [medline]
AID - 10.1007/s10067-014-2573-7 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2014 Jul;33(7):931-7. doi: 10.1007/s10067-014-2573-7. Epub 2014 
      Mar 21.

PMID- 24635564
OWN - NLM
STAT- MEDLINE
DCOM- 20140609
LR  - 20220410
IS  - 1365-2869 (Electronic)
IS  - 0962-1105 (Linking)
VI  - 23
IP  - 2
DP  - 2014 Apr
TI  - Insomnia as a risk factor for ill health: results from the large population-based 
      prospective HUNT Study in Norway.
PG  - 124-32
AB  - Insomnia co-occurs with many health problems, but less is known about the 
      prospective associations. The aim of the current study was to investigate if 
      insomnia predicts cumulative incidence of mental and physical conditions. 
      Prospective population-based data from the two last Nord-Trøndelag Health Studies 
      (HUNT2 in 1995–97 and HUNT3 in 2006–08), comprising 24 715 people in the working 
      population, were used to study insomnia as a risk factor for incidence of 
      physical and mental conditions. Insomnia was defined according to the 4th edition 
      of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). Insomnia 
      at HUNT2 was a significant risk factor for incidence of a range of both mental 
      and physical conditions at HUNT3 11 years later. Most effects were only slightly 
      attenuated when adjusting for confounding factors, and insomnia remained a 
      significant risk factor for the following conditions in the adjusted analyses: 
      depression [odds ratio (OR): 2.38, 95% confidence interval (CI): 1.91–2.98], 
      anxiety (OR: 2.08, 95% CI: 1.63–2.64), fibromyalgia (OR: 2.05, 95% CI: 
      1.51–2.79), rheumatoidarthritis (OR: 1.87, 95% CI: 1.29–2.52), whiplash (OR: 
      1.71, 95% CI: 1.21–2.41), arthrosis (OR: 1.68, 95% CI: 1.43–1.98), osteoporosis 
      (OR:1.52, 95% CI: 1.14–2.01, headache (OR: 1.50, 95% CI: 1.16–1.95,asthma (OR: 
      1.47, 95% CI: 1.16–1.86 and myocardial infarction (OR:1.46, 95% CI: 1.06–2.00). 
      Insomnia was also associated significantly with incidence of angina, 
      hypertension, obesity and stroke in the crude analyses, but not after adjusting 
      for confounders. We conclude that insomnia predicts cumulative incidence of 
      several physical and mental conditions. These results may have important clinical 
      implications, and whether or not treatment of insomnia would have a preventive 
      value for both physical and mental conditions should be studied further.
FAU - Sivertsen, Børge
AU  - Sivertsen B
FAU - Lallukka, Tea
AU  - Lallukka T
FAU - Salo, Paula
AU  - Salo P
FAU - Pallesen, Ståle
AU  - Pallesen S
FAU - Hysing, Mari
AU  - Hysing M
FAU - Krokstad, Steinar
AU  - Krokstad S
FAU - Simon Øverland
AU  - Simon Øverland
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Sleep Res
JT  - Journal of sleep research
JID - 9214441
SB  - IM
CIN - J Sleep Res. 2014 Apr;23(2):121-3. doi: 10.1111/jsr.12145. PMID: 24628696
MH  - Adult
MH  - Anxiety/epidemiology
MH  - Arthritis, Rheumatoid/epidemiology
MH  - Asthma/epidemiology
MH  - Chronic Disease/*epidemiology/prevention & control
MH  - Confounding Factors, Epidemiologic
MH  - Depression/epidemiology
MH  - Female
MH  - Fibromyalgia/epidemiology
MH  - Headache/epidemiology
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Mental Disorders/epidemiology
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology
MH  - Norway/epidemiology
MH  - Obesity/epidemiology
MH  - Osteoporosis/epidemiology
MH  - Prospective Studies
MH  - Risk Factors
MH  - Sleep Initiation and Maintenance Disorders/*complications/epidemiology
MH  - Whiplash Injuries/epidemiology
EDAT- 2014/03/19 06:00
MHDA- 2014/06/10 06:00
CRDT- 2014/03/19 06:00
PHST- 2013/06/21 00:00 [received]
PHST- 2013/09/15 00:00 [accepted]
PHST- 2014/03/19 06:00 [entrez]
PHST- 2014/03/19 06:00 [pubmed]
PHST- 2014/06/10 06:00 [medline]
AID - 10.1111/jsr.12102 [doi]
PST - ppublish
SO  - J Sleep Res. 2014 Apr;23(2):124-32. doi: 10.1111/jsr.12102.

PMID- 24458537
OWN - NLM
STAT- MEDLINE
DCOM- 20150728
LR  - 20220316
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 74
IP  - 6
DP  - 2015 Jun
TI  - The effect of disease duration and disease activity on the risk of cardiovascular 
      disease in rheumatoid arthritis patients.
PG  - 998-1003
LID - 10.1136/annrheumdis-2013-204531 [doi]
AB  - OBJECTIVE: Disease duration and disease activity may be associated with an 
      increased risk of cardiovascular disease (CVD) in rheumatoid arthritis (RA). The 
      objectives of this study were to investigate (1) the relationship between 
      duration of inflammation and the development of CVD in RA patients and (2) the 
      relationship between RA disease activity over time and CVD in patients with RA. 
      METHODS: RA patients with a follow-up of ≥6 months in the Nijmegen early RA 
      cohort without prior CVD were included. Disease activity over time was calculated 
      using the time-averaged  28 joint disease activity score (DAS28) for each 
      patient. Kaplan-Meier survival analysis and Cox proportional hazards regression 
      were used for the analyses. RESULTS: During follow-up of the 855 patients that 
      were included, 154 CV events occurred. The course of hazards over time did not 
      indicate a change in the risk of CVD over the course of RA (disease duration), 
      which is also reflected by the absence of a deflection in the survival curves. 
      The survival distributions did not differ between patients with a disease 
      duration of <10 years or >10 years (Log-rank test: p=0.82). Time-averaged DAS28 
      was significantly associated with CVD (p=0.002) after correction for confounders. 
      CONCLUSIONS: Disease duration does not appear to independently affect the risk of 
      CVD. The risk of CVD in RA patients was not increased after 10 years of disease 
      duration compared with the first 10 years. Disease activity over time may 
      contribute to the risk of CVD.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://group.bmj.com/group/rights-licensing/permissions.
FAU - Arts, Elke E A
AU  - Arts EE
AD  - Department of Rheumatology, Radboud University Medical Centre, Nijmegen, The 
      Netherlands.
FAU - Fransen, Jaap
AU  - Fransen J
AD  - Department of Rheumatology, Radboud University Medical Centre, Nijmegen, The 
      Netherlands.
FAU - den Broeder, Alfons A
AU  - den Broeder AA
AD  - Department of Rheumatology, Sint Maartenskliniek, Nijmegen, The Netherlands.
FAU - Popa, Calin D
AU  - Popa CD
AD  - Department of Rheumatology, Radboud University Medical Centre, Nijmegen, The 
      Netherlands.
FAU - van Riel, Piet L C M
AU  - van Riel PL
AD  - Department of Rheumatology, Radboud University Medical Centre, Nijmegen, The 
      Netherlands.
LA  - eng
PT  - Journal Article
DEP - 20140123
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
MH  - Acute Coronary Syndrome/epidemiology
MH  - Adult
MH  - Aged
MH  - Angina, Stable/epidemiology
MH  - Arthritis, Rheumatoid/*epidemiology/physiopathology
MH  - Cardiovascular Diseases/*epidemiology
MH  - Cerebral Revascularization/statistics & numerical data
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Ischemic Attack, Transient/epidemiology
MH  - Kaplan-Meier Estimate
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Myocardial Revascularization/statistics & numerical data
MH  - Netherlands/epidemiology
MH  - Peripheral Arterial Disease/epidemiology
MH  - Proportional Hazards Models
MH  - Prospective Studies
MH  - Risk
MH  - Severity of Illness Index
MH  - Smoking/epidemiology
MH  - Stroke/epidemiology
MH  - Time Factors
OTO - NOTNLM
OT  - Cardiovascular Disease
OT  - DAS28
OT  - Disease Activity
OT  - Rheumatoid Arthritis
EDAT- 2014/01/25 06:00
MHDA- 2015/07/29 06:00
CRDT- 2014/01/25 06:00
PHST- 2013/08/28 00:00 [received]
PHST- 2014/01/03 00:00 [accepted]
PHST- 2014/01/25 06:00 [entrez]
PHST- 2014/01/25 06:00 [pubmed]
PHST- 2015/07/29 06:00 [medline]
AID - annrheumdis-2013-204531 [pii]
AID - 10.1136/annrheumdis-2013-204531 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2015 Jun;74(6):998-1003. doi: 10.1136/annrheumdis-2013-204531. 
      Epub 2014 Jan 23.

PMID- 24389293
OWN - NLM
STAT- MEDLINE
DCOM- 20150528
LR  - 20220408
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 74
IP  - 4
DP  - 2015 Apr
TI  - Performance of four current risk algorithms in predicting cardiovascular events 
      in patients with early rheumatoid arthritis.
PG  - 668-74
LID - 10.1136/annrheumdis-2013-204024 [doi]
AB  - OBJECTIVE: This study was undertaken to assess the predictive ability of 4 
      established cardiovascular (CV) risk models for the 10-year risk of fatal and 
      non-fatal CV diseases in European patients with rheumatoid arthritis. METHODS: 
      Prospectively collected data from the Nijmegen early rheumatoid arthritis (RA) 
      inception cohort was used. Discriminatory ability for CV risk prediction was 
      estimated by the area under the receiver operating characteristic curve. 
      Calibration was assessed by comparing the observed versus expected number of 
      events using Hosmer-Lemeshov tests and calibration plots. Sensitivity and 
      specificity were calculated for the cut-off values of 10% and 20% predicted risk. 
      RESULTS: Areas under the receiver operating characteristic curve were 0.78-0.80, 
      indicating moderate to good discrimination between patients with and without a CV 
      event. The CV risk models Systematic Coronary Risk Evaluation (SCORE), Framingham 
      risk score (FRS) and Reynolds risk score (RRS) primarily underestimated CV risk 
      at low and middle observed risk levels, and mostly overestimated CV risk at 
      higher observed risk levels. The QRisk II primarily overestimated observed CV 
      risk. For the 10% and 20% cut-off values used as indicators for CV preventive 
      treatment, sensitivity ranged from 68-87% and 40-65%, respectively and 
      specificity ranged from 55-76% and 77-88%, respectively. Depending on the model, 
      up to 32% of observed CV events occurred in patients with RA who were classified 
      as low risk (<10%) for CV disease. CONCLUSIONS: Established risk models generally 
      underestimate (Systematic Coronary Risk Evaluation score, Framingham Risk Score, 
      Reynolds risk score) or overestimate (QRisk II) CV risk in patients with RA.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not 
      already granted under a licence) please go to 
      http://group.bmj.com/group/rights-licensing/permissions.
FAU - Arts, E E A
AU  - Arts EE
AD  - Department of Rheumatology, Radboud University Medical Centre, Nijmegen, The 
      Netherlands.
FAU - Popa, C
AU  - Popa C
AD  - Department of Rheumatology, Radboud University Medical Centre, Nijmegen, The 
      Netherlands.
FAU - Den Broeder, A A
AU  - Den Broeder AA
AD  - Department of Rheumatology, Radboud University Medical Centre, Nijmegen, The 
      Netherlands.
FAU - Semb, A G
AU  - Semb AG
AD  - Department of Rheumatology, Maartenskliniek, Nijmegen, The Netherlands.
FAU - Toms, T
AU  - Toms T
AD  - Department of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway.
FAU - Kitas, G D
AU  - Kitas GD
AD  - Department of Rheumatology, Dudley NHS Hospital Group, Dudley, UK.
FAU - van Riel, P L
AU  - van Riel PL
AD  - Department of Rheumatology, Dudley NHS Hospital Group, Dudley, UK.
FAU - Fransen, J
AU  - Fransen J
AD  - Department of Rheumatology, Radboud University Medical Centre, Nijmegen, The 
      Netherlands.
LA  - eng
PT  - Journal Article
DEP - 20140103
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
MH  - Acute Coronary Syndrome/epidemiology
MH  - Adult
MH  - Aged
MH  - *Algorithms
MH  - Angina, Stable/epidemiology
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Cardiovascular Diseases/*epidemiology
MH  - Cohort Studies
MH  - Female
MH  - Heart Failure/epidemiology
MH  - Humans
MH  - Ischemic Attack, Transient/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Models, Theoretical
MH  - Peripheral Vascular Diseases/epidemiology
MH  - Prognosis
MH  - Prospective Studies
MH  - ROC Curve
MH  - Risk Assessment/methods
MH  - Stroke/epidemiology
OTO - NOTNLM
OT  - Arthritis Rheumatoid
OT  - Cardiovascular Disease
OT  - Models Cardiovascular
EDAT- 2014/01/07 06:00
MHDA- 2015/05/29 06:00
CRDT- 2014/01/07 06:00
PHST- 2014/01/07 06:00 [entrez]
PHST- 2014/01/07 06:00 [pubmed]
PHST- 2015/05/29 06:00 [medline]
AID - annrheumdis-2013-204024 [pii]
AID - 10.1136/annrheumdis-2013-204024 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2015 Apr;74(4):668-74. doi: 10.1136/annrheumdis-2013-204024. Epub 
      2014 Jan 3.

PMID- 24338532
OWN - NLM
STAT- MEDLINE
DCOM- 20140811
LR  - 20131216
IS  - 1898-018X (Electronic)
IS  - 1898-018X (Linking)
VI  - 20
IP  - 6
DP  - 2013
TI  - Autoimmune diseases, their pharmacological treatment and the cardiovascular 
      system.
PG  - 569-76
LID - 10.5603/CJ.2013.0156 [doi]
AB  - Cardiovascular system involvement is a frequent complication of autoimmune 
      diseases (AD) such as systemic lupus erythematosus, scleroderma, rheumatoid 
      arthritis, spondyloarthropaties or psoriatic arthritis. The most common forms of 
      such involvement are pericarditis, myocarditis, accelerated atherosclerosis 
      resulting in myocardial infarction or stroke, arrhythmias, conduction 
      abnormalities or congestive heart failure. Some of these manifestations may be 
      dramatic in their course and ultimately fatal. The treatment of AD may further 
      affect the cardiovascular system and result in a lower quality of life, higher 
      mortality and increased cost of healthcare. The aim of this review is to discuss 
      possible cardiac complications of various AD and the related treatment of these 
      diseases.
FAU - Jastrzębska, Marta
AU  - Jastrzębska M
FAU - Czok, Michael E
AU  - Czok ME
FAU - Guzik, Przemysław
AU  - Guzik P
AD  - Department of Cardiology and Intensive Therapy, Heliodor Swiecicki University 
      Hospital, Poznan, Poland Department of Cardiology and Intensive Therapy, Poznan 
      University of Medical Sciences, Poznan, Poland. pguzik@ptkardio.pl.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Poland
TA  - Cardiol J
JT  - Cardiology journal
JID - 101392712
RN  - 0 (Anti-Inflammatory Agents)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/adverse effects/*therapeutic use
MH  - Autoimmune Diseases/*drug therapy/immunology/mortality/physiopathology
MH  - Autoimmunity/*drug effects
MH  - Cardiovascular Diseases/*immunology/mortality/physiopathology/prevention & 
      control
MH  - Humans
MH  - Prognosis
MH  - Risk Factors
EDAT- 2013/12/18 06:00
MHDA- 2014/08/12 06:00
CRDT- 2013/12/17 06:00
PHST- 2013/12/11 00:00 [received]
PHST- 2013/12/11 00:00 [accepted]
PHST- 2013/12/17 06:00 [entrez]
PHST- 2013/12/18 06:00 [pubmed]
PHST- 2014/08/12 06:00 [medline]
AID - VM/OJS/J/36488 [pii]
AID - 10.5603/CJ.2013.0156 [doi]
PST - ppublish
SO  - Cardiol J. 2013;20(6):569-76. doi: 10.5603/CJ.2013.0156.

PMID- 24281789
OWN - NLM
STAT- MEDLINE
DCOM- 20140922
LR  - 20220408
IS  - 1179-1888 (Electronic)
IS  - 1175-0561 (Linking)
VI  - 15
IP  - 1
DP  - 2014 Feb
TI  - Effect of treating psoriasis on cardiovascular co-morbidities: focus on TNF 
      inhibitors.
PG  - 45-50
LID - 10.1007/s40257-013-0052-6 [doi]
AB  - Psoriasis patients are at increased risk for cardiovascular disease. Literature 
      on rheumatoid arthritis has shown the association of treatment with tumor 
      necrosis factor (TNF) inhibitors and improvement of cardiovascular disease. 
      Recent literature has also shown similar findings in psoriasis patients. We 
      present a review of the literature on the effect of TNF inhibitors for psoriasis 
      treatment on cardiovascular disease, cardiovascular biomarkers, and insulin 
      resistance. We conclude that TNF inhibitors may be especially beneficial in 
      preventing myocardial infarction, to a degree greater than methotrexate, 
      especially in the Caucasian population. The effects of TNF inhibitors in altering 
      insulin sensitivity or preventing new onset diabetes have been contradictory. 
      Case reports of both hyperglycemia and hypoglycemia developing in patients under 
      TNF inhibitor treatment teach us to warn patients about these side effects. More 
      robust clinical studies are needed to evaluate the true effect of TNF inhibitors 
      in diabetic psoriasis patients. More studies are also needed to assess the effect 
      of TNF inhibitors on hypertension, dyslipidemia, and stroke.
FAU - Famenini, Shannon
AU  - Famenini S
AD  - David Geffen School of Medicine at University of California, Los Angeles (UCLA), 
      Los Angeles, CA, USA.
FAU - Sako, Eric Y
AU  - Sako EY
FAU - Wu, Jashin J
AU  - Wu JJ
LA  - eng
PT  - Journal Article
PT  - Review
PL  - New Zealand
TA  - Am J Clin Dermatol
JT  - American journal of clinical dermatology
JID - 100895290
RN  - 0 (Biomarkers)
RN  - 0 (Dermatologic Agents)
RN  - 0 (Immunologic Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Biomarkers/metabolism
MH  - Cardiovascular Diseases/*drug therapy/etiology/prevention & control
MH  - Dermatologic Agents/adverse effects/pharmacology/therapeutic use
MH  - Humans
MH  - Immunologic Factors/adverse effects/pharmacology/therapeutic use
MH  - Insulin Resistance
MH  - Psoriasis/complications/*drug therapy
MH  - Risk
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
EDAT- 2013/11/28 06:00
MHDA- 2014/09/23 06:00
CRDT- 2013/11/28 06:00
PHST- 2013/11/28 06:00 [entrez]
PHST- 2013/11/28 06:00 [pubmed]
PHST- 2014/09/23 06:00 [medline]
AID - 10.1007/s40257-013-0052-6 [doi]
PST - ppublish
SO  - Am J Clin Dermatol. 2014 Feb;15(1):45-50. doi: 10.1007/s40257-013-0052-6.

PMID- 24272316
OWN - NLM
STAT- MEDLINE
DCOM- 20150519
LR  - 20240507
IS  - 1468-2869 (Electronic)
IS  - 1099-3460 (Print)
IS  - 1099-3460 (Linking)
VI  - 91
IP  - 4
DP  - 2014 Aug
TI  - Oral health among residents of publicly supported housing in Boston.
PG  - 809-21
LID - 10.1007/s11524-013-9845-4 [doi]
AB  - Tooth loss in adults diminishes quality of daily life, affecting eating, 
      speaking, appearance, and social interactions. Tooth loss is linked to severe 
      periodontitis and caries; and to risk of stroke, cardiovascular disease, 
      rheumatoid arthritis, and dementia. At the national (USA) level, poverty and 
      African-American race have been linked to lower utilization of dental services, 
      suggesting that the 7.5 million residents of publicly supported housing may be at 
      risk of tooth loss and poor overall oral health. We assessed whether residence in 
      publicly supported housing in Boston was associated with four oral health-related 
      indicators. Compared to residents of nonpublicly supported housing, after 
      adjusting for covariates residents of both public housing developments (PHDs) and 
      rental assistance units (RAUs) had significantly lower odds of having had a 
      dental cleaning in the past year (PHD, OR = 0.64 (95 % CI, 0.44-0.93); RAU, 
      OR = 0.67 (95 % CI, 0.45-0.99))-despite parity in having had a past year dental 
      visit. Further, residents of RAUs had double the odds of having had six or more 
      teeth removed (OR = 2.20 (95 % CI, 1.39-3.50)). Associations of race/ethnicity 
      and housing type with dental insurance were interrelated. Unadjusted results 
      document a deficit in oral health-related indicators among public housing 
      residents, taken as a group, giving a clear picture of an oral health care gap 
      and identifying a defined real-world population that could benefit from services. 
      Existing public housing infrastructure could provide both a venue and a 
      foundation for interventions to reduce oral health disparities on a broad scale.
FAU - Maxwell, Nancy Irwin
AU  - Maxwell NI
AD  - Department of Environmental Health, Boston University School of Public Health, 
      Boston, MA, USA, nimaxwell@comcast.net.
FAU - Shah, Snehal
AU  - Shah S
FAU - Dooley, Daniel
AU  - Dooley D
FAU - Henshaw, Michelle
AU  - Henshaw M
FAU - Bowen, Deborah J
AU  - Bowen DJ
LA  - eng
GR  - R43 DP000019/DP/NCCDPHP CDC HHS/United States
GR  - R44 DP000019/DP/NCCDPHP CDC HHS/United States
GR  - 5 U48 DP0019-22/DP/NCCDPHP CDC HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Urban Health
JT  - Journal of urban health : bulletin of the New York Academy of Medicine
JID - 9809909
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Boston/epidemiology
MH  - Dental Care/*statistics & numerical data
MH  - Dental Caries/epidemiology
MH  - Dental Health Surveys/*statistics & numerical data
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Oral Health/*statistics & numerical data
MH  - Prevalence
MH  - Public Housing/*statistics & numerical data
MH  - Socioeconomic Factors
MH  - Urban Health/*statistics & numerical data
MH  - Young Adult
PMC - PMC4134450
EDAT- 2013/11/26 06:00
MHDA- 2015/05/20 06:00
PMCR- 2015/08/01
CRDT- 2013/11/26 06:00
PHST- 2013/11/26 06:00 [entrez]
PHST- 2013/11/26 06:00 [pubmed]
PHST- 2015/05/20 06:00 [medline]
PHST- 2015/08/01 00:00 [pmc-release]
AID - 9845 [pii]
AID - 10.1007/s11524-013-9845-4 [doi]
PST - ppublish
SO  - J Urban Health. 2014 Aug;91(4):809-21. doi: 10.1007/s11524-013-9845-4.

PMID- 24229049
OWN - NLM
STAT- MEDLINE
DCOM- 20140929
LR  - 20211021
IS  - 1471-2377 (Electronic)
IS  - 1471-2377 (Linking)
VI  - 13
DP  - 2013 Nov 14
TI  - Risk of subarachnoid haemorrhage in people admitted to hospital with selected 
      immune-mediated diseases: record-linkage studies.
PG  - 176
LID - 10.1186/1471-2377-13-176 [doi]
AB  - BACKGROUND: Subarachnoid hemorrhage (SAH) is a devastating cause of stroke, 
      occurring in relatively young people. It has been suggested that some 
      immune-mediated diseases may be associated with an increased risk of SAH. 
      METHODS: We analysed a database of linked statistical records of hospital 
      admissions and death certificates for the whole of England (1999-2011). Rate 
      ratios for SAH were determined, comparing immune-mediated disease cohorts with 
      comparison cohorts. RESULTS: There were significantly elevated risks of SAH after 
      hospital admission for the following individual immune-mediated diseases: 
      Addison's disease, ankylosing spondylitis, autoimmune haemolytic anaemia, Crohn's 
      disease, diabetes mellitus, idiopathic thrombocytopenia purpura, myxoedema, 
      pernicious anaemia, primary biliary cirrhosis, psoriasis, rheumatoid arthritis, 
      scleroderma, Sjogren's syndrome, SLE and thyrotoxicosis. Elevated risks that were 
      greater than 2-fold were found for Addison's disease (rate ratio (RR) = 2.01, 95% 
      confidence interval 1.3-2.97), idiopathic thrombocytopenia purpura (RR = 2.42, 
      1.86-3.11), primary biliary cirrhosis (RR = 2.21, 1.43-3.16) and SLE (RR = 3.76, 
      3.08-4.55). CONCLUSIONS: Our findings strongly support the suggestion that 
      patients with some immune-mediated diseases have an increased risk of SAH. 
      Further studies of the mechanisms behind this association are warranted.
FAU - Ramagopalan, Sreeram V
AU  - Ramagopalan SV
FAU - Pakpoor, Julia
AU  - Pakpoor J
FAU - Seminog, Olena
AU  - Seminog O
FAU - Goldacre, Raph
AU  - Goldacre R
FAU - Graham, Lee
AU  - Graham L
FAU - Goldacre, Michael J
AU  - Goldacre MJ
AD  - Unit of Health-Care Epidemiology, Department of Public Health, University of 
      Oxford, Oxford, UK. michael.goldacre@dph.ox.ac.uk.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131114
PL  - England
TA  - BMC Neurol
JT  - BMC neurology
JID - 100968555
SB  - IM
MH  - Cohort Studies
MH  - Female
MH  - Hospitalization/trends
MH  - Humans
MH  - Immune System Diseases/*diagnosis/*epidemiology
MH  - Male
MH  - Medical Record Linkage/*methods
MH  - Patient Admission/*trends
MH  - Risk Factors
MH  - Subarachnoid Hemorrhage/*diagnosis/*epidemiology
PMC - PMC3833635
EDAT- 2013/11/16 06:00
MHDA- 2014/09/30 06:00
PMCR- 2013/11/14
CRDT- 2013/11/16 06:00
PHST- 2013/11/09 00:00 [received]
PHST- 2013/11/11 00:00 [accepted]
PHST- 2013/11/16 06:00 [entrez]
PHST- 2013/11/16 06:00 [pubmed]
PHST- 2014/09/30 06:00 [medline]
PHST- 2013/11/14 00:00 [pmc-release]
AID - 1471-2377-13-176 [pii]
AID - 10.1186/1471-2377-13-176 [doi]
PST - epublish
SO  - BMC Neurol. 2013 Nov 14;13:176. doi: 10.1186/1471-2377-13-176.

PMID- 24204921
OWN - NLM
STAT- MEDLINE
DCOM- 20140805
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 10
DP  - 2013
TI  - SMAD3 rs17228212 gene polymorphism is associated with reduced risk to 
      cerebrovascular accidents and subclinical atherosclerosis in anti-CCP negative 
      Spanish rheumatoid arthritis patients.
PG  - e77695
LID - 10.1371/journal.pone.0077695 [doi]
LID - e77695
AB  - Rheumatoid arthritis (RA) is a complex polygenic inflammatory disease associated 
      with accelerated atherosclerosis and increased risk of cardiovascular (CV) 
      disease. Previous genome-wide association studies have described SMAD3 rs17228212 
      polymorphism as an important signal associated with CV events. The aim of the 
      present study was to evaluate for the first time the relationship between this 
      gene polymorphism and the susceptibility to CV manifestations and its potential 
      association with the presence of subclinical atherosclerosis assessed by the 
      evaluation of carotid intima-media thickness (cIMT) in patients with RA. METHODS: 
      One thousand eight hundred and ninety-seven patients fulfilling classification 
      criteria for RA were genotyped for SMAD3 rs17228212 gene polymorphism through 
      TaqMan genotyping assay. Also, subclinical atherosclerosis determined by the 
      assessment of cIMT was analyzed in a subgroup of these patients by carotid 
      ultrasonography. RESULTS: No statistically significant differences were observed 
      when allele frequencies of RA patients with or without CV events were compared. 
      Nevertheless, when RA patients were stratified according to anti-cyclic 
      citrullinated peptide (anti-CCP) status, we found that in RA patients who were 
      negative for anti-CCP antibodies, the presence of C allele of SMAD3 rs17228212 
      polymorphism conferred a protective effect against the risk of cerebrovascular 
      accident (CVA) after adjustment for demographic and classic CV risk factors (HR 
      [95%CI]=0.36 [0.14-0.94], p=0.038) in a Cox regression model. Additionally, 
      correlation between the presence of C allele of SMAD3 rs17228212 polymorphism and 
      lower values of cIMT was found after adjustment for demographic and classic CV 
      risk factors (p-value=0.0094) in the anti-CCP negative RA patients. CONCLUSIONS: 
      Our results revealed that SMAD3 rs17228212 gene variant is associated with lower 
      risk of CVA and less severe subclinical atherosclerosis in RA patients negative 
      for anti-CCP antibodies. These findings may have importance to establish 
      predictive models of CV disease in RA patients according to anti-CCP status.
FAU - García-Bermúdez, Mercedes
AU  - García-Bermúdez M
AD  - Instituto de Parasitología y Biomedicina López-Neyra, IPBLN-CSIC, Granada, Spain.
FAU - López-Mejías, Raquel
AU  - López-Mejías R
FAU - Genre, Fernanda
AU  - Genre F
FAU - Castañeda, Santos
AU  - Castañeda S
FAU - González-Juanatey, Carlos
AU  - González-Juanatey C
FAU - Llorca, Javier
AU  - Llorca J
FAU - Corrales, Alfonso
AU  - Corrales A
FAU - Miranda-Filloy, José A
AU  - Miranda-Filloy JA
FAU - Rueda-Gotor, Javier
AU  - Rueda-Gotor J
FAU - Gómez-Vaquero, Carmen
AU  - Gómez-Vaquero C
FAU - Rodríguez-Rodríguez, Luis
AU  - Rodríguez-Rodríguez L
FAU - Fernández-Gutiérrez, Benjamín
AU  - Fernández-Gutiérrez B
FAU - Pascual-Salcedo, Dora
AU  - Pascual-Salcedo D
FAU - Balsa, Alejandro
AU  - Balsa A
FAU - López-Longo, Francisco J
AU  - López-Longo FJ
FAU - Carreira, Patricia
AU  - Carreira P
FAU - Blanco, Ricardo
AU  - Blanco R
FAU - González-Álvaro, Isidoro
AU  - González-Álvaro I
FAU - Martín, Javier
AU  - Martín J
FAU - González-Gay, Miguel A
AU  - González-Gay MA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131021
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (SMAD3 protein, human)
RN  - 0 (Smad3 Protein)
SB  - IM
EIN - PLoS One. 2013;8(11). doi:10.1371/annotation/3fc037c1-2585-4d2b-a781-e04ab7b3bfeb
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications/*genetics
MH  - Atherosclerosis/etiology/genetics
MH  - Cardiovascular Diseases/etiology/genetics
MH  - Carotid Intima-Media Thickness
MH  - Female
MH  - Gene Frequency/genetics
MH  - Genetic Predisposition to Disease/*genetics
MH  - Genotype
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Polymorphism, Single Nucleotide/*genetics
MH  - Risk
MH  - Smad3 Protein/*genetics
MH  - Spain
MH  - Stroke/*etiology/*genetics
PMC - PMC3804609
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/11/10 06:00
MHDA- 2014/08/06 06:00
PMCR- 2013/10/21
CRDT- 2013/11/09 06:00
PHST- 2013/06/26 00:00 [received]
PHST- 2013/09/03 00:00 [accepted]
PHST- 2013/11/09 06:00 [entrez]
PHST- 2013/11/10 06:00 [pubmed]
PHST- 2014/08/06 06:00 [medline]
PHST- 2013/10/21 00:00 [pmc-release]
AID - PONE-D-13-26409 [pii]
AID - 10.1371/journal.pone.0077695 [doi]
PST - epublish
SO  - PLoS One. 2013 Oct 21;8(10):e77695. doi: 10.1371/journal.pone.0077695. 
      eCollection 2013.

PMID- 24166794
OWN - NLM
STAT- MEDLINE
DCOM- 20140102
LR  - 20220410
IS  - 1529-0131 (Electronic)
IS  - 0004-3591 (Linking)
VI  - 65
IP  - 11
DP  - 2013 Nov
TI  - Clinically significant renal involvement in primary Sjögren's syndrome: clinical 
      presentation and outcome.
PG  - 2945-53
LID - 10.1002/art.38100 [doi]
AB  - OBJECTIVE: To estimate the prevalence and investigate the clinical features and 
      the outcome of clinically significant renal involvement in a large cohort of 
      patients with primary Sjögren's syndrome (SS). METHODS: Among 715 patients who 
      met the American-European Consensus Group criteria for primary SS, those with 
      clinically significant renal involvement were identified and their clinical and 
      immunologic features were recorded. The prognosis in patients with primary SS 
      with renal involvement was assessed by the clinical appearance of any of the 
      following major outcomes: death, hemodialysis, chronic renal failure (CRF), and 
      lymphoma. Kaplan-Meier analysis was applied to compare death rates between 
      patients without and those with renal involvement. RESULTS: Thirty-five patients 
      with primary SS (4.9%) had clinically significant renal involvement, representing 
      a total followup time after renal diagnosis of 252.2 person-years. Thirteen 
      patients (37.1%) had interstitial nephritis alone, 17 patients (48.6%) had 
      glomerulonephritis (GN) alone, and 5 patients (14.3%) had both entities. Nine 
      patients died (25.7%), 11 developed CRF (including 4 requiring chronic 
      hemodialysis) (31.4%), and 9 developed lymphoma (25.7%). The overall 5-year 
      survival rate was 85%. Kaplan-Meier analysis showed statistically significant 
      reduced survival for patients with primary SS with renal involvement compared to 
      those without renal involvement (P < 0.0001 by log rank test), with GN patients 
      displaying increased mortality. Eight of 9 reported deaths (89%) and 8 of 9 
      lymphomas (89%) were observed among patients with GN. CONCLUSION: The long-term 
      prognosis varies for patients with primary SS who have clinically significant 
      renal involvement. Patients with interstitial nephritis display a favorable 
      prognosis, while patients with GN are at high risk of developing lymphoma and 
      have poor survival.
CI  - Copyright © 2013 by the American College of Rheumatology.
FAU - Goules, Andreas V
AU  - Goules AV
AD  - National University of Athens, School of Medicine, Athens, Greece.
FAU - Tatouli, Ioanna P
AU  - Tatouli IP
FAU - Moutsopoulos, Haralampos M
AU  - Moutsopoulos HM
FAU - Tzioufas, Athanasios G
AU  - Tzioufas AG
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
SB  - IM
MH  - Adult
MH  - Aged
MH  - Biopsy
MH  - Female
MH  - Follow-Up Studies
MH  - Glomerulonephritis/*mortality/pathology/therapy
MH  - Heart Failure/mortality
MH  - Humans
MH  - Kaplan-Meier Estimate
MH  - Lymphoma/mortality
MH  - Male
MH  - Middle Aged
MH  - Neoplasms/mortality
MH  - Nephritis, Interstitial/*mortality/pathology/therapy
MH  - Prognosis
MH  - Renal Dialysis
MH  - Renal Insufficiency, Chronic/*mortality/pathology/therapy
MH  - Risk Factors
MH  - Sjogren's Syndrome/*mortality
MH  - Stroke/mortality
EDAT- 2013/10/30 06:00
MHDA- 2014/01/03 06:00
CRDT- 2013/10/30 06:00
PHST- 2013/03/30 00:00 [received]
PHST- 2013/07/18 00:00 [accepted]
PHST- 2013/10/30 06:00 [entrez]
PHST- 2013/10/30 06:00 [pubmed]
PHST- 2014/01/03 06:00 [medline]
AID - 10.1002/art.38100 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2013 Nov;65(11):2945-53. doi: 10.1002/art.38100.

PMID- 24095940
OWN - NLM
STAT- MEDLINE
DCOM- 20140211
LR  - 20220409
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Print)
IS  - 0003-4967 (Linking)
VI  - 73
IP  - 1
DP  - 2014 Jan
TI  - Prevalence of comorbidities in rheumatoid arthritis and evaluation of their 
      monitoring: results of an international, cross-sectional study (COMORA).
PG  - 62-8
LID - 10.1136/annrheumdis-2013-204223 [doi]
AB  - BACKGROUND: PATIENTS with rheumatoid arthritis (RA) are at increased risk of 
      developing comorbid conditions. OBJECTIVES: To evaluate the prevalence of 
      comorbidities and compare their management in RA patients from different 
      countries worldwide. STUDY DESIGN: international, cross-sectional. PATIENTS: 
      consecutive RA patients. DATA COLLECTED: demographics, disease characteristics 
      (activity, severity, treatment), comorbidities (cardiovascular, infections, 
      cancer, gastrointestinal, pulmonary, osteoporosis and psychiatric disorders). 
      RESULTS: Of 4586 patients recruited in 17 participating countries, 3920 were 
      analysed (age, 56±13 years; disease duration, 10±9 years (mean±SD); female 
      gender, 82%; DAS28 (Disease Activity Score using 28 joints)-erythrocyte 
      sedimentation rate, 3.7±1.6 (mean±SD); Health Assessment Questionnaire, 1.0±0.7 
      (mean±SD); past or current methotrexate use, 89%; past or current use of 
      biological agents, 39%. The most frequently associated diseases (past or current) 
      were: depression, 15%; asthma, 6.6%; cardiovascular events (myocardial 
      infarction, stroke), 6%; solid malignancies (excluding basal cell carcinoma), 
      4.5%; chronic obstructive pulmonary disease, 3.5%. High intercountry variability 
      was observed for both the prevalence of comorbidities and the proportion of 
      subjects complying with recommendations for preventing and managing 
      comorbidities. The systematic evaluation of comorbidities in this study detected 
      abnormalities in vital signs, such as elevated blood pressure in 11.2%, and 
      identified conditions that manifest as laboratory test abnormalities, such as 
      hyperglycaemia in 3.3% and hyperlipidaemia in 8.3%. CONCLUSIONS: Among RA 
      patients, there is a high prevalence of comorbidities and their risk factors. In 
      this multinational sample, variability among countries was wide, not only in 
      prevalence but also in compliance with recommendations for preventing and 
      managing these comorbidities. Systematic measurement of vital signs and 
      laboratory testing detects otherwise unrecognised comorbid conditions.
FAU - Dougados, Maxime
AU  - Dougados M
AD  - Medicine Faculty, Paris-Descartes University, , Paris, France.
FAU - Soubrier, Martin
AU  - Soubrier M
FAU - Antunez, Anna
AU  - Antunez A
FAU - Balint, Peter
AU  - Balint P
FAU - Balsa, Alejandro
AU  - Balsa A
FAU - Buch, Maya H
AU  - Buch MH
FAU - Casado, Gustavo
AU  - Casado G
FAU - Detert, Jacqueline
AU  - Detert J
FAU - El-Zorkany, Bassel
AU  - El-Zorkany B
FAU - Emery, Paul
AU  - Emery P
FAU - Hajjaj-Hassouni, Najia
AU  - Hajjaj-Hassouni N
FAU - Harigai, Masayoshi
AU  - Harigai M
FAU - Luo, Shue-Fen
AU  - Luo SF
FAU - Kurucz, Reka
AU  - Kurucz R
FAU - Maciel, Gabriel
AU  - Maciel G
FAU - Mola, Emilio Martin
AU  - Mola EM
FAU - Montecucco, Carlo Maurizio
AU  - Montecucco CM
FAU - McInnes, Iain
AU  - McInnes I
FAU - Radner, Helga
AU  - Radner H
FAU - Smolen, Josef S
AU  - Smolen JS
FAU - Song, Yeong-Wook
AU  - Song YW
FAU - Vonkeman, Harald Erwin
AU  - Vonkeman HE
FAU - Winthrop, Kevin
AU  - Winthrop K
FAU - Kay, Jonathan
AU  - Kay J
LA  - eng
GR  - 18475/ARC_/Arthritis Research UK/United Kingdom
GR  - 18475/VAC_/Versus Arthritis/United Kingdom
GR  - UL1 TR000128/TR/NCATS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131004
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
CIN - Ann Rheum Dis. 2014 Mar;73(3):e15. doi: 10.1136/annrheumdis-2013-204954. PMID: 
      24336333
CIN - Ann Rheum Dis. 2014 Mar;73(3):e14. doi: 10.1136/annrheumdis-2013-204895. PMID: 
      24336339
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*epidemiology/therapy
MH  - Cardiovascular Diseases/*epidemiology/therapy
MH  - Comorbidity
MH  - Cross-Sectional Studies
MH  - Female
MH  - Gastrointestinal Diseases/*epidemiology/therapy
MH  - *Global Health
MH  - Humans
MH  - Infections/*epidemiology/therapy
MH  - Internationality
MH  - Lung Diseases/epidemiology/therapy
MH  - Male
MH  - Mental Disorders/epidemiology/therapy
MH  - Middle Aged
MH  - Neoplasms/*epidemiology/therapy
MH  - Osteoporosis/epidemiology/therapy
MH  - Prevalence
MH  - Risk Factors
MH  - Severity of Illness Index
PMC - PMC3888623
OTO - NOTNLM
OT  - Cardiovascular Disease
OT  - Epidemiology
OT  - Lipids
OT  - Rheumatoid Arthritis
OT  - Vaccination
EDAT- 2013/10/08 06:00
MHDA- 2014/02/12 06:00
CRDT- 2013/10/08 06:00
PHST- 2013/10/08 06:00 [entrez]
PHST- 2013/10/08 06:00 [pubmed]
PHST- 2014/02/12 06:00 [medline]
AID - annrheumdis-2013-204223 [pii]
AID - 10.1136/annrheumdis-2013-204223 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2014 Jan;73(1):62-8. doi: 10.1136/annrheumdis-2013-204223. Epub 
      2013 Oct 4.

PMID- 24030041
OWN - NLM
STAT- MEDLINE
DCOM- 20140114
LR  - 20161125
IS  - 1028-768X (Print)
IS  - 1028-768X (Linking)
VI  - 22
IP  - 2
DP  - 2013 Jun
TI  - Sjogren's syndrome with acute cerebellar ataxia and massive lymphadenopathy : a 
      case report.
PG  - 81-6
AB  - PURPOSE: Common etiologies of acute acquired cerebellar ataxia include 
      cerebrovascular diseases, toxin or drugs, infections/para-infections, and 
      autoimmune diseases. It is a rare manifestation of Sjögren's syndrome, which is a 
      common autoimmune disease but is often missed as a differential diagnosis. CASE 
      REPORT: This is a report of a patient with acute onset cerebellar ataxia for one 
      month. She also had massive neck lymphadenopathy. After a series of studies and 
      the exclusion of other common causes of acute cerebellar ataxia, she was 
      diagnosed as having Sjögren's syndrome. Patients with Sjögren's syndrome have 
      higher risk for lymphoma, which leads to poorer prognosis. After lymph node 
      biopsy, the patient was proven to have sinus histiocytosis, which is another rare 
      finding in Sjögren's syndrome. DISCUSSION: For patients with acute acquired 
      cerebellar ataxia, immune-mediated cerebellar ataxia should be an important 
      differential diagnosis aside from the more common causes like stroke or drugs.
FAU - Chen, Yen-Wen
AU  - Chen YW
AD  - Department of Neurology, E-Da Hospital/I-Shou University, Kaohsiung, Taiwan.
FAU - Lee, Kuan-Chiao
AU  - Lee KC
FAU - Chang, I-Wei
AU  - Chang IW
FAU - Chang, Chen-Sheng
AU  - Chang CS
FAU - Hsu, Shih-Pin
AU  - Hsu SP
FAU - Kuo, Hung-Chang
AU  - Kuo HC
LA  - eng
PT  - Case Reports
PT  - Journal Article
PL  - China (Republic : 1949- )
TA  - Acta Neurol Taiwan
JT  - Acta neurologica Taiwanica
JID - 9815355
SB  - IM
MH  - Adult
MH  - Cerebellar Ataxia/*complications/diagnostic imaging
MH  - Female
MH  - Humans
MH  - Lymph Nodes/pathology
MH  - Lymphatic Diseases/*complications/diagnostic imaging
MH  - Magnetic Resonance Imaging
MH  - Sjogren's Syndrome/*complications/diagnostic imaging
MH  - Tomography, X-Ray Computed
EDAT- 2013/09/14 06:00
MHDA- 2014/01/15 06:00
CRDT- 2013/09/14 06:00
PHST- 2013/09/14 06:00 [entrez]
PHST- 2013/09/14 06:00 [pubmed]
PHST- 2014/01/15 06:00 [medline]
AID - 10196099/222081 [pii]
PST - ppublish
SO  - Acta Neurol Taiwan. 2013 Jun;22(2):81-6.

PMID- 24023053
OWN - NLM
STAT- MEDLINE
DCOM- 20140422
LR  - 20140304
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Linking)
VI  - 66
IP  - 3
DP  - 2014 Mar
TI  - Tumor necrosis factor α inhibitor use and decreased risk for incident coronary 
      events in rheumatoid arthritis.
PG  - 355-63
LID - 10.1002/acr.22166 [doi]
AB  - OBJECTIVE: To determine the association of tumor necrosis factor α (TNFα) 
      inhibitors with risk for cardiovascular disease (CVD) in rheumatoid arthritis 
      (RA) patients. METHODS: A retrospective cohort of 2,101 incident RA patients was 
      established. Medication exposure was categorized into the following groups: TNFα 
      inhibitors alone or in combination with methotrexate (MTX; aTNF group); MTX alone 
      or in combination with other nonbiologic disease-modifying antirheumatic drugs 
      (DMARDs; MTX group); and no MTX, nonbiologic DMARDs (reference group). Primary 
      outcome was adjudicated incident coronary artery disease (CAD), defined as 
      myocardial infarction, unstable angina, or coronary revascularization procedure. 
      Secondary outcome was adjudicated incident CVD, defined as a composite of CAD, 
      stroke, transient ischemic attack, abdominal aortic aneurysm, peripheral arterial 
      disease, or arterial revascularization procedure. Cox regression models were used 
      to calculate the hazard ratio for CAD and CVD for the aTNF and MTX groups 
      compared to the reference group. RESULTS: There were 46 incident CAD and 82 
      incident CVD events. Adjusting for covariates associated with CAD and CVD, the 
      hazard ratio for incident CAD was 0.45 (95% confidence interval [95% CI] 
      0.21-0.96) for the aTNF group and 0.54 (95% CI 0.27-1.09) for the MTX group 
      compared to the reference group. Use of TNFα inhibitors for >16.1 months was 
      associated with a relative risk for CAD of 0.18 (95% CI 0.06-0.50) and for CVD of 
      0.31 (95% CI 0.15-0.65) compared to the reference group. A similar, although not 
      significant, trend was seen with the MTX group. CONCLUSION: Use of TNFα 
      inhibitors is associated with a decreased risk for CAD in RA; the risk decreases 
      further with long-term use. This should be considered when weighing the risks 
      versus benefits of these medications.
CI  - Copyright © 2014 by the American College of Rheumatology.
FAU - Bili, Androniki
AU  - Bili A
AD  - Geisinger Medical Center, Danville, Pennsylvania.
FAU - Tang, Xiaoqin
AU  - Tang X
FAU - Pranesh, Shruthi
AU  - Pranesh S
FAU - Bozaite, Rasa
AU  - Bozaite R
FAU - Morris, Stephanie J
AU  - Morris SJ
FAU - Antohe, Jana L
AU  - Antohe JL
FAU - Kirchner, H Lester
AU  - Kirchner HL
FAU - Wasko, Mary Chester M
AU  - Wasko MC
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antirheumatic Agents/pharmacology/*therapeutic use
MH  - Arthritis, Rheumatoid/complications/*drug therapy
MH  - Coronary Artery Disease/*prevention & control
MH  - Female
MH  - Humans
MH  - Male
MH  - Methotrexate/therapeutic use
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
EDAT- 2013/09/12 06:00
MHDA- 2014/04/23 06:00
CRDT- 2013/09/12 06:00
PHST- 2013/01/05 00:00 [received]
PHST- 2013/09/03 00:00 [accepted]
PHST- 2013/09/12 06:00 [entrez]
PHST- 2013/09/12 06:00 [pubmed]
PHST- 2014/04/23 06:00 [medline]
AID - 10.1002/acr.22166 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2014 Mar;66(3):355-63. doi: 10.1002/acr.22166.

PMID- 23889823
OWN - NLM
STAT- MEDLINE
DCOM- 20131028
LR  - 20211021
IS  - 1471-2377 (Electronic)
IS  - 1471-2377 (Linking)
VI  - 13
DP  - 2013 Jul 29
TI  - Spontaneous intracranial hemorrhage as an initial manifestation of primary 
      Sjögren's syndrome: a case report.
PG  - 100
LID - 10.1186/1471-2377-13-100 [doi]
AB  - BACKGROUND: Sjögren's syndrome can involve the central nervous system; however, 
      spontaneous intracranial hemorrhage has rarely been reported as the initial 
      manifestation. CASE PRESENTATION: We report a 39-year-old woman with primary 
      Sjögren's syndrome presenting with intracranial hemorrhage. The diagnosis of 
      primary Sjögren's syndrome was based on the presence of ocular dryness, salivary 
      gland secretory and excretory dysfunction confirmed with dynamic tracer emission 
      CT, and positive anti-Sjögren's syndrome A and anti-Sjögren's syndrome B 
      antibodies. CONCLUSION: Primary Sjögren's syndrome can present with variable 
      central nervous system signs, which may precede the classic sicca symptoms. 
      Therefore, Sjögren's syndrome-associated indicators should be investigated in 
      patients without the common risk factors for stroke who present with spontaneous 
      intracranial hemorrhage.
FAU - Wang, Guo-Qiang
AU  - Wang GQ
AD  - Department of Neurology, General Hospital of Beijing Military Region, Beijing 
      100700, China. wgqbj@163.com
FAU - Zhang, Wei-Wei
AU  - Zhang WW
LA  - eng
PT  - Case Reports
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130729
PL  - England
TA  - BMC Neurol
JT  - BMC neurology
JID - 100968555
SB  - IM
MH  - Adult
MH  - Brain/diagnostic imaging/pathology
MH  - Cerebral Angiography
MH  - Female
MH  - Humans
MH  - Intracranial Hemorrhages/*diagnosis
MH  - Magnetic Resonance Imaging
MH  - Salivary Glands/pathology
MH  - Sialography
MH  - Sjogren's Syndrome/*physiopathology
MH  - Tomography, X-Ray Computed
PMC - PMC3729598
EDAT- 2013/07/31 06:00
MHDA- 2013/10/29 06:00
PMCR- 2013/07/29
CRDT- 2013/07/30 06:00
PHST- 2013/02/28 00:00 [received]
PHST- 2013/07/26 00:00 [accepted]
PHST- 2013/07/30 06:00 [entrez]
PHST- 2013/07/31 06:00 [pubmed]
PHST- 2013/10/29 06:00 [medline]
PHST- 2013/07/29 00:00 [pmc-release]
AID - 1471-2377-13-100 [pii]
AID - 10.1186/1471-2377-13-100 [doi]
PST - epublish
SO  - BMC Neurol. 2013 Jul 29;13:100. doi: 10.1186/1471-2377-13-100.

PMID- 23885678
OWN - NLM
STAT- MEDLINE
DCOM- 20130923
LR  - 20220311
IS  - 1555-7162 (Electronic)
IS  - 0002-9343 (Print)
IS  - 0002-9343 (Linking)
VI  - 126
IP  - 8
DP  - 2013 Aug
TI  - Cardiovascular risk in rheumatoid arthritis: comparing TNF-α blockade with 
      nonbiologic DMARDs.
PG  - 730.e9-730.e17
LID - S0002-9343(13)00227-1 [pii]
LID - 10.1016/j.amjmed.2013.02.016 [doi]
AB  - BACKGROUND: Elevated tumor necrosis factor (TNF)-α likely contributes to the 
      excess cardiovascular risk observed in rheumatoid arthritis. We compared the 
      cardiovascular risk in rheumatoid arthritis patients starting a TNF-α blocking 
      agent versus a nonbiologic disease-modifying antirheumatic drug (nbDMARD). 
      METHODS: Subjects with rheumatoid arthritis participating in several different US 
      insurance programs between 1998 and 2007 who received methotrexate were eligible. 
      Those who added a TNF-α blocking agent were compared with subjects who added a 
      nbDMARD in Cox regression models stratified by propensity score decile and 
      adjusted for oral glucocorticoid dosage. We examined the composite cardiovascular 
      end point of myocardial infarction, stroke, or coronary re-vascularization after 
      6 months. RESULTS: We compared 8656 new users of a nbDMARD with 11,587 new users 
      of a TNF-α blocking agent with similar baseline covariates. Incidence rates per 
      100 person-years for the composite cardiovascular end point were 3.05 (95% 
      confidence interval [CI], 2.54-3.65) for nbDMARDs and 2.52 (95% CI, 2.12-2.98) 
      for TNF-α blocking agents. The hazard ratio (HR) for the TNF-α blocking agent 
      compared with nbDMARD carrying the first exposure forward was 0.80 (95%, CI 
      0.62-1.04), while the HR for the as-treated analysis was 0.71 (95% CI, 
      0.52-0.97). The potential cardiovascular benefit of TNF-α blocking agents was 
      strongest among individuals ≥65 years of age (HR 0.52; 95% CI, 0.34 -0.77; P for 
      interaction = 0.075). CONCLUSION: Among subjects with rheumatoid arthritis, TNF-α 
      blocking agents may be associated with a reduced risk of cardiovascular events 
      compared with an nbDMARD. Randomized controlled clinical trials should be 
      considered to test this hypothesis.
CI  - Copyright © 2013 Elsevier Inc. All rights reserved.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - Brigham and Women's Hospital, Boston, MA 02115, USA. dhsolomon@partners.org
FAU - Curtis, Jeffrey R
AU  - Curtis JR
FAU - Saag, Kenneth G
AU  - Saag KG
FAU - Lii, Joyce
AU  - Lii J
FAU - Chen, Lang
AU  - Chen L
FAU - Harrold, Leslie R
AU  - Harrold LR
FAU - Herrinton, Lisa J
AU  - Herrinton LJ
FAU - Graham, David J
AU  - Graham DJ
FAU - Kowal, Mary K
AU  - Kowal MK
FAU - Kuriya, Bindee
AU  - Kuriya B
FAU - Liu, Liyan
AU  - Liu L
FAU - Griffin, Marie R
AU  - Griffin MR
FAU - Lewis, James D
AU  - Lewis JD
FAU - Rassen, Jeremy A
AU  - Rassen JA
LA  - eng
GR  - K23 AR053351/AR/NIAMS NIH HHS/United States
GR  - U18 HS017919/HS/AHRQ HHS/United States
GR  - 1U18 HSO17919-0/PHS HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Med
JT  - The American journal of medicine
JID - 0267200
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/complications/*drug therapy
MH  - Cardiovascular Diseases/complications/*prevention & control
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Kaplan-Meier Estimate
MH  - Male
MH  - Methotrexate/*therapeutic use
MH  - Middle Aged
MH  - Myocardial Infarction/prevention & control
MH  - Myocardial Revascularization
MH  - Proportional Hazards Models
MH  - Retrospective Studies
MH  - Risk
MH  - Stroke/prevention & control
MH  - Treatment Outcome
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
PMC - PMC4674813
MID - NIHMS739450
OTO - NOTNLM
OT  - Cardiovascular disease
OT  - Rheumatoid arthritis
OT  - TNF-α blocking agents
EDAT- 2013/07/28 06:00
MHDA- 2013/09/24 06:00
PMCR- 2015/12/10
CRDT- 2013/07/27 06:00
PHST- 2012/10/22 00:00 [received]
PHST- 2013/01/17 00:00 [revised]
PHST- 2013/02/04 00:00 [accepted]
PHST- 2013/07/27 06:00 [entrez]
PHST- 2013/07/28 06:00 [pubmed]
PHST- 2013/09/24 06:00 [medline]
PHST- 2015/12/10 00:00 [pmc-release]
AID - S0002-9343(13)00227-1 [pii]
AID - 10.1016/j.amjmed.2013.02.016 [doi]
PST - ppublish
SO  - Am J Med. 2013 Aug;126(8):730.e9-730.e17. doi: 10.1016/j.amjmed.2013.02.016.

PMID- 23874021
OWN - NLM
STAT- MEDLINE
DCOM- 20140311
LR  - 20211021
IS  - 0065-7778 (Print)
IS  - 0065-7778 (Linking)
VI  - 124
DP  - 2013
TI  - Closing the loop on inflammation and atherothrombosis: why perform the CIRT and 
      CANTOS trials?
PG  - 174-90
AB  - Inflammation contributes to all phases of the atherothrombotic process, patients 
      with elevated inflammatory biomarkers such as high-sensitivity C-reactive protein 
      (hsCRP) have increased cardiovascular risk, and recent work directly implicates 
      the interleukin-1 (IL-1) and interleukin-6 (IL-6) pathways in atherogenesis. Yet, 
      it remains unknown whether targeted inhibition of inflammation will reduce 
      cardiovascular event rates. To address directly this fundamental hypothesis, our 
      research group has initiated two large-scale, randomized, placebo-controlled 
      trials using targeted anti-inflammatory agents for the secondary prevention of 
      myocardial infarction. The first trial, the Cardiovascular Inflammation Reduction 
      Trial (CIRT), has been funded by the NHLBI and will evaluate whether low-dose 
      methotrexate (target dose, 20 mg/wk) as compared to placebo will reduce major 
      vascular events among a group of post-myocardial infarction patients with either 
      diabetes or metabolic syndrome, groups known to have high risk on the basis of a 
      persistent pro-inflammatory response. CIRT is based, in part, on observational 
      evidence of reduced vascular event rates among those treated with methotrexate in 
      the setting of rheumatoid arthritis or psoriatic arthritis and on the ability of 
      methotrexate to reduce TNF, IL-6, and CRP levels. The second trial, the 
      Canakinumab Anti-Inflammatory Thrombosis Outcomes Study (CANTOS), will evaluate 
      whether interleukin-1β (IL-1β) inhibition as compared to placebo can reduce rates 
      of recurrent myocardial infarction, stroke, and cardiovascular death among stable 
      coronary artery disease patients who remain at high vascular risk due to 
      persistent elevations of hsCRP (_2 mg/L) despite contemporary secondary 
      prevention strategies. Canakinumab is a human monoclonal antibody that 
      selectively neutralizes IL-1β, a pro-inflammatory cytokine that plays multiple 
      roles in the atherothrombotic process and that undergoes activation by the NLRP3 
      inflammasome, a process promoted by cholesterol crystals that in turn leads 
      directly to increased production of IL-1 and IL-6. Together, CIRT and CANTOS will 
      enroll more than 25,000 patients worldwide and provide a fundamental test of the 
      inflammatory hypothesis of atherothrombosis.
FAU - Ridker, Paul M
AU  - Ridker PM
AD  - Center for Cardiovascular Disease Prevention, Brigham and Women’s Hospital, 900 
      Commonwealth Avenue East, Boston, MA 02215, USA. pridker@partners.org
LA  - eng
GR  - U01 HL101422/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Trans Am Clin Climatol Assoc
JT  - Transactions of the American Clinical and Climatological Association
JID - 7507559
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Biomarkers)
RN  - 0 (Cytokines)
RN  - 37CQ2C7X93 (canakinumab)
RN  - 935E97BOY8 (Folic Acid)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Anti-Inflammatory Agents/*therapeutic use
MH  - Antibodies, Monoclonal/*therapeutic use
MH  - Antibodies, Monoclonal, Humanized
MH  - Biomarkers
MH  - Cytokines/genetics/metabolism
MH  - Female
MH  - Folic Acid/therapeutic use
MH  - Gene Expression Regulation/physiology
MH  - Humans
MH  - Inflammation/*pathology
MH  - Male
MH  - Methotrexate/administration & dosage/therapeutic use
MH  - Randomized Controlled Trials as Topic
MH  - Thrombosis/*pathology/*prevention & control
PMC - PMC3715939
COIS- Potential Conflicts of Interest: None disclosed.
EDAT- 2013/07/23 06:00
MHDA- 2014/03/13 06:00
PMCR- 2013/01/01
CRDT- 2013/07/23 06:00
PHST- 2013/07/23 06:00 [entrez]
PHST- 2013/07/23 06:00 [pubmed]
PHST- 2014/03/13 06:00 [medline]
PHST- 2013/01/01 00:00 [pmc-release]
PST - ppublish
SO  - Trans Am Clin Climatol Assoc. 2013;124:174-90.

PMID- 23790244
OWN - NLM
STAT- MEDLINE
DCOM- 20140407
LR  - 20130820
IS  - 1473-4877 (Electronic)
IS  - 0300-7995 (Linking)
VI  - 29
IP  - 9
DP  - 2013 Sep
TI  - What do we know about the safety of corticosteroids in rheumatoid arthritis?
PG  - 1147-60
LID - 10.1185/03007995.2013.818531 [doi]
AB  - BACKGROUND: Clear information is still lacking on the safety of corticosteroids 
      (GCs) therapy in RA despite six decades of clinical experience. SCOPE: We 
      performed a literature search in Ovid MEDLINE from January 2000 to December 2012. 
      Our Population Intervention Comparator Outcomes (PICO) strategy search was: 
      rheumatoid arthritis [Population], corticosteroids or glucocorticoids 
      [Intervention], any comparison [Comparator], adverse effects [Outcome]. Studies 
      were selected if they reported any measure of association between GCs intake and 
      potential adverse effects in RA patients. FINDINGS: We identified 1030 papers and 
      selected for analysis 26 observational studies and six systematic reviews. The 
      major side effects of GCs in RA are bone loss, risk of cardiovascular events and 
      risk of infections as evidenced by large observational studies and not 
      necessarily RCTs. Others associations were reported with herpes zoster, 
      tuberculosis, hyperglycemia, cutaneous abnormalities, gastrointestinal 
      perforation, respiratory infection and self-reported health problems such as 
      cushingoid phenotype, ecchymosis, parchment-like skin, epistaxis, weight gain and 
      sleep disturbance. Other potential adverse effects of GCs were studied but no 
      association was found. These included psychological disorders, dermatophytosis, 
      brain diseases, interstitial lung disease, memory deficit, metabolic syndrome, 
      lymphoma, non-Hodgkin's lymphoma, renal function and cerebrovascular accidents. 
      Most of the evidence emanates from observational researches and the inherent 
      limitations of such data should be kept in mind. CONCLUSION: Recent observational 
      data and systematic reviews suggest that GCs can lead to relatively alarming and 
      burdensome side effects in RA. This is particularly true for patients who have 
      longer term and higher dose therapies. GCs are largely used in RA and knowing 
      their safety profile is essential to improve patients care. The design of new 
      therapeutic strategies intended to minimize the daily dosing of GCs while 
      conserving their beneficial effect should be encouraged.
FAU - Ethgen, Olivier
AU  - Ethgen O
AD  - Department of Public Health Sciences, Epidemiology and Health Economics, 
      University of Liège, Liège, Belgium. o.ethgen@ulg.ac.be
FAU - de Lemos Esteves, Frédéric
AU  - de Lemos Esteves F
FAU - Bruyere, Olivier
AU  - Bruyere O
FAU - Reginster, Jean-Yves
AU  - Reginster JY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20130703
PL  - England
TA  - Curr Med Res Opin
JT  - Current medical research and opinion
JID - 0351014
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Glucocorticoids)
SB  - IM
MH  - Antirheumatic Agents/*adverse effects/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy/pathology/physiopathology
MH  - Female
MH  - Glucocorticoids/*adverse effects/*therapeutic use
MH  - Humans
MH  - MEDLINE
MH  - Male
EDAT- 2013/06/25 06:00
MHDA- 2014/04/08 06:00
CRDT- 2013/06/25 06:00
PHST- 2013/06/25 06:00 [entrez]
PHST- 2013/06/25 06:00 [pubmed]
PHST- 2014/04/08 06:00 [medline]
AID - 10.1185/03007995.2013.818531 [doi]
PST - ppublish
SO  - Curr Med Res Opin. 2013 Sep;29(9):1147-60. doi: 10.1185/03007995.2013.818531. 
      Epub 2013 Jul 3.

PMID- 23749610
OWN - NLM
STAT- Publisher
LR  - 20191120
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 73
IP  - 8
DP  - 2014 Aug
TI  - Non-steroidal anti-inflammatory drugs and risk of cardiovascular disease in 
      patients with rheumatoid arthritis: a nationwide cohort study.
PG  - 1515-1521
LID - 10.1136/annrheumdis-2012-203137 [doi]
AB  - OBJECTIVE: To examine the risk of major cardiovascular disease associated with 
      non-steroidal anti-inflammatory drugs (NSAIDs) in a large 'real-world' 
      contemporary rheumatoid arthritis (RA) cohort. METHODS: A longitudinal cohort 
      study was conducted with use of Danish nationwide individual-level registry data 
      on inpatient and outpatient health care provision, pharmacotherapy and income 
      during 1997-2009. 17 320 RA patients were identified and matched with 69 280 
      controls (4 : 1) by age and sex. NSAID-associated risk of major cardiovascular 
      disease defined as the combined endpoint of myocardial infarction, stroke or 
      cardiovascular mortality was assessed in multivariable survival models. RESULTS: 
      During follow-up (median 4.9 years) 6283 events occurred. The cardiovascular risk 
      associated with overall NSAID use was significantly lower in RA patients than in 
      controls (HR 1.22 (95% CI 1.09 to 1.37) vs 1.51 (1.36 to 1.66), p<0.01). The 
      pattern of lower NSAID-associated risk in RA patients was generally found with 
      the individual NSAIDs investigated. While use of rofecoxib (HR 1.57 (1.16 to 
      2.12)) and diclofenac (HR 1.35 (1.11 to 1.64)) was associated with increased 
      cardiovascular risk in RA patients, there was no significant risk increase 
      associated with use of other NSAIDs in these patients. CONCLUSIONS: The 
      cardiovascular risk associated with NSAID use in RA patients was modest and 
      significantly lower than in non-RA individuals. Moreover, only a few of the 
      individual NSAIDs were associated with increased cardiovascular risk. NSAID use 
      should be assessed in the individual patient based on the indication for pain 
      relief and risk factors for adverse effects, and not automatically be avoided due 
      to concerns of severe cardiovascular outcomes alone.
FAU - Lindhardsen, Jesper
AU  - Lindhardsen J
AD  - Department of Cardiology, Copenhagen University Hospital Gentofte, Hellerup, 
      Denmark.
FAU - Gislason, Gunnar Hilmar
AU  - Gislason GH
FAU - Jacobsen, Søren
AU  - Jacobsen S
FAU - Ahlehoff, Ole
AU  - Ahlehoff O
FAU - Olsen, Anne-Marie Schjerning
AU  - Olsen AM
FAU - Madsen, Ole Rintek
AU  - Madsen OR
FAU - Torp-Pedersen, Christian
AU  - Torp-Pedersen C
FAU - Hansen, Peter Riis
AU  - Hansen PR
LA  - eng
PT  - Journal Article
DEP - 20130608
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
OTO - NOTNLM
OT  - Cardiovascular Disease
OT  - NSAIDs
OT  - Rheumatoid Arthritis
EDAT- 2013/06/12 06:00
MHDA- 2013/06/12 06:00
CRDT- 2013/06/11 06:00
PHST- 2013/06/11 06:00 [entrez]
PHST- 2013/06/12 06:00 [pubmed]
PHST- 2013/06/12 06:00 [medline]
AID - annrheumdis-2012-203137 [pii]
AID - 10.1136/annrheumdis-2012-203137 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2014 Aug;73(8):1515-1521. doi: 10.1136/annrheumdis-2012-203137. 
      Epub 2013 Jun 8.

PMID- 23641033
OWN - NLM
STAT- MEDLINE
DCOM- 20130625
LR  - 20220321
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Print)
IS  - 0959-8138 (Linking)
VI  - 346
DP  - 2013 May 2
TI  - Derivation and validation of QStroke score for predicting risk of ischaemic 
      stroke in primary care and comparison with other risk scores: a prospective open 
      cohort study.
PG  - f2573
LID - bmj.f2573 [pii]
LID - 10.1136/bmj.f2573 [doi]
LID - f2573
AB  - OBJECTIVE: To develop and validate a risk algorithm (QStroke) to estimate risk of 
      stroke or transient ischaemic attack in patients without prior stroke or 
      transient ischaemic attack at baseline; to compare (a) QStroke with CHADS2 and 
      CHA2DS2VASc scores in patients with atrial fibrillation and (b) the performance 
      of QStroke with the Framingham stroke score in the full population free of stroke 
      or transient ischaemic attack. DESIGN: Prospective open cohort study using 
      routinely collected data from general practice during the study period 1 January 
      1998 to 1 August 2012. SETTING: 451 general practices in England and Wales 
      contributing to the national QResearch database to develop the algorithm and 225 
      different QResearch practices to validate the algorithm. PARTICIPANTS: 3.5 
      million patients aged 25-84 years with 24.8 million person years in the 
      derivation cohort who experienced 77,578 stroke events. For the validation 
      cohort, we identified 1.9 million patients aged 25-84 years with 12.7 million 
      person years who experienced 38,404 stroke events. We excluded patients with a 
      prior diagnosis of stroke or transient ischaemic attack and those prescribed oral 
      anticoagulants at study entry. MAIN OUTCOME MEASURES: Incident diagnosis of 
      stroke or transient ischaemic attack recorded in general practice records or 
      linked death certificates during follow-up. RISK FACTORS: Self assigned 
      ethnicity, age, sex, smoking status, systolic blood pressure, ratio of total 
      serum cholesterol to high density lipoprotein cholesterol concentrations, body 
      mass index, family history of coronary heart disease in first degree relative 
      under 60 years, Townsend deprivation score, treated hypertension, type 1 
      diabetes, type 2 diabetes, renal disease, rheumatoid arthritis, coronary heart 
      disease, congestive cardiac failure, valvular heart disease, and atrial 
      fibrillation RESULTS: The QStroke algorithm explained 57% of the variation in 
      women and 55% in men without a prior stroke. The D statistic for QStroke was 2.4 
      in women and 2.3 in men. QStroke had improved performance on all measures of 
      discrimination and calibration compared with the Framingham score in patients 
      without a prior stroke. Among patients with atrial fibrillation, levels of 
      discrimination were lower, but QStroke had some improved performance on all 
      measures of discrimination compared with CHADS2 and CHA2DS2VASc. CONCLUSION: 
      QStroke provides a valid measure of absolute stroke risk in the general 
      population of patients free of stroke or transient ischaemic attack as shown by 
      its performance in a separate validation cohort. QStroke also shows some 
      improvement on current risk scoring methods, CHADS2 and CHA2DS2VASc, for the 
      subset of patients with atrial fibrillation for whom anticoagulation may be 
      required. Further research is needed to evaluate the cost effectiveness of using 
      these algorithms in primary care.
FAU - Hippisley-Cox, Julia
AU  - Hippisley-Cox J
AD  - Division of Primary Care, University Park, Nottingham NG2 7RD, UK. 
      Julia.hippisley-cox@nottingham.ac.uk
FAU - Coupland, Carol
AU  - Coupland C
FAU - Brindle, Peter
AU  - Brindle P
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Validation Study
DEP - 20130502
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
RN  - 0 (Cholesterol, HDL)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Age Factors
MH  - Aged
MH  - Aged, 80 and over
MH  - Algorithms
MH  - Arthritis, Rheumatoid/epidemiology
MH  - Atrial Fibrillation/epidemiology
MH  - Blood Pressure
MH  - Body Mass Index
MH  - Cholesterol/blood
MH  - Cholesterol, HDL/blood
MH  - Coronary Disease/epidemiology/genetics
MH  - Diabetes Mellitus/epidemiology
MH  - Female
MH  - Heart Failure/epidemiology
MH  - Heart Valve Diseases/epidemiology
MH  - Humans
MH  - Hypertension/epidemiology
MH  - Incidence
MH  - Ischemic Attack, Transient/*epidemiology
MH  - Kidney Diseases/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Primary Health Care
MH  - Prospective Studies
MH  - Racial Groups
MH  - Regression Analysis
MH  - Risk Assessment/*methods
MH  - Risk Factors
MH  - Sex Factors
MH  - Smoking/epidemiology
MH  - Stroke/*epidemiology
MH  - United Kingdom/epidemiology
PMC - PMC3641809
COIS- Competing interests: All authors have completed the ICMJE uniform disclosure form 
      at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding 
      author) and declare: JHC is professor of clinical epidemiology at the University 
      of Nottingham and co-director of QResearch, a not-for-profit organisation which 
      is a joint partnership between the University of Nottingham and EMIS (commercial 
      supplier of IT for 60% of general practices in the UK). JHC is also director of 
      ClinRisk, which produces open and closed source software to ensure reliable and 
      updatable implementation of clinical risk algorithms within clinical computer 
      systems. CC is associate professor of Medical Statistics at the University of 
      Nottingham and a consultant statistician for ClinRisk. This work and any views 
      expressed within it are solely those of the authors and not of any affiliated 
      bodies or organisations. There are no other relationships or activities that 
      could appear to have influenced the submitted work.
EDAT- 2013/05/04 06:00
MHDA- 2013/06/26 06:00
PMCR- 2013/05/02
CRDT- 2013/05/04 06:00
PHST- 2013/05/04 06:00 [entrez]
PHST- 2013/05/04 06:00 [pubmed]
PHST- 2013/06/26 06:00 [medline]
PHST- 2013/05/02 00:00 [pmc-release]
AID - bmj.f2573 [pii]
AID - hipj009990 [pii]
AID - 10.1136/bmj.f2573 [doi]
PST - epublish
SO  - BMJ. 2013 May 2;346:f2573. doi: 10.1136/bmj.f2573.

PMID- 23562414
OWN - NLM
STAT- MEDLINE
DCOM- 20140224
LR  - 20191210
IS  - 1532-821X (Electronic)
IS  - 0003-9993 (Linking)
VI  - 95
IP  - 1
DP  - 2014 Jan
TI  - Economic evaluation of adult rehabilitation: a systematic review and 
      meta-analysis of randomized controlled trials in a variety of settings.
PG  - 94-116.e4
LID - S0003-9993(13)00278-5 [pii]
LID - 10.1016/j.apmr.2013.03.017 [doi]
AB  - OBJECTIVES: To report if there is a difference in costs from a societal 
      perspective between adults receiving rehabilitation in an inpatient 
      rehabilitation setting versus an alternative setting. If there are cost 
      differences, to report whether opting for the least expensive program setting 
      adversely affects patient outcomes. DATA SOURCES: Electronic databases from the 
      earliest possible date until May 2011. All languages were included. STUDY 
      SELECTION: Multiple reviewers identified randomized controlled trials with a full 
      economic evaluation that compared adult inpatient rehabilitation with an 
      alternative. There were 29 included trials with 6746 participants. DATA 
      EXTRACTION: Multiple observers extracted data independently. Trial appraisal 
      included a risk of bias assessment and a checklist to report the strength of the 
      economic evaluation. DATA SYNTHESIS: Results were synthesized using standardized 
      mean differences (SMDs) and meta-analyses for the primary outcome of cost. The 
      Grading of Recommendations Assessment, Development, and Evaluation was applied to 
      assess for risk of bias across studies for meta-analyses. There was high-quality 
      evidence that cost was significantly reduced for rehabilitation in the home 
      versus inpatient rehabilitation in a meta-analysis of 732 patients poststroke 
      (pooled SMD [δ]=-.28; 95% confidence interval [CI], -.47 to -.09), without 
      compromise to patient outcomes. Results of individual trials in other patient 
      groups (orthopedic, rheumatoid arthritis, and geriatric) receiving rehabilitation 
      in the home or community were generally consistent with the meta-analysis. There 
      was moderate quality evidence that cost was significantly reduced for inpatient 
      rehabilitation (stroke unit) versus general acute care in a meta-analysis of 463 
      patients poststroke (δ=.31; 95% CI, .15-.48), with improvement to patient 
      outcomes. These results were not replicated in 2 individual trials with a 
      geriatric and a mixed cohort, where costs did not differ between general acute 
      care and inpatient rehabilitation. Three of the 4 individual trials, inclusive of 
      a stroke or orthopedic population, reported less cost for an intensive inpatient 
      rehabilitation program compared with usual inpatient rehabilitation. Sensitivity 
      analysis included a health service perspective and varied inflation rates with no 
      change to the significant findings of the meta-analyses. CONCLUSIONS: Based on 
      this systematic review and meta-analyses, a single rehabilitation service may not 
      provide health economic benefits for all patient groups and situations. For some 
      patients, inpatient rehabilitation may be the most cost-effective method of 
      providing rehabilitation; yet, for other patients, rehabilitation in the home or 
      community may be the most cost-effective model of care. To achieve cost-effective 
      outcomes, the ideal combination of rehabilitation services and patient inclusion 
      criteria, as well as further data for nonstroke populations, warrants further 
      research.
CI  - Copyright © 2014 American Congress of Rehabilitation Medicine. Published by 
      Elsevier Inc. All rights reserved.
FAU - Brusco, Natasha Kareem
AU  - Brusco NK
AD  - Department of Physiotherapy, La Trobe University, Melbourne, Australia; 
      Physiotherapy Services, Cabrini Health, Melbourne, Australia. Electronic address: 
      nbrusco@cabrini.com.au.
FAU - Taylor, Nicholas F
AU  - Taylor NF
AD  - Department of Physiotherapy, La Trobe University, Melbourne, Australia; Allied 
      Health Clinical Research Office, Eastern Health, Melbourne, Australia.
FAU - Watts, Jennifer J
AU  - Watts JJ
AD  - School of Health and Social Development, Deakin University, Melbourne, Australia.
FAU - Shields, Nora
AU  - Shields N
AD  - Department of Physiotherapy, La Trobe University, Melbourne, Australia.
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PT  - Systematic Review
DEP - 20130403
PL  - United States
TA  - Arch Phys Med Rehabil
JT  - Archives of physical medicine and rehabilitation
JID - 2985158R
SB  - IM
MH  - Community Health Services/*economics
MH  - Costs and Cost Analysis
MH  - Disabled Persons/*rehabilitation
MH  - Home Care Services/*economics
MH  - Humans
MH  - Inpatients/statistics & numerical data
MH  - Outcome Assessment, Health Care
MH  - Outpatients/statistics & numerical data
MH  - Randomized Controlled Trials as Topic
MH  - Rehabilitation Centers/*economics
OTO - NOTNLM
OT  - CI
OT  - Economics
OT  - GRADE
OT  - Grading of Recommendations Assessment, Development, and Evaluation
OT  - Hospitals
OT  - MD
OT  - NPV
OT  - Randomized controlled trials as topic
OT  - Rehabilitation
OT  - SMD
OT  - confidence interval
OT  - mean difference
OT  - net present value
OT  - standardized mean difference
EDAT- 2013/04/09 06:00
MHDA- 2014/02/25 06:00
CRDT- 2013/04/09 06:00
PHST- 2013/02/13 00:00 [received]
PHST- 2013/03/14 00:00 [revised]
PHST- 2013/03/14 00:00 [accepted]
PHST- 2013/04/09 06:00 [entrez]
PHST- 2013/04/09 06:00 [pubmed]
PHST- 2014/02/25 06:00 [medline]
AID - S0003-9993(13)00278-5 [pii]
AID - 10.1016/j.apmr.2013.03.017 [doi]
PST - ppublish
SO  - Arch Phys Med Rehabil. 2014 Jan;95(1):94-116.e4. doi: 10.1016/j.apmr.2013.03.017. 
      Epub 2013 Apr 3.

PMID- 23547211
OWN - NLM
STAT- MEDLINE
DCOM- 20140124
LR  - 20211021
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 40
IP  - 6
DP  - 2013 Jun
TI  - Cardiovascular events are not associated with MTHFR polymorphisms, but are 
      associated with methotrexate use and traditional risk factors in US veterans with 
      rheumatoid arthritis.
PG  - 809-17
LID - 10.3899/jrheum.121012 [doi]
AB  - OBJECTIVE: C677T and A1298C polymorphisms in the enzyme methylenetetrahydrofolate 
      reductase (MTHFR) have been associated with increased cardiovascular (CV) events 
      in non-rheumatoid arthritis (RA) populations. We investigated potential 
      associations of MTHFR polymorphisms and use of methotrexate (MTX) with time-to-CV 
      event in data from the Veterans Affairs Rheumatoid Arthritis (VARA) registry. 
      METHODS: VARA participants were genotyped for MTHFR polymorphisms. Variables 
      included demographic information, baseline comorbidities, RA duration, 
      autoantibody status, and disease activity. Patients' comorbidities and outcome 
      variables were defined using International Classification of Diseases-9 and 
      Current Procedural Terminology codes. The combined CV event outcome included 
      myocardial infarction (MI), percutaneous coronary intervention, coronary artery 
      bypass graft surgery, and stroke. Cox proportional hazards regression was used to 
      model the time-to-CV event. RESULTS: Data were available for 1047 subjects. 
      Post-enrollment CV events occurred in 97 patients (9.26%). Although there was a 
      trend toward reduced risk of CV events, MTHFR polymorphisms were not 
      significantly associated with time-to-CV event. Time-to-CV event was associated 
      with prior stroke (HR 2.01, 95% CI 1.03-3.90), prior MI (HR 1.70, 95% CI 
      1.06-2.71), hyperlipidemia (HR 1.57, 95% CI 1.01-2.43), and increased modified 
      Charlson-Deyo index (HR 1.23, 95% CI 1.13-1.34). MTX use (HR 0.66, 95% CI 
      0.44-0.99) and increasing education (HR 0.87, 95% CI 0.80-0.95) were associated 
      with a lower risk for CV events. CONCLUSION: Although MTHFR polymorphisms were 
      previously associated with CV events in non-RA populations, we found only a trend 
      toward decreased association with CV events in RA. Traditional risk factors 
      conferred substantial CV risk, while MTX use and increasing years of education 
      were protective.
FAU - Davis, Lisa A
AU  - Davis LA
AD  - Department of Rheumatology, University of Colorado School of Medicine, Denver, 
      CO, USA. lisa.davis@ucdenver.edu
FAU - Cannon, Grant W
AU  - Cannon GW
FAU - Pointer, Lauren F
AU  - Pointer LF
FAU - Haverhals, Leah M
AU  - Haverhals LM
FAU - Wolff, Roger K
AU  - Wolff RK
FAU - Mikuls, Ted R
AU  - Mikuls TR
FAU - Reimold, Andreas M
AU  - Reimold AM
FAU - Kerr, Gail S
AU  - Kerr GS
FAU - Richards, J Steuart
AU  - Richards JS
FAU - Johnson, Dannette S
AU  - Johnson DS
FAU - Valuck, Robert
AU  - Valuck R
FAU - Prochazka, Allan
AU  - Prochazka A
FAU - Caplan, Liron
AU  - Caplan L
LA  - eng
GR  - T32 AR007534/AR/NIAMS NIH HHS/United States
GR  - T32 AR007534-24/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20130401
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Antirheumatic Agents)
RN  - EC 1.5.1.20 (MTHFR protein, human)
RN  - EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2))
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Antirheumatic Agents/*adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Cardiovascular Diseases/chemically induced/*etiology/genetics
MH  - Female
MH  - Genotype
MH  - Humans
MH  - Male
MH  - Methotrexate/*adverse effects/therapeutic use
MH  - Methylenetetrahydrofolate Reductase (NADPH2)/*genetics
MH  - Middle Aged
MH  - Polymorphism, Single Nucleotide
MH  - Registries
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Veterans
PMC - PMC4097095
MID - NIHMS608659
OTO - NOTNLM
OT  - CARDIOVASCULAR DISEASES
OT  - METHOTREXATE
OT  - METHYLENETETRAHYDROFOLATE REDUCTASE
OT  - RHEUMATOID ARTHRITIS
OT  - SINGLE-NUCLEOTIDE POLYMORPHISM
EDAT- 2013/04/03 06:00
MHDA- 2014/01/25 06:00
PMCR- 2014/07/15
CRDT- 2013/04/03 06:00
PHST- 2013/04/03 06:00 [entrez]
PHST- 2013/04/03 06:00 [pubmed]
PHST- 2014/01/25 06:00 [medline]
PHST- 2014/07/15 00:00 [pmc-release]
AID - jrheum.121012 [pii]
AID - 10.3899/jrheum.121012 [doi]
PST - ppublish
SO  - J Rheumatol. 2013 Jun;40(6):809-17. doi: 10.3899/jrheum.121012. Epub 2013 Apr 1.

PMID- 23352423
OWN - NLM
STAT- MEDLINE
DCOM- 20140609
LR  - 20161125
IS  - 1532-8511 (Electronic)
IS  - 1052-3057 (Linking)
VI  - 22
IP  - 7
DP  - 2013 Oct
TI  - Vertebral artery dissection in rheumatoid arthritis with cervical spine disease.
PG  - e245-6
LID - S1052-3057(13)00005-0 [pii]
LID - 10.1016/j.jstrokecerebrovasdis.2012.11.023 [doi]
AB  - A 59-year-old woman with long-standing active rheumatoid arthritis presented with 
      posterior circulation ischemic stroke after vertebral dissection. She had severe 
      multilevel degenerative changes of her cervical spine. She did not have classic 
      stroke risk factors nor evidence of atherosclerotic disease or other systemic 
      diseases. The most likely mechanism appears to be injury of the artery wall by an 
      osteophyte, causing dissection that resulted in thrombosis and subsequent embolic 
      strokes.
CI  - Copyright © 2013 National Stroke Association. Published by Elsevier Inc. All 
      rights reserved.
FAU - Mahajan, Ritika
AU  - Mahajan R
AD  - Department of Neurology, University of New Mexico School of Medicine, 
      Albuquerque, New Mexico.
FAU - Huisa, Branko N
AU  - Huisa BN
LA  - eng
PT  - Case Reports
PT  - Journal Article
DEP - 20130123
PL  - United States
TA  - J Stroke Cerebrovasc Dis
JT  - Journal of stroke and cerebrovascular diseases : the official journal of National 
      Stroke Association
JID - 9111633
SB  - IM
MH  - Arthritis, Rheumatoid/*complications/diagnostic imaging
MH  - Brain Ischemia/*complications/diagnostic imaging
MH  - Cervical Vertebrae/*diagnostic imaging
MH  - Female
MH  - Humans
MH  - Middle Aged
MH  - Radiography
MH  - Spinal Diseases/*complications/diagnostic imaging
MH  - Stroke/*complications/diagnostic imaging
MH  - Vertebral Artery Dissection/*complications/diagnostic imaging
OTO - NOTNLM
OT  - Acute ischemic stroke
OT  - inflammatory disease
OT  - neuroimaging
OT  - rheumatoid arthritis
OT  - stroke diagnosis
EDAT- 2013/01/29 06:00
MHDA- 2014/06/10 06:00
CRDT- 2013/01/29 06:00
PHST- 2012/09/24 00:00 [received]
PHST- 2012/11/01 00:00 [revised]
PHST- 2012/11/07 00:00 [accepted]
PHST- 2013/01/29 06:00 [entrez]
PHST- 2013/01/29 06:00 [pubmed]
PHST- 2014/06/10 06:00 [medline]
AID - S1052-3057(13)00005-0 [pii]
AID - 10.1016/j.jstrokecerebrovasdis.2012.11.023 [doi]
PST - ppublish
SO  - J Stroke Cerebrovasc Dis. 2013 Oct;22(7):e245-6. doi: 
      10.1016/j.jstrokecerebrovasdis.2012.11.023. Epub 2013 Jan 23.

PMID- 23250099
OWN - NLM
STAT- MEDLINE
DCOM- 20130731
LR  - 20160815
IS  - 1806-9282 (Electronic)
IS  - 0104-4230 (Linking)
VI  - 58
IP  - 6
DP  - 2012 Nov-Dec
TI  - Infliximab reduces cardiac output in rheumatoid arthritis patients without heart 
      failure.
PG  - 698-702
LID - S0104-42302012000600015 [pii]
AB  - OBJECTIVE: Human anti-tumor necrosis factor (TNF-α) monoclonal antibody 
      (infliximab) is used to treat autoimmune diseases such as rheumatoid arthritis 
      (RA). Although the risk of worsening heart failure has been described in patients 
      under chronic treatment, the acute cardiovascular effects of this drug are 
      unknown in RA patients without heart failure. METHODS: 14 RA patients with normal 
      echocardiography and no history of heart failure were evaluated during the 2-hour 
      infliximab (3-5 mg/kg) infusion period, using a noninvasive hemodynamic 
      beat-to-beat system (Portapres). Stroke volume (SV); systolic, diastolic and mean 
      blood pressures (SBP, DBP and MBP, respectively); cardiac output (CO); heart rate 
      (HR); and total peripheral vascular resistance (PVR) were recorded. All patients 
      also received saline infusion instead of infliximab as a control. Significant 
      differences in hemodynamic parameters were determined using Tuckey's test. All 
      values were expressed as mean ± standard deviation (SD). RESULTS: Fourteen RA 
      patients (6M/8F) with mean age of 47.2 ± 8.8 years were evaluated. A significant 
      decrease was found in cardiac output and stroke volume (7.04 ± 2.3 to 6.12 ± 2.1 
      l/min and 91 ± 29.0 to 83 ± 28.8 mL/beat, respectively) after infliximab 
      infusion. Although not statistically significant, a progressive increase was 
      detected in SBP, DBP and total PVR during infusion. Saline infusion did not cause 
      significant hemodynamic changes in the same group of RA patients. No adverse 
      effects were observed during the infusion period. CONCLUSION: Acute infliximab 
      administration decreased cardiac output due to low stroke volume in RA patients 
      without heart disease. The results also demonstrated that, in spite of its 
      negative inotropic effect, infliximab enhanced BP, probably by increasing PVR.
FAU - Santos, Rodrigo Cardoso
AU  - Santos RC
AD  - Department of Medicine, Faculty of Medical Sciences, Universidade Estadual de 
      Campinas, Campinas, SP, Brazil.
FAU - Figueiredo, Valéria Nasser
AU  - Figueiredo VN
FAU - Martins, Luiz Cláudio
AU  - Martins LC
FAU - Moraes, Carolina de Haro
AU  - Moraes Cde H
FAU - Quinaglia, Thiago
AU  - Quinaglia T
FAU - Boer-Martins, Leandro
AU  - Boer-Martins L
FAU - Ferreira-Melo, Sílvia Elaine
AU  - Ferreira-Melo SE
FAU - Yazbek, Michel Alexandre
AU  - Yazbek MA
FAU - Bertolo, Manoel
AU  - Bertolo M
FAU - Moreno, Heitor Jr
AU  - Moreno H Jr
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Brazil
TA  - Rev Assoc Med Bras (1992)
JT  - Revista da Associacao Medica Brasileira (1992)
JID - 9308586
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antirheumatic Agents)
RN  - B72HH48FLU (Infliximab)
SB  - IM
MH  - Adult
MH  - Antibodies, Monoclonal/*administration & dosage/adverse effects
MH  - Antirheumatic Agents/*administration & dosage
MH  - Arthritis, Rheumatoid/*drug therapy/physiopathology
MH  - Blood Pressure/physiology
MH  - Cardiac Output/*drug effects
MH  - Echocardiography
MH  - Female
MH  - *Heart Failure/diagnosis
MH  - Heart Rate/drug effects
MH  - Humans
MH  - Infliximab
MH  - Male
MH  - Middle Aged
MH  - Stroke Volume/physiology
EDAT- 2012/12/20 06:00
MHDA- 2013/08/01 06:00
CRDT- 2012/12/20 06:00
PHST- 2011/01/20 00:00 [received]
PHST- 2012/07/24 00:00 [accepted]
PHST- 2012/12/20 06:00 [entrez]
PHST- 2012/12/20 06:00 [pubmed]
PHST- 2013/08/01 06:00 [medline]
AID - S0104-42302012000600015 [pii]
PST - ppublish
SO  - Rev Assoc Med Bras (1992). 2012 Nov-Dec;58(6):698-702.

PMID- 23218811
OWN - NLM
STAT- MEDLINE
DCOM- 20130424
LR  - 20220311
IS  - 1873-2585 (Electronic)
IS  - 1047-2797 (Linking)
VI  - 23
IP  - 2
DP  - 2013 Feb
TI  - Arthritis: its prevalence, risk factors, and association with cardiovascular 
      diseases in the United States, 1999 to 2008.
PG  - 80-6
LID - S1047-2797(12)00428-0 [pii]
LID - 10.1016/j.annepidem.2012.11.008 [doi]
AB  - OBJECTIVE: Arthritis is associated with cardiovascular diseases (CVDs). However, 
      there are limited epidemiologic studies on arthritis in a national survey study. 
      We therefore investigated the prevalence of self-reported arthritis and its 
      association with CVDs. METHODS: Data from 15,888 subjects aged 40 years or older 
      in the United States National Health and Nutrition Examination Survey 1999 
      through 2008 were analyzed. CVD was defined as a self-reported history of heart 
      attack, congestive heart failure, coronary heart disease, angina, or stroke. 
      RESULTS: The overall prevalence of self-reported arthritis in subjects aged 40 
      years or older increased from 33.5% in 1999 through 2000 to 37.0% in 2007 through 
      2008 (P for trend = 0.017). Among subjects with arthritis in 1999 through 2008, 
      35.3% had osteoarthritis (OA), 17.9% had rheumatoid arthritis (RA), and 10.2% had 
      other types of arthritis, but 36.6% were unaware of their type of arthritis. 
      Compared with subjects without OA, subjects with OA had higher odds for CVDs 
      (odds ratio [OR], 1.53; P < .001), especially angina (OR, 2.18: P < .001). 
      Compared with subjects without RA, subjects with RA had higher odds for CVDs 
      (adjusted OR, 2.39; P < .001), especially congestive heart failure (OR, 3.59; P < 
      .001). CONCLUSIONS: Both RA and OA are strongly associated with CVDs in the 
      general population. Further studies are needed to investigate their causal 
      relationship.
CI  - Copyright © 2013 Elsevier Inc. All rights reserved.
FAU - Ong, Kwok Leung
AU  - Ong KL
AD  - Lipid Research Group, Heart Research Institute, Sydney, New South Wales, 
      Australia. ongk@hri.org.au
FAU - Wu, Ben J
AU  - Wu BJ
FAU - Cheung, Bernard M Y
AU  - Cheung BM
FAU - Barter, Philip J
AU  - Barter PJ
FAU - Rye, Kerry-Anne
AU  - Rye KA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121205
PL  - United States
TA  - Ann Epidemiol
JT  - Annals of epidemiology
JID - 9100013
SB  - IM
MH  - Adult
MH  - Age Distribution
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis/complications/*epidemiology
MH  - Cardiovascular Diseases/complications/*epidemiology
MH  - Cross-Sectional Studies
MH  - Female
MH  - Health Surveys
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Odds Ratio
MH  - Prevalence
MH  - Risk Factors
MH  - Sex Distribution
MH  - Socioeconomic Factors
MH  - United States/epidemiology
EDAT- 2012/12/12 06:00
MHDA- 2013/04/25 06:00
CRDT- 2012/12/11 06:00
PHST- 2012/09/23 00:00 [received]
PHST- 2012/11/14 00:00 [revised]
PHST- 2012/11/19 00:00 [accepted]
PHST- 2012/12/11 06:00 [entrez]
PHST- 2012/12/12 06:00 [pubmed]
PHST- 2013/04/25 06:00 [medline]
AID - S1047-2797(12)00428-0 [pii]
AID - 10.1016/j.annepidem.2012.11.008 [doi]
PST - ppublish
SO  - Ann Epidemiol. 2013 Feb;23(2):80-6. doi: 10.1016/j.annepidem.2012.11.008. Epub 
      2012 Dec 5.

PMID- 23157913
OWN - NLM
STAT- MEDLINE
DCOM- 20131204
LR  - 20121127
IS  - 1578-2190 (Electronic)
IS  - 0001-7310 (Linking)
VI  - 103
IP  - 10
DP  - 2012 Dec
TI  - Cardiovascular risk and psoriasis: the role of biologic therapy.
PG  - 853-62
LID - S1578-2190(12)00303-4 [pii]
LID - 10.1016/j.adengl.2012.02.004 [doi]
AB  - One of the most clinically important aspects of recent advances in our 
      understanding of psoriasis has been the detection of an association between this 
      disease and an increased prevalence of cardiovascular risk factors. This increase 
      in prevalence is, in turn, linked to a greater risk of morbidity and mortality 
      related to acute myocardial infarction, cerebrovascular accident, and peripheral 
      arterial disease. The chronic systemic inflammation present in psoriasis could 
      explain why moderate to severe psoriasis is an independent risk factor for 
      cardiovascular disease. The introduction of biologic therapies has greatly 
      improved the expectations of treatment as well as the long-term control of 
      psoriasis, and there is epidemiological evidence that these therapies may lower 
      cardiovascular risk in psoriasis as they do in rheumatoid arthritis. Caution 
      should, however, be exercised when prescribing biologic drugs in this setting, 
      because adverse effects have been reported in association with the use of tumor 
      necrosis factor inhibitors in patients with advanced congestive heart failure. 
      Furthermore, a numerical imbalance (without statistical significance) between the 
      groups receiving the biologic drug and the placebo groups was recently observed 
      in the incidence of major cardiovascular events (nonfatal myocardial infarction 
      and cerebrovascular accident and cardiovascular death) during the controlled 
      periods of clinical trials of briakinumab and ustekinumab, 2 monoclonal 
      antibodies that target the p40 subunit shared by IL-12 and IL-23. We review the 
      current scientific evidence on this topic.
CI  - Copyright © 2011 Elsevier España, S.L. and AEDV. All rights reserved.
FAU - Puig, L
AU  - Puig L
AD  - Servicio de Dermatología, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. 
      lpuig@santpau.cat
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20121115
PL  - Spain
TA  - Actas Dermosifiliogr
JT  - Actas dermo-sifiliograficas
JID - 0373062
RN  - 0 (Interleukin-17)
SB  - IM
MH  - Atherosclerosis/chemically induced
MH  - *Biological Therapy/adverse effects
MH  - Cardiovascular Diseases/*epidemiology/*etiology/therapy
MH  - Humans
MH  - Interleukin-17/adverse effects/therapeutic use
MH  - Prevalence
MH  - Psoriasis/*complications
MH  - Risk Factors
EDAT- 2012/11/20 06:00
MHDA- 2013/12/16 06:00
CRDT- 2012/11/20 06:00
PHST- 2011/11/08 00:00 [received]
PHST- 2012/02/08 00:00 [accepted]
PHST- 2012/11/20 06:00 [entrez]
PHST- 2012/11/20 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
AID - S1578-2190(12)00303-4 [pii]
AID - 10.1016/j.adengl.2012.02.004 [doi]
PST - ppublish
SO  - Actas Dermosifiliogr. 2012 Dec;103(10):853-62. doi: 10.1016/j.adengl.2012.02.004. 
      Epub 2012 Nov 15.

PMID- 23136242
OWN - NLM
STAT- MEDLINE
DCOM- 20131017
LR  - 20240323
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Print)
IS  - 0003-4967 (Linking)
VI  - 72
IP  - 9
DP  - 2013 Sep 1
TI  - Long-term safety of rituximab in rheumatoid arthritis: 9.5-year follow-up of the 
      global clinical trial programme with a focus on adverse events of interest in RA 
      patients.
PG  - 1496-502
LID - 10.1136/annrheumdis-2012-201956 [doi]
AB  - OBJECTIVES: Evaluation of long-term safety of rituximab in rheumatoid arthritis 
      (RA). METHODS: Pooled observed case analysis of data from patients with 
      moderate-to-severe, active RA treated with rituximab in a global clinical trial 
      programme. RESULTS: As of September 2010, 3194 patients had received up to 17 
      rituximab courses over 9.5 years (11 962 patient-years). Of these, 627 had >5 
      years' follow-up (4418 patient-years). A pooled placebo population (n=818) 
      (placebo+methotrexate (MTX)) was also analysed. Serious adverse event and 
      infection rates generally remained stable over time and multiple courses. The 
      overall serious infection event (SIE) rate was 3.94/100 patient-years (3.26/100 
      patient-years in patients observed for >5 years) and was comparable with 
      placebo+MTX (3.79/100 patient-years). Serious opportunistic infections were rare. 
      Overall, 22.4% (n=717) of rituximab-treated patients developed low immunoglobulin 
      (Ig)M and 3.5% (n=112) low IgG levels for ≥4 months after ≥1 course. SIE rates 
      were similar before and during/after development of low Ig levels; however, in 
      patients with low IgG, rates were higher than in patients who never developed low 
      IgG. Rates of myocardial infarction and stroke were consistent with rates in the 
      general RA population. No increased risk of malignancy over time was observed. 
      CONCLUSIONS: This analysis demonstrates that rituximab remains generally well 
      tolerated over time and multiple courses, with a safety profile consistent with 
      published data and clinical trial experience. Overall, the findings indicate that 
      there was no evidence of an increased safety risk or increased reporting rates of 
      any types of adverse events with prolonged exposure to rituximab during the 9.5 
      years of observation.
FAU - van Vollenhoven, Ronald F
AU  - van Vollenhoven RF
AD  - Unit for Clinical Therapy Research, The Karolinska Institute, Stockholm, Sweden. 
      ronald.van.vollenhoven@ki.se
FAU - Emery, Paul
AU  - Emery P
FAU - Bingham, Clifton O 3rd
AU  - Bingham CO 3rd
FAU - Keystone, Edward C
AU  - Keystone EC
FAU - Fleischmann, Roy M
AU  - Fleischmann RM
FAU - Furst, Daniel E
AU  - Furst DE
FAU - Tyson, Nicola
AU  - Tyson N
FAU - Collinson, Neil
AU  - Collinson N
FAU - Lehane, Patricia B
AU  - Lehane PB
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20121107
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Antibodies, Monoclonal, Murine-Derived)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Immunoglobulins)
RN  - 4F4X42SYQ6 (Rituximab)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Antibodies, Monoclonal, Murine-Derived/*adverse effects
MH  - Antirheumatic Agents/*adverse effects
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Drug Therapy, Combination
MH  - Female
MH  - Humans
MH  - Immunoglobulins
MH  - International Cooperation
MH  - Male
MH  - Methotrexate/therapeutic use
MH  - Middle Aged
MH  - Opportunistic Infections/chemically induced/epidemiology
MH  - Rituximab
PMC - PMC3756452
OTO - NOTNLM
OT  - B cells
OT  - Rheumatoid Arthritis
OT  - Treatment
EDAT- 2012/11/09 06:00
MHDA- 2013/10/18 06:00
CRDT- 2012/11/09 06:00
PHST- 2012/11/09 06:00 [entrez]
PHST- 2012/11/09 06:00 [pubmed]
PHST- 2013/10/18 06:00 [medline]
AID - annrheumdis-2012-201956 [pii]
AID - 10.1136/annrheumdis-2012-201956 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2013 Sep 1;72(9):1496-502. doi: 10.1136/annrheumdis-2012-201956. 
      Epub 2012 Nov 7.

PMID- 23106832
OWN - NLM
STAT- MEDLINE
DCOM- 20130726
LR  - 20230829
IS  - 1538-7836 (Electronic)
IS  - 1538-7836 (Linking)
VI  - 11
IP  - 1
DP  - 2013 Jan
TI  - Risk of venous thrombosis in patients with major illnesses: results from the MEGA 
      study.
PG  - 116-23
LID - 10.1111/jth.12043 [doi]
AB  - BACKGROUND: The risk of venous thrombosis associated with major illnesses is not 
      well known, and neither is the risk associated with the combined effect of 
      immobilization and thrombophilia. The aim of this study was to assess the effect 
      on the development of venous thrombosis of several major illnesses in combination 
      with immobilization, body mass index, and thrombophilia, to identify high-risk 
      groups that may provide a basis for personalized prevention. METHODS: This study 
      included 4311 consecutive patients with a first episode of venous thrombosis, and 
      5768 controls from a case-control study (MEGA study). We calculated odds ratios 
      (ORs) for venous thrombosis for patients with a self-reported history of major 
      illnesses. RESULTS: Venous thrombosis risk was increased for all investigated 
      major illnesses: liver disease, OR 1.7 (95% confidence interval [CI]1.0-2.9); 
      kidney disease, OR 3.7 (95% CI 2.3-5.9); rheumatoid arthritis, OR 1.5 (95% CI 
      1.2-1.9); multiple sclerosis, OR 2.4 (95% CI 1.3-4.3); heart failure, OR 1.7 (95% 
      CI 1.2-2.3); hemorrhagic stroke, OR 4.9 (95% CI 2.4-9.9); arterial thrombosis, OR 
      1.5 (95% CI 1.2-1.8); and the presence of any of the above major illnesses, OR 
      1.7 (95% CI 1.5-1.9). Combinations of major illnesses with immobilization and 
      increased factor VIII (OR 79.9; 95% CI 33.2-192.2), increased FIX (OR 35.3; 95% 
      CI 14.2-87.8), increased von Willebrand factor (OR 88.0; 95% CI 33.9-228.3), FV 
      Leiden (OR 84.2; 95% CI 19.5-363.6), and blood group non-O (OR 53.1; 95% CI 
      30.9-91.4) were associated with increased venous thrombosis risks. CONCLUSIONS: 
      All of the major illnesses reported here were associated with an increased risk 
      of venous thrombosis. These risks were most pronounced at the time of 
      immobilization or in the presence of thrombophilia.
CI  - © 2012 International Society on Thrombosis and Haemostasis.
FAU - Ocak, G
AU  - Ocak G
AD  - Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, 
      The Netherlands.
FAU - Vossen, C Y
AU  - Vossen CY
FAU - Verduijn, M
AU  - Verduijn M
FAU - Dekker, F W
AU  - Dekker FW
FAU - Rosendaal, F R
AU  - Rosendaal FR
FAU - Cannegieter, S C
AU  - Cannegieter SC
FAU - Lijfering, W M
AU  - Lijfering WM
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Thromb Haemost
JT  - Journal of thrombosis and haemostasis : JTH
JID - 101170508
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/epidemiology
MH  - Body Mass Index
MH  - Cardiovascular Diseases/epidemiology
MH  - Case-Control Studies
MH  - Female
MH  - Humans
MH  - Immobilization/adverse effects
MH  - Kidney Diseases/epidemiology
MH  - Liver Diseases/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Multiple Sclerosis/epidemiology
MH  - Netherlands/epidemiology
MH  - Odds Ratio
MH  - Risk Assessment
MH  - Risk Factors
MH  - Thrombophilia/epidemiology
MH  - Venous Thrombosis/blood/diagnosis/*epidemiology
EDAT- 2012/10/31 06:00
MHDA- 2013/07/28 06:00
CRDT- 2012/10/31 06:00
PHST- 2012/10/31 06:00 [entrez]
PHST- 2012/10/31 06:00 [pubmed]
PHST- 2013/07/28 06:00 [medline]
AID - S1538-7836(22)05237-0 [pii]
AID - 10.1111/jth.12043 [doi]
PST - ppublish
SO  - J Thromb Haemost. 2013 Jan;11(1):116-23. doi: 10.1111/jth.12043.

PMID- 23091653
OWN - NLM
STAT- MEDLINE
DCOM- 20131210
LR  - 20211021
IS  - 2233-4521 (Electronic)
IS  - 1975-8375 (Print)
IS  - 1975-8375 (Linking)
VI  - 45
IP  - 5
DP  - 2012 Sep
TI  - Effect of preexisting musculoskeletal diseases on the 1-year incidence of 
      fall-related injuries.
PG  - 283-90
LID - 10.3961/jpmph.2012.45.5.283 [doi]
AB  - OBJECTIVES: People who have chronic diseases, as well as gait imbalance or 
      psychiatric drug use, may be susceptible to injuries from falls and slips. The 
      purpose of this study was to evaluate the effect of musculoskeletal diseases on 
      incidental fall-related injuries among adults in Korea. METHODS: We analyzed data 
      from the 4th Korea National Health and Nutrition Examination Survey (2007-2009), 
      which are national data obtained by a rolling survey sampling method. The 1-year 
      incidence of fall-related injuries was defined by health service utilization 
      within the last year due to injury occurring after a slip and fall, and 
      musculoskeletal diseases included osteoarthritis, rheumatoid arthritis, 
      osteoporosis, and back pain. To evaluate the effects of preexisting 
      musculoskeletal diseases, adults diagnosed before the last year were considered 
      the exposed group, and adults who had never been diagnosed were the unexposed 
      group. RESULTS: The weighted lifetime prevalence of musculoskeletal disease was 
      32 540 per 100 000 persons. Musculoskeletal diseases were associated with a 
      higher risk of fall-related injury after adjustment for sex, age, residence, 
      household income, education, occupation, visual disturbance, paralysis due to 
      stroke, and medication for depression (odds ratio [OR], 1.41; 95% confidence 
      interval [CI], 1.03 to 1.93). As the number of comorbid musculoskeletal diseases 
      increased, the risk of fall-induced injuries increased (p-value for trend 
      <0.001). In particular, patients who had any musculoskeletal condition were at 
      much higher risk of recurrent fall-related injuries (OR, 6.20; 95% CI, 1.06 to 
      36.08). CONCLUSIONS: One must take into account the risk of fall-related injuries 
      and provide prevention strategies among adults who have musculoskeletal diseases.
FAU - Lee, Won Kyung
AU  - Lee WK
AD  - Department of Preventive Medicine, Ewha Womans University School of Medicine, 
      Seoul, Korea.
FAU - Kong, Kyoung Ae
AU  - Kong KA
FAU - Park, Hyesook
AU  - Park H
LA  - eng
PT  - Journal Article
DEP - 20120928
PL  - Korea (South)
TA  - J Prev Med Public Health
JT  - Journal of preventive medicine and public health = Yebang Uihakhoe chi
JID - 101242972
SB  - IM
MH  - Accidental Falls/*statistics & numerical data
MH  - Adolescent
MH  - Adult
MH  - Age Factors
MH  - Aged
MH  - Arthritis, Rheumatoid/complications/epidemiology
MH  - Back Pain/complications/epidemiology
MH  - Female
MH  - Health Surveys
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Musculoskeletal Diseases/*complications
MH  - Osteoarthritis/complications/epidemiology
MH  - Osteoporosis/complications/epidemiology
MH  - Republic of Korea/epidemiology
MH  - Risk Factors
MH  - Sex Factors
MH  - Socioeconomic Factors
MH  - Young Adult
PMC - PMC3469810
OTO - NOTNLM
OT  - Accidental falls
OT  - Arthritis
OT  - Back pain
OT  - Osteoporosis
OT  - Wounds and injuries
COIS- The authors have no conflicts of interest with the material presented in this 
      paper.
EDAT- 2012/10/24 06:00
MHDA- 2013/12/16 06:00
PMCR- 2012/09/01
CRDT- 2012/10/24 06:00
PHST- 2011/11/23 00:00 [received]
PHST- 2012/03/14 00:00 [accepted]
PHST- 2012/10/24 06:00 [entrez]
PHST- 2012/10/24 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
PHST- 2012/09/01 00:00 [pmc-release]
AID - 10.3961/jpmph.2012.45.5.283 [doi]
PST - ppublish
SO  - J Prev Med Public Health. 2012 Sep;45(5):283-90. doi: 
      10.3961/jpmph.2012.45.5.283. Epub 2012 Sep 28.

PMID- 23086517
OWN - NLM
STAT- MEDLINE
DCOM- 20130226
LR  - 20220409
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 52
IP  - 1
DP  - 2013 Jan
TI  - A study of baseline prevalence and cumulative incidence of comorbidity and 
      extra-articular manifestations in RA and their impact on outcome.
PG  - 99-110
LID - 10.1093/rheumatology/kes262 [doi]
AB  - OBJECTIVES: To study the prevalence at diagnosis and cumulative incidence of 
      comorbidity in RA, associations with clinical features and impact on outcome. 
      METHODS: Standard clinical, laboratory and radiological measures of RA, and 
      details of comorbidity and extra-articular features were recorded at baseline and 
      yearly in an inception cohort of 1460 patients with recently diagnosed RA from 
      nine regions in the UK. The General Practice Research Database was used to 
      compare the incidence of common comorbid conditions (International Classification 
      for Disease-10 codes). RESULTS: Baseline prevalence was 31.6% and 8.6% for all 
      comorbidities and extra-articular features, respectively, and 15-year cumulative 
      incidence was 81% and 53%, respectively. Rates of hypertension [standardized 
      incidence ratio (SIR) = 1.61; 95% CI 1.43, 1.79] and ischaemic heart disease (SIR 
      = 1.60; 95% CI 1.35, 1.84) were raised compared with figures for the general 
      population, as was stroke in females (SIR = 1.34; 95% CI 1.02, 1.77) and chronic 
      obstructive pulmonary disorder in males (SIR = 1.63; 95% CI 1.17, 2.26). 
      Comorbidity was associated with risk of both all-cause and cardiovascular 
      mortality (hazard ratio = 1.09; 95% CI 1.02, 1.17) and increased rates of 
      functional decline over 10 years (b = 0.011; 95% CI 0.004, 0.019). Comorbidity 
      was not related to disease activity or structural damage. CONCLUSION: Significant 
      comorbidity was present at the outset of RA, increasing with follow-up, mainly in 
      cardiovascular, non-cardiac vascular and respiratory systems. Specific conditions 
      (e.g. hypertension) occurred more frequently than in the general population. 
      Comorbidity was related to mortality and functional decline, and more intensive 
      therapies may need consideration in these patients. As many co-existent 
      conditions are amenable to preventative/therapeutic measures, comorbidity needs 
      earlier detection and management in order to reduce its impact on outcome in RA.
FAU - Norton, Sam
AU  - Norton S
AD  - ERAS, Rheumatology Department, St Albans City Hospital, St Albans, Hertfordshire 
      AL3 5PN, UK. eras@whht.nhs.uk
FAU - Koduri, Gouri
AU  - Koduri G
FAU - Nikiphorou, Elena
AU  - Nikiphorou E
FAU - Dixey, Josh
AU  - Dixey J
FAU - Williams, Peter
AU  - Williams P
FAU - Young, Adam
AU  - Young A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121019
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Hypertension/*epidemiology
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Myocardial Ischemia/*epidemiology
MH  - Prevalence
MH  - Pulmonary Disease, Chronic Obstructive/*epidemiology
MH  - Risk
MH  - Stroke/*epidemiology
EDAT- 2012/10/23 06:00
MHDA- 2013/02/27 06:00
CRDT- 2012/10/23 06:00
PHST- 2012/10/23 06:00 [entrez]
PHST- 2012/10/23 06:00 [pubmed]
PHST- 2013/02/27 06:00 [medline]
AID - kes262 [pii]
AID - 10.1093/rheumatology/kes262 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2013 Jan;52(1):99-110. doi: 10.1093/rheumatology/kes262. 
      Epub 2012 Oct 19.

PMID- 23085014
OWN - NLM
STAT- MEDLINE
DCOM- 20130513
LR  - 20211203
IS  - 1873-1244 (Electronic)
IS  - 0899-9007 (Linking)
VI  - 29
IP  - 1
DP  - 2013 Jan
TI  - Vitamin D: health panacea or false prophet?
PG  - 37-41
LID - S0899-9007(12)00252-3 [pii]
LID - 10.1016/j.nut.2012.05.010 [doi]
AB  - Vitamin D deficiency, diagnosed when the serum 25-hydroxyvitamin D (25-OHD(3)) 
      concentration is less than 20 ng/mL, has joined vitamin A deficiency as two of 
      the most common nutrition-responsive medical conditions worldwide. There have 
      been more scientific articles published about vitamin D in the 21st century than 
      about any other vitamin, reflecting the massive expansion of the field of vitamin 
      D research. Adequate vitamin D status has been linked to decreased risks of 
      developing specific cancers, including cancers of the esophagus, stomach, colon, 
      rectum, gallbladder, pancreas, lung, breast, uterus, ovary, prostate, urinary 
      bladder, kidney, skin, thyroid, and hematopoietic system (e.g., Hodgkin's 
      lymphoma, non-Hodgkin's lymphoma, multiple myeloma); bacterial infections; 
      rheumatoid arthritis; Crohn's disease; periodontal disease; multiple sclerosis; 
      asthma; type 2 diabetes; cardiovascular disease; stroke; peripheral artery 
      disease; hypertension; chronic kidney disease; muscle weakness; cognitive 
      impairment; Alzheimer's disease; clinical depression; and premature death. On the 
      other hand, inadequate vitamin D status during human pregnancy may be associated 
      with increased risk for the development of type 1 diabetes in the offspring. 
      However, this point of view may be excessively optimistic. There also is evidence 
      that despite the current heavy reliance on serum 25-OHD(3) concentration for the 
      diagnosis of an individual's vitamin D status, local tissue vitamin D 
      intoxication may be present in individuals with much lower serum 25-OHD(3) 
      concentrations than are currently appreciated. Only rarely are the symptoms of 
      local tissue vitamin D intoxication associated with vitamin D status or intake. 
      An individual's serum 25-OHD(3) concentration may appear to be "low" for reasons 
      totally independent of sunlight exposure or vitamin D intake. Serum 25-OHD(3) 
      concentration is only poorly responsive to increases in vitamin D intake, and the 
      prolonged routine consumption of thousands of international units of vitamin D 
      may interfere with the regulation of phosphate homeostasis by fibroblast growth 
      factor-23 (FGF23) and the Klotho gene product, with consequences that are 
      detrimental to human health. In light of these counterbalancing observations, 
      curbing excessive enthusiasm for universally increasing vitamin D intake 
      recommendations may be in order.
CI  - Copyright © 2013 Elsevier Inc. All rights reserved.
FAU - Glade, Michael J
AU  - Glade MJ
AD  - The Nutrition Doctor, Skokie, Illinois, USA. the_nutrition_doctor@yahoo.com
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20121022
PL  - United States
TA  - Nutrition
JT  - Nutrition (Burbank, Los Angeles County, Calif.)
JID - 8802712
RN  - 0 (FGF23 protein, human)
RN  - 0 (Fgf23 protein, mouse)
RN  - 1406-16-2 (Vitamin D)
RN  - 7Q7P4S7RRE (Fibroblast Growth Factor-23)
RN  - EC 3.2.1.31 (Glucuronidase)
RN  - EC 3.2.1.31 (Klotho Proteins)
SB  - IM
CIN - Nutrition. 2013 May;29(5):809-10. doi: 10.1016/j.nut.2013.01.008. PMID: 23582081
CIN - Nutrition. 2013 May;29(5):810. doi: 10.1016/j.nut.2013.02.017. PMID: 23582082
MH  - Animals
MH  - Female
MH  - Fibroblast Growth Factor-23
MH  - Glucuronidase/genetics/metabolism
MH  - Humans
MH  - Klotho Proteins
MH  - Male
MH  - Mice
MH  - Nutrition Policy
MH  - Pregnancy
MH  - Preventive Medicine
MH  - Risk Factors
MH  - Vitamin D/*administration & dosage/*metabolism
MH  - Vitamin D Deficiency/diet therapy/metabolism
EDAT- 2012/10/23 06:00
MHDA- 2013/05/15 06:00
CRDT- 2012/10/23 06:00
PHST- 2012/03/27 00:00 [received]
PHST- 2012/05/09 00:00 [revised]
PHST- 2012/05/11 00:00 [accepted]
PHST- 2012/10/23 06:00 [entrez]
PHST- 2012/10/23 06:00 [pubmed]
PHST- 2013/05/15 06:00 [medline]
AID - S0899-9007(12)00252-3 [pii]
AID - 10.1016/j.nut.2012.05.010 [doi]
PST - ppublish
SO  - Nutrition. 2013 Jan;29(1):37-41. doi: 10.1016/j.nut.2012.05.010. Epub 2012 Oct 
      22.

PMID- 22925480
OWN - NLM
STAT- MEDLINE
DCOM- 20130312
LR  - 20240512
IS  - 1471-2474 (Electronic)
IS  - 1471-2474 (Linking)
VI  - 13
DP  - 2012 Aug 27
TI  - Rheumatoid arthritis and the incidence of influenza and influenza-related 
      complications: a retrospective cohort study.
PG  - 158
LID - 10.1186/1471-2474-13-158 [doi]
AB  - BACKGROUND: Patients with rheumatoid arthritis (RA) are known to be at increased 
      risk of infection, particularly if they are taking drugs with immunomodulatory 
      effects. There is a need for more information on the risk of influenza in 
      patients with RA. METHODS: A retrospective cohort study was carried out using 
      data gathered from a large US commercial health insurance database (Thomson 
      Reuters Medstat MarketScan) from 1 January 2000 to 31 December 2007. Patients 
      were ≥18 years of age, with at least two RA claims diagnoses. The database was 
      scanned for incidence of seasonal influenza and its complications on or up to 30 
      days after an influenza diagnosis in RA patients and matched controls. Other 
      factors accounted for included medical conditions, use of disease-modifying 
      anti-rheumatic drugs (DMARDs), use of biological agents, influenza vaccination 
      and high- or low-dose corticosteroids. Incidence rate ratios (IRRs) were 
      calculated for influenza and its complications in patients with RA. RESULTS: 
      46,030 patients with RA and a matching number of controls had a median age of 57 
      years. The incidence of influenza was higher in RA patients than in controls 
      (409.33 vs 306.12 cases per 100,000 patient-years), and there was a 2.75-fold 
      increase in incidence of complications in RA. Presence or absence of DMARDs or 
      biologics had no significant effect. The adjusted IRR of influenza was 
      statistically significant in patients aged 60-69 years, and especially among men. 
      A significantly increased rate of influenza complications was observed in women 
      and in both genders combined (but not in men only) when all age groups were 
      combined. In general, the risk of influenza complications was similar in RA 
      patients not receiving DMARDs or biologics to that in all RA patients. Pneumonia 
      rates were significantly higher in women with RA. Rates of stroke/myocardial 
      infarction (MI) were higher in men, although statistical significance was 
      borderline. CONCLUSIONS: RA is associated with increased incidence of seasonal 
      influenza and its complications. Gender- and age-specific subgroup data indicate 
      that women generally have a greater rate of complications than men, but that men 
      primarily have an increased rate of stroke and MI complications. Concomitant 
      DMARD or biological use appears not to significantly affect the rate of influenza 
      or its complications.
FAU - Blumentals, William A
AU  - Blumentals WA
AD  - Hoffmann-La Roche, Inc, Nutley, NJ, USA.
FAU - Arreglado, Anna
AU  - Arreglado A
FAU - Napalkov, Pavel
AU  - Napalkov P
FAU - Toovey, Stephen
AU  - Toovey S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120827
PL  - England
TA  - BMC Musculoskelet Disord
JT  - BMC musculoskeletal disorders
JID - 100968565
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Influenza Vaccines)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/diagnosis/drug therapy/*epidemiology
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Immunization
MH  - Incidence
MH  - Influenza Vaccines/therapeutic use
MH  - Influenza, Human/complications/diagnosis/*epidemiology/prevention & control
MH  - Male
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Seasons
MH  - Time Factors
MH  - United States/epidemiology
MH  - Young Adult
PMC - PMC3495205
EDAT- 2012/08/29 06:00
MHDA- 2013/03/13 06:00
PMCR- 2012/08/27
CRDT- 2012/08/29 06:00
PHST- 2011/11/15 00:00 [received]
PHST- 2012/08/09 00:00 [accepted]
PHST- 2012/08/29 06:00 [entrez]
PHST- 2012/08/29 06:00 [pubmed]
PHST- 2013/03/13 06:00 [medline]
PHST- 2012/08/27 00:00 [pmc-release]
AID - 1471-2474-13-158 [pii]
AID - 10.1186/1471-2474-13-158 [doi]
PST - epublish
SO  - BMC Musculoskelet Disord. 2012 Aug 27;13:158. doi: 10.1186/1471-2474-13-158.

PMID- 22732955
OWN - NLM
STAT- MEDLINE
DCOM- 20121113
LR  - 20130702
IS  - 1699-5198 (Electronic)
IS  - 0212-1611 (Linking)
VI  - 27
IP  - 2
DP  - 2012 Mar-Apr
TI  - [Enteral nutrition in neurological patients: is there enough vitamin D content in 
      commonly used formulas?].
PG  - 341-8
LID - S0212-16112012000200003 [pii]
LID - 10.1590/S0212-16112012000200003 [doi]
AB  - INTRODUCTION: Vitamin D deficiency produces inadequate bone mineralization, 
      proximal muscle weakness, abnormal gait and increased risk of falls and 
      fractures. Moreover, in epidemiological studies, has been associated with 
      increased risk of cancer, autoimmune diseases, type 1 and 2 diabetes, rheumatoid 
      arthritis, multiple sclerosis, infectious diseases, cardiovascular diseases and 
      depression. When synthesis through the skin by sun exposure is not possible and 
      the patient can not eat by mouth, as in the advanced stages of various 
      neurological diseases, the supply of vitamin D has to be done by enteral 
      nutrition. OBJECTIVES: The aim of this study is to review the role of vitamin D 
      in a common group of neurological conditions that often require artificial 
      nutrition and analyze whether the vitamin D of different enteral nutrition 
      formulas is adequate to meet the needs of this group of patients. RESULTS: 
      Numerous studies have shown the association between vitamin D deficiency and 
      increased incidence of dementia, stroke and other neurodegenerative diseases. 
      Interventions aimed to increase levels of vit. D and its effects on functional 
      (falls, pain, quality of life) and cardiovascular goals (cardiovascular death, 
      stroke, myocardial infarction, cardiovascular risk factors) have obtained as 
      highlight data a clear reduction of falls and fractures, while the evidence for 
      the other parameters studied is still limited and inconsistent. The content of 
      calcium and vitamin D of enteral formulas is legislated in our country. The total 
      amount of vitamin D for a daily intake of 1,500-2,000 kcal ranges between 300 and 
      1,600 IU/d (mean ± SD: 32.9 ± 8.5 mg/100 kcal) in the complete formulas for 
      enteral nutrition most commonly used. 50% of the diets studied, for an intake of 
      2,000 kcal/d, and 90% for an intake of 1,500 kcal/d, provide less than 600 IU/d 
      of vitamin D. DISCUSSION: Some revised recently guidelines published 
      recommendations of daily intake of vitamin D. The document published by the U.S. 
      Institute of Medicine recommended for adults between 19 and 70 years, 600 IU/d 
      and up from 70, proposes 800 IU/d of vitamin D. These amounts are deemed 
      insufficient by other scientific societies to state that to achieve blood levels 
      of 25 (OH) D equal or greater than 30 ng/ml may be required a daily intake of 
      1,500-2,000 IU and a number two or three times higher if previous deficiency 
      exists. CONCLUSIONS: Further controlled studies are needed to ascertain which is 
      the appropriate dose of vitamin D in advanced stages of neurological disease, 
      where sun exposure is difficult and unlikely. We suggest that the vitamin D 
      content should probably be reconsidered in enteral nutrition formulas, which, in 
      light of recent publications appear as clearly insufficient for standard energy 
      intakes (1,500-2,000 kcal).
FAU - Botella Romero, F
AU  - Botella Romero F
AD  - Servicio de Endocrinología y Nutrición, Complejo Hospitalario Universitario de 
      Albacete, Albacete, España. fbotellar@sescam.jccm.es
FAU - Alfaro Martínez, J J
AU  - Alfaro Martínez JJ
FAU - Luna López, V
AU  - Luna López V
FAU - Galicia Martín, I
AU  - Galicia Martín I
CN  - Grupo de Trabajo sobre Calcio y Vitamina D en Nutrición Enteral
LA  - spa
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - Nutrición enteral en el paciente neurológico: ¿es suficiente el contenido en 
      vitamina D en las fórmulas de uso habitual?
PL  - Spain
TA  - Nutr Hosp
JT  - Nutricion hospitalaria
JID - 9100365
RN  - 0 (Parenteral Nutrition Solutions)
RN  - 0 (Vitamins)
RN  - 1406-16-2 (Vitamin D)
SB  - IM
MH  - Aged
MH  - Alzheimer Disease/therapy
MH  - Amyotrophic Lateral Sclerosis/therapy
MH  - *Enteral Nutrition
MH  - Epilepsy/therapy
MH  - Humans
MH  - Multiple Sclerosis/therapy
MH  - Nervous System Diseases/*therapy
MH  - Nutrition Policy
MH  - Parenteral Nutrition Solutions/chemistry
MH  - Parkinson Disease/therapy
MH  - Spinocerebellar Degenerations/therapy
MH  - Vitamin D/administration & dosage/*therapeutic use
MH  - Vitamins/administration & dosage/*therapeutic use
EDAT- 2012/06/27 06:00
MHDA- 2012/11/14 06:00
CRDT- 2012/06/27 06:00
PHST- 2011/11/02 00:00 [received]
PHST- 2011/11/27 00:00 [accepted]
PHST- 2012/06/27 06:00 [entrez]
PHST- 2012/06/27 06:00 [pubmed]
PHST- 2012/11/14 06:00 [medline]
AID - S0212-16112012000200003 [pii]
AID - 10.1590/S0212-16112012000200003 [doi]
PST - ppublish
SO  - Nutr Hosp. 2012 Mar-Apr;27(2):341-8. doi: 10.1590/S0212-16112012000200003.

PMID- 22708578
OWN - NLM
STAT- MEDLINE
DCOM- 20130131
LR  - 20211021
IS  - 1471-2377 (Electronic)
IS  - 1471-2377 (Linking)
VI  - 12
DP  - 2012 Jun 18
TI  - Risk of subsequent ischemic and hemorrhagic stroke in patients hospitalized for 
      immune-mediated diseases: a nationwide follow-up study from Sweden.
PG  - 41
LID - 10.1186/1471-2377-12-41 [doi]
AB  - BACKGROUND: Certain immune-mediated diseases (IMDs) have been associated with 
      increased risk for cardiovascular disorders. The aim of the present study was to 
      examine whether there is an association between 32 different IMDs and first 
      hospitalization for ischemic or hemorrhagic stroke. METHODS: All individuals in 
      Sweden hospitalized with a main diagnosis of IMD (without previous or coexisting 
      stroke), between January 1, 1987 and December 31, 2008 (n = 216,291), were 
      followed for first hospitalization for ischemic or hemorrhagic stroke. The 
      reference population was the total population of Sweden. Adjusted standardized 
      incidence ratios (SIRs) for ischemic and hemorrhagic stroke were calculated. 
      RESULTS: Totally 20 and 15 of the 32 IMDs studied, respectively, were associated 
      with an increased risk of ischemic and hemorrhagic stroke during the follow-up. 
      The overall risks of ischemic and hemorrhagic stroke during the first year after 
      hospitalization for IMD were 2.02 (95% CI 1.90-2.14) and 2.65 (95% CI 2.27-3.08), 
      respectively. The overall risk of ischemic or hemorrhagic stroke decreased over 
      time, to 1.50 (95% CI 1.46-1.55) and 1.83 (95% CI 1.69-1.98), respectively, after 
      1-5 years, and 1.29 (95% CI 1.23-1.35) and 1.47 (95% CI 1.31-1.65), respectively, 
      after 10+ years. The risk of hemorrhagic stroke was ≥2 during the first year 
      after hospitalization for seven IMDs: ankylosing spondylitis (SIR = 8.11), immune 
      thrombocytopenic purpura (SIR = 8.60), polymyalgia rheumatica (SIR = 2.06), 
      psoriasis (SIR = 2.88), rheumatoid arthritis (SIR = 3.27), systemic lupus 
      erythematosus (SIR = 8.65), and Wegener's granulomatosis (SIR = 5.83). The risk 
      of ischemic stroke was ≥2 during the first year after hospitalization for twelve 
      IMDs: Addison's disease (SIR = 2.71), Crohn's disease (SIR = 2.15), Grave's 
      disease (SIR = 2.15), Hashimoto's thyroiditis (SIR = 2.99), immune 
      thrombocytopenic purpura (SIR = 2.35), multiple sclerosis (SIR = 3.05), 
      polymyositis/dermatomyositis (SIR = 3.46), rheumatic fever (SIR = 3.91), 
      rheumatoid arthritis (SIR = 2.08), Sjögren's syndrome (SIR = 2.57), systemic 
      lupus erythematosus (SIR = 2.21), and ulcerative colitis (SIR = 2.15). 
      CONCLUSIONS: Hospitalization for many IMDs is associated with increased risk of 
      ischemic or hemorrhagic stroke. The findings suggest that several IMDs are linked 
      to cerebrovascular disease.
FAU - Zöller, Bengt
AU  - Zöller B
AD  - Center for Primary Health Care Research, Lund University/Region Skåne, Clinical 
      Research Centre, Floor 11, Building 28, Entrance 72, Skåne University Hospital, 
      205 02, Malmö, Sweden. bengt.zoller@med.lu.se
FAU - Li, Xinjun
AU  - Li X
FAU - Sundquist, Jan
AU  - Sundquist J
FAU - Sundquist, Kristina
AU  - Sundquist K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120618
PL  - England
TA  - BMC Neurol
JT  - BMC neurology
JID - 100968555
SB  - IM
MH  - Adult
MH  - Age Distribution
MH  - Aged
MH  - Aged, 80 and over
MH  - Brain Ischemia/*epidemiology
MH  - Cerebral Hemorrhage/*epidemiology
MH  - Comorbidity
MH  - Female
MH  - Follow-Up Studies
MH  - Hospitalization/*statistics & numerical data
MH  - Humans
MH  - Immune System Diseases/diagnosis/*epidemiology/*therapy
MH  - Incidence
MH  - Male
MH  - Risk Assessment
MH  - Sex Distribution
MH  - Stroke/*epidemiology
MH  - Sweden/epidemiology
MH  - Young Adult
PMC - PMC3430565
EDAT- 2012/06/20 06:00
MHDA- 2013/02/01 06:00
PMCR- 2012/06/18
CRDT- 2012/06/20 06:00
PHST- 2011/11/22 00:00 [received]
PHST- 2012/06/18 00:00 [accepted]
PHST- 2012/06/20 06:00 [entrez]
PHST- 2012/06/20 06:00 [pubmed]
PHST- 2013/02/01 06:00 [medline]
PHST- 2012/06/18 00:00 [pmc-release]
AID - 1471-2377-12-41 [pii]
AID - 10.1186/1471-2377-12-41 [doi]
PST - epublish
SO  - BMC Neurol. 2012 Jun 18;12:41. doi: 10.1186/1471-2377-12-41.

PMID- 22692396
OWN - NLM
STAT- MEDLINE
DCOM- 20130317
LR  - 20211021
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 31
IP  - 9
DP  - 2012 Sep
TI  - Lupus anticoagulant: a marker for stroke and venous thrombosis in primary 
      Sjögren's syndrome.
PG  - 1331-8
LID - 10.1007/s10067-012-2019-z [doi]
AB  - Antiphospholipid antibodies (aPL) and antiphospholipid syndrome (APS) have been 
      described in primary Sjögren's syndrome (pSS) with controversial findings 
      regarding aPL prevalence and their association with thrombotic events. We 
      evaluated 100 consecutive pSS patients (American-European criteria) and 89 
      age-gender-ethnicity-matched healthy controls for IgG/IgM anticardiolipin (aCL), 
      IgG/IgM anti-beta2-glycoprotein-I (aβ2GPI), and lupus anticoagulant (LA) 
      (positivity according to APS Sydney's criteria). Clinical analysis followed 
      standardized interview and physical examination assessing thrombotic and 
      nonthrombotic APS manifestations and thrombosis risk factors. aPLs were detected 
      in 16 % patients and 5.6 % controls (p = 0.035). LA was the most common aPL in 
      patients (9 %), followed by aβ2GPI (5 %) and aCL (4 %). Thrombotic events 
      occurred in five patients [stroke in two, myocardial infarction in one and 
      deep-vein thrombosis (DVT) in four], but in none of controls (p = 0.061). Mean 
      age at time of stroke was 35 years. Three patients with thrombotic events 
      (including the two with stroke) had APS (Sydney's criteria) and were positive 
      exclusively for LA. Comparison of patients with (n = 16) and without (n = 84) aPL 
      revealed similar mean age, female predominance, and ethnicity (p > =0.387). 
      Frequencies of livedo reticularis (25 vs. 4.8 %, p = 0.021), stroke (12.5 vs. 
      0 %, p = 0.024), and DVT (18.8 vs. 1.2 %, p = 0.013) were significantly higher in 
      APL + patients. Conversely, frequencies of hypertension, dyslipidemia, diabetes, 
      obesity, smoking, sedentarism, and hormonal contraception were similar in 
      patients with or without aPL (p ≥ 0.253). Our study identified LA as an important 
      marker for APS in pSS, particularly for stroke in young patients, warranting 
      routine evaluation of these antibodies and rigorous intervention in modifiable 
      risk factors.
FAU - Pasoto, Sandra Gofinet
AU  - Pasoto SG
AD  - Rheumatology Division, Hospital das Clínicas da Faculdade de Medicina, 
      Universidade de São Paulo, São Paulo, Brazil. sandrapasoto@yahoo.com.br
FAU - Chakkour, Henrique Pires
AU  - Chakkour HP
FAU - Natalino, Renato Romera
AU  - Natalino RR
FAU - Viana, Vilma S T
AU  - Viana VS
FAU - Bueno, Cleonice
AU  - Bueno C
FAU - Lianza, Alessandro Cavalcanti
AU  - Lianza AC
FAU - de Andrade, José Lázaro
AU  - de Andrade JL
FAU - Neto, Mauricio Levy
AU  - Neto ML
FAU - Fuller, Ricardo
AU  - Fuller R
FAU - Bonfa, Eloisa
AU  - Bonfa E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120613
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
RN  - 0 (Antibodies, Antiphospholipid)
RN  - 0 (Cardiolipins)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Immunoglobulin M)
RN  - 0 (Lupus Coagulation Inhibitor)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Antibodies, Antiphospholipid/chemistry
MH  - Antiphospholipid Syndrome/metabolism
MH  - Cardiolipins/chemistry
MH  - Case-Control Studies
MH  - Female
MH  - Humans
MH  - Immunoglobulin G/immunology
MH  - Immunoglobulin M/immunology
MH  - Lupus Coagulation Inhibitor/*blood/*immunology
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - Sjogren's Syndrome/*complications/*immunology
MH  - Stroke/complications/*immunology
MH  - Time Factors
MH  - Venous Thrombosis/complications/*immunology
EDAT- 2012/06/14 06:00
MHDA- 2013/03/19 06:00
CRDT- 2012/06/14 06:00
PHST- 2012/03/27 00:00 [received]
PHST- 2012/05/30 00:00 [accepted]
PHST- 2012/05/18 00:00 [revised]
PHST- 2012/06/14 06:00 [entrez]
PHST- 2012/06/14 06:00 [pubmed]
PHST- 2013/03/19 06:00 [medline]
AID - 10.1007/s10067-012-2019-z [doi]
PST - ppublish
SO  - Clin Rheumatol. 2012 Sep;31(9):1331-8. doi: 10.1007/s10067-012-2019-z. Epub 2012 
      Jun 13.

PMID- 22684631
OWN - NLM
STAT- MEDLINE
DCOM- 20130111
LR  - 20231105
IS  - 1436-6215 (Electronic)
IS  - 1436-6207 (Print)
IS  - 1436-6207 (Linking)
VI  - 51
IP  - 6
DP  - 2012 Sep
TI  - Critical review: vegetables and fruit in the prevention of chronic diseases.
PG  - 637-63
LID - 10.1007/s00394-012-0380-y [doi]
AB  - BACKGROUND: Vegetables and fruit provide a significant part of human nutrition, 
      as they are important sources of nutrients, dietary fibre, and phytochemicals. 
      However, it is uncertain whether the risk of certain chronic diseases can be 
      reduced by increased consumption of vegetables or fruit by the general public, 
      and what strength of evidence has to be allocated to such an association. 
      METHODS: Therefore, a comprehensive analysis of the studies available in the 
      literature and the respective study results has been performed and evaluated 
      regarding obesity, type 2 diabetes mellitus, hypertension, coronary heart disease 
      (CHD), stroke, cancer, chronic inflammatory bowel disease (IBD), rheumatoid 
      arthritis (RA), chronic obstructive pulmonary disease (COPD), asthma, 
      osteoporosis, eye diseases, and dementia. For judgement, the strength of evidence 
      for a risk association, the level of evidence, and the number of studies were 
      considered, the quality of the studies and their estimated relevance based on 
      study design and size. RESULTS: For hypertension, CHD, and stroke, there is 
      convincing evidence that increasing the consumption of vegetables and fruit 
      reduces the risk of disease. There is probable evidence that the risk of cancer 
      in general is inversely associated with the consumption of vegetables and fruit. 
      In addition, there is possible evidence that an increased consumption of 
      vegetables and fruit may prevent body weight gain. As overweight is the most 
      important risk factor for type 2 diabetes mellitus, an increased consumption of 
      vegetables and fruit therefore might indirectly reduces the incidence of type 2 
      diabetes mellitus. Independent of overweight, there is probable evidence that 
      there is no influence of increased consumption on the risk of type 2 diabetes 
      mellitus. There is possible evidence that increasing the consumption of 
      vegetables and fruit lowers the risk of certain eye diseases, dementia and the 
      risk of osteoporosis. Likewise, current data on asthma, COPD, and RA indicate 
      that an increase in vegetable and fruit consumption may contribute to the 
      prevention of these diseases. For IBD, glaucoma, and diabetic retinopathy, there 
      was insufficient evidence regarding an association with the consumption of 
      vegetables and fruit. CONCLUSIONS: This critical review on the associations 
      between the intake of vegetables and fruit and the risk of several chronic 
      diseases shows that a high daily intake of these foods promotes health. 
      Therefore, from a scientific point of view, national campaigns to increase 
      vegetable and fruit consumption are justified. The promotion of vegetable and 
      fruit consumption by nutrition and health policies is a preferable strategy to 
      decrease the burden of several chronic diseases in Western societies.
FAU - Boeing, Heiner
AU  - Boeing H
AD  - Department of Epidemiology, German Institute of Human Nutrition, 
      Potsdam-Rehbrücke, Germany.
FAU - Bechthold, Angela
AU  - Bechthold A
FAU - Bub, Achim
AU  - Bub A
FAU - Ellinger, Sabine
AU  - Ellinger S
FAU - Haller, Dirk
AU  - Haller D
FAU - Kroke, Anja
AU  - Kroke A
FAU - Leschik-Bonnet, Eva
AU  - Leschik-Bonnet E
FAU - Müller, Manfred J
AU  - Müller MJ
FAU - Oberritter, Helmut
AU  - Oberritter H
FAU - Schulze, Matthias
AU  - Schulze M
FAU - Stehle, Peter
AU  - Stehle P
FAU - Watzl, Bernhard
AU  - Watzl B
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20120609
PL  - Germany
TA  - Eur J Nutr
JT  - European journal of nutrition
JID - 100888704
SB  - IM
MH  - Animals
MH  - Chronic Disease/*prevention & control
MH  - Evidence-Based Medicine
MH  - *Fruit
MH  - *Health Promotion
MH  - Humans
MH  - *Vegetables
PMC - PMC3419346
EDAT- 2012/06/12 06:00
MHDA- 2013/01/12 06:00
PMCR- 2012/06/09
CRDT- 2012/06/12 06:00
PHST- 2012/02/13 00:00 [received]
PHST- 2012/05/09 00:00 [accepted]
PHST- 2012/06/12 06:00 [entrez]
PHST- 2012/06/12 06:00 [pubmed]
PHST- 2013/01/12 06:00 [medline]
PHST- 2012/06/09 00:00 [pmc-release]
AID - 380 [pii]
AID - 10.1007/s00394-012-0380-y [doi]
PST - ppublish
SO  - Eur J Nutr. 2012 Sep;51(6):637-63. doi: 10.1007/s00394-012-0380-y. Epub 2012 Jun 
      9.

PMID- 22610975
OWN - NLM
STAT- MEDLINE
DCOM- 20130430
LR  - 20220331
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 72
IP  - 4
DP  - 2013 Apr
TI  - Occurrence and relative risk of stroke in incident and prevalent contemporary 
      rheumatoid arthritis.
PG  - 541-6
LID - 10.1136/annrheumdis-2012-201387 [doi]
AB  - OBJECTIVE: In contrast with the wealth of data on ischaemic heart disease in 
      rheumatoid arthritis (RA), data on stroke are scarce and contradictory. Despite 
      the high clinical and aetiological relevance, there is no data regarding when (if 
      ever) after RA diagnosis there is an increased risk. Our objective was to assess 
      the risk of stroke (by subtype) in contemporary patients with RA, particularly in 
      relation to time since RA diagnosis. METHODS: One incident RA cohort diagnosed 
      between 1997 and 2009 (n=8077) and one nationwide prevalent RA cohort followed at 
      Swedish rheumatology clinics between 2005 and 2009 ((n=39 065) were assembled). 
      Each cohort member was matched to a general population comparator. Information on 
      first-time hospitalisations for stroke up to 2009 was retrieved from the Swedish 
      Patient Register. HR and 95% CI were estimated using Cox models. RESULTS: In 
      prevalent unselected RA, the HR of ischaemic stroke was 1.29 (95% CI 1.18 to 
      1.41). In the incident RA cohort, the overall risk increase was small and 
      non-significant (overall HR 1.11, 95% CI 0.95 to 1.30). When stratified by RA 
      disease duration, an increased risk of ischaemic stroke was indeed detectable but 
      only after 10 or more years since RA diagnosis (HR>10 years: 2.33, 95% CI 1.25 to 
      4.34). Risk of haemorrhagic stroke was increased in prevalent but not in incident 
      RA. CONCLUSION: The magnitude of stroke risk is lower than for ischaemic heart 
      disease in RA, and the evolvement of this risk from RA diagnosis may be slower. 
      This suggests different driving forces behind these two RA co-morbidities and has 
      implications for the clinical follow-up of patients with RA.
FAU - Holmqvist, Marie
AU  - Holmqvist M
AD  - Karolinska Institutet, Clinical Epidemiology Unit, Department of Medicine Solna, 
      T2, Karolinska Universitetssjukhuset, Stockholm 17176, Sweden. 
      marie.holmqvist@ki.se
FAU - Gränsmark, Emma
AU  - Gränsmark E
FAU - Mantel, Angla
AU  - Mantel A
FAU - Alfredsson, Lars
AU  - Alfredsson L
FAU - Jacobsson, Lennart T H
AU  - Jacobsson LT
FAU - Wallberg-Jonsson, Solveig
AU  - Wallberg-Jonsson S
FAU - Askling, Johan
AU  - Askling J
LA  - eng
PT  - Journal Article
DEP - 20120518
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/diagnosis/*epidemiology
MH  - Brain Ischemia/diagnosis/*epidemiology
MH  - Cohort Studies
MH  - Comorbidity
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Myocardial Ischemia/diagnosis/epidemiology
MH  - Prevalence
MH  - Proportional Hazards Models
MH  - Registries/statistics & numerical data
MH  - Risk Factors
MH  - Stroke/diagnosis/*epidemiology
MH  - Sweden/epidemiology
EDAT- 2012/05/23 06:00
MHDA- 2013/05/01 06:00
CRDT- 2012/05/22 06:00
PHST- 2012/05/22 06:00 [entrez]
PHST- 2012/05/23 06:00 [pubmed]
PHST- 2013/05/01 06:00 [medline]
AID - annrheumdis-2012-201387 [pii]
AID - 10.1136/annrheumdis-2012-201387 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2013 Apr;72(4):541-6. doi: 10.1136/annrheumdis-2012-201387. Epub 
      2012 May 18.

PMID- 22592810
OWN - NLM
STAT- MEDLINE
DCOM- 20130813
LR  - 20211021
IS  - 1433-2965 (Electronic)
IS  - 0937-941X (Linking)
VI  - 24
IP  - 2
DP  - 2013 Feb
TI  - Association between osteoporosis and urinary calculus: evidence from a 
      population-based study.
PG  - 651-7
LID - 10.1007/s00198-012-2019-5 [doi]
AB  - SUMMARY: This population-based case-control analysis investigated the association 
      between osteoporosis and prior urinary calculus (UC) in Taiwan. We succeeded in 
      detecting an association between osteoporosis and prior UC (adjusted odds 
      ratio = 1.66). This association was consistent and significant regardless of 
      stone location. INTRODUCTION: UC has been demonstrated to be a risk factor for 
      osteoporotic fractures, but no studies to date have directly investigated the 
      association between UC and osteoporosis. This case-control analysis aimed to 
      investigate the association of osteoporosis with prior UC using a 
      population-based dataset in Taiwan. METHODS: We first identified 39,840 cases ≥40 
      years who received their first-time diagnosis of osteoporosis between 2002 and 
      2009 and then randomly selected 79,680 controls. We used conditional logistic 
      regression analyses to compute the odds ratio (OR) and the corresponding 95 % 
      confidence interval (CI) for having been previously diagnosed with UC between 
      cases and controls. RESULTS: The OR of having been previously diagnosed with UC 
      for patients with osteoporosis was 1.66 (95 % CI = 1.59-1.73) when compared to 
      controls after adjusting for geographic location, urbanization level, type I 
      diabetes mellitus, coronary heart disease, hyperlipidemia, rheumatoid arthritis, 
      stroke, renal disease, Parkinson's disease, hyperthyroidism, chronic hepatopathy, 
      Cushing's syndrome, malabsorption, gastrectomy, obesity, and alcohol 
      abuse/alcohol dependence syndrome. The results consistently showed that 
      osteoporosis was significantly associated with a previous diagnosis of UC 
      regardless of stone location; the adjusted ORs of prior kidney calculus, ureter 
      calculus, bladder calculus, and unspecified calculus when compared to controls 
      were 1.71 (95 % CI = 1.61-1.81), 1.60 (95 % CI = 1.47-1.74), 1.59 (95 % 
      CI = 1.23-2.04), and 1.69 (95 % CI = 1.59-1.80), respectively. CONCLUSIONS: This 
      study succeeded in detecting an association between osteoporosis and prior UC. In 
      addition, our findings were consistent and significant regardless of stone 
      location.
FAU - Keller, J J
AU  - Keller JJ
AD  - School of Public Health, Taipei Medical University, 250 Wu-Hsing St, Taipei, 110, 
      Taiwan.
FAU - Lin, C-C
AU  - Lin CC
FAU - Kang, J-H
AU  - Kang JH
FAU - Lin, H-C
AU  - Lin HC
LA  - eng
PT  - Journal Article
DEP - 20120517
PL  - England
TA  - Osteoporos Int
JT  - Osteoporosis international : a journal established as result of cooperation 
      between the European Foundation for Osteoporosis and the National Osteoporosis 
      Foundation of the USA
JID - 9100105
SB  - IM
MH  - Adult
MH  - Aged
MH  - Case-Control Studies
MH  - Comorbidity
MH  - Databases, Factual
MH  - Evidence-Based Medicine/methods
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Osteoporosis/*complications/epidemiology
MH  - Socioeconomic Factors
MH  - Taiwan/epidemiology
MH  - Urinary Calculi/*complications/epidemiology
EDAT- 2012/05/18 06:00
MHDA- 2013/08/14 06:00
CRDT- 2012/05/18 06:00
PHST- 2012/03/19 00:00 [received]
PHST- 2012/03/30 00:00 [accepted]
PHST- 2012/05/18 06:00 [entrez]
PHST- 2012/05/18 06:00 [pubmed]
PHST- 2013/08/14 06:00 [medline]
AID - 10.1007/s00198-012-2019-5 [doi]
PST - ppublish
SO  - Osteoporos Int. 2013 Feb;24(2):651-7. doi: 10.1007/s00198-012-2019-5. Epub 2012 
      May 17.

PMID- 22591655
OWN - NLM
STAT- Publisher
LR  - 20191120
IS  - 1578-2190 (Electronic)
IS  - 0001-7310 (Linking)
VI  - 103
IP  - 10
DP  - 2012 Dec
TI  - Cardiovascular Risk and Psoriasis: the Role of Biologic Therapy.
PG  - 853-862
LID - S0001-7310(12)00107-X [pii]
LID - 10.1016/j.ad.2012.02.003 [doi]
AB  - One of the most clinically important aspects of recent advances in our 
      understanding of psoriasis has been the detection of an association between this 
      disease and an increased prevalence of cardiovascular risk factors. This increase 
      in prevalence is, in turn, linked to a greater risk of morbidity and mortality 
      related to acute myocardial infarction, cerebrovascular accident, and peripheral 
      arterial disease. The chronic systemic inflammation present in psoriasis could 
      explain why moderate to severe psoriasis is an independent risk factor for 
      cardiovascular disease. The introduction of biologic therapies has greatly 
      improved the expectations of treatment as well as the long-term control of 
      psoriasis, and there is epidemiological evidence that these therapies may lower 
      cardiovascular risk in psoriasis as they do in rheumatoid arthritis. Caution 
      should, however, be exercised when prescribing biologic drugs in this setting, 
      because adverse effects have been reported in association with the use of tumor 
      necrosis factor inhibitors in patients with advanced congestive heart failure. 
      Furthermore, a numerical imbalance (without statistical significance) between the 
      groups receiving the biologic drug and the placebo groups was recently observed 
      in the incidence of major cardiovascular events (nonfatal myocardial infarction 
      and cerebrovascular accident and cardiovascular death) during the controlled 
      periods of clinical trials of briakinumab and ustekinumab, 2 monoclonal 
      antibodies that target the p40 subunit shared by IL 12 and IL-23. We review the 
      current scientific evidence on this topic.
CI  - Copyright © 2011 Elsevier España, S.L. and AEDV. All rights reserved.
FAU - Puig, L
AU  - Puig L
AD  - Servicio de Dermatología, Hospital de la Santa Creu i Sant Pau, Barcelona, 
      España. Electronic address: lpuig@santpau.cat.
LA  - eng
LA  - spa
PT  - Journal Article
TT  - Riesgo cardiovascular y psoriasis: papel de la terapia biológica.
DEP - 20120514
PL  - Spain
TA  - Actas Dermosifiliogr
JT  - Actas dermo-sifiliograficas
JID - 0373062
EDAT- 2012/05/18 06:00
MHDA- 2012/05/18 06:00
CRDT- 2012/05/18 06:00
PHST- 2011/11/08 00:00 [received]
PHST- 2012/02/06 00:00 [revised]
PHST- 2012/02/08 00:00 [accepted]
PHST- 2012/05/18 06:00 [entrez]
PHST- 2012/05/18 06:00 [pubmed]
PHST- 2012/05/18 06:00 [medline]
AID - S0001-7310(12)00107-X [pii]
AID - 10.1016/j.ad.2012.02.003 [doi]
PST - ppublish
SO  - Actas Dermosifiliogr. 2012 Dec;103(10):853-862. doi: 10.1016/j.ad.2012.02.003. 
      Epub 2012 May 14.

PMID- 22521305
OWN - NLM
STAT- MEDLINE
DCOM- 20120926
LR  - 20220408
IS  - 1879-1913 (Electronic)
IS  - 0002-9149 (Print)
IS  - 0002-9149 (Linking)
VI  - 110
IP  - 3
DP  - 2012 Aug 1
TI  - Usefulness of risk scores to estimate the risk of cardiovascular disease in 
      patients with rheumatoid arthritis.
PG  - 420-4
LID - 10.1016/j.amjcard.2012.03.044 [doi]
AB  - Patients with rheumatoid arthritis (RA) have an excess burden of cardiovascular 
      (CV) disease (CVD). CV risk scores for the general population may not accurately 
      predict CV risk for patients with RA. A population-based inception cohort of 
      patients who fulfilled 1987 American College of Rheumatology criteria for RA from 
      1988 to 2007 was followed until death, migration, or December 31, 2008. CV risk 
      factors and CVD (myocardial infarction, CV death, angina, stroke, intermittent 
      claudication, and heart failure) were ascertained by medical record review. 
      Ten-year predicted CVD risk was calculated using the general Framingham and the 
      Reynolds risk scores. Standardized incidence ratios were calculated to compare 
      observed and predicted CVD risks. The study included 525 patients with RA aged 
      ≥30 years without previous CVD. The mean follow-up period was 8.4 years, during 
      which 84 patients developed CVD. The observed CVD risk was 2-fold higher than the 
      Framingham risk score predicted in women and 65% higher in men, and the Reynolds 
      risk score revealed similar deficits. Patients aged ≥75 years had observed CVD 
      risk >3 times the Framingham-predicted risk. Patients with positive rheumatoid 
      factor or persistently elevated erythrocyte sedimentation rates also experienced 
      more CVD events than predicted. In conclusion, the Framingham and Reynolds risk 
      scores substantially underestimated CVD risk in patients with RA of both genders, 
      especially in older ages and in patients with positive rheumatoid factor. These 
      data underscore the need for more accurate tools to predict CVD risk in patients 
      with RA.
CI  - Copyright © 2012 Elsevier Inc. All rights reserved.
FAU - Crowson, Cynthia S
AU  - Crowson CS
AD  - Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. 
      crowson@mayo.edu
FAU - Matteson, Eric L
AU  - Matteson EL
FAU - Roger, Veronique L
AU  - Roger VL
FAU - Therneau, Terry M
AU  - Therneau TM
FAU - Gabriel, Sherine E
AU  - Gabriel SE
LA  - eng
GR  - R01 AR046849/AR/NIAMS NIH HHS/United States
GR  - R01 AG034676/AG/NIA NIH HHS/United States
GR  - R01 AR46849/AR/NIAMS NIH HHS/United States
GR  - R01 AR046849-11A1/AR/NIAMS NIH HHS/United States
GR  - R01 AG034676-47/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20120420
PL  - United States
TA  - Am J Cardiol
JT  - The American journal of cardiology
JID - 0207277
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications
MH  - Cardiovascular Diseases/*epidemiology/*etiology
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Prognosis
MH  - Reproducibility of Results
MH  - Retrospective Studies
MH  - Risk Assessment
PMC - PMC3398213
MID - NIHMS367850
EDAT- 2012/04/24 06:00
MHDA- 2012/09/27 06:00
PMCR- 2013/08/01
CRDT- 2012/04/24 06:00
PHST- 2012/01/12 00:00 [received]
PHST- 2012/03/15 00:00 [revised]
PHST- 2012/03/15 00:00 [accepted]
PHST- 2012/04/24 06:00 [entrez]
PHST- 2012/04/24 06:00 [pubmed]
PHST- 2012/09/27 06:00 [medline]
PHST- 2013/08/01 00:00 [pmc-release]
AID - S0002-9149(12)01060-0 [pii]
AID - 10.1016/j.amjcard.2012.03.044 [doi]
PST - ppublish
SO  - Am J Cardiol. 2012 Aug 1;110(3):420-4. doi: 10.1016/j.amjcard.2012.03.044. Epub 
      2012 Apr 20.

PMID- 22505696
OWN - NLM
STAT- MEDLINE
DCOM- 20130204
LR  - 20171116
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
VI  - 39
IP  - 5
DP  - 2012 May
TI  - Polymorphisms of the genes encoding CD40 and growth differentiation factor 15 and 
      in the 9p21.3 region in patients with rheumatoid arthritis and cardiovascular 
      disease.
PG  - 939-45
LID - 10.3899/jrheum.111336 [doi]
AB  - OBJECTIVE: Genes or gene products associated with coronary artery disease in the 
      general population were analyzed in rheumatoid arthritis (RA) patients with 
      atherothrombotic manifestations (ATM). METHODS: A cross-sectional study of 681 
      individuals (498 women; 183 men) with RA (American College of Rheumatology 
      criteria), a mean age of 60.6 ± 13.2 years, and mean disease duration of 15.5 ± 
      12.6 years who were consecutively recruited and followed for 6 years. The 
      prevalence of ATM [i.e., myocardial infarction, angina pectoris with 
      intervention, deep vein thrombosis/pulmonary embolism (DVT/PE), and/or 
      stroke/transient ischemic attack (TIA)] was recorded. Polymorphisms were analyzed 
      in the genes coding for growth differentiation factor 15 (GDF15)/monocyte 
      inhibitory cytokine-1 (MIC-1; rs1058587), CD40 (rs1535045 and rs3765459), and the 
      9p21.3 locus (rs1333049). Controls were randomly selected (n = 687; matched for 
      age and sex). RESULTS: The distribution of genotypes of GDF15/MIC-1 differed 
      significantly between patients with RA and controls (chi-squared = 6.40, 2 df, p 
      = 0.041). ATM were associated with polymorphism of the GDF15/MIC-1 G allele (OR 
      2.21, 95% CI 1.17-4.18), and with CC genotype of the 9p21.3 locus (rs1333049; OR 
      1.92, 95% CI 1.15-3.19). Stroke/TIA in women was associated with GDF15/MIC-1 GG 
      genotype (OR 3.75, 95% CI 1.06-13.33), while stroke/TIA in men was associated 
      with CD40 homozygous major alleles (OR 6.48, 95% CI 1.31-32.0 and OR 2.78, 95% CI 
      0.78-9.91, respectively). DVT/PE was associated with polymorphism in the 
      GDF15/MIC-1 gene (rs1058587) minor allele (OR 3.53, 95% CI 1.30-9.58). 
      CONCLUSION: The gene polymorphisms analyzed were associated with different ATM in 
      RA. The GDF15/MIC-1 gene polymorphism was also associated with RA per se, 
      suggesting a common etiology for RA and ATM.
FAU - Ärlestig, Lisbeth
AU  - Ärlestig L
AD  - Department of Public Health and Clinical Medicine, Rheumatology, Umeå University, 
      Umeå, Sweden.
FAU - Rantapää-Dahlqvist, Solbritt
AU  - Rantapää-Dahlqvist S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120415
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (CD40 Antigens)
RN  - 0 (GDF15 protein, human)
RN  - 0 (Growth Differentiation Factor 15)
SB  - IM
MH  - Aged
MH  - Arteriosclerosis/epidemiology/genetics
MH  - Arthritis, Rheumatoid/epidemiology/*genetics
MH  - CD40 Antigens/*genetics
MH  - Cardiovascular Diseases/epidemiology/*genetics
MH  - Cross-Sectional Studies
MH  - Female
MH  - Genetic Predisposition to Disease/epidemiology/genetics
MH  - Genotype
MH  - Growth Differentiation Factor 15/*genetics
MH  - Humans
MH  - Hypertension/epidemiology/genetics
MH  - Ischemic Attack, Transient/epidemiology/genetics
MH  - Male
MH  - Middle Aged
MH  - Polymorphism, Genetic/*genetics
MH  - Prevalence
MH  - Pulmonary Embolism/epidemiology/genetics
MH  - Risk Factors
MH  - Stroke/epidemiology/genetics
MH  - Venous Thrombosis/epidemiology/genetics
EDAT- 2012/04/17 06:00
MHDA- 2013/02/05 06:00
CRDT- 2012/04/17 06:00
PHST- 2012/04/17 06:00 [entrez]
PHST- 2012/04/17 06:00 [pubmed]
PHST- 2013/02/05 06:00 [medline]
AID - jrheum.111336 [pii]
AID - 10.3899/jrheum.111336 [doi]
PST - ppublish
SO  - J Rheumatol. 2012 May;39(5):939-45. doi: 10.3899/jrheum.111336. Epub 2012 Apr 15.

PMID- 23798298
OWN - NLM
STAT- MEDLINE
DCOM- 20131105
LR  - 20220410
IS  - 2040-4603 (Electronic)
IS  - 2040-4603 (Linking)
VI  - 2
IP  - 2
DP  - 2012 Apr
TI  - Lack of exercise is a major cause of chronic diseases.
PG  - 1143-211
LID - 10.1002/cphy.c110025 [doi]
AB  - Chronic diseases are major killers in the modern era. Physical inactivity is a 
      primary cause of most chronic diseases. The initial third of the article 
      considers: activity and prevention definitions; historical evidence showing 
      physical inactivity is detrimental to health and normal organ functional 
      capacities; cause versus treatment; physical activity and inactivity mechanisms 
      differ; gene-environment interaction (including aerobic training adaptations, 
      personalized medicine, and co-twin physical activity); and specificity of 
      adaptations to type of training. Next, physical activity/exercise is examined as 
      primary prevention against 35 chronic conditions [accelerated biological 
      aging/premature death, low cardiorespiratory fitness (VO2max), sarcopenia, 
      metabolic syndrome, obesity, insulin resistance, prediabetes, type 2 diabetes, 
      nonalcoholic fatty liver disease, coronary heart disease, peripheral artery 
      disease, hypertension, stroke, congestive heart failure, endothelial dysfunction, 
      arterial dyslipidemia, hemostasis, deep vein thrombosis, cognitive dysfunction, 
      depression and anxiety, osteoporosis, osteoarthritis, balance, bone 
      fracture/falls, rheumatoid arthritis, colon cancer, breast cancer, endometrial 
      cancer, gestational diabetes, pre-eclampsia, polycystic ovary syndrome, erectile 
      dysfunction, pain, diverticulitis, constipation, and gallbladder diseases]. The 
      article ends with consideration of deterioration of risk factors in longer-term 
      sedentary groups; clinical consequences of inactive childhood/adolescence; and 
      public policy. In summary, the body rapidly maladapts to insufficient physical 
      activity, and if continued, results in substantial decreases in both total and 
      quality years of life. Taken together, conclusive evidence exists that physical 
      inactivity is one important cause of most chronic diseases. In addition, physical 
      activity primarily prevents, or delays, chronic diseases, implying that chronic 
      disease need not be an inevitable outcome during life.
CI  - © 2012 American Physiological Society. Compr Physiol 2:1143-1211, 2012.
FAU - Booth, Frank W
AU  - Booth FW
AD  - Departments of Biomedical Sciences, Medical Pharmacology and Physiology, and 
      Nutrition and Exercise Physiology, Dalton Cardiovascular Institute, University of 
      Missouri, Columbia, Missouri, USA. boothf@missouri.edu
FAU - Roberts, Christian K
AU  - Roberts CK
FAU - Laye, Matthew J
AU  - Laye MJ
LA  - eng
GR  - R01 AR019393/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Compr Physiol
JT  - Comprehensive Physiology
JID - 101574442
SB  - IM
MH  - Adaptation, Physiological/physiology
MH  - Chronic Disease/*prevention & control
MH  - Exercise/*physiology
MH  - Gene-Environment Interaction
MH  - Humans
MH  - Metabolic Syndrome/physiopathology
MH  - Motor Activity/physiology
MH  - Pharmacogenetics
MH  - Physical Fitness
MH  - Risk Factors
MH  - *Sedentary Behavior
MH  - Twin Studies as Topic
PMC - PMC4241367
MID - NIHMS603913
EDAT- 2012/04/01 00:00
MHDA- 2013/11/06 06:00
PMCR- 2014/11/23
CRDT- 2013/06/27 06:00
PHST- 2013/06/27 06:00 [entrez]
PHST- 2012/04/01 00:00 [pubmed]
PHST- 2013/11/06 06:00 [medline]
PHST- 2014/11/23 00:00 [pmc-release]
AID - 10.1002/cphy.c110025 [doi]
PST - ppublish
SO  - Compr Physiol. 2012 Apr;2(2):1143-211. doi: 10.1002/cphy.c110025.

PMID- 22453881
OWN - NLM
STAT- MEDLINE
DCOM- 20120612
LR  - 20181201
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Linking)
VI  - 344
DP  - 2012 Mar 27
TI  - Atrial fibrillation and rheumatoid arthritis are cardiovascular risk factors.
PG  - e2259
LID - bmj.e2259 [pii]
LID - 10.1136/bmj.e2259 [doi]
FAU - Hippisley-Cox, Julia
AU  - Hippisley-Cox J
FAU - Coupland, Carol
AU  - Coupland C
FAU - Robson, John
AU  - Robson J
FAU - Brindle, Peter
AU  - Brindle P
LA  - eng
PT  - Comment
PT  - Letter
DEP - 20120327
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
SB  - IM
CON - BMJ. 2012 Mar 08;344:e1257. doi: 10.1136/bmj.e1257. PMID: 22403267
MH  - Arthritis, Rheumatoid/*complications
MH  - Atrial Fibrillation/*epidemiology
MH  - Female
MH  - Humans
MH  - Male
MH  - Stroke/*epidemiology
EDAT- 2012/03/29 06:00
MHDA- 2012/06/13 06:00
CRDT- 2012/03/29 06:00
PHST- 2012/03/29 06:00 [entrez]
PHST- 2012/03/29 06:00 [pubmed]
PHST- 2012/06/13 06:00 [medline]
AID - bmj.e2259 [pii]
AID - 10.1136/bmj.e2259 [doi]
PST - epublish
SO  - BMJ. 2012 Mar 27;344:e2259. doi: 10.1136/bmj.e2259.

PMID- 22425941
OWN - NLM
STAT- MEDLINE
DCOM- 20121016
LR  - 20220410
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 71
IP  - 9
DP  - 2012 Sep
TI  - Risk of incident cardiovascular events in patients with rheumatoid arthritis: a 
      meta-analysis of observational studies.
PG  - 1524-9
LID - 10.1136/annrheumdis-2011-200726 [doi]
AB  - OBJECTIVE: To determine the magnitude of the risk of incident cardiovascular 
      disease (CVD; fatal and non-fatal), including acute myocardial infarction (MI), 
      cerebrovascular accidents (CVA) and congestive heart failure (CHF), in patients 
      with rheumatoid arthritis (RA) compared to the general population through a 
      meta-analysis of controlled observational studies. METHODS: The authors searched 
      the Medline, Embase, LILACS and Cochrane databases from their inception to June 
      2011. Observational studies meeting the following criteria were included: (1) 
      prespecified RA criteria; (2) predefined CVD criteria for incident CVD (MI, CVA 
      or CHF); (3) a comparison group; and (4) RR estimates, 95% CI or data for 
      calculating them. The authors calculated the pooled RR using the random-effects 
      model and tested for heterogeneity using the bootstrap version of the Q 
      statistic. RESULTS: Fourteen studies comprising 41 490 patients met the inclusion 
      criteria. Overall, there was a 48% increased risk of incident CVD in patients 
      with RA (pooled RR 1.48 (95% CI 1.36 to 1.62)). The risks of MI and CVA were 
      increased by 68% (pooled RR 1.68 (95% CI 1.40 to 2.03)) and 41% (pooled RR 1.41 
      (95% CI 1.14 to 1.74)). The risk of CHF was assessed in only one study (RR 1.87 
      (95% CI 1.47 to 2.39)). Significant heterogeneity existed in all main analyses. 
      Subgroup analyses showed that inception cohort studies were the only group that 
      did not show a significantly increased risk of CVD (pooled RR 1.12 (95% CI 0.97 
      to 1.65)). CONCLUSIONS: Published data indicate that the risk of incident CVD is 
      increased by 48% in patients with RA compared to the general population. Sample 
      and cohort type influenced the estimates of RR.
FAU - Avina-Zubieta, Juan Antonio
AU  - Avina-Zubieta JA
AD  - Arthritis Research Centre of Canada, 895 West 10th Avenue, Vancouver, British 
      Columbia, Canada V5Z 1L7. azubieta@arthritisresearch.ca
FAU - Thomas, Jamie
AU  - Thomas J
FAU - Sadatsafavi, Mohsen
AU  - Sadatsafavi M
FAU - Lehman, Allen J
AU  - Lehman AJ
FAU - Lacaille, Diane
AU  - Lacaille D
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
DEP - 20120316
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
MH  - Arthritis, Rheumatoid/*complications
MH  - Cardiovascular Diseases/*epidemiology/*etiology
MH  - Humans
MH  - Observation
MH  - Risk Factors
EDAT- 2012/03/20 06:00
MHDA- 2012/10/17 06:00
CRDT- 2012/03/20 06:00
PHST- 2012/03/20 06:00 [entrez]
PHST- 2012/03/20 06:00 [pubmed]
PHST- 2012/10/17 06:00 [medline]
AID - annrheumdis-2011-200726 [pii]
AID - 10.1136/annrheumdis-2011-200726 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2012 Sep;71(9):1524-9. doi: 10.1136/annrheumdis-2011-200726. Epub 
      2012 Mar 16.

PMID- 22421340
OWN - NLM
STAT- MEDLINE
DCOM- 20120410
LR  - 20240615
IS  - 1474-547X (Electronic)
IS  - 0140-6736 (Print)
IS  - 0140-6736 (Linking)
VI  - 379
IP  - 9822
DP  - 2012 Mar 31
TI  - The interleukin-6 receptor as a target for prevention of coronary heart disease: 
      a mendelian randomisation analysis.
PG  - 1214-24
LID - 10.1016/S0140-6736(12)60110-X [doi]
AB  - BACKGROUND: A high circulating concentration of interleukin 6 is associated with 
      increased risk of coronary heart disease. Blockade of the interleukin-6 receptor 
      (IL6R) with a monoclonal antibody (tocilizumab) licensed for treatment of 
      rheumatoid arthritis reduces systemic and articular inflammation. However, 
      whether IL6R blockade also reduces risk of coronary heart disease is unknown. 
      METHODS: Applying the mendelian randomisation principle, we used single 
      nucleotide polymorphisms (SNPs) in the gene IL6R to evaluate the likely efficacy 
      and safety of IL6R inhibition for primary prevention of coronary heart disease. 
      We compared genetic findings with the effects of tocilizumab reported in 
      randomised trials in patients with rheumatoid arthritis. FINDINGS: In 40 studies 
      including up to 133,449 individuals, an IL6R SNP (rs7529229) marking a 
      non-synonymous IL6R variant (rs8192284; p.Asp358Ala) was associated with 
      increased circulating log interleukin-6 concentration (increase per allele 9·45%, 
      95% CI 8·34-10·57) as well as reduced C-reactive protein (decrease per allele 
      8·35%, 95% CI 7·31-9·38) and fibrinogen concentrations (decrease per allele 
      0·85%, 95% CI 0·60-1·10). This pattern of effects was consistent with IL6R 
      blockade from infusions of tocilizumab (4-8 mg/kg every 4 weeks) in patients with 
      rheumatoid arthritis studied in randomised trials. In 25,458 coronary heart 
      disease cases and 100,740 controls, the IL6R rs7529229 SNP was associated with a 
      decreased odds of coronary heart disease events (per allele odds ratio 0·95, 95% 
      CI 0·93-0·97, p=1·53×10(-5)). INTERPRETATION: On the basis of genetic evidence in 
      human beings, IL6R signalling seems to have a causal role in development of 
      coronary heart disease. IL6R blockade could provide a novel therapeutic approach 
      to prevention of coronary heart disease that warrants testing in suitably powered 
      randomised trials. Genetic studies in populations could be used more widely to 
      help to validate and prioritise novel drug targets or to repurpose existing 
      agents and targets for new therapeutic uses. FUNDING: UK Medical Research 
      Council; British Heart Foundation; Rosetrees Trust; US National Heart, Lung, and 
      Blood Institute; Du Pont Pharma; Chest, Heart and Stroke Scotland; Wellcome 
      Trust; Coronary Thrombosis Trust; Northwick Park Institute for Medical Research; 
      UCLH/UCL Comprehensive Medical Research Centre; US National Institute on Aging; 
      Academy of Finland; Netherlands Organisation for Health Research and Development; 
      SANCO; Dutch Ministry of Public Health, Welfare and Sports; World Cancer Research 
      Fund; Agentschap NL; European Commission; Swedish Heart-Lung Foundation; Swedish 
      Research Council; Strategic Cardiovascular Programme of the Karolinska 
      Institutet; Stockholm County Council; US National Institute of Neurological 
      Disorders and Stroke; MedStar Health Research Institute; GlaxoSmithKline; Dutch 
      Kidney Foundation; US National Institutes of Health; Netherlands Interuniversity 
      Cardiology Institute of the Netherlands; Diabetes UK; European Union Seventh 
      Framework Programme; National Institute for Healthy Ageing; Cancer Research UK; 
      MacArthur Foundation.
CI  - Copyright © 2012 Elsevier Ltd. All rights reserved.
CN  - Interleukin-6 Receptor Mendelian Randomisation Analysis (IL6R MR) Consortium
FAU - Swerdlow, Daniel I
AU  - Swerdlow DI
FAU - Holmes, Michael V
AU  - Holmes MV
FAU - Kuchenbaecker, Karoline B
AU  - Kuchenbaecker KB
FAU - Engmann, Jorgen E L
AU  - Engmann JE
FAU - Shah, Tina
AU  - Shah T
FAU - Sofat, Reecha
AU  - Sofat R
FAU - Guo, Yiran
AU  - Guo Y
FAU - Chung, Christina
AU  - Chung C
FAU - Peasey, Anne
AU  - Peasey A
FAU - Pfister, Roman
AU  - Pfister R
FAU - Mooijaart, Simon P
AU  - Mooijaart SP
FAU - Ireland, Helen A
AU  - Ireland HA
FAU - Leusink, Maarten
AU  - Leusink M
FAU - Langenberg, Claudia
AU  - Langenberg C
FAU - Li, Ka Wah
AU  - Li KW
FAU - Palmen, Jutta
AU  - Palmen J
FAU - Howard, Philip
AU  - Howard P
FAU - Cooper, Jackie A
AU  - Cooper JA
FAU - Drenos, Fotios
AU  - Drenos F
FAU - Hardy, John
AU  - Hardy J
FAU - Nalls, Michael A
AU  - Nalls MA
FAU - Li, Yun Rose
AU  - Li YR
FAU - Lowe, Gordon
AU  - Lowe G
FAU - Stewart, Marlene
AU  - Stewart M
FAU - Bielinski, Suzette J
AU  - Bielinski SJ
FAU - Peto, Julian
AU  - Peto J
FAU - Timpson, Nicholas J
AU  - Timpson NJ
FAU - Gallacher, John
AU  - Gallacher J
FAU - Dunlop, Malcolm
AU  - Dunlop M
FAU - Houlston, Richard
AU  - Houlston R
FAU - Tomlinson, Ian
AU  - Tomlinson I
FAU - Tzoulaki, Ioanna
AU  - Tzoulaki I
FAU - Luan, Jian'an
AU  - Luan J
FAU - Boer, Jolanda M A
AU  - Boer JM
FAU - Forouhi, Nita G
AU  - Forouhi NG
FAU - Onland-Moret, N Charlotte
AU  - Onland-Moret NC
FAU - van der Schouw, Yvonne T
AU  - van der Schouw YT
FAU - Schnabel, Renate B
AU  - Schnabel RB
FAU - Hubacek, Jaroslav A
AU  - Hubacek JA
FAU - Kubinova, Ruzena
AU  - Kubinova R
FAU - Baceviciene, Migle
AU  - Baceviciene M
FAU - Tamosiunas, Abdonas
AU  - Tamosiunas A
FAU - Pajak, Andrzej
AU  - Pajak A
FAU - Topor-Madry, Roman
AU  - Topor-Madry R
FAU - Malyutina, Sofia
AU  - Malyutina S
FAU - Baldassarre, Damiano
AU  - Baldassarre D
FAU - Sennblad, Bengt
AU  - Sennblad B
FAU - Tremoli, Elena
AU  - Tremoli E
FAU - de Faire, Ulf
AU  - de Faire U
FAU - Ferrucci, Luigi
AU  - Ferrucci L
FAU - Bandenelli, Stefania
AU  - Bandenelli S
FAU - Tanaka, Toshiko
AU  - Tanaka T
FAU - Meschia, James F
AU  - Meschia JF
FAU - Singleton, Andrew
AU  - Singleton A
FAU - Navis, Gerjan
AU  - Navis G
FAU - Mateo Leach, Irene
AU  - Mateo Leach I
FAU - Bakker, Stephan J L
AU  - Bakker SJ
FAU - Gansevoort, Ron T
AU  - Gansevoort RT
FAU - Ford, Ian
AU  - Ford I
FAU - Epstein, Stephen E
AU  - Epstein SE
FAU - Burnett, Mary Susan
AU  - Burnett MS
FAU - Devaney, Joe M
AU  - Devaney JM
FAU - Jukema, J Wouter
AU  - Jukema JW
FAU - Westendorp, Rudi G J
AU  - Westendorp RG
FAU - Jan de Borst, Gert
AU  - Jan de Borst G
FAU - van der Graaf, Yolanda
AU  - van der Graaf Y
FAU - de Jong, Pim A
AU  - de Jong PA
FAU - Mailand-van der Zee, Anke-Hilse
AU  - Mailand-van der Zee AH
FAU - Klungel, Olaf H
AU  - Klungel OH
FAU - de Boer, Anthonius
AU  - de Boer A
FAU - Doevendans, Pieter A
AU  - Doevendans PA
FAU - Stephens, Jeffrey W
AU  - Stephens JW
FAU - Eaton, Charles B
AU  - Eaton CB
FAU - Robinson, Jennifer G
AU  - Robinson JG
FAU - Manson, JoAnn E
AU  - Manson JE
FAU - Fowkes, F Gerry
AU  - Fowkes FG
FAU - Frayling, Timonthy M
AU  - Frayling TM
FAU - Price, Jackie F
AU  - Price JF
FAU - Whincup, Peter H
AU  - Whincup PH
FAU - Morris, Richard W
AU  - Morris RW
FAU - Lawlor, Debbie A
AU  - Lawlor DA
FAU - Smith, George Davey
AU  - Smith GD
FAU - Ben-Shlomo, Yoav
AU  - Ben-Shlomo Y
FAU - Redline, Susan
AU  - Redline S
FAU - Lange, Leslie A
AU  - Lange LA
FAU - Kumari, Meena
AU  - Kumari M
FAU - Wareham, Nick J
AU  - Wareham NJ
FAU - Verschuren, W M Monique
AU  - Verschuren WM
FAU - Benjamin, Emelia J
AU  - Benjamin EJ
FAU - Whittaker, John C
AU  - Whittaker JC
FAU - Hamsten, Anders
AU  - Hamsten A
FAU - Dudbridge, Frank
AU  - Dudbridge F
FAU - Delaney, J A Chris
AU  - Delaney JA
FAU - Wong, Andrew
AU  - Wong A
FAU - Kuh, Diana
AU  - Kuh D
FAU - Hardy, Rebecca
AU  - Hardy R
FAU - Castillo, Berta Almoguera
AU  - Castillo BA
FAU - Connolly, John J
AU  - Connolly JJ
FAU - van der Harst, Pim
AU  - van der Harst P
FAU - Brunner, Eric J
AU  - Brunner EJ
FAU - Marmot, Michael G
AU  - Marmot MG
FAU - Wassel, Christina L
AU  - Wassel CL
FAU - Humphries, Steve E
AU  - Humphries SE
FAU - Talmud, Philippa J
AU  - Talmud PJ
FAU - Kivimaki, Mika
AU  - Kivimaki M
FAU - Asselbergs, Folkert W
AU  - Asselbergs FW
FAU - Voevoda, Mikhail
AU  - Voevoda M
FAU - Bobak, Martin
AU  - Bobak M
FAU - Pikhart, Hynek
AU  - Pikhart H
FAU - Wilson, James G
AU  - Wilson JG
FAU - Hakonarson, Hakon
AU  - Hakonarson H
FAU - Reiner, Alex P
AU  - Reiner AP
FAU - Keating, Brendan J
AU  - Keating BJ
FAU - Sattar, Naveed
AU  - Sattar N
FAU - Hingorani, Aroon D
AU  - Hingorani AD
FAU - Casas, Juan Pablo
AU  - Casas JP
LA  - eng
SI  - ClinicalTrials.gov/NCT00000611
GR  - N01HC95160/HL/NHLBI NIH HHS/United States
GR  - R37 AG013196/AG/NIA NIH HHS/United States
GR  - R01 LM010098/LM/NLM NIH HHS/United States
GR  - WT_/Wellcome Trust/United Kingdom
GR  - U01 HG005152/HG/NHGRI NIH HHS/United States
GR  - 12076/CRUK_/Cancer Research UK/United Kingdom
GR  - 081081/Z/06/Z/WT_/Wellcome Trust/United Kingdom
GR  - RG/07/008/23674/BHF_/British Heart Foundation/United Kingdom
GR  - N01HC-95169/HC/NHLBI NIH HHS/United States
GR  - G8802774/MRC_/Medical Research Council/United Kingdom
GR  - 1R01 AG23522-01/AG/NIA NIH HHS/United States
GR  - G19/35/MRC_/Medical Research Council/United Kingdom
GR  - RG/04/003/BHF_/British Heart Foundation/United Kingdom
GR  - N01HC-95163/HC/NHLBI NIH HHS/United States
GR  - AG000954-06/AG/NIA NIH HHS/United States
GR  - R01 NS042733/NS/NINDS NIH HHS/United States
GR  - R01 HL036310/HL/NHLBI NIH HHS/United States
GR  - G0100222/MRC_/Medical Research Council/United Kingdom
GR  - N01HC-95168/HC/NHLBI NIH HHS/United States
GR  - MC_UP_A100_1003/MRC_/Medical Research Council/United Kingdom
GR  - FS 05/125/BHF_/British Heart Foundation/United Kingdom
GR  - RG/08/013/25942/BHF_/British Heart Foundation/United Kingdom
GR  - 064947/Z/01/Z/WT_/Wellcome Trust/United Kingdom
GR  - N01HC95163/HL/NHLBI NIH HHS/United States
GR  - Z01 AG000015/ImNIH/Intramural NIH HHS/United States
GR  - RFP-NHLBI-WH-11-10/WH/WHI NIH HHS/United States
GR  - RG/08/008/25291/BHF_/British Heart Foundation/United Kingdom
GR  - C150/A5660/CRUK_/Cancer Research UK/United Kingdom
GR  - N01HC-95165/HC/NHLBI NIH HHS/United States
GR  - AG1764406S1/AG/NIA NIH HHS/United States
GR  - U01HG005152/HG/NHGRI NIH HHS/United States
GR  - RR-024156/RR/NCRR NIH HHS/United States
GR  - N01HC95169/HL/NHLBI NIH HHS/United States
GR  - MC_U123092720/MRC_/Medical Research Council/United Kingdom
GR  - MC_U127527198/MRC_/Medical Research Council/United Kingdom
GR  - AG13196/AG/NIA NIH HHS/United States
GR  - N01HC-95159/HC/NHLBI NIH HHS/United States
GR  - DH_/Department of Health/United Kingdom
GR  - UL1 RR024156/RR/NCRR NIH HHS/United States
GR  - PG/09/022/26739/BHF_/British Heart Foundation/United Kingdom
GR  - N01HC-95166/HC/NHLBI NIH HHS/United States
GR  - HHSN268200625226C/PHS HHS/United States
GR  - N01HC95164/HL/NHLBI NIH HHS/United States
GR  - Z01 AG000954/ImNIH/Intramural NIH HHS/United States
GR  - N01HC95162/HL/NHLBI NIH HHS/United States
GR  - G0902037/MRC_/Medical Research Council/United Kingdom
GR  - HHSN268200960009C/PHS HHS/United States
GR  - N01HC-95162/HC/NHLBI NIH HHS/United States
GR  - N01HC95168/HL/NHLBI NIH HHS/United States
GR  - MC_U123092721/MRC_/Medical Research Council/United Kingdom
GR  - FS/07/011/BHF_/British Heart Foundation/United Kingdom
GR  - R01 AG023522/AG/NIA NIH HHS/United States
GR  - HL36310/HL/NHLBI NIH HHS/United States
GR  - G0600705/MRC_/Medical Research Council/United Kingdom
GR  - R01 NS039987/NS/NINDS NIH HHS/United States
GR  - G1000718/MRC_/Medical Research Council/United Kingdom
GR  - N01HC95165/HL/NHLBI NIH HHS/United States
GR  - N01HC95161/HL/NHLBI NIH HHS/United States
GR  - 090532/WT_/Wellcome Trust/United Kingdom
GR  - N01HC-95161/HC/NHLBI NIH HHS/United States
GR  - N01HC65226/HL/NHLBI NIH HHS/United States
GR  - RG08/008/BHF_/British Heart Foundation/United Kingdom
GR  - RG/10/12/28456/BHF_/British Heart Foundation/United Kingdom
GR  - HHSN268200900009C/HL/NHLBI NIH HHS/United States
GR  - N01HC-95167/HC/NHLBI NIH HHS/United States
GR  - N01HC95167/HL/NHLBI NIH HHS/United States
GR  - F30 AR066486/AR/NIAMS NIH HHS/United States
GR  - R01 AG013196/AG/NIA NIH HHS/United States
GR  - HS06516/HS/AHRQ HHS/United States
GR  - G0802432/MRC_/Medical Research Council/United Kingdom
GR  - N01HC-95160/HC/NHLBI NIH HHS/United States
GR  - G0701075/MRC_/Medical Research Council/United Kingdom
GR  - N01HC95166/HL/NHLBI NIH HHS/United States
GR  - MC_U106179471/MRC_/Medical Research Council/United Kingdom
GR  - G0500877/MRC_/Medical Research Council/United Kingdom
GR  - N01HC-95164/HC/NHLBI NIH HHS/United States
GR  - 5215810-55000000041/PHS HHS/United States
GR  - PG/07/133/24260/BHF_/British Heart Foundation/United Kingdom
GR  - R01 NS39987/NS/NINDS NIH HHS/United States
GR  - C1298/A8362/CRUK_/Cancer Research UK/United Kingdom
GR  - R01 NS42733/NS/NINDS NIH HHS/United States
GR  - N01 HC095159/HC/NHLBI NIH HHS/United States
GR  - NHLBI 33014/PHS HHS/United States
GR  - LM010098/LM/NLM NIH HHS/United States
GR  - N01-HC-65226/HC/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, N.I.H., Intramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20120314
PL  - England
TA  - Lancet
JT  - Lancet (London, England)
JID - 2985213R
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (IL6R protein, human)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Receptors, Interleukin-6)
RN  - I031V2H011 (tocilizumab)
SB  - IM
CIN - Lancet. 2012 Mar 31;379(9822):1176-8. doi: 10.1016/S0140-6736(12)60361-4. PMID: 
      22421338
CIN - Nat Rev Cardiol. 2012 Apr 03;9(6):313. doi: 10.1038/nrcardio.2012.46. PMID: 
      22473076
CIN - Lancet. 2012 Jul 28;380(9839):338. doi: 10.1016/S0140-6736(12)61246-X. PMID: 
      22841333
MH  - Antibodies, Monoclonal, Humanized/adverse effects/*therapeutic use
MH  - Coronary Disease/*genetics/*prevention & control
MH  - Gene Frequency/genetics
MH  - Genetic Association Studies
MH  - Genetic Variation/genetics
MH  - Genotype
MH  - Humans
MH  - Inflammation Mediators/blood
MH  - *Mendelian Randomization Analysis
MH  - Phenotype
MH  - Polymorphism, Single Nucleotide/genetics
MH  - Randomized Controlled Trials as Topic
MH  - Receptors, Interleukin-6/*antagonists & inhibitors/*genetics
MH  - Signal Transduction/drug effects/genetics
MH  - Treatment Outcome
PMC - PMC3316968
EDAT- 2012/03/17 06:00
MHDA- 2012/04/11 06:00
PMCR- 2012/03/31
CRDT- 2012/03/17 06:00
PHST- 2012/03/17 06:00 [entrez]
PHST- 2012/03/17 06:00 [pubmed]
PHST- 2012/04/11 06:00 [medline]
PHST- 2012/03/31 00:00 [pmc-release]
AID - S0140-6736(12)60110-X [pii]
AID - 10.1016/S0140-6736(12)60110-X [doi]
PST - ppublish
SO  - Lancet. 2012 Mar 31;379(9822):1214-24. doi: 10.1016/S0140-6736(12)60110-X. Epub 
      2012 Mar 14.

PMID- 22403267
OWN - NLM
STAT- MEDLINE
DCOM- 20120423
LR  - 20220330
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Print)
IS  - 0959-8138 (Linking)
VI  - 344
DP  - 2012 Mar 8
TI  - Risk of atrial fibrillation and stroke in rheumatoid arthritis: Danish nationwide 
      cohort study.
PG  - e1257
LID - bmj.e1257 [pii]
LID - 10.1136/bmj.e1257 [doi]
LID - e1257
AB  - OBJECTIVES: To determine if patients with rheumatoid arthritis have increased 
      risk of atrial fibrillation and stroke. DESIGN: Longitudinal nationwide register 
      based cohort study. SETTING: Inpatient and outpatient hospital care in Denmark 
      from 1997 to 2009. PARTICIPANTS: Entire Danish population aged over 15 years 
      without rheumatoid arthritis, atrial fibrillation, or stroke before 1997. 
      Participants with rheumatoid arthritis were identified by individual level 
      linkage of diagnoses and rheumatoid arthritis treatment. MAIN OUTCOME MEASURES: 
      Rates of atrial fibrillation and stroke. RESULTS: Of 4,182,335 participants 
      included in the cohort, 18,247 were identified as having rheumatoid arthritis 
      during follow-up, with a mean age at disease onset of 59.2 years and a median 
      follow-up of 4.8 years. A total of 156,484 people, including 774 with rheumatoid 
      arthritis, were diagnosed as having atrial fibrillation (age and sex matched 
      event rates of 8.2 per 1000 person years in rheumatoid arthritis patients and 6.0 
      per 1000 person years in the general population), with an adjusted incidence rate 
      ratio of 1.41 (95% confidence interval 1.31 to 1.51). In addition, 165,343 
      people, including 718 with rheumatoid arthritis, had a stroke (7.6 per 1000 
      person years in rheumatoid arthritis and 5.7 per 1000 person years in the general 
      population), with a resultant rate ratio of 1.32 (1.22 to 1.42). For both atrial 
      fibrillation and stroke, relative risks were increased in all strata based on 
      thirds of sex and age, with higher relative risks in younger patients but higher 
      absolute risk differences in older patients. CONCLUSIONS: Rheumatoid arthritis 
      was associated with an increased incidence of atrial fibrillation and stroke. The 
      novel finding of increased risk of atrial fibrillation in rheumatoid arthritis 
      suggests that this arrhythmia is relevant in cardiovascular risk assessment of 
      these patients.
FAU - Lindhardsen, Jesper
AU  - Lindhardsen J
AD  - Department of Cardiology, Copenhagen University Hospital Gentofte, 2900 Hellerup, 
      Denmark. jeslin01@geh.regionh.dk
FAU - Ahlehoff, Ole
AU  - Ahlehoff O
FAU - Gislason, Gunnar Hilmar
AU  - Gislason GH
FAU - Madsen, Ole Rintek
AU  - Madsen OR
FAU - Olesen, Jonas Bjerring
AU  - Olesen JB
FAU - Svendsen, Jesper Hastrup
AU  - Svendsen JH
FAU - Torp-Pedersen, Christian
AU  - Torp-Pedersen C
FAU - Hansen, Peter Riis
AU  - Hansen PR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120308
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
SB  - IM
CIN - BMJ. 2012 Mar 27;344:e2259. doi: 10.1136/bmj.e2259. PMID: 22453881
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications
MH  - Atrial Fibrillation/*epidemiology/etiology
MH  - Cohort Studies
MH  - Denmark/epidemiology
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - Stroke/*epidemiology/etiology
PMC - PMC3297675
COIS- Competing interests: All authors have completed the Unified Competing Interest 
      form at www.icmje.org/coi_disclosure.pdf (available on request from the 
      corresponding author) and declare: no support from any organisation for the 
      submitted work; no financial relationships with any organisations that might have 
      an interest in the submitted work in the previous three years; no other 
      relationships or activities that could appear to have influenced the submitted 
      work.
EDAT- 2012/03/10 06:00
MHDA- 2012/04/24 06:00
PMCR- 2012/03/08
CRDT- 2012/03/10 06:00
PHST- 2012/03/10 06:00 [entrez]
PHST- 2012/03/10 06:00 [pubmed]
PHST- 2012/04/24 06:00 [medline]
PHST- 2012/03/08 00:00 [pmc-release]
AID - bmj.e1257 [pii]
AID - linj003076 [pii]
AID - 10.1136/bmj.e1257 [doi]
PST - epublish
SO  - BMJ. 2012 Mar 8;344:e1257. doi: 10.1136/bmj.e1257.

PMID- 22391030
OWN - NLM
STAT- MEDLINE
DCOM- 20120809
LR  - 20131121
IS  - 1532-2777 (Electronic)
IS  - 0306-9877 (Linking)
VI  - 78
IP  - 5
DP  - 2012 May
TI  - Glutamate-based depression GBD.
PG  - 675-81
LID - 10.1016/j.mehy.2012.02.009 [doi]
AB  - We describe a new term: glutamate-based depression (GBD). GBD is defined as a 
      chronic depressive illness associated with environmental stress and diseases 
      associated with altered glutamate neurotransmission. We hypothesize that 
      glutamate-induced over-activation of extrasynaptic NMDA receptors in the 
      subgenual cingulate area called Brodmann's 25 plays an important role in the 
      etiology of depression and may be responsible for the high incidence of co-morbid 
      depression associated in diseases with glutamate etiology. While depression is a 
      syndrome with multiple possible etiologies, we propose that a disruption in 
      glutamatergic neurotransmission may underline a substantial proportion of 
      clinically observed depression. The high rates of depressive symptoms associated 
      with various disorders in which altered glutamatergic functions have been 
      identified, may suggest a common pathophysiological mechanism is underlying the 
      diverse clinical presentations.
CI  - Copyright © 2012 Elsevier Ltd. All rights reserved.
FAU - McCarthy, Dennis J
AU  - McCarthy DJ
AD  - Clinical Neuroscience AstraZeneca Pharmaceuticals LP, Wilmington, DE, USA. 
      dennis.mccarthy@astrazeneca.com
FAU - Alexander, Robert
AU  - Alexander R
FAU - Smith, Mark A
AU  - Smith MA
FAU - Pathak, Sanjeev
AU  - Pathak S
FAU - Kanes, Stephen
AU  - Kanes S
FAU - Lee, Chi-Ming
AU  - Lee CM
FAU - Sanacora, Gerard
AU  - Sanacora G
LA  - eng
PT  - Journal Article
DEP - 20120304
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - 9008-11-1 (Interferons)
SB  - IM
MH  - Affect/physiology
MH  - Alzheimer Disease/complications
MH  - Arthritis, Rheumatoid/complications
MH  - Chronic Pain/complications
MH  - Cognition/physiology
MH  - Coronary Artery Disease/complications
MH  - Depression/*etiology/*metabolism/physiopathology
MH  - Diabetes Complications/etiology/psychology
MH  - Fibromyalgia/complications
MH  - Glutamic Acid/*metabolism
MH  - Gyrus Cinguli/metabolism/physiopathology
MH  - Humans
MH  - Huntington Disease/complications
MH  - Inflammation/complications
MH  - Interferons/metabolism
MH  - Models, Neurological
MH  - Models, Psychological
MH  - Parkinson Disease/complications
MH  - Receptors, N-Methyl-D-Aspartate/metabolism
MH  - Risk Factors
MH  - Stroke/complications
MH  - Synaptic Transmission
EDAT- 2012/03/07 06:00
MHDA- 2012/08/10 06:00
CRDT- 2012/03/07 06:00
PHST- 2011/11/02 00:00 [received]
PHST- 2012/01/15 00:00 [revised]
PHST- 2012/02/09 00:00 [accepted]
PHST- 2012/03/07 06:00 [entrez]
PHST- 2012/03/07 06:00 [pubmed]
PHST- 2012/08/10 06:00 [medline]
AID - S0306-9877(12)00075-8 [pii]
AID - 10.1016/j.mehy.2012.02.009 [doi]
PST - ppublish
SO  - Med Hypotheses. 2012 May;78(5):675-81. doi: 10.1016/j.mehy.2012.02.009. Epub 2012 
      Mar 4.

PMID- 22364129
OWN - NLM
STAT- MEDLINE
DCOM- 20120730
LR  - 20190728
IS  - 1873-4286 (Electronic)
IS  - 1381-6128 (Linking)
VI  - 18
IP  - 11
DP  - 2012
TI  - Rheumatoid arthritis: cardiovascular manifestations, pathogenesis, and therapy.
PG  - 1450-6
AB  - Rheumatoid Arthritis (RA) is a chronic progressive inflammatory joint disorder 
      that affects 0.5% - 1% of the general population. This review article discusses 
      cardiovascular manifestations of rheumatoid arthritis, pathogenesis of these 
      manifestations, and therapy. This disease not only affects the joints, but it 
      also involves other organ systems. The majority of these patients suffer 
      significant morbidity and mortality from cardiovascular disease. Cardiovascular 
      manifestations of RA include predilection for accelerated atherosclerosis and 
      endothelial dysfunction resulting in coronary artery disease (CAD), stroke, 
      congestive heart failure, and peripheral arterial disease. Some studies have 
      shown that the risk of developing CAD in RA patients is the same as for patients 
      with diabetes mellitus. These patients should be treated with aggressive medical 
      therapy such as disease modifying antirheumatic drugs, tumor necrosis factor 
      alpha inhibitors, and corticosteroids and with appropriate control of risk 
      factors such as smoking, dyslipidemia, hypertension, and obesity. Other 
      manifestations include pericarditis, myocarditis, and vasculitis.
FAU - Mellana, William M
AU  - Mellana WM
AD  - Cardiology Division, New York Medical College, Macy Pavilion, Room 138, Valhalla, 
      NY 10595, USA.
FAU - Aronow, Wilbert S
AU  - Aronow WS
FAU - Palaniswamy, Chandrasekar
AU  - Palaniswamy C
FAU - Khera, Sahil
AU  - Khera S
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United Arab Emirates
TA  - Curr Pharm Des
JT  - Current pharmaceutical design
JID - 9602487
RN  - 0 (Anti-Inflammatory Agents)
SB  - IM
MH  - Anti-Inflammatory Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*complications/*drug therapy
MH  - Cardiovascular Diseases/*etiology/*prevention & control
MH  - Humans
MH  - Risk Assessment
EDAT- 2012/03/01 06:00
MHDA- 2012/07/31 06:00
CRDT- 2012/02/28 06:00
PHST- 2011/12/16 00:00 [received]
PHST- 2012/01/10 00:00 [accepted]
PHST- 2012/02/28 06:00 [entrez]
PHST- 2012/03/01 06:00 [pubmed]
PHST- 2012/07/31 06:00 [medline]
AID - CPD-EPUB-20120224-002 [pii]
AID - 10.2174/138161212799504795 [doi]
PST - ppublish
SO  - Curr Pharm Des. 2012;18(11):1450-6. doi: 10.2174/138161212799504795.

PMID- 22290761
OWN - NLM
STAT- MEDLINE
DCOM- 20120418
LR  - 20211021
IS  - 1557-0681 (Electronic)
IS  - 1478-2189 (Linking)
VI  - 10
IP  - 1
DP  - 2012 Mar
TI  - Factors associated with the severity and progression of self-reported hand pain 
      and functional difficulty in community-dwelling older adults: a systematic 
      review.
PG  - 51-62
LID - 10.1002/msc.1007 [doi]
AB  - BACKGROUND: Hand problems are common in older adults and cause significant pain 
      and disruption to everyday living. The aim of this systematic review was to 
      summarize evidence on the factors associated with the severity and progression of 
      self-reported hand pain and functional difficulty in population-based studies of 
      older adults. METHODS: MEDLINE, EMBASE, CINAL, BNI, AMED, HMIC, PsycINFO and ISI 
      Web of Knowledge were searched up to January 2011 for relevant articles. The 
      search strategy combined text words for hand, pain, function and epidemiological 
      study. Inclusion criteria were applied and articles in the review assessed for 
      quality using the QUality In Prognosis Studies (QUIPS) assessment tool. Data 
      extraction included: author, year of publication, study location, participant 
      inclusion criteria, risk factor and outcome measurement, and association with 
      hand pain and/or function. RESULTS: Seven articles from five studies met the 
      inclusion criteria from 5,679 citations. All studies were cross-sectional and 
      provided no information on progression of hand pain and function over time. 
      Factors associated with limited hand function were older age, female gender, 
      manual occupation, neck or shoulder pain, clinical and radiographic 
      osteoarthritis, weaker hand strength, hand pain, history of Parkinson's disease, 
      stroke, diabetes or rheumatoid arthritis, and illness perceptions (namely, 
      frustration, impact and symptom count). Key factors associated with hand pain 
      severity were age, impact, frustration, patient expectation of a long disease 
      time course and self-reported diagnosis of the cause of the hand problem. 
      CONCLUSIONS: Both demographic and clinical factors were found to be related to 
      self-reported hand pain severity and functional difficulty in older adults; 
      however, the results were derived from a small number of studies, with no 
      information on progression of hand pain and functional difficulty over time.
CI  - Copyright © 2012 John Wiley & Sons, Ltd.
FAU - Nicholls, Elaine E
AU  - Nicholls EE
AD  - Arthritis Research UK Primary Care Centre, Keele University, Keele, UK. 
      e.nicholls@cphc.keele.ac.uk
FAU - van der Windt, Danielle A W M
AU  - van der Windt DA
FAU - Jordan, Joanne L
AU  - Jordan JL
FAU - Dziedzic, Krysia S
AU  - Dziedzic KS
FAU - Thomas, Elaine
AU  - Thomas E
LA  - eng
GR  - G0501798/MRC_/Medical Research Council/United Kingdom
GR  - 18174/ARC_/Arthritis Research UK/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PT  - Systematic Review
DEP - 20120131
PL  - England
TA  - Musculoskeletal Care
JT  - Musculoskeletal care
JID - 101181344
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthralgia/*epidemiology
MH  - Female
MH  - *Hand
MH  - *Hand Joints
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Musculoskeletal Pain/*epidemiology
EDAT- 2012/02/01 06:00
MHDA- 2012/04/19 06:00
CRDT- 2012/02/01 06:00
PHST- 2012/02/01 06:00 [entrez]
PHST- 2012/02/01 06:00 [pubmed]
PHST- 2012/04/19 06:00 [medline]
AID - 10.1002/msc.1007 [doi]
PST - ppublish
SO  - Musculoskeletal Care. 2012 Mar;10(1):51-62. doi: 10.1002/msc.1007. Epub 2012 Jan 
      31.

PMID- 22043258
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20111110
LR  - 20220311
IS  - 1918-3011 (Electronic)
IS  - 1918-3003 (Print)
IS  - 1918-3003 (Linking)
VI  - 2
IP  - 6
DP  - 2010 Dec 11
TI  - Bilirubin as a Protective Factor for Rheumatoid Arthritis: An NHANES Study of 
      2003 - 2006 Data.
PG  - 256-60
LID - 10.4021/jocmr444w [doi]
AB  - BACKGROUND: Rheumatoid arthritis(RA) is a chronic inflammatory, autoimmune 
      polyarthritis, with a prevalence estimated at one percent of the United 
      States(US) population. Serum bilirubin, because of its antioxidant nature, has 
      been conjectured to exert an anti-inflammatory biologic effect. The objective of 
      this study is to discern whether higher serum Total Bilirubin(TBili) levels are 
      protective against RA. METHODS: This is a secondary analysis of National Health 
      and Nutrition Examination Survey (NHANES) data collected between 2003-2006. Study 
      participants completed a comprehensive questionnaire regarding their health 
      history, underwent a physical examination, and had body fluids collected for 
      laboratory studies. In NHANES, to assess for the presence of RA, the following 
      questions were asked: Doctor ever said you had arthritis?" If so, Which type of 
      arthritis. Statistical analysis was performed, using SAS version 9.1, proc survey 
      methods. Participant data were adjusted for demographic characteristics as well 
      as risk factors for RA. RESULTS: NHANES 2003-2006 included 20,470 individuals, 
      chosen as a representative sampling of the entire US population. Exclusion 
      criteria included age less than twenty years or liver dysfunction, defined as 
      history of abnormal liver function tests or liver disease. 8,147 subjects did not 
      have any exclusion criteria and were included in the data analysis. RA is 
      inversely related to the serum level of TBili with an odds ratio of 0.679 (95% CI 
      0.533-0.865) and remained significant even after adjusting for age, gender, race, 
      education, and tobacco history, with an odds ratio 0.749 (95% CI 0.575 - 0.976). 
      CONCLUSIONS: Our study supports the hypothesis that higher TBili levels are 
      protective against RA. A plausible mechanism for this association would be that 
      the anti-oxidant effects of TBili exert a physiologic anti-inflammatory effect, 
      which provides protection against RA. This explanation is supported by prior 
      studies which show that higher TBili levels are protective against stroke, 
      atherosclerosis, and vasculitis. Further studies are needed to delineate the 
      exact nature of the protective properties of TBili. KEYWORDS: Bilirubin; 
      Rheumatoid arthritis; Antioxidant; Protective.
FAU - Fischman, Daniel
AU  - Fischman D
AD  - Pinnacle Health/Harrisburg Hospital, 205 S Front Street, Harrisburg, PA 17104, 
      USA.
FAU - Valluri, Ashok
AU  - Valluri A
FAU - Gorrepati, Venkata Subhash
AU  - Gorrepati VS
FAU - Murphy, Megan E
AU  - Murphy ME
FAU - Peters, Ian
AU  - Peters I
FAU - Cheriyath, Pramil
AU  - Cheriyath P
LA  - eng
PT  - Journal Article
PL  - Canada
TA  - J Clin Med Res
JT  - Journal of clinical medicine research
JID - 101538301
PMC - PMC3194029
EDAT- 2011/11/02 06:00
MHDA- 2011/11/02 06:01
PMCR- 2010/12/01
CRDT- 2011/11/02 06:00
PHST- 2010/10/08 00:00 [accepted]
PHST- 2011/11/02 06:00 [entrez]
PHST- 2011/11/02 06:00 [pubmed]
PHST- 2011/11/02 06:01 [medline]
PHST- 2010/12/01 00:00 [pmc-release]
AID - 10.4021/jocmr444w [doi]
PST - ppublish
SO  - J Clin Med Res. 2010 Dec 11;2(6):256-60. doi: 10.4021/jocmr444w.

PMID- 21885031
OWN - NLM
STAT- MEDLINE
DCOM- 20120925
LR  - 20131121
IS  - 1768-3181 (Electronic)
IS  - 0003-3928 (Linking)
VI  - 61
IP  - 2
DP  - 2012 Apr
TI  - [Rheumatoid arthritis: a cardiovascular disease?].
PG  - 111-7
LID - 10.1016/j.ancard.2011.07.008 [doi]
AB  - Mortality in rheumatoid arthritis (RA) is doubled when compared to the general 
      population. This excess in mortality can be explained in half of cases by 
      cardiovascular (CV) events. The risk of myocardial infarction is increased by 
      about 60% in RA. Mortality secondary to cerebrovascular stroke is increased by 
      50% even if the incidence of stroke is not increased. Indeed, the risk of fatal 
      CV events is increased in RA when compared to the general population. The 
      increased CV risk cannot be explained only by traditional CV risk factors, even 
      if smoking and changes in lipid profile may be implied. It is mainly related to 
      the chronic inflammatory condition that causes many metabolic disturbances. Other 
      parameters such as treatments used in RA also play a role. Thus, it is essential 
      for proper management of RA patients to be aware of this risk and to treat any 
      modifiable CV risk factors.
CI  - Copyright © 2011 Elsevier Masson SAS. All rights reserved.
FAU - Daïen, C I
AU  - Daïen CI
AD  - Service d'immuno-rhumatologie, CHU Lapeyronie, Montpellier, France.
FAU - Fesler, P
AU  - Fesler P
LA  - fre
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - La polyarthrite rhumatoïde : une maladie cardiovasculaire ?
DEP - 20110817
PL  - France
TA  - Ann Cardiol Angeiol (Paris)
JT  - Annales de cardiologie et d'angeiologie
JID - 0142167
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal/administration & dosage/adverse effects
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/drug therapy/*epidemiology
MH  - Cardiovascular Diseases/*epidemiology
MH  - Humans
MH  - Inflammation/epidemiology
MH  - Methotrexate/therapeutic use
MH  - Risk Factors
MH  - Stroke/epidemiology
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
EDAT- 2011/09/03 06:00
MHDA- 2012/09/26 06:00
CRDT- 2011/09/03 06:00
PHST- 2011/01/11 00:00 [received]
PHST- 2011/07/24 00:00 [accepted]
PHST- 2011/09/03 06:00 [entrez]
PHST- 2011/09/03 06:00 [pubmed]
PHST- 2012/09/26 06:00 [medline]
AID - S0003-3928(11)00118-1 [pii]
AID - 10.1016/j.ancard.2011.07.008 [doi]
PST - ppublish
SO  - Ann Cardiol Angeiol (Paris). 2012 Apr;61(2):111-7. doi: 
      10.1016/j.ancard.2011.07.008. Epub 2011 Aug 17.

PMID- 21756157
OWN - NLM
STAT- MEDLINE
DCOM- 20130717
LR  - 20181202
IS  - 1471-1753 (Electronic)
IS  - 0954-6634 (Linking)
VI  - 24
IP  - 2
DP  - 2013 Apr
TI  - Comparing the lifetime risks of TNF-alpha inhibitor use to common benchmarks of 
      risk.
PG  - 101-6
LID - 10.3109/09546634.2011.595574 [doi]
AB  - OBJECTIVE: The study aims to illustrate the range of lifetime risks of lymphoma, 
      tuberculosis (TB), and demyelinating diseases with TNF-α inhibitors in psoriasis 
      patients. METHODS: Previously published data and online resources were used to 
      determine the risk of the TB, demyelinating disease, and lymphoma with and 
      without TNF-α inhibitor treatment. Lifetime risks for heart disease and stroke 
      were collected using a Medline search. All cancer, trauma, and environmental 
      statistics were obtained from the data published by National Cancer Institute, 
      National Safety Council, and the National Oceanic and Atmospheric Administration, 
      respectively. RESULTS: The lifetime risks of TNF-α-inhibitor-linked conditions 
      and comparators are as follows: TNF-α inhibitor-linked conditions: lymphoma with: 
      without TNF-α inhibitors (0.5-4.8%:2.3%), TB with:without TNF-α inhibitors 
      (0-17.1%:0.3%), and demyelinating disease with:without TNF-α inhibitors 
      (0.1-1.7%:0.15%). Comparators: cancer (40.4%), heart disease (36.2%), stroke 
      (18.4%), accidental death (3.0%), motor vehicle death (1.2%), and lightning 
      strike (0.033%). LIMITATIONS: Much of the data on lifetime risks of disease with 
      TNF-α inhibitor were for patients with rheumatoid arthritis and not psoriasis. 
      CONCLUSIONS: The risks of lymphoma, demyelinating diseases, and tuberculosis with 
      TNF-α inhibitors are lower than risks patients face on a regular basis. Screening 
      reduces the risk of tuberculosis in patients receiving TNF-α inhibitors.
FAU - Kaminska, Edi
AU  - Kaminska E
AD  - Department of Dermatology, University of Chicago, 5841 S. Maryland Avenue, MC 
      5067, Chicago, IL, USA.
FAU - Patel, Isha
AU  - Patel I
FAU - Dabade, Tushar S
AU  - Dabade TS
FAU - Chang, Jongwha
AU  - Chang J
FAU - Qureshi, Ayub A
AU  - Qureshi AA
FAU - O'Neill, Jenna L
AU  - O'Neill JL
FAU - Balkrishnan, Rajesh
AU  - Balkrishnan R
FAU - Feldman, Steven R
AU  - Feldman SR
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20110714
PL  - England
TA  - J Dermatolog Treat
JT  - The Journal of dermatological treatment
JID - 8918133
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - B72HH48FLU (Infliximab)
RN  - FYS6T7F842 (Adalimumab)
RN  - OP401G7OJC (Etanercept)
SB  - IM
MH  - Adalimumab
MH  - Antibodies, Monoclonal/adverse effects
MH  - Antibodies, Monoclonal, Humanized/adverse effects
MH  - Antirheumatic Agents/*adverse effects
MH  - Benchmarking
MH  - Demyelinating Diseases/*chemically induced
MH  - Etanercept
MH  - Humans
MH  - Immunoglobulin G/adverse effects
MH  - Infliximab
MH  - Lymphoma/*chemically induced
MH  - Psoriasis/drug therapy
MH  - Receptors, Tumor Necrosis Factor
MH  - Risk Assessment
MH  - Risk Factors
MH  - Tuberculosis/*chemically induced
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
EDAT- 2011/07/16 06:00
MHDA- 2013/07/19 06:00
CRDT- 2011/07/16 06:00
PHST- 2011/07/16 06:00 [entrez]
PHST- 2011/07/16 06:00 [pubmed]
PHST- 2013/07/19 06:00 [medline]
AID - 10.3109/09546634.2011.595574 [doi]
PST - ppublish
SO  - J Dermatolog Treat. 2013 Apr;24(2):101-6. doi: 10.3109/09546634.2011.595574. Epub 
      2011 Jul 14.

PMID- 21733721
OWN - NLM
STAT- MEDLINE
DCOM- 20130423
LR  - 20121105
IS  - 1532-8511 (Electronic)
IS  - 1052-3057 (Linking)
VI  - 21
IP  - 8
DP  - 2012 Nov
TI  - Risk of stroke in 28,000 patients with celiac disease: a nationwide cohort study 
      in Sweden.
PG  - 860-7
LID - S1052-3057(11)00115-7 [pii]
LID - 10.1016/j.jstrokecerebrovasdis.2011.05.008 [doi]
AB  - BACKGROUND: Earlier studies on stroke in celiac disease (CD) have been 
      underpowered, but a recent study suggested that childhood CD is associated with a 
      10-fold increased risk of death from stroke, although it was based on small 
      numbers. We examined the risk of stroke in patients with biopsy-verified CD. 
      METHODS: We collected biopsy data from all 28 pathology departments in Sweden and 
      identified 28,676 individuals with CD diagnosed between 1969 and 2007 (Marsh 3: 
      villous atrophy). In the main analyses, we used Cox regression to estimate hazard 
      ratios (HRs) for stroke in patients with CD compared with HRs for stroke in 
      141,806 sex- and age-matched controls. RESULTS: During follow-up, there were 785 
      first-stroke diagnoses in patients with CD and 2937 in reference individuals. 
      Patients with CD were at increased risk of stroke (HR 1.10; 95% confidence 
      interval [CI] 1.01-1.19). HRs were similar for ischemic stroke and brain 
      hemorrhage and were not affected by adjustment for type 1 diabetes, rheumatoid 
      arthritis, use of medication against hypertension, or dyslipidemia. The absolute 
      risk of stroke in patients with CD was 267 per 100,000 person-years (excess risk 
      24/100,000). The highest risk estimates occurred in the first year, with 
      virtually no increased risk after more than 5 years of follow-up after CD 
      diagnosis. The HR for stroke in childhood CD was 1.10 (95% CI 0.37-3.22). 
      CONCLUSIONS: Patients with CD are at only a small increased risk of stroke, which 
      persists only for a brief period after diagnosis. CD does not seem to be a major 
      risk factor for stroke.
CI  - Copyright © 2012 National Stroke Association. Published by Elsevier Inc. All 
      rights reserved.
FAU - Ludvigsson, Jonas F
AU  - Ludvigsson JF
AD  - Department of Pediatrics, Örebro University Hospital, Örebro, Sweden. 
      jonasludvigsson@yahoo.com
FAU - West, Joe
AU  - West J
FAU - Card, Tim
AU  - Card T
FAU - Appelros, Peter
AU  - Appelros P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110705
PL  - United States
TA  - J Stroke Cerebrovasc Dis
JT  - Journal of stroke and cerebrovascular diseases : the official journal of National 
      Stroke Association
JID - 9111633
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Biopsy
MH  - Brain Ischemia/diagnosis/*epidemiology/mortality
MH  - Case-Control Studies
MH  - Celiac Disease/diagnosis/*epidemiology/mortality
MH  - Child
MH  - Child, Preschool
MH  - Comorbidity
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Infant
MH  - Infant, Newborn
MH  - Intracranial Hemorrhages/diagnosis/*epidemiology/mortality
MH  - Male
MH  - Middle Aged
MH  - Prognosis
MH  - Proportional Hazards Models
MH  - Registries
MH  - Risk Assessment
MH  - Risk Factors
MH  - Stroke/diagnosis/*epidemiology
MH  - Sweden/epidemiology
MH  - Time Factors
MH  - Young Adult
EDAT- 2011/07/08 06:00
MHDA- 2013/04/24 06:00
CRDT- 2011/07/08 06:00
PHST- 2010/12/02 00:00 [received]
PHST- 2011/05/07 00:00 [revised]
PHST- 2011/05/07 00:00 [accepted]
PHST- 2011/07/08 06:00 [entrez]
PHST- 2011/07/08 06:00 [pubmed]
PHST- 2013/04/24 06:00 [medline]
AID - S1052-3057(11)00115-7 [pii]
AID - 10.1016/j.jstrokecerebrovasdis.2011.05.008 [doi]
PST - ppublish
SO  - J Stroke Cerebrovasc Dis. 2012 Nov;21(8):860-7. doi: 
      10.1016/j.jstrokecerebrovasdis.2011.05.008. Epub 2011 Jul 5.

PMID- 21567119
OWN - NLM
STAT- MEDLINE
DCOM- 20120426
LR  - 20211020
IS  - 1434-9949 (Electronic)
IS  - 0770-3198 (Linking)
VI  - 31
IP  - 1
DP  - 2012 Jan
TI  - Assessment of cardiovascular risk in rheumatoid arthritis: impact of the new 
      EULAR recommendations on the score cardiovascular risk index.
PG  - 35-9
LID - 10.1007/s10067-011-1774-6 [doi]
AB  - To assess the impact of the application of the European League against Rheumatism 
      (EULAR) task force recommendations in the cardiovascular (CV) risk of a series of 
      Spanish patients diagnosed with rheumatoid arthritis (RA). Two hundred 
      consecutive RA patients seen at the rheumatology outpatient clinics of Bellvitge 
      Hospital, Barcelona, were studied. Information on clinical features of the 
      disease, classic CV risk factors, and history of CV events was assessed. Both the 
      systematic coronary risk evaluation (SCORE) CV risk index and the modified SCORE 
      (mSCORE) according to the last EULAR recommendations were calculated. Based on 
      the classic CV risk factors, the mean ± standard deviation SCORE was 2.1 ± 2.3% 
      (median, 2; interquartile range [IQR], 1-3). Twenty-three (11%) patients were 
      above the threshold of high CV risk for the Spanish population (≥5%). Following 
      the EULAR recommendations, a change in the score was required in 119 (59%) 
      patients. Therefore, the mean mSCORE was 2.7 ± 2.9% (median, 2; IQR, 1-3) and, 
      due to this, 28 (14%) patients were above the threshold of high CV risk. Nine 
      (5%) had at least one ischemic CV event. Patients with CV events were older and 
      had more CV risk factors and higher SCORE and mSCORE than those without CV 
      events. Although a large proportion of patients from this series fulfilled the 
      criteria for the application of the EULAR recommendations, the final impact on 
      the calculated CV risk was low and clinically significant in only a few patients. 
      However, an association between the mSCORE and the presence of ischemic CV events 
      was observed.
FAU - Gómez-Vaquero, Carmen
AU  - Gómez-Vaquero C
AD  - Rheumatology Division, IDIBELL-Hospital Universitari de Bellvitge, Barcelona, 
      Spain.
FAU - Robustillo, Montserrat
AU  - Robustillo M
FAU - Narváez, Javier
AU  - Narváez J
FAU - Rodríguez-Moreno, Jesús
AU  - Rodríguez-Moreno J
FAU - González-Juanatey, Carlos
AU  - González-Juanatey C
FAU - Llorca, Javier
AU  - Llorca J
FAU - Nolla, Joan Miquel
AU  - Nolla JM
FAU - González-Gay, Miguel Angel
AU  - González-Gay MA
LA  - eng
PT  - Journal Article
DEP - 20110513
PL  - Germany
TA  - Clin Rheumatol
JT  - Clinical rheumatology
JID - 8211469
SB  - IM
MH  - Arthritis, Rheumatoid/diagnosis/*epidemiology
MH  - Comorbidity
MH  - Evidence-Based Medicine/methods
MH  - Female
MH  - Hospitals, University
MH  - Humans
MH  - International Cooperation
MH  - Male
MH  - Middle Aged
MH  - Myocardial Ischemia/diagnosis/*epidemiology
MH  - Peripheral Arterial Disease/diagnosis/*epidemiology
MH  - Practice Guidelines as Topic
MH  - Risk Assessment
MH  - Spain/epidemiology
MH  - Stroke/diagnosis/*epidemiology
EDAT- 2011/05/14 06:00
MHDA- 2012/04/27 06:00
CRDT- 2011/05/14 06:00
PHST- 2011/03/21 00:00 [received]
PHST- 2011/05/04 00:00 [accepted]
PHST- 2011/05/01 00:00 [revised]
PHST- 2011/05/14 06:00 [entrez]
PHST- 2011/05/14 06:00 [pubmed]
PHST- 2012/04/27 06:00 [medline]
AID - 10.1007/s10067-011-1774-6 [doi]
PST - ppublish
SO  - Clin Rheumatol. 2012 Jan;31(1):35-9. doi: 10.1007/s10067-011-1774-6. Epub 2011 
      May 13.

PMID- 21459935
OWN - NLM
STAT- MEDLINE
DCOM- 20111013
LR  - 20181201
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
VI  - 38
IP  - 6
DP  - 2011 Jun
TI  - Evaluation of NT-proBNP and high sensitivity C-reactive protein for predicting 
      cardiovascular risk in patients with arthritis taking longterm nonsteroidal 
      antiinflammatory drugs.
PG  - 1071-8
LID - 10.3899/jrheum.100880 [doi]
AB  - OBJECTIVE: Patients with arthritis frequently are at increased risk for future 
      cardiovascular (CV) events. We investigated the performance of the cardiac 
      biomarkers N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high 
      sensitivity C-reactive protein (hsCRP) for predicting CV events in patients with 
      arthritis taking chronic nonsteroidal antiinflammatory drugs (NSAID). METHODS: We 
      evaluated 2-year CV outcomes in a prospective, nested biomarker study among 
      patients (N = 6273) with rheumatoid arthritis and osteoarthritis treated with 
      NSAID in the MEDAL (Multinational Etoricoxib and Diclofenac Arthritis Long-term) 
      trial. Patients were stratified by quartiles of baseline NT-proBNP and 
      established cutpoints of NT-proBNP and hsCRP. RESULTS: NT-proBNP demonstrated a 
      strong graded relationship with CV outcomes, including CV death (p for trend < 
      0.0001), myocardial infarction (MI) (p for trend = 0.02), heart failure (HF) (p 
      for trend < 0.0001), and a composite of thrombotic events (CV death, MI, stroke) 
      or HF (p for trend < 0.0001). Baseline levels of hsCRP were not associated with 
      CV events (CV death/MI/stroke/HF; p for trend = 0.65). NT-proBNP remained 
      strongly predictive of CV events after adjustment for age, sex, diabetes, 
      hypertension, hyperlipidemia, smoking, type of arthritis, body mass index, 
      creatinine clearance, history of CV disease, and hsCRP (CV death/MI/stroke/HF: Q4 
      vs Q1 hazard ratio 3.53, 95% CI 1.89-6.58). Patients with a NT-proBNP level below 
      100 pg/ml had a 0.94% rate of thrombotic events or heart failure at 2 years. 
      CONCLUSION: NT-proBNP is a simple and robust noninvasive indicator of CV risk in 
      patients with arthritis. Risk stratification based on NT-proBNP may facilitate 
      identification of patients with arthritis who are at low CV risk during chronic 
      NSAID treatment.
FAU - Ruff, Christian T
AU  - Ruff CT
AD  - TIMI Study Group, 350 Longwood Avenue, Boston, MA 02115, USA. cruff@partners.org
FAU - Morrow, David A
AU  - Morrow DA
FAU - Jarolim, Peter
AU  - Jarolim P
FAU - Ren, Fang
AU  - Ren F
FAU - Contant, Charles F
AU  - Contant CF
FAU - Kaur, Amarjot
AU  - Kaur A
FAU - Curtis, Sean P
AU  - Curtis SP
FAU - Laine, Loren
AU  - Laine L
FAU - Cannon, Christopher P
AU  - Cannon CP
FAU - Brune, Kay
AU  - Brune K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110401
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Biomarkers)
RN  - 0 (Peptide Fragments)
RN  - 0 (Pyridines)
RN  - 0 (Sulfones)
RN  - 0 (pro-brain natriuretic peptide (1-76))
RN  - 114471-18-0 (Natriuretic Peptide, Brain)
RN  - 144O8QL0L1 (Diclofenac)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - WRX4NFY03R (Etoricoxib)
SB  - IM
CIN - Orthopade. 2012 Nov;41(11):923-4. doi: 10.1007/s00132-012-1975-y. PMID: 23135376
MH  - Aged
MH  - Anti-Inflammatory Agents, Non-Steroidal/*therapeutic use
MH  - Arthritis, Rheumatoid/blood/*drug therapy
MH  - Biomarkers/blood
MH  - C-Reactive Protein/*metabolism
MH  - Cardiovascular Diseases/*epidemiology
MH  - Diclofenac/therapeutic use
MH  - Etoricoxib
MH  - Female
MH  - Heart Failure/epidemiology
MH  - Humans
MH  - Longitudinal Studies
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology
MH  - Natriuretic Peptide, Brain/*blood
MH  - Osteoarthritis/blood/*drug therapy
MH  - Peptide Fragments/*blood
MH  - Prospective Studies
MH  - Pyridines/therapeutic use
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Sulfones/therapeutic use
MH  - Thrombosis
MH  - Treatment Outcome
EDAT- 2011/04/05 06:00
MHDA- 2011/10/14 06:00
CRDT- 2011/04/05 06:00
PHST- 2011/04/05 06:00 [entrez]
PHST- 2011/04/05 06:00 [pubmed]
PHST- 2011/10/14 06:00 [medline]
AID - jrheum.100880 [pii]
AID - 10.3899/jrheum.100880 [doi]
PST - ppublish
SO  - J Rheumatol. 2011 Jun;38(6):1071-8. doi: 10.3899/jrheum.100880. Epub 2011 Apr 1.

PMID- 21407167
OWN - NLM
STAT- MEDLINE
DCOM- 20110712
LR  - 20220330
IS  - 0172-780X (Print)
IS  - 0172-780X (Linking)
VI  - 32
IP  - 1
DP  - 2011
TI  - Depression's multiple comorbidities explained by (neuro)inflammatory and 
      oxidative & nitrosative stress pathways.
PG  - 7-24
AB  - There is now evidence that depression, as characterized by melancholic symptoms, 
      anxiety, and fatigue and somatic (F&S) symptoms, is the clinical expression of 
      peripheral cell-mediated activation, inflammation and induction of oxidative and 
      nitrosative stress (IO&NS) pathways and of central microglial activation, 
      decreased neurogenesis and increased apoptosis. This review gives an explanation 
      for the multiple "co-morbidities" between depression and a large variety of a) 
      brain disorders related to neurodegeneration, e.g. Alzheimer's, Parkinson's and 
      Huntington's disease, multiple sclerosis and stroke; b) medical disorders, such 
      as cardiovascular disorder, chronic fatigue syndrome, chronic obstructive 
      pulmonary disease, rheumatoid arthritis, psoriasis, systemic lupus erythematosus, 
      inflammatory bowel disease, irritable bowel syndrome, leaky gut, diabetes type 1 
      and 2, obesity and the metabolic syndrome, and HIV infection; and c) conditions, 
      such as hemodialysis, interferon-α-based immunotherapy, the postnatal period and 
      psychosocial stressors. The common denominator of all those disorders/conditions 
      is the presence of microglial activation and/or activation of peripheral IO&NS 
      pathways. There is evidence that shared peripheral and / or central IO&NS 
      pathways underpin the pathophysiology of depression and the previously mentioned 
      disorders and that activation of these IO&NS pathways contributes to shared risk. 
      The IO&NS pathways function as a smoke sensor that detect threats in the 
      peripheral and central parts of the body and signal these threats as melancholic, 
      anxiety, and fatigue and somatic (F&S) symptoms. The presence of concomitant 
      depression is strongly associated with a lower quality of life and increased 
      morbidity and mortality in medical disorders. This may be explained since 
      depression contributes to increased (neuro)inflammatory burden and may therefore 
      drive the inflammatory and degenerative progression. It is concluded that the 
      activation of peripheral and / or central IO&NS pathways may explain the 
      co-occurrence of depression with the above disorders. This shows that depression 
      belongs to the spectrum of inflammatory and degenerative disorders.
FAU - Maes, Michael
AU  - Maes M
AD  - Maes Clinics @ TRIA, Bangkok, Thailand, Thailand.
FAU - Kubera, Marta
AU  - Kubera M
FAU - Obuchowiczwa, Ewa
AU  - Obuchowiczwa E
FAU - Goehler, Lisa
AU  - Goehler L
FAU - Brzeszcz, Joanna
AU  - Brzeszcz J
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Sweden
TA  - Neuro Endocrinol Lett
JT  - Neuro endocrinology letters
JID - 8008373
RN  - 0 (Reactive Nitrogen Species)
SB  - IM
MH  - Animals
MH  - Comorbidity
MH  - *Depression/epidemiology/immunology/metabolism
MH  - Humans
MH  - *Inflammation/epidemiology/immunology/metabolism
MH  - Neuroimmunomodulation/*physiology
MH  - Oxidative Stress/*immunology
MH  - Reactive Nitrogen Species/metabolism
MH  - Signal Transduction/immunology
MH  - *Stress, Psychological/epidemiology/immunology/metabolism
EDAT- 2011/03/17 06:00
MHDA- 2011/07/13 06:00
CRDT- 2011/03/17 06:00
PHST- 2011/01/09 00:00 [received]
PHST- 2011/01/27 00:00 [accepted]
PHST- 2011/03/17 06:00 [entrez]
PHST- 2011/03/17 06:00 [pubmed]
PHST- 2011/07/13 06:00 [medline]
AID - NEL320111R02 [pii]
PST - ppublish
SO  - Neuro Endocrinol Lett. 2011;32(1):7-24.

PMID- 21388351
OWN - NLM
STAT- MEDLINE
DCOM- 20110627
LR  - 20111117
IS  - 1399-0039 (Electronic)
IS  - 0001-2815 (Linking)
VI  - 77
IP  - 4
DP  - 2011 Apr
TI  - Vascular endothelial growth factor A and cardiovascular disease in rheumatoid 
      arthritis patients.
PG  - 291-7
LID - 10.1111/j.1399-0039.2010.01625.x [doi]
AB  - To determine the contribution of the vascular endothelial growth factor A (VEGFA) 
      rs2010963 (-634 G>C) and rs1570360 (-1154 G>A) polymorphisms to the risk of 
      cardiovascular (CV) disease in a series of patients with rheumatoid arthritis 
      (RA). Six hundred sixty-one patients fulfilling the 1987 American College of 
      Rheumatology classification criteria for RA, seen at the rheumatology outpatient 
      clinics of the Hospital Xeral-Calde, Lugo, and the Hospital San Carlos, Madrid, 
      Spain, were studied. Patients were genotyped for the VEGFA rs2010963 (-634 G>C) 
      and rs1570360 (-1154 G>A) polymorphisms using predesigned TaqMan single 
      nucleotide polymorphism (SNP) genotyping assay (Applied Biosystems, Foster City, 
      CA). Also, human leukocyte antigen (HLA) DRB1 genotyping was performed using 
      molecular-based methods. Clinical histories of the patients were reviewed for the 
      presence of CV events that were considered to be present if the patient had 
      ischemic heart disease, heart failure, cerebrovascular accident, or peripheral 
      arteriopathy. Also, a subgroup of patients without the history of CV events was 
      assessed for the presence of subclinical atherosclerosis manifested by the 
      presence of endothelial dysfunction by brachial artery reactivity (n = 126) and 
      increased carotid artery intima-media thickness (n = 105) using high resolution 
      Doppler ultrasonography. No significant association between the VEGFA rs2010963 
      and the rs1570360 polymorphisms (neither isolated nor joined as allelic 
      combinations) with clinically evident CV disease was found in this series of 
      patients with RA. It was also the case when we examined the contribution of these 
      polymorphisms to the development of subclinical atherosclerosis. VEGFA 
      polymorphisms do not seem to exert a significant influence on the risk of CV 
      disease in patients with RA.
CI  - © 2011 John Wiley & Sons A/S.
FAU - Rodríguez-Rodríguez, L
AU  - Rodríguez-Rodríguez L
AD  - Instituto de Parasitología y Biomedicina Lopez-Neyra, CSIC, Armilla, Granada, 
      Spain.
FAU - García-Bermúdez, M
AU  - García-Bermúdez M
FAU - González-Juanatey, C
AU  - González-Juanatey C
FAU - Vazquez-Rodriguez, T R
AU  - Vazquez-Rodriguez TR
FAU - Miranda-Filloy, J A
AU  - Miranda-Filloy JA
FAU - Fernández-Gutierrez, B
AU  - Fernández-Gutierrez B
FAU - Llorca, J
AU  - Llorca J
FAU - Martín, J
AU  - Martín J
FAU - González-Gay, M A
AU  - González-Gay MA
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (HLA-DR Antigens)
RN  - 0 (HLA-DRB1 Chains)
RN  - 0 (VEGFA protein, human)
RN  - 0 (Vascular Endothelial Growth Factor A)
SB  - IM
MH  - Aged
MH  - Alleles
MH  - Arthritis, Rheumatoid/blood/diagnosis/etiology/*genetics
MH  - Cardiovascular Diseases/blood/complications/diagnosis/*genetics
MH  - HLA-DR Antigens/blood/genetics
MH  - HLA-DRB1 Chains
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Polymorphism, Single Nucleotide
MH  - Risk Factors
MH  - Spain
MH  - Vascular Endothelial Growth Factor A/*genetics/metabolism
EDAT- 2011/03/11 06:00
MHDA- 2011/06/28 06:00
CRDT- 2011/03/11 06:00
PHST- 2011/03/11 06:00 [entrez]
PHST- 2011/03/11 06:00 [pubmed]
PHST- 2011/06/28 06:00 [medline]
AID - 10.1111/j.1399-0039.2010.01625.x [doi]
PST - ppublish
SO  - Tissue Antigens. 2011 Apr;77(4):291-7. doi: 10.1111/j.1399-0039.2010.01625.x.

PMID- 21375196
OWN - NLM
STAT- MEDLINE
DCOM- 20110317
LR  - 20151119
IS  - 0030-9982 (Print)
IS  - 0030-9982 (Linking)
VI  - 60
IP  - 11
DP  - 2010 Nov
TI  - Association of visfatin with chronic kidney disease in a cohort of patients with 
      and without diabetes.
PG  - 922-6
AB  - OBJECTIVE: To evaluate association of serum visfatin with CKD secondary to 
      diabetic nephropathy and to compare it with patients of CKD secondary to other 
      risk factors. METHODS: Seventy eight individuals including 28 healthy controls 
      and 50 patients of CKD were included in this study. Patients with CKD were 
      further grouped based on etiology of CKD into diabetics and non-diabetics. 
      Patients with type 1 diabetes mellitus, urinary tract infection, urolithiasis, 
      liver cirrhosis, stroke, ischaemic heart disease, and rheumatoid arthritis were 
      excluded. Measurement of Serum visfatin was done through EIA Kit (Phoenix 
      pharmaceuticals Burlingame CA). RESULTS: Visfatin concentration was significantly 
      high in patients with CKD compared to controls (8.7 +/- 4.7 vs. 5.2 +/- 3.3 p = 
      0.001). No significant difference in Visfatin concentrations between patients of 
      CKD with and without diabetes was detected (9.2 +/- 5.5 vs. 8.3 +/- 3.2 p = 
      0.694). A significant negative correlation of visfatin with estimated GFR (r2= 
      -0.383, p = 0.01) and a positive correlation with degree of proteinuria (p = 
      0.01) was observed. CONCLUSION: The present study confirms the association of 
      visfatin with CKD, however further studies at molecular level to check its 
      expression within renal tissue may clarify its definitive role in CKD
FAU - Mahmood, Nosheen
AU  - Mahmood N
AD  - Department of Pathology, Ziauddin University, Pakistan.
FAU - Junejo, Abdul Manan
AU  - Junejo AM
FAU - Jamal, Qamar
AU  - Jamal Q
FAU - Awan, Rashid
AU  - Awan R
LA  - eng
PT  - Journal Article
PL  - Pakistan
TA  - J Pak Med Assoc
JT  - JPMA. The Journal of the Pakistan Medical Association
JID - 7501162
RN  - 0 (Biomarkers)
RN  - 0 (Cytokines)
RN  - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase)
RN  - EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, human)
SB  - IM
MH  - Adult
MH  - Biomarkers/blood
MH  - Body Mass Index
MH  - Case-Control Studies
MH  - Chronic Disease
MH  - Cohort Studies
MH  - Cytokines/*blood
MH  - Diabetes Mellitus, Type 2/*blood/physiopathology
MH  - Diabetic Nephropathies/complications
MH  - Female
MH  - Humans
MH  - Kidney Failure, Chronic/*blood/physiopathology
MH  - Male
MH  - Middle Aged
MH  - Nicotinamide Phosphoribosyltransferase/*blood
MH  - Pakistan
EDAT- 2011/03/08 06:00
MHDA- 2011/03/18 06:00
CRDT- 2011/03/08 06:00
PHST- 2011/03/08 06:00 [entrez]
PHST- 2011/03/08 06:00 [pubmed]
PHST- 2011/03/18 06:00 [medline]
PST - ppublish
SO  - J Pak Med Assoc. 2010 Nov;60(11):922-6.

PMID- 21367762
OWN - NLM
STAT- MEDLINE
DCOM- 20110713
LR  - 20110504
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 70
IP  - 6
DP  - 2011 Jun
TI  - Risk of cerebrovascular disease associated with the use of glucocorticoids in 
      patients with incident rheumatoid arthritis: a population-based study.
PG  - 990-5
LID - 10.1136/ard.2010.140210 [doi]
AB  - OBJECTIVES: To determine the effect of glucocorticoids (GC) on the risk of 
      cerebrovascular accidents (CVA) in patients with rheumatoid arthritis (RA). 
      METHODS: A population-based cohort study was carried out using administrative 
      health data on 7051 individuals with RA onset between 1997 and 2001 and no 
      exposure to GC before RA onset. Follow-up was until 2006. GC exposure was defined 
      in four ways: current use (yes/no), current dose (mg/day), cumulative dose 
      (grams) and cumulative duration of use (years). All were used as time-dependent 
      variables updated monthly. CVA were ascertained using hospitalisation and vital 
      statistics data. Transient ischaemic attacks were not considered as CVA. Cox 
      regression models adjusting for demographics, cardiovascular drug use, propensity 
      scores and RA characteristics were used. RESULTS: The mean age of the cohort was 
      56 years and 66% were women. Over 6 years' mean follow-up (43 355 person-years), 
      178 incident CVA cases were identified. GC current use was not associated with a 
      significant increase in the risk of CVA (HR=1.41, 95% CI 0.84 to 2.37). 
      Similarly, the models that accounted for daily dose (HR=1.07, 95% CI 0.94 to 1.21 
      for each 5 mg increase in the daily dose), cumulative duration of use (HR=1.1, 
      95% CI 0.94 to 1.32 for each year accumulated in the past) and total cumulative 
      dose (HR=1.04, 95% CI 0.99 to 1.08 per gram accumulated in the past) were also 
      not significantly associated with CVA. CONCLUSIONS: This large population-based 
      study indicates that GC use is not associated with an increased risk of CVA in 
      cases with RA.
FAU - Aviña-Zubieta, J Antonio
AU  - Aviña-Zubieta JA
AD  - Arthritis Research Centre of Canada, 895 West 10th Avenue, Vancouver, BC V5Z 1L7, 
      Canada. azubieta@arthritisresearch.ca
FAU - Abrahamowicz, Michal
AU  - Abrahamowicz M
FAU - Choi, Hyon K
AU  - Choi HK
FAU - Rahman, M Mushfiqur
AU  - Rahman MM
FAU - Sylvestre, Marie-Pierre
AU  - Sylvestre MP
FAU - Esdaile, John M
AU  - Esdaile JM
FAU - Lacaille, Diane
AU  - Lacaille D
LA  - eng
GR  - 186011/Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110302
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Glucocorticoids)
SB  - IM
MH  - Administration, Oral
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/complications/*drug therapy/epidemiology
MH  - British Columbia/epidemiology
MH  - Dose-Response Relationship, Drug
MH  - Drug Administration Schedule
MH  - Epidemiologic Methods
MH  - Female
MH  - Glucocorticoids/administration & dosage/*adverse effects
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Stroke/*chemically induced/epidemiology/etiology
EDAT- 2011/03/04 06:00
MHDA- 2011/07/14 06:00
CRDT- 2011/03/04 06:00
PHST- 2011/03/04 06:00 [entrez]
PHST- 2011/03/04 06:00 [pubmed]
PHST- 2011/07/14 06:00 [medline]
AID - ard.2010.140210 [pii]
AID - 10.1136/ard.2010.140210 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2011 Jun;70(6):990-5. doi: 10.1136/ard.2010.140210. Epub 2011 Mar 
      2.

PMID- 21279517
OWN - NLM
STAT- MEDLINE
DCOM- 20110923
LR  - 20221207
IS  - 1432-1459 (Electronic)
IS  - 0340-5354 (Linking)
VI  - 258
IP  - 6
DP  - 2011 Jun
TI  - Comorbidity profile of poliomyelitis survivors in a Chinese population: a 
      population-based study.
PG  - 1026-33
LID - 10.1007/s00415-010-5875-y [doi]
AB  - Previous reports of comorbid conditions in poliomyelitis survivors mainly focused 
      on some disease categories, such as respiratory diseases, gastrointestinal 
      diseases, psychiatric diseases, neurological diseases and cancer. Data regarding 
      a wide spectrum of medical comorbidities in patients with poliomyelitis is still 
      sparse. This study aimed to investigate and profile the wide range of 
      comorbidities among the survivors of paralytic poliomyelitis in a Chinese 
      population. In total, 2,032 paralytic poliomyelitis patients were selected as the 
      study group and the comparison group consisted of 10,160 randomly selected 
      enrollees. The comorbidities for analysis were based on a modified version of the 
      Elixhauser Comorbidity Index. Conditional logistic regression analyses were 
      computed to investigate the risk of comorbidities for these two groups. As 
      compared to controls, patients with paralytic poliomyelitis had significantly 
      higher prevalence of hypertension, ischemic heart disease, hyperlipidemia, 
      congestive heart failure, cardiac arrhythmias, peripheral vascular disorder, 
      stroke, paralysis, migraines, Parkinson's disease, rheumatoid arthritis, 
      ankylosing spondylitis, pulmonary circulation disorders, chronic pulmonary 
      disease, liver disease, peptic ulcers, hepatitis B or C, deficiency anemias, 
      depression, and lymphoma. Most of the differences are of clinical interest, ORs 
      often being between 2 and 3. No significant difference between poliomyelitis 
      patients and controls was observed in the prevalence of SLE, tuberculosis, 
      alcohol abuse and drug abuse. Our findings demonstrate that survivors of 
      paralytic poliomyelitis in Taiwan are at higher risk of having multiple medical 
      comorbidities although some potential confounding factors including educational 
      level, marital status, obesity and physical activity are not available in our 
      database. The pattern is generally consistent with previous observations from 
      Western populations. Nevertheless, we found several novel associations which have 
      rarely, if ever, been reported previously.
FAU - Kang, Jiunn-Horng
AU  - Kang JH
AD  - Department of Rehabilitation, Taipei Medical University Hospital, Taipei, Taiwan.
FAU - Lin, Herng-Ching
AU  - Lin HC
LA  - eng
PT  - Journal Article
DEP - 20110130
PL  - Germany
TA  - J Neurol
JT  - Journal of neurology
JID - 0423161
SB  - IM
MH  - Asian People
MH  - Cardiovascular Diseases/epidemiology
MH  - Community Health Planning
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Kidney Diseases, Cystic/epidemiology
MH  - Logistic Models
MH  - Male
MH  - Mental Disorders/epidemiology
MH  - National Health Programs/statistics & numerical data
MH  - Nervous System Diseases/epidemiology
MH  - Poliomyelitis/*epidemiology/*mortality
MH  - Survivors/*statistics & numerical data
MH  - Taiwan/epidemiology
EDAT- 2011/02/01 06:00
MHDA- 2011/09/29 06:00
CRDT- 2011/02/01 06:00
PHST- 2010/10/14 00:00 [received]
PHST- 2010/12/08 00:00 [accepted]
PHST- 2010/12/06 00:00 [revised]
PHST- 2011/02/01 06:00 [entrez]
PHST- 2011/02/01 06:00 [pubmed]
PHST- 2011/09/29 06:00 [medline]
AID - 10.1007/s00415-010-5875-y [doi]
PST - ppublish
SO  - J Neurol. 2011 Jun;258(6):1026-33. doi: 10.1007/s00415-010-5875-y. Epub 2011 Jan 
      30.

PMID- 21109516
OWN - NLM
STAT- MEDLINE
DCOM- 20110421
LR  - 20220316
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 70
IP  - 4
DP  - 2011 Apr
TI  - Tumour necrosis factor antagonist use and associated risk reduction of 
      cardiovascular events among patients with rheumatoid arthritis.
PG  - 576-82
LID - 10.1136/ard.2010.129916 [doi]
AB  - OBJECTIVE: To examine the association of cardiovascular events with tumour 
      necrosis factor (TNF) α antagonist use compared with non-biological 
      disease-modifying antirheumatic drug (DMARD) utilisation in patients with 
      rheumatoid arthritis (RA). METHODS: The study population included 10 156 patients 
      enrolled in the Consortium of Rheumatology Researchers of North America RA 
      registry. Three study cohorts were defined based on three mutually exclusive drug 
      use categories, including TNF antagonists, methotrexate and other non-biological 
      DMARDs. HR were calculated adjusting for cardiovascular risk factors, RA disease 
      characteristics and prednisone use. The primary study outcome was a composite of 
      non-fatal myocardial infarction (MI), transient ischaemic attack (TIA) or stroke 
      and cardiovascular-related death. RESULTS: There were 88 cardiovascular events, 
      including 26 MI, 45 TIA/strokes and 17 cardiovascular-related deaths. After 
      adjusting for age, gender, cardiovascular risk factors and RA disease 
      characteristics, patients using a TNF antagonist experienced a reduced risk of 
      the primary composite cardiovascular endpoint (HR 0.39, 95% CI 0.19 to 0.82) 
      compared with users of non-biological DMARDs. Methotrexate was not associated 
      with a reduced risk (HR 0.94, 95% CI 0.49 to 1.80). Prednisone use was associated 
      with a dose-dependent increased risk (p=0.04). The risk reduction associated with 
      TNF antagonists was also observed for non-fatal cardiovascular events (HR 0.35, 
      95% CI 0.16 to 0.74). CONCLUSION: TNF antagonist use was associated with a 
      reduced risk of cardiovascular events in patients with RA.
FAU - Greenberg, Jeffrey D
AU  - Greenberg JD
AD  - Department of Rheumatology, New York University Hospital for Joint Diseases, 301 
      East 17th Street, Suite 1410, New York, NY 10003, USA. 
      jeffrey.greenberg@nyumc.org
FAU - Kremer, Joel M
AU  - Kremer JM
FAU - Curtis, Jeffrey R
AU  - Curtis JR
FAU - Hochberg, Marc C
AU  - Hochberg MC
FAU - Reed, George
AU  - Reed G
FAU - Tsao, Peter
AU  - Tsao P
FAU - Farkouh, Michael E
AU  - Farkouh ME
FAU - Nasir, Adeel
AU  - Nasir A
FAU - Setoguchi, Soko
AU  - Setoguchi S
FAU - Solomon, Daniel H
AU  - Solomon DH
CN  - CORRONA Investigators
LA  - eng
GR  - R01HS018517/HS/AHRQ HHS/United States
GR  - AR047782/AR/NIAMS NIH HHS/United States
GR  - K23 AR053351/AR/NIAMS NIH HHS/United States
GR  - K23 AR054412/AR/NIAMS NIH HHS/United States
GR  - R01 HS018517/HS/AHRQ HHS/United States
GR  - K23AR054412/AR/NIAMS NIH HHS/United States
GR  - AR053351/AR/NIAMS NIH HHS/United States
GR  - AR055989/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20101124
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Immunologic Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
CIN - Ann Rheum Dis. 2011 Apr;70(4):561-2. doi: 10.1136/ard.2010.142174. PMID: 21372192
MH  - Adult
MH  - Aged
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/complications/*drug therapy/epidemiology
MH  - Cardiovascular Diseases/epidemiology/etiology/*prevention & control
MH  - Epidemiologic Methods
MH  - Female
MH  - Humans
MH  - Immunologic Factors/*therapeutic use
MH  - Male
MH  - Middle Aged
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
MH  - United States/epidemiology
EDAT- 2010/11/27 06:00
MHDA- 2011/04/22 06:00
CRDT- 2010/11/27 06:00
PHST- 2010/11/27 06:00 [entrez]
PHST- 2010/11/27 06:00 [pubmed]
PHST- 2011/04/22 06:00 [medline]
AID - ard.2010.129916 [pii]
AID - 10.1136/ard.2010.129916 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2011 Apr;70(4):576-82. doi: 10.1136/ard.2010.129916. Epub 2010 Nov 
      24.

PMID- 21109513
OWN - NLM
STAT- MEDLINE
DCOM- 20110318
LR  - 20220408
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 70
IP  - 1
DP  - 2011 Jan
TI  - Cardiovascular disease in rheumatoid arthritis: state of the art and future 
      perspectives.
PG  - 8-14
LID - 10.1136/ard.2010.142133 [doi]
AB  - Rheumatoid arthritis is associated with an increased risk for cardiovascular 
      events, such as myocardial infarction and stroke. Epidemiological evidence 
      suggests that classic cardiovascular risk factors, such as hypertension, 
      dyslipidaemia, insulin resistance and body composition alterations are important 
      but not sufficient to explain all of the excess risk. High-grade systemic 
      inflammation and its interplay with classic risk factors may also contribute. 
      Some associations between classic risk factors and cardiovascular risk in people 
      with rheumatoid arthritis appear counterintuitive but may be explained on the 
      basis of biological alterations. More research is necessary to uncover the exact 
      mechanisms responsible for this phenomenon, develop accurate systems used to 
      identify patients at high risk, design and assess prevention strategies specific 
      to this population of patients.
FAU - Kitas, George D
AU  - Kitas GD
AD  - Department of Rheumatology, Dudley Group of Hospitals NHS Foundation Trust, 
      Clinical Research Unit, Russells Hall Hospital, Dudley, West Midlands, UK. 
      gd.kitas@dgoh.nhs.uk
FAU - Gabriel, Sherine E
AU  - Gabriel SE
LA  - eng
GR  - Arthritis Research UK/United Kingdom
GR  - British Heart Foundation/United Kingdom
GR  - Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20101124
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Lipids)
SB  - IM
EIN - Ann Rheum Dis. 2011 Aug;70(8):1520
MH  - Arthritis, Rheumatoid/*complications
MH  - Atherosclerosis/etiology
MH  - Body Composition
MH  - Cardiovascular Diseases/*etiology
MH  - Humans
MH  - Hypertension/etiology
MH  - Inflammation/complications
MH  - Lipids/blood
MH  - Risk Factors
EDAT- 2010/11/27 06:00
MHDA- 2011/03/19 06:00
CRDT- 2010/11/27 06:00
PHST- 2010/11/27 06:00 [entrez]
PHST- 2010/11/27 06:00 [pubmed]
PHST- 2011/03/19 06:00 [medline]
AID - ard.2010.142133 [pii]
AID - 10.1136/ard.2010.142133 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2011 Jan;70(1):8-14. doi: 10.1136/ard.2010.142133. Epub 2010 Nov 
      24.

PMID- 21071477
OWN - NLM
STAT- MEDLINE
DCOM- 20120221
LR  - 20220317
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
VI  - 50
IP  - 3
DP  - 2011 Mar
TI  - Tumour necrosis factor antagonists and the risk of cardiovascular disease in 
      patients with rheumatoid arthritis: a systematic literature review.
PG  - 518-31
LID - 10.1093/rheumatology/keq316 [doi]
AB  - OBJECTIVES: RA is associated with early ischaemic heart disease. This appears to 
      be driven largely by the presence of chronic inflammation. Studies suggest that 
      treatment with disease-modifying drugs such as MTX may reduce the incidence of 
      cardiovascular events in RA. Anti-TNF therapies significantly reduce inflammation 
      in RA. However, the extent to which these agents also reduce cardiovascular 
      disease (CVD) is uncertain. The purpose of this study was to explore the effect 
      of anti-TNF agents on CVD in RA using a systematic literature review. METHODS: We 
      searched for studies of adults with RA treated with TNF antagonists where 
      cardiovascular outcomes were recorded using MEDLINE, EMBASE, Cochrane Database, 
      Database of Abstracts and Reviews of Effects, Health Technology Appraisal, 
      Science Citation Index and Clinical Evidence from 1989 to 2010. Conference 
      proceedings for the British Society of Rheumatology, ACR and EULAR between 2005 
      and 2009 were hand searched. Two reviewers assessed abstracts for inclusion and 
      then quality of selected papers was assessed. RESULTS: A total of 1840 abstracts 
      were identified and 20 articles were suitable for inclusion. Information was 
      obtained on the effect of TNF antagonists on overall CVD events, myocardial 
      infarction, strokes and heart failure. CONCLUSION: In many studies, TNF 
      antagonists appear to reduce the likelihood of CVD in individuals with RA. 
      Reassuringly, there does not appear to be an increased risk of cardiac failure. 
      However, the reduction in CVD is not as consistently seen as with studies of MTX.
FAU - Westlake, Sarah L
AU  - Westlake SL
AD  - Department of Rheumatology, Southampton General Hospital, Tremona Road, 
      Southampton SO16 6YD, UK. cedwards@soton.ac.uk.
FAU - Colebatch, Alexandra N
AU  - Colebatch AN
FAU - Baird, Janis
AU  - Baird J
FAU - Curzen, Nick
AU  - Curzen N
FAU - Kiely, Patrick
AU  - Kiely P
FAU - Quinn, Mark
AU  - Quinn M
FAU - Choy, Ernest
AU  - Choy E
FAU - Ostor, Andrew J K
AU  - Ostor AJ
FAU - Edwards, Christopher J
AU  - Edwards CJ
LA  - eng
PT  - Journal Article
PT  - Review
PT  - Systematic Review
DEP - 20101111
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Lymphotoxin-beta)
SB  - IM
MH  - Adult
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/complications/*drug therapy
MH  - Cardiovascular Diseases/complications/*prevention & control
MH  - Humans
MH  - Lymphotoxin-beta/*antagonists & inhibitors
MH  - Risk Factors
MH  - Treatment Outcome
EDAT- 2010/11/13 06:00
MHDA- 2012/02/22 06:00
CRDT- 2010/11/13 06:00
PHST- 2010/11/13 06:00 [entrez]
PHST- 2010/11/13 06:00 [pubmed]
PHST- 2012/02/22 06:00 [medline]
AID - keq316 [pii]
AID - 10.1093/rheumatology/keq316 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2011 Mar;50(3):518-31. doi: 10.1093/rheumatology/keq316. 
      Epub 2010 Nov 11.

PMID- 20957658
OWN - NLM
STAT- MEDLINE
DCOM- 20110526
LR  - 20220321
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Linking)
VI  - 63
IP  - 4
DP  - 2011 Apr
TI  - Systematic review and meta-analysis: anti-tumor necrosis factor α therapy and 
      cardiovascular events in rheumatoid arthritis.
PG  - 522-9
LID - 10.1002/acr.20371 [doi]
AB  - OBJECTIVE: Control of rheumatoid arthritis (RA) may reduce the risk of 
      cardiovascular events. We sought to systematically assess the association between 
      anti-tumor necrosis factor α (anti-TNFα) therapy in RA and cardiovascular event 
      rates. METHODS: Observational cohorts and randomized controlled trials (RCTs) 
      reporting on cardiovascular events (all events, myocardial infarction [MI], 
      congestive heart failure, and cerebrovascular accident [CVA]) in RA patients 
      treated with anti-TNFα therapy compared to traditional disease-modifying 
      antirheumatic drugs were identified from a search of PubMed (1950 to November 
      2009), EMBase (1980 to November 2009), and conference abstracts. Relative risks 
      (RRs) or hazard ratios and 95% confidence intervals (95% CIs) were extracted. If 
      the incidence was reported, additional data were extracted to calculate an 
      incidence density ratio and its variance. RESULTS: The systematic review and 
      meta-analysis include 16 and 11 publications, respectively. In cohort studies, 
      anti-TNFα therapy was associated with a reduced risk for all cardiovascular 
      events (pooled adjusted RR 0.46; 95% CI 0.28, 0.77), MI (pooled adjusted RR 0.81; 
      95% CI 0.68, 0.96), and CVA (pooled adjusted RR 0.69; 95% CI 0.53, 0.89). 
      Meta-analysis of RCTs also produced a point estimate indicating lower risk of 
      cardiovascular events, but this was not statistically significant (pooled RR 
      0.85; 95% CI 0.28, 2.59). CONCLUSION: Anti-TNFα therapy is associated with a 
      reduced risk of all cardiovascular events, MI, and CVA in observational cohorts. 
      There was heterogeneity among cohort studies and possible publication bias. The 
      point estimate of the effect from RCTs is underpowered with wide 95% CIs, and 
      cardiovascular events were secondary outcomes, but RCTs also demonstrated a trend 
      toward decreased risk.
CI  - Copyright © 2011 by the American College of Rheumatology.
FAU - Barnabe, Cheryl
AU  - Barnabe C
AD  - University of Calgary, Calgary, Alberta, Canada. ccbarnab@ucalgary.ca
FAU - Martin, Billie-Jean
AU  - Martin BJ
FAU - Ghali, William A
AU  - Ghali WA
LA  - eng
GR  - Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PT  - Systematic Review
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Antirheumatic Agents/adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/complications/*drug therapy/*metabolism
MH  - Cardiovascular Diseases/*drug therapy/etiology/metabolism
MH  - Cohort Studies
MH  - Humans
MH  - Randomized Controlled Trials as Topic/trends
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors/physiology
EDAT- 2010/10/20 06:00
MHDA- 2011/05/27 06:00
CRDT- 2010/10/20 06:00
PHST- 2010/10/20 06:00 [entrez]
PHST- 2010/10/20 06:00 [pubmed]
PHST- 2011/05/27 06:00 [medline]
AID - 10.1002/acr.20371 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2011 Apr;63(4):522-9. doi: 10.1002/acr.20371.

PMID- 20890982
OWN - NLM
STAT- MEDLINE
DCOM- 20110526
LR  - 20220410
IS  - 2151-4658 (Electronic)
IS  - 2151-464X (Linking)
VI  - 63
IP  - 4
DP  - 2011 Apr
TI  - Cardiovascular profile in ankylosing spondylitis: a systematic review and 
      meta-analysis.
PG  - 557-63
LID - 10.1002/acr.20364 [doi]
AB  - OBJECTIVE: Rheumatoid arthritis is associated with increased cardiovascular risk. 
      In ankylosing spondylitis (AS), there is a paucity of information concerning this 
      risk. Our objective was to assess the incidence of myocardial infarction (MI) or 
      strokes and the cardiovascular risk profile in AS patients. METHODS: We performed 
      a systematic literature review using PubMed, EMBase, and the Cochrane Library up 
      to August 2009. Incidence of MI or stroke was calculated by metaproportion. For 
      cardiovascular risk factors, differences between AS patients and controls were 
      expressed by standardized mean differences using inverse of variance method. 
      RESULTS: For MI, 8 longitudinal studies were included. In controls (n=82,745), 
      1,318 MI cases were observed (4.6%; 95% confidence interval [95% CI] 1.2%, 
      10.0%). In AS patients (n=3,279), 224 MI cases were reported (incidence 7.4%; 95% 
      CI 5.2%, 10.0%). The increase in MI cases in AS patients was not significant 
      (risk ratio 1.88; 95% CI 0.83, 4.28). For stroke, 7 longitudinal studies reported 
      327 strokes in AS patients (n=31,949), which is an incidence of 2.2% (95% CI 
      1.3%, 3.4%). In controls (n=7,372), one study reported 170 strokes (2.3%; 95% CI 
      2.0%, 2.7%). For cardiovascular risk factors, 15 case-control studies and 9 
      abstracts were included (n=1,214 for patients and n=1,000 for controls). AS 
      patients were characterized by a higher weighted mean intima-media thickness and 
      higher risk of metabolic syndrome. In AS patients, there was a significant 
      decrease in triglycerides, total cholesterol, and high-density lipoprotein (HDL) 
      cholesterol. CONCLUSION: AS patients appear to be at higher risk of MI, which 
      could be due to low HDL cholesterol levels or to systemic inflammation. 
      Management of cardiovascular risk factors and control of systemic inflammation 
      should be taken into account in AS.
CI  - Copyright © 2011 by the American College of Rheumatology.
FAU - Mathieu, Sylvain
AU  - Mathieu S
AD  - Clermont 1 University, Centre Hospitalier Universitaire Gabriel Montpied, 
      Clermont-Ferrand, France. smathieu@chu-clermontferrand.fr
FAU - Gossec, Laure
AU  - Gossec L
FAU - Dougados, Maxime
AU  - Dougados M
FAU - Soubrier, Martin
AU  - Soubrier M
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PT  - Systematic Review
PL  - United States
TA  - Arthritis Care Res (Hoboken)
JT  - Arthritis care & research
JID - 101518086
RN  - 0 (Cholesterol, HDL)
SB  - IM
MH  - Animals
MH  - Cardiovascular Diseases/diagnosis/*epidemiology/*etiology
MH  - Cholesterol, HDL/blood
MH  - Humans
MH  - Longitudinal Studies/trends
MH  - Risk Factors
MH  - Spondylitis, Ankylosing/blood/*complications/*epidemiology
EDAT- 2010/10/05 06:00
MHDA- 2011/05/27 06:00
CRDT- 2010/10/05 06:00
PHST- 2010/10/05 06:00 [entrez]
PHST- 2010/10/05 06:00 [pubmed]
PHST- 2011/05/27 06:00 [medline]
AID - 10.1002/acr.20364 [doi]
PST - ppublish
SO  - Arthritis Care Res (Hoboken). 2011 Apr;63(4):557-63. doi: 10.1002/acr.20364.

PMID- 20656636
OWN - NLM
STAT- MEDLINE
DCOM- 20101102
LR  - 20220311
IS  - 1875-2128 (Electronic)
IS  - 1875-2128 (Linking)
VI  - 103
IP  - 4
DP  - 2010 Apr
TI  - High risk of clinical cardiovascular events in rheumatoid arthritis: Levels of 
      associations of myocardial infarction and stroke through a systematic review and 
      meta-analysis.
PG  - 253-61
LID - 10.1016/j.acvd.2010.03.007 [doi]
AB  - BACKGROUND: While there are convergent data suggesting that overall 
      cardiovascular mortality is increased in patients with rheumatoid arthritis, the 
      relative contributions of myocardial infarction and stroke remain unclear. AIMS: 
      We sought to clarify this issue by conducting a meta-analysis of cohort studies 
      on myocardial infarction and stroke in patients with rheumatoid arthritis. 
      METHODS: A MEDLINE search from January 1960 to September 2009 and abstracts from 
      international conferences from 2007 to 2009 were searched for relevant 
      literature. All cohort studies reporting on standardized mortality ratio or 
      incidence rate ratio of myocardial or stroke associated with rheumatoid 
      arthritis, with available crude numbers, were included. STATA meta-analysis 
      software was used to calculate pooled risk estimates. RESULTS: Seventeen papers 
      fulfilled the inclusion criteria, corresponding to a total of 124,894 patients. 
      Ten studies reported on standardized mortality ratio for fatal myocardial 
      infarction, which ranged from 0.99 to 3.82. The overall pooled estimate was 1.77 
      (95% confidence interval [CI] 1.65-1.89). Incidence rate ratio for myocardial 
      infarction was reported in five studies; the pooled estimate was 2.10 (95% CI 
      1.52-2.89). Nine studies reported on fatal stroke, with standardized mortality 
      ratio ranging from 1.08 to 2.00; the pooled estimate was 1.46 (95% CI 1.31-1.63). 
      The pooled incidence rate ratio for stroke (three studies) was 1.91 (95% CI 
      1.73-2.12). CONCLUSION: Our results show that risks of myocardial infarction and 
      stroke are increased in patients with rheumatoid arthritis. In addition, both 
      account for the observed increased mortality in individuals with rheumatoid 
      arthritis.
CI  - Copyright 2010 Elsevier Masson SAS. All rights reserved.
FAU - Meune, Christophe
AU  - Meune C
AD  - Département de cardiologie, université Paris-Descartes, hôpital Cochin, 
      Assistance publique-Hôpitaux de Paris, 75014 Paris, France. 
      christophe.meune@cch.aphp.fr
FAU - Touzé, Emmanuel
AU  - Touzé E
FAU - Trinquart, Ludovic
AU  - Trinquart L
FAU - Allanore, Yannick
AU  - Allanore Y
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Review
PT  - Systematic Review
DEP - 20100518
PL  - Netherlands
TA  - Arch Cardiovasc Dis
JT  - Archives of cardiovascular diseases
JID - 101465655
SB  - IM
MH  - Arthritis, Rheumatoid/*complications/mortality
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*etiology/mortality
MH  - Prognosis
MH  - Risk Assessment
MH  - Risk Factors
MH  - Stroke/*etiology/mortality
EDAT- 2010/07/27 06:00
MHDA- 2010/11/03 06:00
CRDT- 2010/07/27 06:00
PHST- 2009/12/03 00:00 [received]
PHST- 2010/03/26 00:00 [revised]
PHST- 2010/03/29 00:00 [accepted]
PHST- 2010/07/27 06:00 [entrez]
PHST- 2010/07/27 06:00 [pubmed]
PHST- 2010/11/03 06:00 [medline]
AID - S1875-2136(10)00077-X [pii]
AID - 10.1016/j.acvd.2010.03.007 [doi]
PST - ppublish
SO  - Arch Cardiovasc Dis. 2010 Apr;103(4):253-61. doi: 10.1016/j.acvd.2010.03.007. 
      Epub 2010 May 18.

PMID- 20583916
OWN - NLM
STAT- MEDLINE
DCOM- 20110224
LR  - 20220317
IS  - 1943-3670 (Electronic)
IS  - 0022-3492 (Linking)
VI  - 81
IP  - 11
DP  - 2010 Nov
TI  - Increased prevalence of cardiovascular and autoimmune diseases in periodontitis 
      patients: a cross-sectional study.
PG  - 1622-8
LID - 10.1902/jop.2010.100058 [doi]
AB  - BACKGROUND: Associations between periodontitis and cardiovascular and autoimmune 
      diseases are most often assessed in patients with a particular cardiovascular or 
      autoimmune disease. To prevent selection bias, this study assesses the existence 
      of associations between periodontitis and cardiovascular and autoimmune diseases 
      in patients attending a dental or periodontal clinic. METHODS: Data were 
      collected from 1,276 randomly selected dental records from patients attending a 
      dental (n = 588) or periodontal (n = 688) clinic. Data on the prevalence of 
      cardiovascular and autoimmune diseases were obtained from a validated health 
      questionnaire. Data on the presence of periodontitis were taken from patients' 
      dental records. RESULTS: In uncontrolled analyses, the prevalence of 
      hypertension, diabetes mellitus (DM), and rheumatoid arthritis (RA) is 
      significantly increased in patients with periodontitis. Controlled for 
      confounding, periodontitis was associated with DM, with an odds ratio of 4 (1.03 
      to 15.3), in the dental clinic. DM was not associated with periodontitis in 
      periodontal clinics. Hypertension does not seem to be associated with 
      periodontitis when controlling for confounders. Periodontitis may be associated 
      with RA in both clinic types. CONCLUSIONS: The increased prevalence of 
      cardiovascular and autoimmune diseases among patients with periodontitis 
      attending dental or periodontal clinics may, at least in part, be influenced by 
      confounding. However, the increased prevalence of DM and RA in patients with 
      periodontitis could not be explained by confounding.
FAU - Nesse, Willem
AU  - Nesse W
AD  - Department of Oral and Maxillofacial Surgery, University Medical Center 
      Groningen, University of Groningen, Groningen, The Netherlands.
FAU - Dijkstra, Pieter U
AU  - Dijkstra PU
FAU - Abbas, Frank
AU  - Abbas F
FAU - Spijkervet, Fred K L
AU  - Spijkervet FK
FAU - Stijger, Astrid
AU  - Stijger A
FAU - Tromp, Jan A H
AU  - Tromp JA
FAU - van Dijk, Johan L
AU  - van Dijk JL
FAU - Vissink, Arjan
AU  - Vissink A
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20100628
PL  - United States
TA  - J Periodontol
JT  - Journal of periodontology
JID - 8000345
SB  - IM
MH  - Adult
MH  - Age Factors
MH  - Arthritis, Rheumatoid/epidemiology
MH  - Autoimmune Diseases/*epidemiology
MH  - Cardiovascular Diseases/*epidemiology
MH  - Confounding Factors, Epidemiologic
MH  - Cross-Sectional Studies
MH  - Dental Records/statistics & numerical data
MH  - Diabetes Mellitus/epidemiology
MH  - Female
MH  - Humans
MH  - Hypertension/epidemiology
MH  - Hypothyroidism/epidemiology
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology
MH  - Netherlands/epidemiology
MH  - Periodontal Index
MH  - Periodontitis/*epidemiology
MH  - Prevalence
MH  - Risk Factors
MH  - Sex Factors
MH  - Smoking/epidemiology
MH  - Stroke/epidemiology
MH  - Surveys and Questionnaires
EDAT- 2010/06/30 06:00
MHDA- 2011/02/25 06:00
CRDT- 2010/06/30 06:00
PHST- 2010/06/30 06:00 [entrez]
PHST- 2010/06/30 06:00 [pubmed]
PHST- 2011/02/25 06:00 [medline]
AID - 10.1902/jop.2010.100058 [doi]
PST - ppublish
SO  - J Periodontol. 2010 Nov;81(11):1622-8. doi: 10.1902/jop.2010.100058. Epub 2010 
      Jun 28.

PMID- 20551156
OWN - NLM
STAT- MEDLINE
DCOM- 20101112
LR  - 20151119
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 69
IP  - 11
DP  - 2010 Nov
TI  - Lipids, myocardial infarction and ischaemic stroke in patients with rheumatoid 
      arthritis in the Apolipoprotein-related Mortality RISk (AMORIS) Study.
PG  - 1996-2001
LID - 10.1136/ard.2009.126128 [doi]
AB  - OBJECTIVES: To examine the rates of acute myocardial infarction (AMI) and 
      ischaemic stroke (IS) and to examine the predictive value of total cholesterol 
      (TC) and triglycerides (TG) for AMI and IS in patients with rheumatoid arthritis 
      (RA) and people without RA. METHODS: In the Apolipoprotein MOrtality RISk 
      (AMORIS) Study 480 406 people (including 1779 with RA, of whom 214 had an AMI and 
      165 an IS) were followed for 11.8 (range 7-17) years. Cox regression analysis was 
      used to calculate HR per SD increase in TC or TG with 95% CI. All values were 
      adjusted for age, diabetes and hypertension. RESULTS: The levels of TC and TG 
      were significantly lower in patients with RA than in people without RA. Despite 
      this, the rate of AMI and IS per 1000 years was at least 1.6 times higher in RA 
      than non-RA. TC was nearly significantly predictive for AMI (HR/SD 1.13 (95% CI 
      0.99 to 1.29), p=0.07) and significantly predictive for future IS in RA (HR/SD 
      1.20 (95% CI 1.03 to 1.40), p=0.02). TG had no relationship to development of AMI 
      (1.07, 0.94 to 1.21, p=0.29), but was weakly related to IS (1.13, 0.99 to 1.27, 
      p=0.06). In contrast, both TC and TG were significant predictors of AMI and IS in 
      people without RA. CONCLUSIONS: Patients with RA had 1.6 times higher rate of AMI 
      and IS than people without RA. TC and TG were significant predictors of AMI and 
      IS in people without RA, whereas the predictive value in RA was not consistent.
FAU - Semb, A G
AU  - Semb AG
AD  - Department of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway. 
      a-semb@diakonsyk.no
FAU - Kvien, T K
AU  - Kvien TK
FAU - Aastveit, A H
AU  - Aastveit AH
FAU - Jungner, I
AU  - Jungner I
FAU - Pedersen, T R
AU  - Pedersen TR
FAU - Walldius, G
AU  - Walldius G
FAU - Holme, I
AU  - Holme I
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20100615
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Biomarkers)
RN  - 0 (Lipids)
RN  - 0 (Triglycerides)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/blood/*complications/epidemiology
MH  - Biomarkers/blood
MH  - Cholesterol/blood
MH  - Epidemiologic Methods
MH  - Female
MH  - Humans
MH  - Lipids/*blood
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/blood/epidemiology/*etiology
MH  - Prognosis
MH  - Stroke/blood/epidemiology/*etiology
MH  - Sweden/epidemiology
MH  - Triglycerides/blood
EDAT- 2010/06/17 06:00
MHDA- 2010/11/13 06:00
CRDT- 2010/06/17 06:00
PHST- 2010/06/17 06:00 [entrez]
PHST- 2010/06/17 06:00 [pubmed]
PHST- 2010/11/13 06:00 [medline]
AID - ard.2009.126128 [pii]
AID - 10.1136/ard.2009.126128 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2010 Nov;69(11):1996-2001. doi: 10.1136/ard.2009.126128. Epub 2010 
      Jun 15.

PMID- 20511601
OWN - NLM
STAT- MEDLINE
DCOM- 20110204
LR  - 20220409
IS  - 1475-3901 (Electronic)
IS  - 1475-3898 (Linking)
VI  - 19
IP  - 5
DP  - 2010 Oct
TI  - Patient-held medical records for patients with chronic disease: a systematic 
      review.
PG  - e41
LID - 10.1136/qshc.2009.037531 [doi]
AB  - OBJECTIVES: To determine whether in patients with chronic disease a patient-held 
      medical record (PHR), compared to usual care, improves clinical care, patient 
      outcomes or satisfaction. DESIGN: Systematic review. DATA SOURCES: Databases 
      searched were All EBM (The Cochrane Database of Systematic Reviews, DARE 
      CENTRAL), Medline, CINAHL and EMBASE from 1980 to 16 February 2009. STUDY 
      SELECTION: Two reviewers assessed comparative studies that compared paper-based 
      PHR to usual care for inclusion using a priori study selection criteria. STUDIES 
      REVIEWED: Four hundred and eighty-one articles were reviewed by title and 
      abstract. Full text was retrieved for 120 articles. Fourteen studies met the 
      inclusion and exclusion criteria and were appraised using a priori criteria for 
      methodological quality. RESULTS: Fourteen studies were included in diabetes, 
      oncology, mental health, rheumatoid arthritis, stroke and palliative care. The 
      studies used a variety of designs of PHR and compared this with usual care. PHR 
      were implemented with varying degrees of patient and staff support and education, 
      mainly for six months or less. Outcomes included attitudes on the usefulness of 
      PHR, the quality of information exchange, process indicators, and clinical and 
      physiological indicators. The effectiveness of PHRs is generally of low or very 
      low quality, with the majority of studies having a high risk of bias. These 
      studies do not demonstrate a significant benefit of introducing PHR. CONCLUSIONS: 
      There is no clear benefit of implementing a PHR, and due to medium to high risk 
      of bias these findings should be interpreted with caution. More high quality 
      studies are needed to evaluate properly the effectiveness of PHRs in chronic 
      disease populations.
FAU - Ko, Henry
AU  - Ko H
AD  - Centre for Clinical Effectiveness, Southern Health, 43-51 Kanooka Grove, Clayton, 
      VIC 3168, Australia. henry.ko@med.monash.edu.au
FAU - Turner, Tari
AU  - Turner T
FAU - Jones, Christine
AU  - Jones C
FAU - Hill, Caron
AU  - Hill C
LA  - eng
PT  - Journal Article
PT  - Review
PT  - Systematic Review
DEP - 20100528
PL  - England
TA  - Qual Saf Health Care
JT  - Quality & safety in health care
JID - 101136980
MH  - *Chronic Disease
MH  - Humans
MH  - *Medical Records
MH  - *Patient Access to Records
MH  - *Patient Participation
EDAT- 2010/06/01 06:00
MHDA- 2011/02/05 06:00
CRDT- 2010/06/01 06:00
PHST- 2010/06/01 06:00 [entrez]
PHST- 2010/06/01 06:00 [pubmed]
PHST- 2011/02/05 06:00 [medline]
AID - qshc.2009.037531 [pii]
AID - 10.1136/qshc.2009.037531 [doi]
PST - ppublish
SO  - Qual Saf Health Care. 2010 Oct;19(5):e41. doi: 10.1136/qshc.2009.037531. Epub 
      2010 May 28.

PMID- 27789992
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1179-156X (Print)
IS  - 1179-156X (Electronic)
IS  - 1179-156X (Linking)
VI  - 2
DP  - 2010
TI  - Association of periodontitis with rheumatoid arthritis and atherosclerosis: Novel 
      paradigms in etiopathogeneses and management?
PG  - 1-16
AB  - There is increasing documentation of a link between inflammatory periodontal 
      disease affecting the supporting structure of teeth, rheumatoid arthritis, and 
      coronary artery disease. Periodontitis is initiated predominantly by 
      Gram-negative bacteria and progresses as a consequence of the host inflammatory 
      response to periodontal pathogens. Lipopolysaccharide, a cell wall constituent 
      stimulates the production of inflammatory cytokines via the activation of 
      signaling pathways perpetuating inflammatory pathogenesis in a cyclical manner in 
      susceptible individuals; with an element of autoimmune stimulation, not 
      dissimilar to the sequential events seen in RA. Periodontitis, also implicated as 
      a risk factor for cardiovascular disease, promotes mechanisms for atherosclerosis 
      by enhancing an imbalance in systemic inflammatory mediators; more direct 
      mechanisms attributed to microbial products are also implicated in both RA and 
      atherogenesis. Severe periodontal disease characterized by clinical and 
      radiographic parameters has been associated with ischemic stroke risk, 
      significant levels of C-reactive protein and serum amyloid A, amongst others 
      common to both periodontitis and atherosclerosis. Existing data supports the 
      hypothesis that persistent localized infection in periodontitis may influence 
      systemic levels of inflammatory markers and pose a risk for RA and 
      atherosclerosis. A common nucleus of activity in their pathogeneses provides 
      novel paradigms of therapeutic targeting for reciprocal benefit.
FAU - Soory, Mena
AU  - Soory M
AD  - King's College London Dental Institute, Denmark Hill, London UK.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20100528
PL  - New Zealand
TA  - Open Access Rheumatol
JT  - Open access rheumatology : research and reviews
JID - 101688698
PMC - PMC5074770
OTO - NOTNLM
OT  - RA
OT  - atherosclerosis
OT  - cytokines
OT  - periodontal pathogens
OT  - periodontitis
OT  - therapeutic targets
COIS- The author report no conflicts of interest in this work.
EDAT- 2010/05/28 00:00
MHDA- 2010/05/28 00:01
PMCR- 2010/05/28
CRDT- 2010/05/28 00:00
PHST- 2010/05/28 00:00 [pubmed]
PHST- 2010/05/28 00:01 [medline]
PHST- 2010/05/28 00:00 [entrez]
PHST- 2010/05/28 00:00 [pmc-release]
AID - oarrr-2-001 [pii]
AID - 10.2147/oarrr.s10928 [doi]
PST - epublish
SO  - Open Access Rheumatol. 2010 May 28;2:1-16. doi: 10.2147/oarrr.s10928. eCollection 
      2010.

PMID- 20471897
OWN - NLM
STAT- MEDLINE
DCOM- 20110503
LR  - 20220331
IS  - 1778-7254 (Electronic)
IS  - 1297-319X (Linking)
VI  - 78
IP  - 1
DP  - 2011 Jan
TI  - Cardiovascular risk induced by low-dose corticosteroids in rheumatoid arthritis: 
      a systematic literature review.
PG  - 23-30
LID - 10.1016/j.jbspin.2010.02.040 [doi]
AB  - OBJECTIVES: To assess the association between cardiovascular (CV) risk and 
      low-dose corticosteroids (LD-CT, defined as a daily dose <10mg/day of prednisone) 
      in rheumatoid arthritis (RA) patients. DATA SOURCE: A systematic review of the 
      literature up to June 2009 was performed. DATA EXTRACTION: (1) cardiovascular 
      risk factors: high blood pressure, glycemia and lipid profile, carotid 
      intima-media thickness, pulse-wave velocity, ventricular function; (2) "hard" 
      outcomes: heart failure (HF), stroke, myocardial infarction (MI) or mortality. 
      DATA ANALYSIS: descriptive, comparing CV risk between LD-CT-treated RA patients 
      and LD-CT-non-treated RA patients. RESULTS: Of the 1138 screened reports, the 
      literature search identified 37 assessing CV risk in LD-CT treated RA. The 
      analysis showed a protective effect on serum lipid profile, an increase of 
      insulin resistance or glycemia, probably no effect on blood pressure, no effect 
      on atherosclerosis, discrepancies regarding arterial stiffness and no effect on 
      ventricular function or heart rate variability. An association of LD-CT with 
      major CV events was found in 4/6 studies. This included MI (HR=1.7 [1.2-2.3]), 
      stroke (OR=4.36 [1.60-11.90] for LDC between 6 and 10mg/day), mortality (HR=2.03 
      [1.25-3.32]) and a composite index of CV events (in the group of rheumatoid 
      factor positive RA, HR=2.21 [1.22-4.00]). Two studies did not find any 
      significant association between LD-CT exposure and mortality (OR=2.25 
      [0.29-102.5]) or a composite index of CV events (OR=1.3 [0.8-2.0]). CONCLUSION: 
      Although the literature review showed poor association between LDC exposure and 
      CV risk factors, a trend of increasing major CV events was identified.
CI  - Copyright Â© 2010 Société française de rhumatologie. Published by Elsevier SAS. 
      All rights reserved.
FAU - Ruyssen-Witrand, Adeline
AU  - Ruyssen-Witrand A
AD  - Service de rhumatologie B, hôpital Cochin, AP-HP, université Paris-V 
      René-Descartes, 27, rue du Faubourg-Saint-Jacques, 75014 Paris, France. 
      adruyssen@hotmail.com
FAU - Fautrel, Bruno
AU  - Fautrel B
FAU - Saraux, Alain
AU  - Saraux A
FAU - Le Loët, Xavier
AU  - Le Loët X
FAU - Pham, Thao
AU  - Pham T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PT  - Systematic Review
DEP - 20100514
PL  - France
TA  - Joint Bone Spine
JT  - Joint bone spine
JID - 100938016
RN  - 0 (Adrenal Cortex Hormones)
SB  - IM
MH  - Adrenal Cortex Hormones/administration & dosage/*adverse effects
MH  - Arthritis, Rheumatoid/*drug therapy/*epidemiology
MH  - Cardiovascular Diseases/*epidemiology
MH  - Dose-Response Relationship, Drug
MH  - Humans
MH  - Risk Factors
EDAT- 2010/05/18 06:00
MHDA- 2011/05/04 06:00
CRDT- 2010/05/18 06:00
PHST- 2009/09/21 00:00 [received]
PHST- 2010/02/03 00:00 [accepted]
PHST- 2010/05/18 06:00 [entrez]
PHST- 2010/05/18 06:00 [pubmed]
PHST- 2011/05/04 06:00 [medline]
AID - S1297-319X(10)00113-2 [pii]
AID - 10.1016/j.jbspin.2010.02.040 [doi]
PST - ppublish
SO  - Joint Bone Spine. 2011 Jan;78(1):23-30. doi: 10.1016/j.jbspin.2010.02.040. Epub 
      2010 May 14.

PMID- 20444756
OWN - NLM
STAT- MEDLINE
DCOM- 20101112
LR  - 20220408
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Print)
IS  - 0003-4967 (Linking)
VI  - 69
IP  - 11
DP  - 2010 Nov
TI  - Explaining the cardiovascular risk associated with rheumatoid arthritis: 
      traditional risk factors versus markers of rheumatoid arthritis severity.
PG  - 1920-5
LID - 10.1136/ard.2009.122226 [doi]
AB  - BACKGROUND: Cardiovascular (CV) disease has a major impact on patients with 
      rheumatoid arthritis (RA), however, the relative contributions of traditional CV 
      risk factors and markers of RA severity are unclear. The authors examined the 
      relative importance of traditional CV risk factors and RA markers in predicting 
      CV events. METHODS: A prospective longitudinal cohort study was conducted in the 
      setting of the CORRONA registry in the USA. Baseline data from subjects with RA 
      enrolled in the CORRONA registry were examined to determine predictors of CV 
      outcomes, including myocardial infarction, stroke or transient ischemic attack. 
      Possible predictors were of two types: traditional CV risk factors and markers of 
      RA severity. The discriminatory value of these variables was assessed by 
      calculating the area under the receiver operating characteristic curve 
      (c-statistic) in logistic regression. The authors then assessed the incidence 
      rate for CV events among subjects with an increasing number of traditional CV 
      risk factors and/or RA severity markers. RESULTS: The cohort consisted of 10 156 
      patients with RA followed for a median of 22 months. The authors observed 76 
      primary CV events during follow-up for a composite event rate of 3.98 (95% CI 
      3.08 to 4.88) per 1000 patient-years. The c-statistic improved from 0.57 for 
      models with only CV risk factors to 0.67 for models with CV risk factors plus age 
      and gender. The c-statistic improved further to 0.71 when markers of RA severity 
      were also added. The incidence rate for CV events was 0 (95% CI 0 to 5.98) for 
      persons without any CV risk factors or markers of RA severity, while in the group 
      with two or more CV risk factors and three or more markers of RA severity the 
      incidence was 7.47 (95% CI 4.21 to 10.73) per 1000 person-years. CONCLUSIONS: 
      Traditional CV risk factors and markers of RA severity both contribute to models 
      predicting CV events. Increasing numbers of both types of factors are associated 
      with greater risk.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - Brigham and Women's Hospital, Boston Massachusetts 02115, USA. 
      dhsolomon@partners.org
FAU - Kremer, Joel
AU  - Kremer J
FAU - Curtis, Jeffrey R
AU  - Curtis JR
FAU - Hochberg, Marc C
AU  - Hochberg MC
FAU - Reed, George
AU  - Reed G
FAU - Tsao, Peter
AU  - Tsao P
FAU - Farkouh, Michael E
AU  - Farkouh ME
FAU - Setoguchi, Soko
AU  - Setoguchi S
FAU - Greenberg, Jeffrey D
AU  - Greenberg JD
LA  - eng
GR  - K24 AR055989-04/AR/NIAMS NIH HHS/United States
GR  - P60 AR047782-06A10006/AR/NIAMS NIH HHS/United States
GR  - K24 AR055989-02/AR/NIAMS NIH HHS/United States
GR  - K23 AR053351-04/AR/NIAMS NIH HHS/United States
GR  - K23 AR054412-05/AR/NIAMS NIH HHS/United States
GR  - U01 HL071988-01A1/HL/NHLBI NIH HHS/United States
GR  - K23 AR053351/AR/NIAMS NIH HHS/United States
GR  - P60 AR047782-090006/AR/NIAMS NIH HHS/United States
GR  - P60 AR047782-080006/AR/NIAMS NIH HHS/United States
GR  - K24 AR055989-03/AR/NIAMS NIH HHS/United States
GR  - U01 HL071988/HL/NHLBI NIH HHS/United States
GR  - R01 HL092989-02/HL/NHLBI NIH HHS/United States
GR  - HL092989/HL/NHLBI NIH HHS/United States
GR  - AR 047782/AR/NIAMS NIH HHS/United States
GR  - K23 AR053351-03/AR/NIAMS NIH HHS/United States
GR  - K24 AR055989-01/AR/NIAMS NIH HHS/United States
GR  - P60 AR047782/AR/NIAMS NIH HHS/United States
GR  - R01 HL092989/HL/NHLBI NIH HHS/United States
GR  - K24 AR055989/AR/NIAMS NIH HHS/United States
GR  - HL071988/HL/NHLBI NIH HHS/United States
GR  - AR053351/AR/NIAMS NIH HHS/United States
GR  - AR055989/AR/NIAMS NIH HHS/United States
GR  - K23 AR053351-03S1/AR/NIAMS NIH HHS/United States
GR  - P60 AR047782-070006/AR/NIAMS NIH HHS/United States
GR  - K23 AR054412/AR/NIAMS NIH HHS/United States
GR  - K23 AR053351-01A1/AR/NIAMS NIH HHS/United States
GR  - K23 AR053351-02/AR/NIAMS NIH HHS/United States
GR  - K23AR054412/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20100505
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
MH  - Age Factors
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications/epidemiology
MH  - Cardiovascular Diseases/epidemiology/*etiology
MH  - Epidemiologic Methods
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Sex Factors
MH  - United States/epidemiology
PMC - PMC2963658
MID - NIHMS227235
EDAT- 2010/05/07 06:00
MHDA- 2010/11/13 06:00
PMCR- 2010/11/01
CRDT- 2010/05/07 06:00
PHST- 2010/05/07 06:00 [entrez]
PHST- 2010/05/07 06:00 [pubmed]
PHST- 2010/11/13 06:00 [medline]
PHST- 2010/11/01 00:00 [pmc-release]
AID - ard.2009.122226 [pii]
AID - 10.1136/ard.2009.122226 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2010 Nov;69(11):1920-5. doi: 10.1136/ard.2009.122226. Epub 2010 
      May 5.

PMID- 20131277
OWN - NLM
STAT- MEDLINE
DCOM- 20100504
LR  - 20211020
IS  - 1529-0131 (Electronic)
IS  - 0004-3591 (Print)
IS  - 0004-3591 (Linking)
VI  - 62
IP  - 4
DP  - 2010 Apr
TI  - Left ventricular structure and function in patients with rheumatoid arthritis, as 
      assessed by cardiac magnetic resonance imaging.
PG  - 940-51
LID - 10.1002/art.27349 [doi]
AB  - OBJECTIVE: Heart failure is a major contributor to cardiovascular morbidity and 
      mortality in patients with rheumatoid arthritis (RA), but little is known about 
      myocardial structure and function in this population. This study was undertaken 
      to assess the factors associated with progression to heart failure in patients 
      with RA. METHODS: With the use of cardiac magnetic resonance imaging, measures of 
      myocardial structure and function were assessed in men and women with RA enrolled 
      in the Evaluation of Subclinical Cardiovascular Disease and Predictors of Events 
      in Rheumatoid Arthritis study, a cohort study of subclinical cardiovascular 
      disease in patients with RA, in comparison with non-RA control subjects from a 
      cohort enrolled in the Baltimore Multi-Ethnic Study of Atherosclerosis. RESULTS: 
      Measures of myocardial structure and function were compared between 75 patients 
      with RA and 225 frequency-matched controls. After adjustment for confounders, the 
      mean left ventricular mass was found to be 26 gm lower in patients with RA 
      compared with controls (P < 0.001), an 18% difference. In addition, the mean left 
      ventricular ejection fraction, cardiac output, and stroke volume were modestly 
      lower in the RA group compared with controls. The mean left ventricular end 
      systolic and end diastolic volumes did not differ between the groups. In patients 
      with RA, higher levels of anti-cyclic citrullinated peptide (anti-CCP) antibodies 
      and current use of biologic agents, but not other measures of disease activity or 
      severity, were associated with significantly lower adjusted mean values for the 
      left ventricular mass, end diastolic volume, and stroke volume, but not with 
      ejection fraction. The combined associations of anti-CCP antibody level and 
      biologic agent use with myocardial measures were additive, without evidence of 
      interaction. CONCLUSION: These findings suggest that the progression to heart 
      failure in RA may occur through reduced myocardial mass rather than hypertrophy. 
      Both modifiable and nonmodifiable factors may contribute to lower levels of left 
      ventricular mass and volume.
FAU - Giles, Jon T
AU  - Giles JT
AD  - Johns Hopkins University, Baltimore, Maryland 21224, USA.
FAU - Malayeri, Ashkan A
AU  - Malayeri AA
FAU - Fernandes, Veronica
AU  - Fernandes V
FAU - Post, Wendy
AU  - Post W
FAU - Blumenthal, Roger S
AU  - Blumenthal RS
FAU - Bluemke, David
AU  - Bluemke D
FAU - Vogel-Claussen, Jens
AU  - Vogel-Claussen J
FAU - Szklo, Moyses
AU  - Szklo M
FAU - Petri, Michelle
AU  - Petri M
FAU - Gelber, Allan C
AU  - Gelber AC
FAU - Brumback, Lyndia
AU  - Brumback L
FAU - Lima, João
AU  - Lima J
FAU - Bathon, Joan M
AU  - Bathon JM
LA  - eng
GR  - ZIA CL090019-01/ImNIH/Intramural NIH HHS/United States
GR  - N01HC95169/HL/NHLBI NIH HHS/United States
GR  - N01-HC-95159/HC/NHLBI NIH HHS/United States
GR  - ZIA EB000072-01/ImNIH/Intramural NIH HHS/United States
GR  - N01-HC-95169/HC/NHLBI NIH HHS/United States
GR  - Z99 CL999999/ImNIH/Intramural NIH HHS/United States
GR  - R01 AR050026-04/AR/NIAMS NIH HHS/United States
GR  - AR-050026/AR/NIAMS NIH HHS/United States
GR  - R01 AR050026/AR/NIAMS NIH HHS/United States
GR  - N01HC95159/HL/NHLBI NIH HHS/United States
GR  - R55 AR050026/AR/NIAMS NIH HHS/United States
GR  - N01HC95166/HL/NHLBI NIH HHS/United States
GR  - N01-HC-95166/HC/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
RN  - 0 (Lipids)
SB  - IM
CIN - Arthritis Rheum. 2010 Dec;62(12):3833-4; author reply 3834-5. doi: 
      10.1002/art.27724. PMID: 21120999
MH  - Aged
MH  - Arthritis, Rheumatoid/complications/*physiopathology
MH  - Body Surface Area
MH  - Cardiovascular Diseases/epidemiology
MH  - Diabetes Complications/epidemiology
MH  - Female
MH  - Heart Failure/epidemiology/etiology
MH  - Heart Rate
MH  - Heart Ventricles/*anatomy & histology
MH  - Humans
MH  - Hypertension/epidemiology
MH  - Lipids/blood
MH  - Magnetic Resonance Imaging
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - Ventricular Function, Left/*physiology
PMC - PMC3008503
MID - NIHMS218994
EDAT- 2010/02/05 06:00
MHDA- 2010/05/05 06:00
PMCR- 2011/04/01
CRDT- 2010/02/05 06:00
PHST- 2010/02/05 06:00 [entrez]
PHST- 2010/02/05 06:00 [pubmed]
PHST- 2010/05/05 06:00 [medline]
PHST- 2011/04/01 00:00 [pmc-release]
AID - 10.1002/art.27349 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2010 Apr;62(4):940-51. doi: 10.1002/art.27349.

PMID- 20107818
OWN - NLM
STAT- MEDLINE
DCOM- 20100524
LR  - 20211020
IS  - 1435-1250 (Electronic)
IS  - 0340-1855 (Linking)
VI  - 69
IP  - 2
DP  - 2010 Mar
TI  - [Pathogenesis of parodontitis in rheumatic diseases].
PG  - 109-12, 114-6
LID - 10.1007/s00393-009-0560-1 [doi]
AB  - Inflammatory periodontal disease (PD) is a common disease worldwide that has a 
      primarily bacterial aetiology and is characterized by dysregulation of the host 
      inflammatory response. The degree of inflammation varies among individuals with 
      PD independently of the degree of bacterial infection, suggesting that alteration 
      of the immune function may substantially contribute to its extent. Factors such 
      as smoking, education, and body mass index (BMI) are discussed as potential risk 
      factors for PD. Most PD patients respond to bacterial invaders by mobilizing 
      their defensive cells and releasing cytokines such as interleukin (IL)-1beta, 
      tumour necrosis factor (TNF)-alpha, and IL-6, which ultimately causes tissue 
      destruction by stimulating the production of collagenolytic enzymes, such matrix 
      metalloproteinases. Recently, there has been growing evidence suggesting an 
      association between PD and the increased risk of systemic diseases, such 
      ateriosclerosis, diabetes mellitus, stroke, and rheumatoid arthritis (RA). PD and 
      rheumatologic diseases such as RA share many pathological aspects and 
      immunological findings.
FAU - Detert, J
AU  - Detert J
AD  - Klinik mit Schwerpunkt Rheumatologie und klinische Immunologie, 
      Charité-Universitätsmedizin Berlin, Berlin, Deutschland. 
      jacqueline.detert@charite.de
FAU - Pischon, N
AU  - Pischon N
FAU - Burmester, G-R
AU  - Burmester GR
FAU - Buttgereit, F
AU  - Buttgereit F
LA  - ger
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - Pathogenese der Parodontitis bei rheumatischen Erkrankungen.
PL  - Germany
TA  - Z Rheumatol
JT  - Zeitschrift fur Rheumatologie
JID - 0414162
SB  - IM
MH  - Arthritis, Rheumatoid/*diagnosis
MH  - Dental Plaque Index
MH  - Humans
MH  - Periodontitis/*diagnosis
MH  - Rheumatic Diseases/*diagnosis
MH  - Risk Factors
MH  - Sjogren's Syndrome/diagnosis
RF  - 169
EDAT- 2010/01/29 06:00
MHDA- 2010/05/25 06:00
CRDT- 2010/01/29 06:00
PHST- 2010/01/29 06:00 [entrez]
PHST- 2010/01/29 06:00 [pubmed]
PHST- 2010/05/25 06:00 [medline]
AID - 10.1007/s00393-009-0560-1 [doi]
PST - ppublish
SO  - Z Rheumatol. 2010 Mar;69(2):109-12, 114-6. doi: 10.1007/s00393-009-0560-1.

PMID- 19822058
OWN - NLM
STAT- MEDLINE
DCOM- 20100223
LR  - 20171116
IS  - 0392-856X (Print)
IS  - 0392-856X (Linking)
VI  - 27
IP  - 4 Suppl 55
DP  - 2009 Jul-Aug
TI  - Comparison of cardiovascular risk in ankylosing spondylitis and rheumatoid 
      arthritis.
PG  - S124-6
AB  - Cardiovascular co-morbidity is now a recognised complication of chronic 
      inflammation and an elevated acute phase response predisposes to hypertension, 
      stroke and myocardial infarction. Dyslipidaemia is a feature of inflammatory 
      joint diseases and is closely related to elevated CRP and Il-6 levels. Rheumatoid 
      arthritis (RA) has an increased standardised mortality ratio largely attributable 
      to cardiovascular risk. An increased although lesser, cardiovascular morbidity 
      has also been observed in ankylosing spondylitis (AS) which has a similar 
      abnormal lipid profile to that seen in RA. There is some evidence that 
      therapeutic agents such as anti-tumour necrosis factor-alpha (TNF-alpha) drugs 
      that down-regulate the acute phase response, also have an effect in reducing 
      cardiovascular complications in RA and AS.
FAU - McCarey, D
AU  - McCarey D
AD  - Centre for Rheumatic Diseases, University of Glasgow, Glasgow, United Kingdom.
FAU - Sturrock, R D
AU  - Sturrock RD
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Clin Exp Rheumatol
JT  - Clinical and experimental rheumatology
JID - 8308521
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Cytokines)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Antibodies, Monoclonal/therapeutic use
MH  - Antirheumatic Agents/therapeutic use
MH  - Arthritis, Rheumatoid/drug therapy/*epidemiology/metabolism
MH  - Cardiovascular Diseases/drug therapy/*epidemiology/metabolism
MH  - Comorbidity
MH  - Cytokines/metabolism
MH  - Dyslipidemias/drug therapy/*epidemiology/metabolism
MH  - Humans
MH  - Metabolic Syndrome/drug therapy/epidemiology/metabolism
MH  - Risk Factors
MH  - Spondylitis, Ankylosing/drug therapy/*epidemiology/metabolism
MH  - Synovitis/metabolism
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
EDAT- 2010/01/27 06:00
MHDA- 2010/02/24 06:00
CRDT- 2009/10/14 06:00
PHST- 2009/10/14 06:00 [entrez]
PHST- 2010/01/27 06:00 [pubmed]
PHST- 2010/02/24 06:00 [medline]
AID - 2775 [pii]
PST - ppublish
SO  - Clin Exp Rheumatol. 2009 Jul-Aug;27(4 Suppl 55):S124-6.

PMID- 20096157
OWN - NLM
STAT- MEDLINE
DCOM- 20100603
LR  - 20191111
IS  - 0001-7310 (Print)
IS  - 0001-7310 (Linking)
VI  - 100 Suppl 2
DP  - 2009 Dec
TI  - Cardiometabolic comorbidities and the approach to patients with psoriasis.
PG  - 14-21
AB  - Psoriasis is a chronic inflammatory, immune-mediated skin disease, which may 
      cause significant deterioration in the quality of life. Recent evidence indicates 
      that psoriasis and psoriatic arthritis are frequently associated with 
      cardiometabolic diseases including myocardial infarction, stroke, diabetes, 
      obesity, dyslipidemia and non-alcoholic fatty liver disease. Although the causal 
      relationship between cardiometabolic comorbidities and psoriasis has not yet been 
      completely proven, it appears that obesity is a relevant risk factor for the 
      development of psoriasis and metabolic syndrome. In addition, moderate to severe 
      psoriasis itself is a risk factor for cardiovascular disease and the metabolic 
      syndrome. Some common genetic traits as well as inflammatory mechanisms may 
      underlie the development of psoriasis and cardiometabolic comorbidities. The 
      presence of comorbidities has important implications in the global approach to 
      patients with psoriasis. Traditional systemic anti-psoriatic agents could 
      negatively affect cardiometabolic comorbidities, and may have important 
      interactions with drugs commonly used by psoriasis patients. In contrast, the 
      recent findings that the risk of myocardial infarction is markedly reduced in 
      rheumatoid arthritis patients who respond to anti-TNF-alpha therapy compared with 
      non-responders supports the hypothesis that the anti-inflammatory effect of 
      TNF-alpha blockers might potentially reduce the cardiovascular risk also in 
      psoriasis patients. Finally, patients with moderate to severe psoriasis should be 
      treated promptly and effectively, should also be encouraged to drastically 
      correct their modifiable cardiovascular risk factors, in particular obesity and 
      smoking habit.
FAU - Gisondi, P
AU  - Gisondi P
AD  - Department of Biomedical and Surgical Science, Section of Dermatology and 
      Venereology, University of Verona. Italy, paolo.gisondi@univr.it
FAU - Girolomoni, G
AU  - Girolomoni G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Spain
TA  - Actas Dermosifiliogr
JT  - Actas dermo-sifiliograficas
JID - 0373062
SB  - IM
MH  - Cardiovascular Diseases/*complications/*metabolism
MH  - Fatty Liver/complications
MH  - Humans
MH  - Metabolic Diseases/*complications
MH  - Psoriasis/*complications/*metabolism
EDAT- 2010/01/26 06:00
MHDA- 2010/06/04 06:00
CRDT- 2010/01/26 06:00
PHST- 2010/01/26 06:00 [entrez]
PHST- 2010/01/26 06:00 [pubmed]
PHST- 2010/06/04 06:00 [medline]
AID - 13146412 [pii]
AID - 10.1016/s0001-7310(09)73373-3 [doi]
PST - ppublish
SO  - Actas Dermosifiliogr. 2009 Dec;100 Suppl 2:14-21. doi: 
      10.1016/s0001-7310(09)73373-3.

PMID- 20091657
OWN - NLM
STAT- MEDLINE
DCOM- 20100416
LR  - 20220409
IS  - 1469-493X (Electronic)
IS  - 1361-6137 (Linking)
IP  - 1
DP  - 2010 Jan 20
TI  - Effect of cyclosporine on blood pressure.
PG  - CD007893
LID - 10.1002/14651858.CD007893.pub2 [doi]
AB  - BACKGROUND: Cyclosporine is an immunosuppressive agent used for different 
      autoimmune diseases. The official Canadian indications for cyclosporine are solid 
      organ transplantation, bone marrow transplantation, psoriasis, rheumatoid 
      arthritis and nephritic syndrome (e-CPS 2008). The expanding range of indications 
      for cyclosporine therapy will lead to more patients receiving chronic therapy 
      with possible side effects, hypertension being one of the most common. Therefore 
      it is essential to know the magnitude of increase of blood pressure (BP) 
      associated with cyclosporine in order to appropriately manage patients receiving 
      the drug. OBJECTIVES: The primary objective of this systematic review is to 
      evaluate the effect of cyclosporine on blood pressure, compared to placebo in 
      randomized trials. SEARCH STRATEGY: We searched The Cochrane Central Register of 
      Controlled Trials (CENTRAL) and bibliographic databases, including MEDLINE 
      (2000-2008) and EMBASE (1980-2008). SELECTION CRITERIA: Selection was made using 
      double-blind, randomized, controlled trials comparing cyclosporine to placebo. 
      All patients treated with cyclosporine were included without restriction by type 
      of disease or by age and sex. DATA COLLECTION AND ANALYSIS: Blood pressure 
      measurements in any setting and by any means were acceptable including the 
      auscultatory or oscillometric method with a preference for the sitting position. 
      Mean blood pressure results were entered as mean change from placebo and standard 
      error of the mean (SEM). If blood pressure data was provided at different times 
      after the initiation of cyclosporine therapy the weighted mean BP change from 
      placebo from all measurements was used. MAIN RESULTS: The search yielded 1340 
      citations, of which 17 trials met the inclusion criteria. We created dose-ranges 
      according to the usual dose administration recommended by the manufacturer and 
      allocated the 17 included trials to the corresponding dose-range. The results 
      demonstrate a highly statistically significant increase in blood pressure 
      associated with cyclosporine. There appears to be a dose-related effect with 
      lower doses (1-4 mg/kg/d) increasing mean BP by an average of 5 mmHg and higher 
      doses (>10 mg/kg/d) increasing mean BP by 11 mmHg on average. Furthermore in 3 
      trials the effect appears to be similar after a single dose as with chronic 
      therapy. AUTHORS' CONCLUSIONS: Cyclosporine statistically significantly increases 
      blood pressure compared to placebo in a dose-related fashion. The magnitude of 
      increase in blood pressure is clinically significant and increases the risk of 
      stroke, myocardial infarction, heart failure and other adverse cardiovascular 
      events associated with elevated BP. Consequently prescribers should try to find 
      the lowest effective dose in all patients receiving cyclosporine chronically.
FAU - Robert, Nadège
AU  - Robert N
AD  - Institut of Social and Preventive Medicine, University of Bern, Finkenhubelweg 
      11, Bern, Bern, Switzerland, CH-3012.
FAU - Wong, Gavin Wk
AU  - Wong GW
FAU - Wright, James M
AU  - Wright JM
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Review
PT  - Systematic Review
DEP - 20100120
PL  - England
TA  - Cochrane Database Syst Rev
JT  - The Cochrane database of systematic reviews
JID - 100909747
RN  - 0 (Immunosuppressive Agents)
RN  - 83HN0GTJ6D (Cyclosporine)
SB  - IM
MH  - Blood Pressure/*drug effects
MH  - Cyclosporine/administration & dosage/*adverse effects
MH  - Dose-Response Relationship, Drug
MH  - Humans
MH  - Hypertension/*chemically induced
MH  - Immunosuppressive Agents/administration & dosage/*adverse effects
MH  - Randomized Controlled Trials as Topic
RF  - 76
EDAT- 2010/01/22 06:00
MHDA- 2010/04/17 06:00
CRDT- 2010/01/22 06:00
PHST- 2010/01/22 06:00 [entrez]
PHST- 2010/01/22 06:00 [pubmed]
PHST- 2010/04/17 06:00 [medline]
AID - 10.1002/14651858.CD007893.pub2 [doi]
PST - epublish
SO  - Cochrane Database Syst Rev. 2010 Jan 20;(1):CD007893. doi: 
      10.1002/14651858.CD007893.pub2.

PMID- 19843413
OWN - NLM
STAT- MEDLINE
DCOM- 20100226
LR  - 20220311
IS  - 1478-5242 (Electronic)
IS  - 0960-1643 (Print)
IS  - 0960-1643 (Linking)
VI  - 59
IP  - 567
DP  - 2009 Oct
TI  - Identification of new risk factors for pneumonia: population-based case-control 
      study.
PG  - e329-38
LID - 10.3399/bjgp09X472629 [doi]
AB  - BACKGROUND: Certain conditions are established as risk factors for 
      community-acquired pneumonia. There are a number of other conditions that may 
      also be risk factors, but information on these is limited. AIM: To determine new 
      independent risk factors for community-acquired pneumonia using a very large 
      primary care database. DESIGN OF STUDY: Nested case-control study. SETTING: Four 
      hundred and forty-three general practices in the UK contributing to the QRESEARCH 
      database. METHOD: A total of 17 172 incident cases of all ages diagnosed with 
      pneumonia between 1996 and 2005 were matched with up to five controls by age, 
      sex, general practice, and calendar year. Associations between pneumonia and each 
      established condition and potential risk factors were determined with odds ratios 
      (ORs), using multiple conditional logistic regression analysis adjusted for 
      smoking, socioeconomic status, and use of influenza and pneumococcal vaccines. 
      RESULTS: The analysis confirmed the higher risk of pneumonia among patients with 
      at least one of the established risk factors; the adjusted OR was 2.29 (95% 
      confidence interval [CI]=2.20 to 2.39). In addition, patients with the following 
      conditions had a higher risk of pneumonia despite adjustment for known risk 
      factors and confounders: stroke or transient ischaemic attack, rheumatoid 
      arthritis, Parkinson's disease, cancers, multiple sclerosis, dementia, and 
      osteoporosis. The adjusted OR for pneumonia among patients without an established 
      risk factor but with at least one of the new conditions was 2.44 (95% CI=2.24 to 
      2.65). CONCLUSION: As well as confirming some established risk factors, this 
      study has determined seven new independent risk factors for community-acquired 
      pneumonia.
FAU - Vinogradova, Yana
AU  - Vinogradova Y
AD  - Division of Primary Care, University of Nottingham, Nottingham. 
      yana.vinogradova@nottingham.ac.uk
FAU - Hippisley-Cox, Julia
AU  - Hippisley-Cox J
FAU - Coupland, Carol
AU  - Coupland C
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br J Gen Pract
JT  - The British journal of general practice : the journal of the Royal College of 
      General Practitioners
JID - 9005323
RN  - 0 (Pneumococcal Vaccines)
SB  - IM
CIN - Br J Gen Pract. 2009 Oct;59(567):716-7. doi: 10.3399/bjgp09X472557. PMID: 
      19843417
MH  - Adolescent
MH  - Adult
MH  - Child
MH  - Child, Preschool
MH  - Community-Acquired Infections/*epidemiology/prevention & control
MH  - Epidemiologic Methods
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Pneumococcal Vaccines
MH  - Pneumonia/*epidemiology/prevention & control
MH  - Young Adult
PMC - PMC2751937
EDAT- 2009/10/22 06:00
MHDA- 2010/02/27 06:00
PMCR- 2010/10/01
CRDT- 2009/10/22 06:00
PHST- 2009/10/22 06:00 [entrez]
PHST- 2009/10/22 06:00 [pubmed]
PHST- 2010/02/27 06:00 [medline]
PHST- 2010/10/01 00:00 [pmc-release]
AID - 10.3399/bjgp09X472629 [doi]
PST - ppublish
SO  - Br J Gen Pract. 2009 Oct;59(567):e329-38. doi: 10.3399/bjgp09X472629.

PMID- 19797557
OWN - NLM
STAT- MEDLINE
DCOM- 20091215
LR  - 20211203
IS  - 1943-4723 (Electronic)
IS  - 0002-8177 (Linking)
VI  - 140
IP  - 10
DP  - 2009 Oct
TI  - Oral health needs among adults in the United States with chronic diseases.
PG  - 1266-74
AB  - BACKGROUND: Oral and dental diseases may be associated with other chronic 
      diseases. METHODS: Using data from the National Health and Nutrition Examination 
      Survey 1999-2004, the authors calculated the prevalence of untreated dental 
      diseases, self-reported poor oral health and the number of missing teeth for 
      adults in the United States who had certain chronic diseases. The authors used 
      multivariate analysis to determine whether these diseases were associated with 
      indicators of dental disease after controlling for common risk factors. RESULTS: 
      Participants with rheumatoid arthritis, diabetes or a liver condition were twice 
      as likely to have an urgent need for dental treatment as were participants who 
      did not have these diseases. After controlling for common risk factors, the 
      authors found that arthritis, cardiovascular disease, diabetes, emphysema, 
      hepatitis C virus, obesity and stroke still were associated with dental disease. 
      CONCLUSIONS: The authors found a high burden of unmet dental care needs among 
      participants with chronic diseases. This association held in the multivariate 
      analysis, suggesting that some chronic diseases may increase the risk of 
      developing dental disease, decrease utilization of dental care or both. CLINICAL 
      IMPLICATIONS: Dental and medical care providers should work together to ensure 
      that adults with chronic diseases receive regular dental care.
FAU - Griffin, Susan O
AU  - Griffin SO
AD  - Surveillance, Investigations, and Research Branch, Division of Oral Health, 
      Centers for Disease Control and Prevention, Chamblee, GA 30341, USA. sig1@cdc.gov
FAU - Barker, Laurie K
AU  - Barker LK
FAU - Griffin, Paul M
AU  - Griffin PM
FAU - Cleveland, Jennifer L
AU  - Cleveland JL
FAU - Kohn, William
AU  - Kohn W
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Am Dent Assoc
JT  - Journal of the American Dental Association (1939)
JID - 7503060
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis/complications
MH  - Cardiovascular Diseases/complications
MH  - DMF Index
MH  - Dental Care for Chronically Ill/*statistics & numerical data
MH  - Dental Caries/*complications/epidemiology
MH  - Diabetes Complications/epidemiology
MH  - Emphysema/complications
MH  - Ethnicity/statistics & numerical data
MH  - Female
MH  - Health Services Needs and Demand/*statistics & numerical data
MH  - Hepatitis C/complications
MH  - Humans
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Obesity/complications
MH  - Periodontal Diseases/*complications/epidemiology
MH  - Poverty/statistics & numerical data
MH  - Referral and Consultation/statistics & numerical data
MH  - Smoking/epidemiology
MH  - Stroke/complications
MH  - Tooth Loss/complications/epidemiology
MH  - United States/epidemiology
MH  - Young Adult
EDAT- 2009/10/03 06:00
MHDA- 2009/12/16 06:00
CRDT- 2009/10/03 06:00
PHST- 2009/10/03 06:00 [entrez]
PHST- 2009/10/03 06:00 [pubmed]
PHST- 2009/12/16 06:00 [medline]
AID - 140/10/1266 [pii]
AID - 10.14219/jada.archive.2009.0050 [doi]
PST - ppublish
SO  - J Am Dent Assoc. 2009 Oct;140(10):1266-74. doi: 10.14219/jada.archive.2009.0050.

PMID- 19743942
OWN - NLM
STAT- MEDLINE
DCOM- 20100420
LR  - 20151119
IS  - 1369-6998 (Print)
IS  - 1369-6998 (Linking)
VI  - 12
IP  - 3
DP  - 2009 Sep
TI  - Cost-utility of celecoxib use in different treatment strategies for 
      osteoarthritis and rheumatoid arthritis from the Quebec healthcare system 
      perspective.
PG  - 246-58
LID - 10.3111/13696990903288970 [doi]
AB  - OBJECTIVE: To assess the cost-utility of celecoxib in three treatment strategies 
      for arthritis in Quebec, considering both upper gastrointestinal (GI) and 
      cardiovascular (CV) events. METHODS: A Markov analytic framework was used to 
      model patients with osteoarthritis and rheumatoid arthritis at low/average and 
      high risk of GI and CV toxicity over 5 years with monthly cycles. Treatment 
      strategies were modelled in line with Canadian clinical practice. In first-line 
      treatment, patients started on celecoxib; second-line, patients started on a 
      non-selective non-steroidal anti-inflammatory drug (NSAID) and switched to 
      celecoxib after a first GI event; third-line, patients started on a non-selective 
      NSAID, added a proton pump inhibitor (PPI) after a first GI event, and switched 
      to celecoxib after a second GI event (while maintaining the PPI). Model inputs 
      were determined through comprehensive literature searches (MEDLINE and EMBASE) 
      from 1995 to 2006. Included studies evaluated GI (dyspepsia, uncomplicated and 
      complicated ulcers, death) and CV (myocardial infarction, stroke, death) events. 
      Drug and procedure costs were derived from Canadian published sources (Can$2005). 
      RESULTS: Total costs per patient for celecoxib first-, second-, and third-line 
      treatment were Can$4,790, $3,390, and $3,466, and total quality-adjusted 
      life-years (QALY) were 3.251, 3.231, and 3.230, respectively. In all risk 
      categories, celecoxib second-line was less costly and as effective as celecoxib 
      third-line, producing savings to the healthcare system. Although celecoxib 
      first-line generated incremental expenditures versus celecoxib second-line, it 
      was also more effective. The resulting cost-utility ratio for the high-risk 
      population was Can$54,696/QALY. Based on this analytical approach, a treatment 
      strategy where celecoxib is used before the combination of a non-selective NSAID 
      plus a PPI possesses cost advantages for the Quebec provincial drug programme. 
      One-way sensitivity analysis (varying GI and CV event rates, utilities, and cost) 
      generally showed second-line treatment with celecoxib as the dominant strategy 
      compared with third-line treatment with celecoxib. CONCLUSION: Although 
      effectiveness of second- and third-line celecoxib use is similar, total cost is 
      lower for second-line. These results suggest that the use of celecoxib before the 
      combination of a non-selective NSAID plus a PPI is relatively cost-effective in 
      the treatment of arthritis pain and support the full benefit listing of celecoxib 
      in Quebec's drug programme.
FAU - Bessette, Louis
AU  - Bessette L
AD  - Laval University Hospital Centre, Sainte-Foy, Quebec, Canada.
FAU - Risebrough, Nancy
AU  - Risebrough N
FAU - Mittmann, Nicole
AU  - Mittmann N
FAU - Roussy, Jean-Pascal
AU  - Roussy JP
FAU - Ho, Joanne
AU  - Ho J
FAU - Zlateva, Gergana
AU  - Zlateva G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Med Econ
JT  - Journal of medical economics
JID - 9892255
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
RN  - 0 (Pyrazoles)
RN  - 0 (Sulfonamides)
RN  - JCX84Q7J1L (Celecoxib)
SB  - IM
MH  - Aged
MH  - Anti-Inflammatory Agents, Non-Steroidal/adverse effects/economics/therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy/*economics
MH  - Cardiovascular Diseases/chemically induced
MH  - Celecoxib
MH  - Cost-Benefit Analysis
MH  - Cyclooxygenase 2 Inhibitors/adverse effects/economics/therapeutic use
MH  - Gastrointestinal Tract/drug effects
MH  - Humans
MH  - Insurance, Pharmaceutical Services/economics
MH  - Markov Chains
MH  - Middle Aged
MH  - Osteoarthritis/*drug therapy/*economics
MH  - Pyrazoles/adverse effects/*economics/*therapeutic use
MH  - Quality-Adjusted Life Years
MH  - Quebec
MH  - Sulfonamides/adverse effects/*economics/*therapeutic use
EDAT- 2009/09/12 06:00
MHDA- 2010/04/21 06:00
CRDT- 2009/09/12 06:00
PHST- 2009/09/12 06:00 [entrez]
PHST- 2009/09/12 06:00 [pubmed]
PHST- 2010/04/21 06:00 [medline]
AID - 10.3111/13696990903288970 [doi]
PST - ppublish
SO  - J Med Econ. 2009 Sep;12(3):246-58. doi: 10.3111/13696990903288970.

PMID- 19630828
OWN - NLM
STAT- MEDLINE
DCOM- 20091201
LR  - 20230829
IS  - 1538-7836 (Electronic)
IS  - 1538-7836 (Linking)
VI  - 7 Suppl 1
DP  - 2009 Jul
TI  - Testing the inflammatory hypothesis of atherothrombosis: scientific rationale for 
      the cardiovascular inflammation reduction trial (CIRT).
PG  - 332-9
LID - 10.1111/j.1538-7836.2009.03404.x [doi]
AB  - While inflammation is a crucial component of atherothrombosis and patients with 
      elevated inflammatory biomarkers such as high sensitivity C-reactive protein 
      (hsCRP) are at increased vascular risk, it remains unknown whether inhibition of 
      inflammation per se will lower vascular event rates. The recently completed 
      JUPITER (N Engl J Med 2008, 359, 2195) trial demonstrates that statins reduce 
      myocardial infarction, stroke, and all-cause mortality among healthy individuals 
      with low cholesterol and elevated hsCRP. However, a direct test of the 
      inflammatory hypothesis of atherothrombosis requires an agent that inhibits 
      inflammation without impacting other components of the atherothrombotic process, 
      and has an acceptable safety profile for a trial setting. On this basis, the 
      cardiovascular inflammation reduction trial (CIRT) proposes to allocate 7000 
      stable coronary artery disease patients with persistent elevations of hsCRP to 
      placebo or very-low-dose-methotrexate (VLDM, 10 mg weekly), a proven 
      anti-inflammatory regimen that reduces TNFalpha, IL-6, and CRP levels and is in 
      wide use among rheumatoid arthritis patients. If successful, CIRT would both 
      confirm the inflammatory hypothesis of atherothrombosis and open novel approaches 
      to the treatment and prevention of cardiovascular disorders.
FAU - Ridker, Paul M
AU  - Ridker PM
AD  - Center for Cardiovascular Disease Prevention, Brigham and Women's Hospital, 
      Harvard Medical School, Boston, MA 02215, USA. pridker@partners.org
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - J Thromb Haemost
JT  - Journal of thrombosis and haemostasis : JTH
JID - 101170508
SB  - IM
MH  - Atherosclerosis/pathology/*prevention & control
MH  - Cardiovascular Diseases/pathology/prevention & control
MH  - Clinical Trials as Topic
MH  - Humans
MH  - Inflammation/*complications/drug therapy
RF  - 44
EDAT- 2009/07/28 09:00
MHDA- 2009/12/16 06:00
CRDT- 2009/07/28 09:00
PHST- 2009/07/28 09:00 [entrez]
PHST- 2009/07/28 09:00 [pubmed]
PHST- 2009/12/16 06:00 [medline]
AID - S1538-7836(22)17423-4 [pii]
AID - 10.1111/j.1538-7836.2009.03404.x [doi]
PST - ppublish
SO  - J Thromb Haemost. 2009 Jul;7 Suppl 1:332-9. doi: 
      10.1111/j.1538-7836.2009.03404.x.

PMID- 19537595
OWN - NLM
STAT- MEDLINE
DCOM- 20090914
LR  - 20090622
IS  - 0040-3660 (Print)
IS  - 0040-3660 (Linking)
VI  - 81
IP  - 5
DP  - 2009
TI  - [Prevention of cardiovascular diseases in rheumatoid arthritis].
PG  - 88-96
AB  - One of the key causes of lethality in rheumatoid arthritis (RA) are 
      cardiovascular catastrophes (myocardial infarction, stroke, sudden cardiac death) 
      resultant from early development and rapid progression of atherosclerotic 
      vascular lesion. The article presents current approaches to prevention of 
      cardiovascular diseases in RA including assessment of overall cardiovascular risk 
      for design of optimal strategy of correction of modification factors increasing 
      probability of cardiovascular complications, strong control over inflammation and 
      adequate use of drugs which may be harmful (glucocorticosteroids, nonsteroid 
      anti-inflammatory drugs). Much attention is paid to perspectives of ACE 
      inhibitors, angiotensin II receptor blockers, statins, TNFalpha inhibitors in 
      prevention of cardiovascular complication in RA
FAU - Novikova, D S
AU  - Novikova DS
FAU - Popkova, T V
AU  - Popkova TV
FAU - Nasonov, E L
AU  - Nasonov EL
LA  - rus
PT  - English Abstract
PT  - Journal Article
PT  - Review
PL  - Russia (Federation)
TA  - Ter Arkh
JT  - Terapevticheskii arkhiv
JID - 2984818R
RN  - 0 (Anti-Inflammatory Agents)
SB  - IM
MH  - Anti-Inflammatory Agents/administration & dosage/adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/blood/*complications/drug therapy
MH  - Cardiovascular Diseases/blood/drug therapy/etiology/*prevention & control
MH  - Diet
MH  - Humans
MH  - Motor Activity
MH  - Treatment Outcome
RF  - 91
EDAT- 2009/06/23 09:00
MHDA- 2009/09/15 06:00
CRDT- 2009/06/23 09:00
PHST- 2009/06/23 09:00 [entrez]
PHST- 2009/06/23 09:00 [pubmed]
PHST- 2009/09/15 06:00 [medline]
PST - ppublish
SO  - Ter Arkh. 2009;81(5):88-96.

PMID- 19349084
OWN - NLM
STAT- MEDLINE
DCOM- 20100426
LR  - 20100201
IS  - 1872-6976 (Electronic)
IS  - 0167-4943 (Linking)
VI  - 50
IP  - 2
DP  - 2010 Mar-Apr
TI  - Prevalence and factors associated with urinary tract infections (UTIs) in very 
      old women.
PG  - 132-5
LID - 10.1016/j.archger.2009.02.013 [doi]
AB  - The aim of this study was to describe the prevalence of urinary tract infection 
      (UTI) and associated factors among very old women. In a cross-sectional, 
      population-based study in Sweden and Finland, 532 women were asked to participate 
      and 395 (74.2%) were possible to evaluate for UTI. Data were collected from 
      structured interviews and assessments made during home visits, from medical 
      charts, caregivers and relatives. UTI diagnosis documented in medical records 
      during the preceding 1 and 5 years was registered. About one-third (117/395, 
      29.6%) were diagnosed as having suffered from at least one UTI in the preceding 
      year and 60% in the preceding 5 years. In a multivariate logistic regression 
      model, UTI in the preceding year, was associated with vertebral fractures (odds 
      ratio (OR) = 3.2; 95% confidence interval (95% CI) = 1.4-7.1), incontinence (OR = 
      2.8; 95% CI = 1.8-4.5), inflammatory rheumatic disease (OR = 2.8; 95% CI = 
      1.4-5.7) and multi-infarct dementia (OR = 2.4; 95% CI = 1.3-4.5). UTI is a major 
      public health problem in very old women and were independently associated with 
      vertebral fractures, urinary incontinence, inflammatory rheumatic disease and 
      multi-infarct dementia which might indicate that UTI is not a harmless disease.
CI  - Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
FAU - Eriksson, Irene
AU  - Eriksson I
AD  - Department of Community Medicine and Rehabilitation, Geriatric Medicine, Umea 
      University, SE-901 85 Umea, Sweden. irene.eriksson@his.se
FAU - Gustafson, Yngve
AU  - Gustafson Y
FAU - Fagerström, Lisbeth
AU  - Fagerström L
FAU - Olofsson, Birgitta
AU  - Olofsson B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090405
PL  - Netherlands
TA  - Arch Gerontol Geriatr
JT  - Archives of gerontology and geriatrics
JID - 8214379
SB  - IM
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/epidemiology
MH  - Cross-Sectional Studies
MH  - Dementia, Multi-Infarct/epidemiology
MH  - Factor Analysis, Statistical
MH  - Female
MH  - Fractures, Bone/epidemiology
MH  - Humans
MH  - Predictive Value of Tests
MH  - Prevalence
MH  - Prospective Studies
MH  - Risk Factors
MH  - Urinary Incontinence/epidemiology
MH  - Urinary Tract Infections/diagnosis/*epidemiology
EDAT- 2009/04/08 09:00
MHDA- 2010/04/27 06:00
CRDT- 2009/04/08 09:00
PHST- 2008/09/02 00:00 [received]
PHST- 2009/02/23 00:00 [revised]
PHST- 2009/02/25 00:00 [accepted]
PHST- 2009/04/08 09:00 [entrez]
PHST- 2009/04/08 09:00 [pubmed]
PHST- 2010/04/27 06:00 [medline]
AID - S0167-4943(09)00052-1 [pii]
AID - 10.1016/j.archger.2009.02.013 [doi]
PST - ppublish
SO  - Arch Gerontol Geriatr. 2010 Mar-Apr;50(2):132-5. doi: 
      10.1016/j.archger.2009.02.013. Epub 2009 Apr 5.

PMID- 19348180
OWN - NLM
STAT- MEDLINE
DCOM- 20090519
LR  - 20190917
IS  - 0009-918X (Print)
IS  - 0009-918X (Linking)
VI  - 49
IP  - 2-3
DP  - 2009 Feb-Mar
TI  - [A young patient with ischemic stroke due to carotid artery dissection in whom 
      number of microembolic signals was followed-up].
PG  - 127-9
AB  - A 23-year-old Japanese man with rheumatoid arthritis experienced attacks of the 
      right hand weakness during the latest month. Megaloblastic anemia was diagnosed 
      and he was admitted in the department of hematology. Seven days after admission, 
      he developed mild consciousness disturbance and hemiparesis on the right side. 
      Brain MRI revealed the cortical watershed infarction in the left cerebral 
      hemisphere. The cause of the infarction was diagnosed spontaneous dissection of 
      the left internal carotid artery. We detected 11 microembolic signals (MES) 
      during 30 minutes' monitoring in the left middle cerebral artery using 
      transcranial Doppler. MES decreased gradually with anticoagulant therapy. 
      However, surgical therapy was performed to prevent progression of dissection or 
      arterial rupture. MES detected on transcranial Doppler would be important to 
      assess the risk of embolism and to discuss therapeutic strategy.
FAU - Sasaki, Mika
AU  - Sasaki M
AD  - Department of Neurology, Graduate School of Medical Sciences, Kumamoto 
      University.
FAU - Nakajima, Makoto
AU  - Nakajima M
FAU - Hirano, Teruyuki
AU  - Hirano T
FAU - Yokoo, Eri
AU  - Yokoo E
FAU - Watanabe, Masaki
AU  - Watanabe M
FAU - Uchino, Makoto
AU  - Uchino M
LA  - jpn
PT  - Case Reports
PT  - Journal Article
PL  - Japan
TA  - Rinsho Shinkeigaku
JT  - Rinsho shinkeigaku = Clinical neurology
JID - 0417466
SB  - IM
MH  - Carotid Artery, Internal, Dissection/*complications
MH  - Humans
MH  - Intracranial Embolism/*diagnostic imaging
MH  - Male
MH  - Stroke/*etiology
MH  - Ultrasonography, Doppler, Transcranial
MH  - Young Adult
EDAT- 2009/04/08 09:00
MHDA- 2009/05/20 09:00
CRDT- 2009/04/08 09:00
PHST- 2009/04/08 09:00 [entrez]
PHST- 2009/04/08 09:00 [pubmed]
PHST- 2009/05/20 09:00 [medline]
AID - 10.5692/clinicalneurol.49.127 [doi]
PST - ppublish
SO  - Rinsho Shinkeigaku. 2009 Feb-Mar;49(2-3):127-9. doi: 
      10.5692/clinicalneurol.49.127.

PMID- 19332185
OWN - NLM
STAT- MEDLINE
DCOM- 20090421
LR  - 20220317
IS  - 1097-6744 (Electronic)
IS  - 0002-8703 (Linking)
VI  - 157
IP  - 4
DP  - 2009 Apr
TI  - Rationale, design, and governance of Prospective Randomized Evaluation of 
      Celecoxib Integrated Safety versus Ibuprofen Or Naproxen (PRECISION), a 
      cardiovascular end point trial of nonsteroidal antiinflammatory agents in 
      patients with arthritis.
PG  - 606-12
LID - 10.1016/j.ahj.2008.12.014 [doi]
AB  - BACKGROUND: Pain management in patients with osteoarthritis or rheumatoid 
      arthritis often requires long-term use of nonsteroidal antiinflammatory drugs 
      (NSAIDs). However, the relative cardiovascular safety of these therapies remains 
      uncertain. METHODS: The Prospective Randomized Evaluation of Celecoxib Integrated 
      Safety versus Ibuprofen Or Naproxen (PRECISION) trial will evaluate the 
      cardiovascular safety of celecoxib, ibuprofen, and naproxen. Approximately 20,000 
      patients with symptomatic osteoarthritis or rheumatoid arthritis at high risk 
      for, or with, established cardiovascular disease will be randomized in this 
      double-blind, triple dummy, multinational, multicenter study. The primary end 
      point is the composite of cardiovascular death, nonfatal myocardial infarction, 
      or nonfatal stroke. The trial will continue until 762 primary events occur with 
      at least 18 months follow-up. Noninferiority of any of the regimens will require 
      a 97.5% upper CI of the hazard ratio (HR) < or =1.33 and point estimate < or 
      =1.12 for both intent-to-treat (ITT) and modified ITT populations. CONCLUSION: 
      PRECISION, the first study of patients with high cardiovascular risk chronically 
      treated with a cyclooxygenase-2 selective inhibitor or nonselective NSAID, will 
      define the relative cardiovascular safety profile of celecoxib, ibuprofen, and 
      naproxen and provide data to help guide NSAID use for pain management for this 
      population.
FAU - Becker, Matthew C
AU  - Becker MC
AD  - Department of Cardiology, Cleveland Clinic Foundation, OH 44195, USA.
FAU - Wang, Thomas H
AU  - Wang TH
FAU - Wisniewski, Lisa
AU  - Wisniewski L
FAU - Wolski, Kathy
AU  - Wolski K
FAU - Libby, Peter
AU  - Libby P
FAU - Lüscher, Thomas F
AU  - Lüscher TF
FAU - Borer, Jeffrey S
AU  - Borer JS
FAU - Mascette, Alice M
AU  - Mascette AM
FAU - Husni, M Elaine
AU  - Husni ME
FAU - Solomon, Daniel H
AU  - Solomon DH
FAU - Graham, David Y
AU  - Graham DY
FAU - Yeomans, Neville D
AU  - Yeomans ND
FAU - Krum, Henry
AU  - Krum H
FAU - Ruschitzka, Frank
AU  - Ruschitzka F
FAU - Lincoff, A Michael
AU  - Lincoff AM
FAU - Nissen, Steven E
AU  - Nissen SE
CN  - PRECISION Investigators
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
DEP - 20090225
PL  - United States
TA  - Am Heart J
JT  - American heart journal
JID - 0370465
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Pyrazoles)
RN  - 0 (Sulfonamides)
RN  - 57Y76R9ATQ (Naproxen)
RN  - JCX84Q7J1L (Celecoxib)
RN  - WK2XYI10QM (Ibuprofen)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal/administration & dosage/therapeutic use
MH  - Arthritis/*drug therapy
MH  - Cardiovascular Diseases/*epidemiology/prevention & control
MH  - Celecoxib
MH  - Cyclooxygenase Inhibitors/administration & dosage/therapeutic use
MH  - Dose-Response Relationship, Drug
MH  - Double-Blind Method
MH  - Follow-Up Studies
MH  - Humans
MH  - Ibuprofen/administration & dosage/*therapeutic use
MH  - Middle Aged
MH  - Naproxen/administration & dosage/*therapeutic use
MH  - Prospective Studies
MH  - Pyrazoles/administration & dosage/*therapeutic use
MH  - Sulfonamides/administration & dosage/*therapeutic use
MH  - Treatment Outcome
EDAT- 2009/04/01 09:00
MHDA- 2009/04/22 09:00
CRDT- 2009/04/01 09:00
PHST- 2008/07/21 00:00 [received]
PHST- 2008/12/12 00:00 [accepted]
PHST- 2009/04/01 09:00 [entrez]
PHST- 2009/04/01 09:00 [pubmed]
PHST- 2009/04/22 09:00 [medline]
AID - S0002-8703(08)01060-0 [pii]
AID - 10.1016/j.ahj.2008.12.014 [doi]
PST - ppublish
SO  - Am Heart J. 2009 Apr;157(4):606-12. doi: 10.1016/j.ahj.2008.12.014. Epub 2009 Feb 
      25.

PMID- 19130662
OWN - NLM
STAT- MEDLINE
DCOM- 20090212
LR  - 20081211
IS  - 1051-5313 (Print)
IS  - 1051-5313 (Linking)
VI  - 18
IP  - 12
DP  - 2008 Aug
TI  - Joint inflammation may point the finger at heart disease. Rheumatoid arthritis 
      and lupus raise the risk of heart attack and stroke.
PG  - 3
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Harv Heart Lett
JT  - Harvard heart letter : from Harvard Medical School
JID - 9425723
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
MH  - Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
MH  - Arthritis, Rheumatoid/*complications/drug therapy/physiopathology
MH  - Autoimmune Diseases
MH  - Heart Failure/*etiology
MH  - Humans
MH  - Lupus Erythematosus, Systemic/*complications/drug therapy/physiopathology
MH  - Risk Assessment
MH  - Stroke/*etiology
EDAT- 2009/01/10 09:00
MHDA- 2009/02/13 09:00
CRDT- 2009/01/10 09:00
PHST- 2009/01/10 09:00 [entrez]
PHST- 2009/01/10 09:00 [pubmed]
PHST- 2009/02/13 09:00 [medline]
PST - ppublish
SO  - Harv Heart Lett. 2008 Aug;18(12):3.

PMID- 19059533
OWN - NLM
STAT- MEDLINE
DCOM- 20090115
LR  - 20131121
IS  - 1532-8600 (Electronic)
IS  - 0026-0495 (Linking)
VI  - 58
IP  - 1
DP  - 2009 Jan
TI  - The role of homocysteine as a significant risk factor for white matter lesions in 
      Japanese women with rheumatoid arthritis.
PG  - 69-73
LID - 10.1016/j.metabol.2008.08.008 [doi]
AB  - The presence of white matter lesions (WML) is an important prognostic factor for 
      the development of stroke. Plasma total homocysteine (tHcy), which increases with 
      diabetes, has been flagged as a novel predictor for cerebrovascular events. We 
      tested the hypothesis that the presence of WML correlates with tHcy in rheumatoid 
      arthritis patients. Based on brain magnetic resonance imaging findings, 65 
      rheumatoid arthritis patients were divided into 2 groups: WML-positive group (61 
      +/- 6 years, mean +/- SD; n = 25) and WML-negative group (60 +/- 7 years, n = 
      40). The level of metabolic parameters was assessed by total cholesterol, 
      triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein 
      cholesterol, fasting plasma glucose, and homocysteine (tHcy). The duration of 
      rheumatoid arthritis was longer in the WML-positive group than in the 
      WML-negative group (P < .05). Plasma levels of triglyceride was higher whereas 
      high-density lipoprotein cholesterol was lower in the WML-positive group than in 
      the WML-negative group (P < .05 and P < .01, respectively). Fasting plasma 
      glucose (P < .05) and tHcy (<.0001) levels were higher in the WML-positive group 
      than in the WML-negative group. Multivariate logistic analysis revealed that WML 
      was independently predicted by the tHcy (odds ratio, 1.35; 95% confidence 
      interval, 1.12-1.63; P < .0001). Our findings indicate that the presence of WML 
      was associated with the tHcy in Japanese patients with rheumatoid arthritis.
FAU - Anan, Futoshi
AU  - Anan F
AD  - Department of Cardiology, Oita Red Cross Hospital, Oita 870-0033, Japan. 
      anan-f@med.oita-u.ac.jp
FAU - Masaki, Takayuki
AU  - Masaki T
FAU - Tatsukawa, Hiroshi
AU  - Tatsukawa H
FAU - Nagano, Shuji
AU  - Nagano S
FAU - Oribe, Motohiro
AU  - Oribe M
FAU - Eshima, Nobuoki
AU  - Eshima N
FAU - Saikawa, Tetsunori
AU  - Saikawa T
FAU - Yoshimatsu, Hironobu
AU  - Yoshimatsu H
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 0 (Blood Glucose)
RN  - 0 (Triglycerides)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Arthritis, Rheumatoid/blood/complications/*metabolism
MH  - Blood Glucose/metabolism
MH  - Blood Pressure/physiology
MH  - Brain Diseases/blood/*metabolism/pathology
MH  - Cholesterol/blood
MH  - Cross-Sectional Studies
MH  - Dyslipidemias/blood/metabolism/pathology
MH  - Female
MH  - Heart Rate/physiology
MH  - Homocysteine/*metabolism
MH  - Humans
MH  - Japan
MH  - Logistic Models
MH  - Magnetic Resonance Imaging
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Stroke/blood/complications/metabolism
MH  - Triglycerides/blood
EDAT- 2008/12/09 09:00
MHDA- 2009/01/16 09:00
CRDT- 2008/12/09 09:00
PHST- 2008/04/12 00:00 [received]
PHST- 2008/08/13 00:00 [accepted]
PHST- 2008/12/09 09:00 [pubmed]
PHST- 2009/01/16 09:00 [medline]
PHST- 2008/12/09 09:00 [entrez]
AID - S0026-0495(08)00322-3 [pii]
AID - 10.1016/j.metabol.2008.08.008 [doi]
PST - ppublish
SO  - Metabolism. 2009 Jan;58(1):69-73. doi: 10.1016/j.metabol.2008.08.008.

PMID- 19035419
OWN - NLM
STAT- MEDLINE
DCOM- 20090127
LR  - 20220410
IS  - 0004-3591 (Print)
IS  - 0004-3591 (Linking)
VI  - 59
IP  - 12
DP  - 2008 Dec 15
TI  - Risk of cardiovascular mortality in patients with rheumatoid arthritis: a 
      meta-analysis of observational studies.
PG  - 1690-7
LID - 10.1002/art.24092 [doi]
AB  - OBJECTIVE: To determine the magnitude of risk of cardiovascular mortality in 
      patients with rheumatoid arthritis (RA) compared with the general population 
      through a meta-analysis of observational studies. METHODS: We searched Medline, 
      EMBase, and Lilacs databases from their inception to July 2005. Observational 
      studies that met the following criteria were assessed by 2 researchers: 1) 
      prespecified RA definition, 2) clearly defined cardiovascular disease (CVD) 
      outcome, including ischemic heart disease (IHD) and cerebrovascular accidents 
      (CVAs), and 3) reported standardized mortality ratios (SMRs) and 95% confidence 
      intervals (95% CIs). We calculated weighted-pooled summary estimates of SMRs 
      (meta-SMRs) for CVD, IHD, and CVAs using the random-effects model, and tested for 
      heterogeneity using the I(2) statistic. RESULTS: Twenty-four studies met the 
      inclusion criteria, comprising 111,758 patients with 22,927 cardiovascular 
      events. Overall, there was a 50% increased risk of CVD death in patients with RA 
      (meta-SMR 1.50, 95% CI 1.39-1.61). Mortality risks for IHD and CVA were increased 
      by 59% and 52%, respectively (meta-SMR 1.59, 95% CI 1.46-1.73 and meta-SMR 1.52, 
      95% CI 1.40-1.67, respectively). We identified asymmetry in the funnel plot 
      (Egger's test P = 0.002), as well as significant heterogeneity in all main 
      analyses (P < 0.0001). Subgroup analyses showed that inception cohort studies (n 
      = 4, comprising 2,175 RA cases) were the only group that did not show a 
      significantly increased risk for CVD (meta-SMR 1.19, 95% CI 0.86-1.68). 
      CONCLUSION: Published data indicate that CVD mortality is increased by 
      approximately 50% in RA patients compared with the general population. However, 
      we found that study characteristics may influence the estimate.
FAU - Aviña-Zubieta, J Antonio
AU  - Aviña-Zubieta JA
AD  - University of British Columbia and Arthritis Research Centre of Canada, British 
      Columbia, Canada. azubieta@arthritisresearch.ca
FAU - Choi, Hyon K
AU  - Choi HK
FAU - Sadatsafavi, Mohsen
AU  - Sadatsafavi M
FAU - Etminan, Mahyar
AU  - Etminan M
FAU - Esdaile, John M
AU  - Esdaile JM
FAU - Lacaille, Diane
AU  - Lacaille D
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
SB  - IM
MH  - Arthritis, Rheumatoid/*complications
MH  - Cardiovascular Diseases/*mortality
MH  - Confidence Intervals
MH  - Humans
MH  - Myocardial Ischemia/mortality
MH  - Stroke/mortality
EDAT- 2008/11/28 09:00
MHDA- 2009/01/28 09:00
CRDT- 2008/11/28 09:00
PHST- 2008/11/28 09:00 [pubmed]
PHST- 2009/01/28 09:00 [medline]
PHST- 2008/11/28 09:00 [entrez]
AID - 10.1002/art.24092 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2008 Dec 15;59(12):1690-7. doi: 10.1002/art.24092.

PMID- 18927458
OWN - NLM
STAT- MEDLINE
DCOM- 20090106
LR  - 20161122
IS  - 1524-4628 (Electronic)
IS  - 0039-2499 (Linking)
VI  - 39
IP  - 12
DP  - 2008 Dec
TI  - Platelet C4d is associated with acute ischemic stroke and stroke severity.
PG  - 3236-41
LID - 10.1161/STROKEAHA.108.514687 [doi]
AB  - BACKGROUND AND PURPOSE: Platelets bearing complement C4d were recently reported 
      to be 99% specific for a diagnosis of systemic lupus erythematosus (SLE) and 
      associated with neuropsychiatric lupus. We compared the prevalence of platelet 
      C4d and investigated the clinical associations of platelet C4d in patients with 
      acute ischemic stroke. METHODS: We recruited 80 patients hospitalized for acute 
      ischemic stroke. Stroke severity was measured by the National Institutes of 
      Health Stroke Scale (NIH-SS). Infarct volume was determined by MRI. Platelet C4d 
      was measured by flow cytometry. RESULTS: Mean age was 57.9 years (range: 24.6 to 
      86.8 years), 58% were male, and 91% were white. Eight patients (10%) with acute 
      ischemic stroke were platelet C4d-positive, which was significantly higher in 
      prevalence compared to healthy controls (0%, P<0.0001) and non-SLE patients with 
      immune/inflammatory disease (2%, P=0.004). The median NIH-SS score and infarct 
      volume for acute stroke patients were 6 (interquartile range [IQR]: 2 to 13) and 
      3.4 cc (IQR: 1.1 to 16.6), respectively. Platelet C4d-positive patients were more 
      likely to have a severe stroke compared to those with negative platelet C4d 
      (NIH-SS median: 17.5 versus 5, P=0.003). Positive platelet C4d was independently 
      associated with stroke severity (P=0.03) after controlling for age, 
      anticardiolipin antibody (aCL) status, and total anterior circulation of stroke 
      involvement, and also with infarct volume (P=0.005) after controlling for age, 
      aCL status, and old stroke by MRI. CONCLUSIONS: Platelet C4d is associated with 
      severe acute ischemic stroke. Platelet C4d may be a biomarker as well as 
      pathogenic clue that links cerebrovascular inflammation and thrombosis.
FAU - Mehta, Nidhi
AU  - Mehta N
AD  - University of Pittsburgh School of the Health Sciences, University of Pittsburgh, 
      PA, USA.
FAU - Uchino, Ken
AU  - Uchino K
FAU - Fakhran, Saeed
AU  - Fakhran S
FAU - Sattar, M Abdus
AU  - Sattar MA
FAU - Branstetter, Barton F 4th
AU  - Branstetter BF 4th
FAU - Au, Karen
AU  - Au K
FAU - Navratil, Jeannine S
AU  - Navratil JS
FAU - Paul, Barbara
AU  - Paul B
FAU - Lee, Melissa
AU  - Lee M
FAU - Gallagher, Katie M
AU  - Gallagher KM
FAU - Manzi, Susan
AU  - Manzi S
FAU - Ahearn, Joseph M
AU  - Ahearn JM
FAU - Kao, Amy H
AU  - Kao AH
LA  - eng
GR  - K23 AR-051044/AR/NIAMS NIH HHS/United States
GR  - K24 AR-02213/AR/NIAMS NIH HHS/United States
GR  - MO1-RR-00056/RR/NCRR NIH HHS/United States
GR  - R01 AR-46588/AR/NIAMS NIH HHS/United States
GR  - R01 AR-4676402/AR/NIAMS NIH HHS/United States
GR  - R01 HL-074335/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20081016
PL  - United States
TA  - Stroke
JT  - Stroke
JID - 0235266
RN  - 0 (Antibodies, Anticardiolipin)
RN  - 0 (Biomarkers)
RN  - 0 (Fibrinolytic Agents)
RN  - 0 (Peptide Fragments)
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - 80295-50-7 (Complement C4b)
RN  - 80295-52-9 (complement C4d)
SB  - IM
MH  - Acute Disease
MH  - Aged
MH  - Antibodies, Anticardiolipin/blood
MH  - Arthritis, Rheumatoid/blood/complications/immunology
MH  - Biomarkers
MH  - Blood Platelets/*chemistry
MH  - Brain Ischemia/*blood/drug therapy/immunology/pathology
MH  - Cardiovascular Diseases/blood/immunology
MH  - Comorbidity
MH  - Complement C4b
MH  - Female
MH  - Fibrinolytic Agents/therapeutic use
MH  - Humans
MH  - Inflammation/blood/immunology
MH  - Lupus Erythematosus, Systemic/blood/complications/immunology
MH  - Male
MH  - Middle Aged
MH  - Peptide Fragments/*blood
MH  - Platelet Aggregation Inhibitors/therapeutic use
MH  - Rheumatic Diseases/blood/immunology
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Thrombolytic Therapy
EDAT- 2008/10/18 09:00
MHDA- 2009/01/07 09:00
CRDT- 2008/10/18 09:00
PHST- 2008/10/18 09:00 [pubmed]
PHST- 2009/01/07 09:00 [medline]
PHST- 2008/10/18 09:00 [entrez]
AID - STROKEAHA.108.514687 [pii]
AID - 10.1161/STROKEAHA.108.514687 [doi]
PST - ppublish
SO  - Stroke. 2008 Dec;39(12):3236-41. doi: 10.1161/STROKEAHA.108.514687. Epub 2008 Oct 
      16.

PMID- 18799105
OWN - NLM
STAT- MEDLINE
DCOM- 20090205
LR  - 20220318
IS  - 0392-856X (Print)
IS  - 0392-856X (Linking)
VI  - 26
IP  - 4
DP  - 2008 Jul-Aug
TI  - Incidence and risk of fatal myocardial infarction and stroke events in rheumatoid 
      arthritis patients. A systematic review of the literature.
PG  - 673-9
AB  - BACKGROUND: There is substantial evidence of excess cardiovascular morbidity and 
      mortality in rheumatoid arthritis (RA) patients, but the related studies showed 
      important variations in the estimation of the risk. We conducted a meta-analysis 
      to evaluate more accurately the incidence of cardiovascular events, and the 
      excess of cardiovascular risk in a population of RA patients. METHODS: The 
      authors searched for observational studies accounting for the number of 
      myocardial infarction or stroke events, using Medline, and congress abstracts 
      published until February 2006. The populations studied were adults and RA 
      diagnosis was based on the American College of Rheumatology (ACR) criteria. We 
      calculated the incidence of myocardial infarction and cerebrovascular fatal 
      events in RA patients and estimated the cardiovascular risk increase for RA 
      patients compared with the control group. RESULTS: 17 publications and abstracts 
      were identified, 15 were selected for the meta-analysis (two publications were 
      excluded because of the lack of person-years information). The incidence of fatal 
      myocardial infarction was 13.3 for 1000 RA patients-year (IC95%=[13-13.6]). The 
      incidence of fatal cerebrovascular accident was 4.5 for 1000 RA patients-year 
      (IC95%=[4.3-4.7]). Risk of myocardial ischemia in RA patients was about 1.63 
      compared to the general population (OR=1.63, IC95%=[1.34-2]). No excess was found 
      for the risk of stroke event in RA patients. CONCLUSION: RA patients were 
      reported to present an excess risk of fatal myocardial infarction compared to the 
      general population. The prevention of cardiovascular complications, including 
      management of cardiovascular risk factors and control of systemic inflammation, 
      should be taken into account by the rheumatologist.
FAU - Lévy, L
AU  - Lévy L
AD  - Department of Rheumatology, University Hospital Pellegrin, Bordeaux, France. 
      levy.lorna@gmail.com
FAU - Fautrel, B
AU  - Fautrel B
FAU - Barnetche, T
AU  - Barnetche T
FAU - Schaeverbeke, T
AU  - Schaeverbeke T
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Systematic Review
PL  - Italy
TA  - Clin Exp Rheumatol
JT  - Clinical and experimental rheumatology
JID - 8308521
SB  - IM
MH  - Arthritis, Rheumatoid/complications/*mortality
MH  - Europe/epidemiology
MH  - Humans
MH  - Incidence
MH  - Myocardial Infarction/complications/*mortality
MH  - Odds Ratio
MH  - Risk
MH  - Stroke/complications/*mortality
MH  - United States/epidemiology
EDAT- 2008/09/19 09:00
MHDA- 2009/02/06 09:00
CRDT- 2008/09/19 09:00
PHST- 2008/09/19 09:00 [pubmed]
PHST- 2009/02/06 09:00 [medline]
PHST- 2008/09/19 09:00 [entrez]
AID - 2409 [pii]
PST - ppublish
SO  - Clin Exp Rheumatol. 2008 Jul-Aug;26(4):673-9.

PMID- 18774002
OWN - NLM
STAT- MEDLINE
DCOM- 20081016
LR  - 20211020
IS  - 0002-9149 (Print)
IS  - 0002-9149 (Linking)
VI  - 102
IP  - 6
DP  - 2008 Sep 15
TI  - C-reactive protein and coronary artery calcium in asymptomatic women with 
      systemic lupus erythematosus or rheumatoid arthritis.
PG  - 755-60
LID - 10.1016/j.amjcard.2008.04.059 [doi]
AB  - Patients with systemic lupus erythematosus (SLE) and those with rheumatoid 
      arthritis (RA) have increased risk for atherosclerotic cardiovascular disease. 
      The aims of this study were to compare the presence of coronary artery calcium 
      (CAC) in age- and race-matched women with SLE, those with RA, and healthy 
      controls without diabetes mellitus or history of myocardial infarction, angina 
      pectoris, or stroke and to investigate its relation with traditional risk 
      factors, inflammation, and endothelial activation. Study subjects completed 
      cardiovascular risk factor assessment and electron-beam computed tomography that 
      measured CAC. The 2 patient groups had similar prevalence and extent of CAC as 
      well as significantly increased odds of having any CAC (odds ratio 1.87, 95% 
      confidence interval 1.09 to 3.21) and more extensive CAC (odds ratio 4.04, 95% 
      confidence interval 1.42 to 11.56 for CAC score >100) compared with healthy 
      controls. After controlling for differences in cardiovascular risk factors, 
      including insulin resistance and hypertension, the results remained statistically 
      significant. After adjustment for differences in levels of C-reactive protein 
      and/or soluble intercellular adhesion molecule-1, however, women with chronic 
      inflammatory diseases no longer had significantly increased odds of having any 
      CAC or more extensive CAC compared with controls. In conclusion, asymptomatic and 
      nondiabetic women with chronic inflammatory diseases had significantly increased 
      odds of having CAC and more extensive CAC compared with age- and race-matched 
      healthy controls. The increased odds for CAC may in part result from higher 
      levels of inflammation and endothelial activation in these patients.
FAU - Kao, Amy H
AU  - Kao AH
AD  - Department of Medicine, Division of Rheumatology and Clinical Immunology, 
      Graduate School of Public Health, University of Pittsburgh, Pittsburgh, 
      Pennsylvania, USA. ahk7@pitt.edu
FAU - Wasko, Mary Chester M
AU  - Wasko MC
FAU - Krishnaswami, Shanthi
AU  - Krishnaswami S
FAU - Wagner, Joseph
AU  - Wagner J
FAU - Edmundowicz, Daniel
AU  - Edmundowicz D
FAU - Shaw, Penny
AU  - Shaw P
FAU - Cunningham, Amy Lynn
AU  - Cunningham AL
FAU - Danchenko, Natalya
AU  - Danchenko N
FAU - Sutton-Tyrrell, Kim
AU  - Sutton-Tyrrell K
FAU - Tracy, Russell P
AU  - Tracy RP
FAU - Kuller, Lewis H
AU  - Kuller LH
FAU - Manzi, Susan
AU  - Manzi S
LA  - eng
GR  - UL1 TR000005/TR/NCATS NIH HHS/United States
GR  - K24 AR002213-06A1/AR/NIAMS NIH HHS/United States
GR  - K24 AR002213-04/AR/NIAMS NIH HHS/United States
GR  - K23 AR51044/AR/NIAMS NIH HHS/United States
GR  - K24 AR002213/AR/NIAMS NIH HHS/United States
GR  - K24 AR002213-01/AR/NIAMS NIH HHS/United States
GR  - K24 AR002213-02/AR/NIAMS NIH HHS/United States
GR  - K23 AR051044-02/AR/NIAMS NIH HHS/United States
GR  - K23 AR047571/AR/NIAMS NIH HHS/United States
GR  - K23 AR047571-02/AR/NIAMS NIH HHS/United States
GR  - K23 AR051044/AR/NIAMS NIH HHS/United States
GR  - K23 AR047571-05/AR/NIAMS NIH HHS/United States
GR  - K24 AR02213-01/AR/NIAMS NIH HHS/United States
GR  - K23 AR47571/AR/NIAMS NIH HHS/United States
GR  - R01 AR046588/AR/NIAMS NIH HHS/United States
GR  - K23 AR047571-03/AR/NIAMS NIH HHS/United States
GR  - K23 AR047571-04/AR/NIAMS NIH HHS/United States
GR  - M01 RR000056/RR/NCRR NIH HHS/United States
GR  - R01 AR46588-01/AR/NIAMS NIH HHS/United States
GR  - K23 AR051044-03/AR/NIAMS NIH HHS/United States
GR  - K23 AR047571-01/AR/NIAMS NIH HHS/United States
GR  - M01-RR000056/RR/NCRR NIH HHS/United States
GR  - K23 AR051044-01/AR/NIAMS NIH HHS/United States
GR  - R01 AR046588-01A2/AR/NIAMS NIH HHS/United States
GR  - 1-P60-AR-44811 01/AR/NIAMS NIH HHS/United States
GR  - K23 AR051044-05/AR/NIAMS NIH HHS/United States
GR  - K23 AR051044-04/AR/NIAMS NIH HHS/United States
GR  - R01 AR046588-03/AR/NIAMS NIH HHS/United States
GR  - K24 AR002213-05/AR/NIAMS NIH HHS/United States
GR  - R01 AR046588-04/AR/NIAMS NIH HHS/United States
GR  - K24 AR002213-07/AR/NIAMS NIH HHS/United States
GR  - K24 AR002213-03/AR/NIAMS NIH HHS/United States
GR  - R01 AR046588-02/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20080626
PL  - United States
TA  - Am J Cardiol
JT  - The American journal of cardiology
JID - 0207277
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Arthritis, Rheumatoid/blood/*epidemiology
MH  - Body Mass Index
MH  - C-Reactive Protein/*analysis
MH  - Calcinosis/diagnostic imaging/*epidemiology
MH  - Case-Control Studies
MH  - Coronary Angiography/methods
MH  - Coronary Artery Disease/diagnostic imaging/*epidemiology
MH  - Female
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/blood
MH  - Lupus Erythematosus, Systemic/blood/*epidemiology
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Tomography, X-Ray Computed
PMC - PMC2563802
MID - NIHMS69879
EDAT- 2008/09/09 09:00
MHDA- 2008/10/17 09:00
PMCR- 2009/09/15
CRDT- 2008/09/09 09:00
PHST- 2008/01/16 00:00 [received]
PHST- 2008/04/29 00:00 [revised]
PHST- 2008/04/29 00:00 [accepted]
PHST- 2008/09/09 09:00 [pubmed]
PHST- 2008/10/17 09:00 [medline]
PHST- 2008/09/09 09:00 [entrez]
PHST- 2009/09/15 00:00 [pmc-release]
AID - S0002-9149(08)00850-3 [pii]
AID - 10.1016/j.amjcard.2008.04.059 [doi]
PST - ppublish
SO  - Am J Cardiol. 2008 Sep 15;102(6):755-60. doi: 10.1016/j.amjcard.2008.04.059. Epub 
      2008 Jun 26.

PMID- 18767411
OWN - NLM
STAT- MEDLINE
DCOM- 20081016
LR  - 20080904
IS  - 1220-4749 (Print)
IS  - 1220-4749 (Linking)
VI  - 45
IP  - 4
DP  - 2007
TI  - Antiphospholipid antibodies and migraine: a retrospective study of 428 patients 
      with inflammatory connective tissue diseases.
PG  - 355-63
AB  - The antiphospholipid syndrome (APS) is defined by the presence of 
      antiphospholipid antibodies (aPL), associated with thrombosis or recurrent 
      spontaneous abortions. APS can occur alone or secondary to other conditions, 
      especially associated to inflammatory systemic autoimmune diseases. Among the 
      neurological manifestations associated with aPL, only ischemic stroke is 
      recognized by the actual classification criteria for APS. Other neurological 
      manifestations have been, however, repeatedly reported in case studies of APS 
      patients. Headache, and especially migraine, was commonly reported in APS 
      patients and is one of the classical features described by Hughes as related to 
      aPL, but studies failed to confirm this association. We studied retrospectively 
      the association between headache syndromes and aPL in 428 patients with 
      inflammatory connective tissue diseases admitted in the Neurology and Internal 
      Medicine Departments of Colentina Hospital-Bucharest. We found that migraine 
      alone, not headache of all types, is significantly associated with aPL in 
      patients with systemic immune disease. We studied the presence of cerebral 
      ischemia in patients with headache and aPL. In SLE patients, headache (all types) 
      is significantly associated with positive titers of aPL, and cerebral ischemic 
      lesions are significantly encountered. Even if both migraine and aPL are 
      conditions with high frequency in patients with immune systemic disease and their 
      association may be coincidental, the presence of ischemic lesions in patients 
      showing this association suggests the need to define a sub-group at risk, for 
      whom headache can be a marker and anticoagulants can be discussed.
FAU - Tănăsescu, R
AU  - Tănăsescu R
AD  - Carol Davila University of Medicine and Pharmacy, Department of Neurology, 
      Colentina Hospital, Bucharest, Romania neuradutanasescu@yahoo.com
FAU - Nicolau, Adriana
AU  - Nicolau A
FAU - Caraiola, Simona
AU  - Caraiola S
FAU - Ticmeanu, Marina
AU  - Ticmeanu M
FAU - Cojocaru, Inimioara Mihaela
AU  - Cojocaru IM
FAU - Frăsineanu, A
AU  - Frăsineanu A
FAU - Ionescu, R
AU  - Ionescu R
FAU - Hristea, Adriana
AU  - Hristea A
FAU - Ene, Amalia
AU  - Ene A
FAU - Anghel, Daniela
AU  - Anghel D
FAU - Tănăsescu, Ruxandra
AU  - Tănăsescu R
FAU - Băicuş, C
AU  - Băicuş C
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Rom J Intern Med
JT  - Romanian journal of internal medicine = Revue roumaine de medecine interne
JID - 9304507
RN  - 0 (Antibodies, Antiphospholipid)
SB  - IM
MH  - Antibodies, Antiphospholipid/*immunology
MH  - Antiphospholipid Syndrome/*complications
MH  - Brain Ischemia/complications/immunology
MH  - Female
MH  - Humans
MH  - Lupus Erythematosus, Systemic/complications/immunology
MH  - Male
MH  - Migraine Disorders/*complications/*immunology
MH  - Odds Ratio
MH  - Retrospective Studies
MH  - Sjogren's Syndrome/complications/immunology
EDAT- 2008/09/05 09:00
MHDA- 2008/10/17 09:00
CRDT- 2008/09/05 09:00
PHST- 2008/09/05 09:00 [pubmed]
PHST- 2008/10/17 09:00 [medline]
PHST- 2008/09/05 09:00 [entrez]
PST - ppublish
SO  - Rom J Intern Med. 2007;45(4):355-63.

PMID- 18724604
OWN - NLM
STAT- MEDLINE
DCOM- 20081209
LR  - 20240426
IS  - 1470-2118 (Print)
IS  - 1473-4893 (Electronic)
IS  - 1470-2118 (Linking)
VI  - 8
IP  - 4
DP  - 2008 Aug
TI  - Cardiovascular disease--the silent killer in rheumatoid arthritis.
PG  - 384-7
AB  - Rheumatoid arthritis (RA) is a multisystem disease with high rates of morbidity 
      and mortality. In recent years, there has been increasing focus on the growing 
      rates of cardiovascular disease (CVD) in RA, over and above expected levels 
      allowing for 'traditional' risk factors. In this paper the impact of CVD in RA, 
      the relative contributions of traditional risk factors and novel risk factors 
      (including homocysteine, oxidised low-density lipoprotein, high-sensitivity 
      C-reactive protein and leptin), and the need to address cardiovascular risk in 
      the fight against premature death from coronary artery and stroke disease in RA 
      are discussed.
FAU - Kumar, Namita
AU  - Kumar N
AD  - University Hospital of North Durham, Durham.
FAU - Armstrong, David J
AU  - Armstrong DJ
LA  - eng
PT  - Journal Article
PL  - England
TA  - Clin Med (Lond)
JT  - Clinical medicine (London, England)
JID - 101092853
RN  - 0 (Cholesterol, LDL)
RN  - 0 (Leptin)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - C-Reactive Protein/analysis
MH  - Cardiovascular Diseases/*epidemiology
MH  - Cholesterol, LDL/blood
MH  - Comorbidity
MH  - Coronary Artery Disease/epidemiology
MH  - Endothelium, Vascular/pathology/physiopathology
MH  - Homocysteine/blood
MH  - Humans
MH  - Leptin/physiology
PMC - PMC4952930
EDAT- 2008/08/30 09:00
MHDA- 2008/12/17 09:00
PMCR- 2008/08/01
CRDT- 2008/08/30 09:00
PHST- 2008/08/30 09:00 [pubmed]
PHST- 2008/12/17 09:00 [medline]
PHST- 2008/08/30 09:00 [entrez]
PHST- 2008/08/01 00:00 [pmc-release]
AID - S1470-2118(24)00185-4 [pii]
AID - clinmedicine [pii]
AID - 10.7861/clinmedicine.8-4-384 [doi]
PST - ppublish
SO  - Clin Med (Lond). 2008 Aug;8(4):384-7. doi: 10.7861/clinmedicine.8-4-384.

PMID- 18668605
OWN - NLM
STAT- MEDLINE
DCOM- 20080918
LR  - 20211020
IS  - 0004-3591 (Print)
IS  - 1529-0131 (Electronic)
IS  - 0004-3591 (Linking)
VI  - 59
IP  - 8
DP  - 2008 Aug 15
TI  - Subgroup analyses to determine cardiovascular risk associated with nonsteroidal 
      antiinflammatory drugs and coxibs in specific patient groups.
PG  - 1097-104
LID - 10.1002/art.23911 [doi]
AB  - OBJECTIVE: To explore the extent to which clinical characteristics influence the 
      association between cyclooxygenase 2 inhibitors (coxibs) and/or nonselective 
      nonsteroidal antiinflammatory drugs (NSAIDs) and increased cardiovascular disease 
      (CVD) risk in specific patient subgroups. There is substantial concern regarding 
      the potential cardiovascular adverse effects of selective coxibs and nonselective 
      NSAIDs, but many patients with arthritis experience important clinical benefits 
      from these agents. METHODS: The study population consisted of Medicare 
      beneficiaries also eligible for a drug benefits program for older adults during 
      the years 1999-2004. We calculated the relative risk (RR) for CVD events 
      (myocardial infarction [MI], stroke, congestive heart failure, and cardiovascular 
      death) among users of coxibs or nonselective NSAIDs in the prior 6 months 
      compared with nonusers. We assessed biologic interaction between these medication 
      exposures and important patient characteristics. RESULTS: In the primary cohort, 
      we identified 76,082 new users of coxibs, 53,014 new users of nonselective 
      NSAIDs, and 46,558 nonusers. Compared with nonusers, the adjusted RR of CVD 
      events for new users of each agent increased for rofecoxib (RR 1.22, 95% 
      confidence interval [95% CI] 1.14, 1.30) and decreased for naproxen (RR 0.79, 95% 
      CI 0.67, 0.93). Several patient characteristics were found to increase the risk 
      of CVD events among users of some agents in both the primary and secondary 
      cohorts, including age >/=80 years, hypertension, prior MI, prior CVD, rheumatoid 
      arthritis, chronic renal disease, and chronic obstructive pulmonary disease. 
      Rofecoxib and ibuprofen appeared to confer an increased risk in multiple patient 
      subgroups. CONCLUSION: Many nonselective NSAIDs and coxibs are not associated 
      with an increased risk of CVD events. However, several patient characteristics 
      identify important subgroups that may be at an increased risk when using specific 
      agents.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - Brigham and Women's Hospital, 1620 Tremont Street, Boston, MA 02120, USA. 
      dhsolomon@partners.org
FAU - Glynn, Robert J
AU  - Glynn RJ
FAU - Rothman, Kenneth J
AU  - Rothman KJ
FAU - Schneeweiss, Sebastian
AU  - Schneeweiss S
FAU - Setoguchi, Soko
AU  - Setoguchi S
FAU - Mogun, Helen
AU  - Mogun H
FAU - Avorn, Jerry
AU  - Avorn J
FAU - Stürmer, Til
AU  - Stürmer T
LA  - eng
GR  - K23 AR048616/AR/NIAMS NIH HHS/United States
GR  - AR 48616/AR/NIAMS NIH HHS/United States
GR  - K24 AR055989/AR/NIAMS NIH HHS/United States
GR  - K23 AR048616-05/AR/NIAMS NIH HHS/United States
GR  - R01 DA015507-03/DA/NIDA NIH HHS/United States
GR  - DA 15507/DA/NIDA NIH HHS/United States
GR  - R01 DA015507/DA/NIDA NIH HHS/United States
GR  - AR 48264/AR/NIAMS NIH HHS/United States
GR  - R55 AR048264-01/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Anti-Inflammatory Agents, Non-Steroidal/administration & dosage/*adverse effects
MH  - Antirheumatic Agents/administration & dosage/*adverse effects
MH  - Arthritis/*drug therapy/*epidemiology
MH  - Cardiovascular Diseases/*epidemiology
MH  - Cohort Studies
MH  - Cyclooxygenase 2 Inhibitors/administration & dosage/*adverse effects
MH  - Databases, Factual/statistics & numerical data
MH  - Female
MH  - Heart Failure/epidemiology
MH  - Humans
MH  - Male
MH  - Myocardial Infarction/epidemiology
MH  - Risk Factors
MH  - Stroke/epidemiology
PMC - PMC2884183
MID - NIHMS205082
EDAT- 2008/08/01 09:00
MHDA- 2008/09/19 09:00
PMCR- 2010/06/14
CRDT- 2008/08/01 09:00
PHST- 2008/08/01 09:00 [pubmed]
PHST- 2008/09/19 09:00 [medline]
PHST- 2008/08/01 09:00 [entrez]
PHST- 2010/06/14 00:00 [pmc-release]
AID - 10.1002/art.23911 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2008 Aug 15;59(8):1097-104. doi: 10.1002/art.23911.

PMID- 18668583
OWN - NLM
STAT- MEDLINE
DCOM- 20080918
LR  - 20220331
IS  - 0004-3591 (Print)
IS  - 1529-0131 (Electronic)
IS  - 0004-3591 (Linking)
VI  - 59
IP  - 8
DP  - 2008 Aug 15
TI  - Cardiovascular, rheumatologic, and pharmacologic predictors of stroke in patients 
      with rheumatoid arthritis: a nested, case-control study.
PG  - 1090-6
LID - 10.1002/art.23935 [doi]
AB  - OBJECTIVE: To determine the risk of stroke in patients with rheumatoid arthritis 
      (RA) and risk factors associated with stroke. METHODS: We performed nested 
      case-control analyses within a longitudinal databank, matching up to 20 controls 
      for age, sex, and time of cohort entry to each patient with stroke. Conditional 
      logistic regression was performed as an estimate of the relative risk of stroke 
      in RA patients compared with those with noninflammatory rheumatic disorders, and 
      to examine severity and anti-tumor necrosis factor (anti-TNF) treatment effects 
      in RA. RESULTS: We identified 269 patients with first-ever all-category strokes 
      and 67 with ischemic stroke, including 41 in RA patients. The odds ratio (OR) for 
      the risk of all-category stroke in RA was 1.64 (95% confidence interval [95% CI] 
      1.16-2.30, P = 0.005), and for ischemic stroke was 2.66 (95% CI 1.24-5.70, P = 
      0.012). Ischemic stroke was predicted by hypertension, myocardial infarction, 
      low-dose aspirin, comorbidity score, Health Assessment Questionnaire score, and 
      presence of total joint replacement, but not by diabetes, smoking, exercise, or 
      body mass index. Adjusted for cardiovascular and RA risk factors, ischemic stroke 
      was associated with rofecoxib (P = 0.060, OR 2.27 [95% CI 0.97-5.28]), and 
      possibly with corticosteroid use. Anti-TNF therapy was not associated with 
      ischemic stroke (P = 0.584, OR 0.80 [95% CI 0.34-1.82]). CONCLUSION: RA is 
      associated with increased risk of stroke, particularly ischemic stroke. Stroke is 
      predicted by RA severity, certain cardiovascular risk factors, and comorbidity. 
      Except for rofecoxib, RA treatment does not appear to be associated with stroke, 
      although the effect of corticosteroids remains uncertain.
FAU - Nadareishvili, Zurab
AU  - Nadareishvili Z
AD  - Georgetown University Hospital, Washington, DC, USA.
FAU - Michaud, Kaleb
AU  - Michaud K
FAU - Hallenbeck, John M
AU  - Hallenbeck JM
FAU - Wolfe, Frederick
AU  - Wolfe F
LA  - eng
GR  - Z01 NS002995-06/ImNIH/Intramural NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
RN  - 0 (Adrenal Cortex Hormones)
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Lactones)
RN  - 0 (Sulfones)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0QTW8Z7MCR (rofecoxib)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
CIN - Arthritis Rheum. 2008 Aug 15;59(8):1051-3. doi: 10.1002/art.23933. PMID: 18668582
MH  - Adrenal Cortex Hormones/therapeutic use
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy/*epidemiology
MH  - Aspirin/therapeutic use
MH  - Brain Ischemia/*epidemiology
MH  - Case-Control Studies
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Hypertension/epidemiology
MH  - Lactones/*therapeutic use
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology
MH  - Predictive Value of Tests
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Stroke/*epidemiology
MH  - Sulfones/*therapeutic use
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
PMC - PMC2778069
MID - NIHMS148211
EDAT- 2008/08/01 09:00
MHDA- 2008/09/19 09:00
PMCR- 2009/11/17
CRDT- 2008/08/01 09:00
PHST- 2008/08/01 09:00 [pubmed]
PHST- 2008/09/19 09:00 [medline]
PHST- 2008/08/01 09:00 [entrez]
PHST- 2009/11/17 00:00 [pmc-release]
AID - 10.1002/art.23935 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2008 Aug 15;59(8):1090-6. doi: 10.1002/art.23935.

PMID- 18668582
OWN - NLM
STAT- MEDLINE
DCOM- 20080918
LR  - 20080807
IS  - 0004-3591 (Print)
IS  - 0004-3591 (Linking)
VI  - 59
IP  - 8
DP  - 2008 Aug 15
TI  - Ischemic stroke: another feature of accelerated atherosclerosis in rheumatoid 
      arthritis?
PG  - 1051-3
LID - 10.1002/art.23933 [doi]
FAU - Symmons, Deborah P M
AU  - Symmons DP
LA  - eng
PT  - Comment
PT  - Editorial
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
SB  - IM
CON - Arthritis Rheum. 2008 Aug 15;59(8):1090-6. doi: 10.1002/art.23935. PMID: 18668583
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Brain Ischemia/*epidemiology
MH  - Humans
MH  - Intracranial Arteriosclerosis/*epidemiology
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Stroke/*epidemiology
EDAT- 2008/08/01 09:00
MHDA- 2008/09/19 09:00
CRDT- 2008/08/01 09:00
PHST- 2008/08/01 09:00 [pubmed]
PHST- 2008/09/19 09:00 [medline]
PHST- 2008/08/01 09:00 [entrez]
AID - 10.1002/art.23933 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2008 Aug 15;59(8):1051-3. doi: 10.1002/art.23933.

PMID- 18573856
OWN - NLM
STAT- MEDLINE
DCOM- 20080725
LR  - 20220331
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Print)
IS  - 0959-8138 (Linking)
VI  - 336
IP  - 7659
DP  - 2008 Jun 28
TI  - Predicting cardiovascular risk in England and Wales: prospective derivation and 
      validation of QRISK2.
PG  - 1475-82
LID - 10.1136/bmj.39609.449676.25 [doi]
AB  - OBJECTIVE: To develop and validate version two of the QRISK cardiovascular 
      disease risk algorithm (QRISK2) to provide accurate estimates of cardiovascular 
      risk in patients from different ethnic groups in England and Wales and to compare 
      its performance with the modified version of Framingham score recommended by the 
      National Institute for Health and Clinical Excellence (NICE). DESIGN: Prospective 
      open cohort study with routinely collected data from general practice, 1 January 
      1993 to 31 March 2008. SETTING: 531 practices in England and Wales contributing 
      to the national QRESEARCH database. PARTICIPANTS: 2.3 million patients aged 35-74 
      (over 16 million person years) with 140,000 cardiovascular events. Overall 
      population (derivation and validation cohorts) comprised 2.22 million people who 
      were white or whose ethnic group was not recorded, 22,013 south Asian, 11,595 
      black African, 10,402 black Caribbean, and 19,792 from Chinese or other Asian or 
      other ethnic groups. MAIN OUTCOME MEASURES: First (incident) diagnosis of 
      cardiovascular disease (coronary heart disease, stroke, and transient ischaemic 
      attack) recorded in general practice records or linked Office for National 
      Statistics death certificates. Risk factors included self assigned ethnicity, 
      age, sex, smoking status, systolic blood pressure, ratio of total serum 
      cholesterol:high density lipoprotein cholesterol, body mass index, family history 
      of coronary heart disease in first degree relative under 60 years, Townsend 
      deprivation score, treated hypertension, type 2 diabetes, renal disease, atrial 
      fibrillation, and rheumatoid arthritis. RESULTS: The validation statistics 
      indicated that QRISK2 had improved discrimination and calibration compared with 
      the modified Framingham score. The QRISK2 algorithm explained 43% of the 
      variation in women and 38% in men compared with 39% and 35%, respectively, by the 
      modified Framingham score. Of the 112,156 patients classified as high risk (that 
      is, >or=20% risk over 10 years) by the modified Framingham score, 46,094 (41.1%) 
      would be reclassified at low risk with QRISK2. The 10 year observed risk among 
      these reclassified patients was 16.6% (95% confidence interval 16.1% to 
      17.0%)-that is, below the 20% treatment threshold. Of the 78 024 patients 
      classified at high risk on QRISK2, 11,962 (15.3%) would be reclassified at low 
      risk by the modified Framingham score. The 10 year observed risk among these 
      patients was 23.3% (22.2% to 24.4%)-that is, above the 20% threshold. In the 
      validation cohort, the annual incidence rate of cardiovascular events among those 
      with a QRISK2 score of >or=20% was 30.6 per 1000 person years (29.8 to 31.5) for 
      women and 32.5 per 1000 person years (31.9 to 33.1) for men. The corresponding 
      figures for the modified Framingham equation were 25.7 per 1000 person years 
      (25.0 to 26.3) for women and 26.4 (26.0 to 26.8) for men). At the 20% threshold, 
      the population identified by QRISK2 was at higher risk of a CV event than the 
      population identified by the Framingham score. CONCLUSIONS: Incorporating 
      ethnicity, deprivation, and other clinical conditions into the QRISK2 algorithm 
      for risk of cardiovascular disease improves the accuracy of identification of 
      those at high risk in a nationally representative population. At the 20% 
      threshold, QRISK2 is likely to be a more efficient and equitable tool for 
      treatment decisions for the primary prevention of cardiovascular disease. As the 
      validation was performed in a similar population to the population from which the 
      algorithm was derived, it potentially has a "home advantage." Further validation 
      in other populations is therefore advised.
FAU - Hippisley-Cox, Julia
AU  - Hippisley-Cox J
AD  - Division of Primary Care, Tower Building, University Park, Nottingham NG2 7RD. 
      Julia.hippisley-cox@nottingham.ac.uk
FAU - Coupland, Carol
AU  - Coupland C
FAU - Vinogradova, Yana
AU  - Vinogradova Y
FAU - Robson, John
AU  - Robson J
FAU - Minhas, Rubin
AU  - Minhas R
FAU - Sheikh, Aziz
AU  - Sheikh A
FAU - Brindle, Peter
AU  - Brindle P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Validation Study
DEP - 20080623
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
SB  - IM
CIN - BMJ. 2008 Jun 28;336(7659):1445-6. doi: 10.1136/bmj.a480. PMID: 18573855
MH  - Adult
MH  - Age Distribution
MH  - Aged
MH  - *Algorithms
MH  - Cardiovascular Diseases/*mortality
MH  - England/epidemiology
MH  - Epidemiologic Studies
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Prognosis
MH  - Sex Distribution
MH  - Wales/epidemiology
PMC - PMC2440904
COIS- Competing interests: JR chaired and PB and RM were members of the NICE guideline 
      development group on cardiovascular risk assessment. JHC is codirector of 
      QRESEARCH—a not for profit organisation that is a joint partnership between the 
      University of Nottingham and EMIS. EMIS is the leading commercial supplier of IT 
      systems for 56% of general practices in England and Wales and it is likely to 
      implement QRISK2 into its clinical management system. EMIS is likely to also 
      distribute the software package for those using it for academic research or other 
      organisations interesting in implementing QRISK2 into practice or 
      (www.qresearch.org/Public/qriskInformationforClinicians.aspx). RM is a 2008 
      Harkness Fellow in healthcare policy and practice and is the chair of the 
      cardiovascular working group of the South Asian Health Foundation (SAHF), which 
      receives unrestricted funding from the Department of Health and BHF and 
      unrestricted grants from the pharmaceutical industry. AS chairs the equality and 
      diversity forum of the National Clinical Assessment Service. AS is PI on NHS 
      Connecting for Health’s evaluation of the implementation of the NHS Care Record 
      Service. QRESEARCH undertakes analyses for the Department of Health and other 
      government organisations.
EDAT- 2008/06/25 09:00
MHDA- 2008/07/26 09:00
PMCR- 2008/06/28
CRDT- 2008/06/25 09:00
PHST- 2008/06/25 09:00 [pubmed]
PHST- 2008/07/26 09:00 [medline]
PHST- 2008/06/25 09:00 [entrez]
PHST- 2008/06/28 00:00 [pmc-release]
AID - bmj.39609.449676.25 [pii]
AID - hipj576058 [pii]
AID - 10.1136/bmj.39609.449676.25 [doi]
PST - ppublish
SO  - BMJ. 2008 Jun 28;336(7659):1475-82. doi: 10.1136/bmj.39609.449676.25. Epub 2008 
      Jun 23.

PMID- 18503132
OWN - NLM
STAT- MEDLINE
DCOM- 20080820
LR  - 20080526
IS  - 1386-0291 (Print)
IS  - 1386-0291 (Linking)
VI  - 39
IP  - 1-4
DP  - 2008
TI  - Plasma viscosity: a forgotten variable.
PG  - 243-6
AB  - Evaluation of plasma viscosity has been underutilized in the clinical practice. 
      Plasma viscosity is determined by water-content and macromolecular components. 
      Plasma is a highly concentrated protein solution, therefore weak protein-protein 
      interactions can play a role that is not characterized by electrophoresis. The 
      effect of a protein on plasma viscosity depends on its molecular weight and 
      structure. The less spheroid shape, the higher molecular weight, the higher 
      aggregating capacity, and the higher temperature or pH sensitivity a protein has, 
      the higher plasma viscosity results. Plasma is a Newtonian fluid, its viscosity 
      does not depend on flow characteristics, therefore it is simple to measure, 
      especially in capillary viscosimeters. Its normal value is 1.10-1.30 mPa s at 37 
      degrees C and independent of age and gender. The measurement has high stability 
      and accuracy, thus little alterations may be pathologically important. 
      Inflammations, tissue injuries resulting in plasma protein changes can increase 
      its value with high sensitivity, though low specificity. It can increase in 
      parallel with erythrocyte sedimentation rate (ESR), but it is not influenced by 
      hematocrit (anemia, polycytemia), or time to analysis. Based on these favorable 
      features, in 1942 plasma viscosity was recommended to substitute ESR. In 
      hyperviscosity syndromes plasma viscosity is better in follow-up than ESR. In 
      rheumatoid arthritis, its sensitivity and specificity are better than that of ESR 
      or C-reactive protein. Plasma fibrinogen concentration and plasma viscosity are 
      elevated in unstable angina pectoris and stroke and their higher values are 
      associated with higher rate of major adverse clinical events. Elevation of plasma 
      viscosity correlates to the progression of coronary and peripheral artery 
      diseases. In conclusion, plasma viscosity should be measured routinely in medical 
      practice.
FAU - Késmárky, Gábor
AU  - Késmárky G
AD  - First Department of Medicine, University of Pecs, Pecs, Hungary. 
      gabor.kesmarky@aok.pte.hu
FAU - Kenyeres, Péter
AU  - Kenyeres P
FAU - Rábai, Miklós
AU  - Rábai M
FAU - Tóth, Kálmán
AU  - Tóth K
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Netherlands
TA  - Clin Hemorheol Microcirc
JT  - Clinical hemorheology and microcirculation
JID - 9709206
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - *Blood Sedimentation
MH  - *Blood Viscosity
MH  - C-Reactive Protein/metabolism
MH  - Cardiovascular Diseases/blood
MH  - *Erythrocyte Aggregation
MH  - Erythrocyte Deformability
MH  - Hematocrit
MH  - Hemorheology/methods
MH  - Humans
MH  - Myocardial Ischemia/pathology
MH  - Plasma/*metabolism/*physiology
MH  - Rheology/methods
MH  - Risk Factors
RF  - 10
EDAT- 2008/05/27 09:00
MHDA- 2008/08/21 09:00
CRDT- 2008/05/27 09:00
PHST- 2008/05/27 09:00 [pubmed]
PHST- 2008/08/21 09:00 [medline]
PHST- 2008/05/27 09:00 [entrez]
PST - ppublish
SO  - Clin Hemorheol Microcirc. 2008;39(1-4):243-6.

PMID- 18417067
OWN - NLM
STAT- MEDLINE
DCOM- 20080515
LR  - 20220316
IS  - 1534-6242 (Electronic)
IS  - 1523-3804 (Linking)
VI  - 10
IP  - 2
DP  - 2008 Apr
TI  - Rheumatoid arthritis and cardiovascular disease.
PG  - 128-33
AB  - Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease affecting 
      approximately 1% of the adult general population. Cardiovascular disease is 
      recognized as the leading cause of death in RA patients, accounting for nearly 
      40% of their mortality. Patients with RA are at a twofold increased risk for 
      myocardial infarction and stroke, with risk increasing to nearly threefold in 
      patients who have had the disease for 10 years or more. Congestive heart failure 
      appears to be a greater contributor to excess mortality than ischemia. This 
      increased cardiovascular disease risk in RA patients seems to be independent of 
      traditional cardiovascular risk factors. Pathogenic mechanisms include 
      pro-oxidative dyslipidemia, insulin resistance, prothrombotic state, 
      hyperhomocysteinemia, and immune mechanisms such as T-cell activation that 
      subsequently lead to endothelial dysfunction, a decrease in endothelial 
      progenitor cells, and arterial stiffness, which are the congeners of accelerated 
      atherosclerosis observed in RA patients. This paper discusses pathogenic 
      mechanisms, effects of methotrexate, tumor necrosis factor antagonists, steroids, 
      and statins, with a perspective on therapy.
FAU - Dhawan, Saurabh S
AU  - Dhawan SS
AD  - Division of Cardiology, Department of Medicine, Emory University, 1364 Clifton 
      Road NE, Suite 403C, Atlanta, GA 30322, USA.
FAU - Quyyumi, Arshed A
AU  - Quyyumi AA
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Curr Atheroscler Rep
JT  - Current atherosclerosis reports
JID - 100897685
RN  - 0 (Cholesterol, HDL)
RN  - 0 (Cholesterol, LDL)
SB  - IM
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - CD4-Positive T-Lymphocytes
MH  - CD8-Positive T-Lymphocytes
MH  - Cardiovascular Diseases/*epidemiology
MH  - Cholesterol, HDL/blood
MH  - Cholesterol, LDL/blood
MH  - Dyslipidemias/blood
MH  - Endothelium, Vascular/physiopathology
MH  - Heart Failure/epidemiology
MH  - Humans
MH  - Hyperhomocysteinemia/epidemiology
MH  - Insulin Resistance/physiology
MH  - Myocardial Infarction/epidemiology
MH  - Risk Assessment
MH  - Stem Cells/physiology
RF  - 69
EDAT- 2008/04/18 09:00
MHDA- 2008/05/16 09:00
CRDT- 2008/04/18 09:00
PHST- 2008/04/18 09:00 [pubmed]
PHST- 2008/05/16 09:00 [medline]
PHST- 2008/04/18 09:00 [entrez]
AID - 10.1007/s11883-008-0019-x [doi]
PST - ppublish
SO  - Curr Atheroscler Rep. 2008 Apr;10(2):128-33. doi: 10.1007/s11883-008-0019-x.

PMID- 18394459
OWN - NLM
STAT- MEDLINE
DCOM- 20080617
LR  - 20080408
IS  - 0002-9149 (Print)
IS  - 0002-9149 (Linking)
VI  - 101
IP  - 8
DP  - 2008 Apr 15
TI  - Cardiovascular outcomes in male veterans with rheumatoid arthritis.
PG  - 1201-5
LID - 10.1016/j.amjcard.2007.11.076 [doi]
AB  - In men with rheumatoid arthritis (RA), the confounding effect of adverse 
      cardiovascular risk profile on the independent association of RA disease activity 
      score (DAS) and major adverse cardiovascular events (MACEs) continues to be 
      debated. The aim was to analyze the association of RA DAS with MACEs in a 
      prospective cohort of men with RA enrolled in the VARA Registry at the Dallas 
      site from January 2003 to October 2006. All subjects met American College of 
      Rheumatology criteria for RA. All events were obtained by reviewing patient 
      clinical data. DAS was categorized as low, 0 to 3.2; moderate, 3.2 to 5.09; and 
      high, > or =5.1. Of 282 men (mean age 66 +/- 11.1 years), 231 had valid DASs 
      (150, low; 60, moderate; and 21, high DAS) and were followed up for 4.4 +/- 2 
      years. Ninety-two subjects (32.6%; 95% confidence interval 27 to 38) experienced 
      an MACE, a composite end point of death (9 patients; 10%), acute coronary 
      syndrome (38 patients; 42%), coronary revascularization (47 patients; 49%), 
      new-onset heart failure (37 patients; 40%), and stroke (15 patients; 16%). DAS 
      was a significant predictor of MACEs (hazard ratio 1.31, 95% confidence interval 
      1.1 to 1.6, p = 0.01) independent of traditional risk factors. Compared with 
      patients with low or moderate DASs, patients with high DASs had a lower mean 
      event-free period (35 and 30 vs 19 years, respectively; p = 0.03). In conclusion, 
      in a population of male US veterans aged >50 years, (1) patients with RA were at 
      high risk of MACEs, and (2) RA DAS was a significant predictor of MACEs 
      independent of traditional cardiovascular risk factors.
FAU - Banerjee, Subhash
AU  - Banerjee S
AD  - Dallas VA Medical Center, Dallas, Texas, USA. subhash.banerjee@usouthwestern.edu
FAU - Compton, Alexander P
AU  - Compton AP
FAU - Hooker, Roderick S
AU  - Hooker RS
FAU - Cipher, Daisha J
AU  - Cipher DJ
FAU - Reimold, Andreas
AU  - Reimold A
FAU - Brilakis, Emmanouil S
AU  - Brilakis ES
FAU - Banerjee, Pooja
AU  - Banerjee P
FAU - Kazi, Salahuddin
AU  - Kazi S
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
DEP - 20080305
PL  - United States
TA  - Am J Cardiol
JT  - The American journal of cardiology
JID - 0207277
SB  - IM
MH  - Acute Coronary Syndrome/epidemiology
MH  - Aged
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Follow-Up Studies
MH  - Heart Failure/epidemiology
MH  - Humans
MH  - Male
MH  - Myocardial Revascularization/statistics & numerical data
MH  - Proportional Hazards Models
MH  - Prospective Studies
MH  - Registries
MH  - Severity of Illness Index
MH  - Stroke/epidemiology
MH  - United States/epidemiology
MH  - *Veterans
EDAT- 2008/04/09 09:00
MHDA- 2008/06/18 09:00
CRDT- 2008/04/09 09:00
PHST- 2007/09/25 00:00 [received]
PHST- 2007/11/21 00:00 [revised]
PHST- 2007/11/21 00:00 [accepted]
PHST- 2008/04/09 09:00 [pubmed]
PHST- 2008/06/18 09:00 [medline]
PHST- 2008/04/09 09:00 [entrez]
AID - S0002-9149(07)02500-3 [pii]
AID - 10.1016/j.amjcard.2007.11.076 [doi]
PST - ppublish
SO  - Am J Cardiol. 2008 Apr 15;101(8):1201-5. doi: 10.1016/j.amjcard.2007.11.076. Epub 
      2008 Mar 5.

PMID- 18336869
OWN - NLM
STAT- MEDLINE
DCOM- 20090518
LR  - 20220321
IS  - 1532-866X (Electronic)
IS  - 0049-0172 (Linking)
VI  - 38
IP  - 5
DP  - 2009 Apr
TI  - Carotid intima-media thickness predicts the development of cardiovascular events 
      in patients with rheumatoid arthritis.
PG  - 366-71
LID - 10.1016/j.semarthrit.2008.01.012 [doi]
AB  - OBJECTIVE: To establish whether carotid intima-media wall thickness (IMT) may be 
      a good predictor for the development of cardiovascular (CV) events in patients 
      with rheumatoid arthritis (RA). METHODS: A series of 47 RA patients who at the 
      time of recruitment did not have traditional CV risk factors or CV disease were 
      assessed by carotid ultrasonography. Carotid IMT and carotid plaques were 
      measured in the right common carotid artery. Then, a prospective assessment of 
      the CV outcome was performed over a 5-year period. Logistic regression models and 
      receiver operating characteristic curves were performed to evaluate the ability 
      of different variables to predict CV events. RESULTS: Carotid IMT was greater in 
      RA patients who over the extended follow-up experienced CV events (1.01 +/- 0.16 
      mm) compared with the remaining RA patients who did not have CV complications 
      (0.74 +/- 0.12 mm) (P < 0.001). Also, carotid IMT categorized in quartiles was 
      strongly associated with CV events. In this regard, none of the patients with 
      carotid IMT less than 0.77 mm had CV events. However, 6 of the 10 patients with 
      carotid IMT greater than 0.91 mm experienced CV events (P value for the trend 
      <0.001). Carotid IMT yielded a high predictive power for the development of CV 
      events over the 5-year follow-up period. The area under the receiver operating 
      characteristic curve was 0.93 for a model that only included carotid IMT and 0.90 
      for carotid plaque. CONCLUSIONS: The results from the present study support the 
      use of carotid ultrasonography as a predictor of CV events in RA.
FAU - Gonzalez-Juanatey, Carlos
AU  - Gonzalez-Juanatey C
AD  - Division of Cardiology, Hospital Xeral-Calde, Lugo, Spain.
FAU - Llorca, Javier
AU  - Llorca J
FAU - Martin, Javier
AU  - Martin J
FAU - Gonzalez-Gay, Miguel A
AU  - Gonzalez-Gay MA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080312
PL  - United States
TA  - Semin Arthritis Rheum
JT  - Seminars in arthritis and rheumatism
JID - 1306053
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Carotid Artery Diseases/*diagnostic imaging/*epidemiology
MH  - Female
MH  - Humans
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Myocardial Ischemia/*epidemiology
MH  - Predictive Value of Tests
MH  - ROC Curve
MH  - Risk Factors
MH  - Stroke/*epidemiology
MH  - Tunica Intima/diagnostic imaging
MH  - Tunica Media/diagnostic imaging
MH  - Ultrasonography
EDAT- 2008/03/14 09:00
MHDA- 2009/05/19 09:00
CRDT- 2008/03/14 09:00
PHST- 2007/10/14 00:00 [received]
PHST- 2007/11/28 00:00 [revised]
PHST- 2008/01/05 00:00 [accepted]
PHST- 2008/03/14 09:00 [pubmed]
PHST- 2009/05/19 09:00 [medline]
PHST- 2008/03/14 09:00 [entrez]
AID - S0049-0172(08)00022-X [pii]
AID - 10.1016/j.semarthrit.2008.01.012 [doi]
PST - ppublish
SO  - Semin Arthritis Rheum. 2009 Apr;38(5):366-71. doi: 
      10.1016/j.semarthrit.2008.01.012. Epub 2008 Mar 12.

PMID- 18325087
OWN - NLM
STAT- MEDLINE
DCOM- 20080923
LR  - 20220409
IS  - 1478-6362 (Electronic)
IS  - 1478-6354 (Print)
IS  - 1478-6354 (Linking)
VI  - 10
IP  - 2
DP  - 2008
TI  - Cardiovascular disease in patients with rheumatoid arthritis: results from the 
      QUEST-RA study.
PG  - R30
LID - 10.1186/ar2383 [doi]
AB  - INTRODUCTION: We analyzed the prevalence of cardiovascular (CV) disease in 
      patients with rheumatoid arthritis (RA) and its association with traditional CV 
      risk factors, clinical features of RA, and the use of disease-modifying 
      antirheumatic drugs (DMARDs) in a multinational cross-sectional cohort of 
      nonselected consecutive outpatients with RA (The Questionnaires in Standard 
      Monitoring of Patients with Rheumatoid Arthritis Program, or QUEST-RA) who were 
      receiving regular clinical care. METHODS: The study involved a clinical 
      assessment by a rheumatologist and a self-report questionnaire by patients. The 
      clinical assessment included a review of clinical features of RA and exposure to 
      DMARDs over the course of RA. Comorbidities were recorded; CV morbidity included 
      myocardial infarction, angina, coronary disease, coronary bypass surgery, and 
      stroke. Traditional risk factors recorded were hypertension, hyperlipidemia, 
      diabetes mellitus, smoking, physical inactivity, and body mass index. Unadjusted 
      and adjusted hazard ratios (HRs) (95% confidence interval [CI]) for CV morbidity 
      were calculated using Cox proportional hazard regression models. RESULTS: Between 
      January 2005 and October 2006, the QUEST-RA project included 4,363 patients from 
      48 sites in 15 countries; 78% were female, more than 90% were Caucasian, and the 
      mean age was 57 years. The prevalence for lifetime CV events in the entire sample 
      was 3.2% for myocardial infarction, 1.9% for stroke, and 9.3% for any CV event. 
      The prevalence for CV risk factors was 32% for hypertension, 14% for 
      hyperlipidemia, 8% for diabetes, 43% for ever-smoking, 73% for physical 
      inactivity, and 18% for obesity. Traditional risk factors except obesity and 
      physical inactivity were significantly associated with CV morbidity. There was an 
      association between any CV event and age and male gender and between 
      extra-articular disease and myocardial infarction. Prolonged exposure to 
      methotrexate (HR 0.85; 95% CI 0.81 to 0.89), leflunomide (HR 0.59; 95% CI 0.43 to 
      0.79), sulfasalazine (HR 0.92; 95% CI 0.87 to 0.98), glucocorticoids (HR 0.95; 
      95% CI 0.92 to 0.98), and biologic agents (HR 0.42; 95% CI 0.21 to 0.81; P < 
      0.05) was associated with a reduction of the risk of CV morbidity; analyses were 
      adjusted for traditional risk factors and countries. CONCLUSION: In conclusion, 
      prolonged use of treatments such as methotrexate, sulfasalazine, leflunomide, 
      glucocorticoids, and tumor necrosis factor-alpha blockers appears to be 
      associated with a reduced risk of CV disease. In addition to traditional risk 
      factors, extra-articular disease was associated with the occurrence of myocardial 
      infarction in patients with RA.
FAU - Naranjo, Antonio
AU  - Naranjo A
AD  - Hospital de Gran Canaria Dr, Negrin, University of Las Palmas de Gran Canaria, 
      Barranco de la Ballena s/n 35011, Spain. anarher@gobiernodecanarias.org
FAU - Sokka, Tuulikki
AU  - Sokka T
FAU - Descalzo, Miguel A
AU  - Descalzo MA
FAU - Calvo-Alén, Jaime
AU  - Calvo-Alén J
FAU - Hørslev-Petersen, Kim
AU  - Hørslev-Petersen K
FAU - Luukkainen, Reijo K
AU  - Luukkainen RK
FAU - Combe, Bernard
AU  - Combe B
FAU - Burmester, Gerd R
AU  - Burmester GR
FAU - Devlin, Joe
AU  - Devlin J
FAU - Ferraccioli, Gianfranco
AU  - Ferraccioli G
FAU - Morelli, Alessia
AU  - Morelli A
FAU - Hoekstra, Monique
AU  - Hoekstra M
FAU - Majdan, Maria
AU  - Majdan M
FAU - Sadkiewicz, Stefan
AU  - Sadkiewicz S
FAU - Belmonte, Miguel
AU  - Belmonte M
FAU - Holmqvist, Ann-Carin
AU  - Holmqvist AC
FAU - Choy, Ernest
AU  - Choy E
FAU - Tunc, Recep
AU  - Tunc R
FAU - Dimic, Aleksander
AU  - Dimic A
FAU - Bergman, Martin
AU  - Bergman M
FAU - Toloza, Sergio
AU  - Toloza S
FAU - Pincus, Theodore
AU  - Pincus T
CN  - QUEST-RA Group
LA  - eng
PT  - Journal Article
DEP - 20080306
PL  - England
TA  - Arthritis Res Ther
JT  - Arthritis research & therapy
JID - 101154438
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Glucocorticoids)
SB  - IM
CIN - Arthritis Res Ther. 2008;10(2):105. doi: 10.1186/ar2364. PMID: 18341711
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*complications/*drug therapy
MH  - Cardiovascular Diseases/*complications/*epidemiology
MH  - Cross-Sectional Studies
MH  - Female
MH  - Glucocorticoids/therapeutic use
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Prevalence
MH  - Surveys and Questionnaires
PMC - PMC2453774
FIR - Hetland, Merete Lund
IR  - Hetland ML
FIR - Linde, Louise
IR  - Linde L
FIR - Hørslev-Petersen, Kim
IR  - Hørslev-Petersen K
FIR - Hansen, Troels Mørk
IR  - Hansen TM
FIR - Knudsen, Lene Surland
IR  - Knudsen LS
FIR - Mäkinen, Heidi
IR  - Mäkinen H
FIR - Immonen, Kai
IR  - Immonen K
FIR - Forsberg, Sinikka
IR  - Forsberg S
FIR - Lähteenmäki, Jukka
IR  - Lähteenmäki J
FIR - Luukkainen, Reijo
IR  - Luukkainen R
FIR - Gossec, Laure
IR  - Gossec L
FIR - Dougados, Maxime
IR  - Dougados M
FIR - Maillefert, Jean Francis
IR  - Maillefert JF
FIR - Combe, Bernard
IR  - Combe B
FIR - Sibilia, Jean
IR  - Sibilia J
FIR - Herborn, Gertraud
IR  - Herborn G
FIR - Rau, Rolf
IR  - Rau R
FIR - Alten, Rieke
IR  - Alten R
FIR - Pohl, Christof
IR  - Pohl C
FIR - Burmester, Gerd R
IR  - Burmester GR
FIR - Marsmann, Bettina
IR  - Marsmann B
FIR - Bresnihan, Barry
IR  - Bresnihan B
FIR - Minnock, Patricia
IR  - Minnock P
FIR - Murphy, Eithne
IR  - Murphy E
FIR - Sheehy, Claire
IR  - Sheehy C
FIR - Quirke, Edel
IR  - Quirke E
FIR - Devlin, Joe
IR  - Devlin J
FIR - Alraqi, Shafeeq
IR  - Alraqi S
FIR - Cazzato, Massimiliano
IR  - Cazzato M
FIR - Bombardieri, Stefano
IR  - Bombardieri S
FIR - Ferraccioli, Gianfranco
IR  - Ferraccioli G
FIR - Morelli, Alessia
IR  - Morelli A
FIR - Cutolo, Maurizio
IR  - Cutolo M
FIR - Salaffi, Fausto
IR  - Salaffi F
FIR - Stancati, Andrea
IR  - Stancati A
FIR - Verstappen, Suzan M M
IR  - Verstappen SM
FIR - Jacobs, Johannes W G
IR  - Jacobs JW
FIR - Huisman, Margriet
IR  - Huisman M
FIR - Hoekstra, Monique
IR  - Hoekstra M
FIR - Sierakowski, Stanislaw
IR  - Sierakowski S
FIR - Majdan, Maria
IR  - Majdan M
FIR - Romanowski, Wojciech
IR  - Romanowski W
FIR - Tlustochowicz, Witold
IR  - Tlustochowicz W
FIR - Kapolka, Danuta
IR  - Kapolka D
FIR - Sadkiewicz, Stefan
IR  - Sadkiewicz S
FIR - Zarowny-Wierzbinska, Danuta
IR  - Zarowny-Wierzbinska D
FIR - Titz-Kosko, Jadwigi
IR  - Titz-Kosko J
FIR - Naranjo, Antonio
IR  - Naranjo A
FIR - Calvo-Alén, Jaime
IR  - Calvo-Alén J
FIR - Rodríguez-Lozano, Carlos
IR  - Rodríguez-Lozano C
FIR - Belmonte, Miguel
IR  - Belmonte M
FIR - Baecklund, Eva
IR  - Baecklund E
FIR - Henrohn, Dan
IR  - Henrohn D
FIR - Oding, Rolf
IR  - Oding R
FIR - Liveborn, Margareth
IR  - Liveborn M
FIR - Holmqvist, Ann-Carin
IR  - Holmqvist AC
FIR - Taylor, Peter
IR  - Taylor P
FIR - McClinton, Catherine
IR  - McClinton C
FIR - Woolf, Anthony
IR  - Woolf A
FIR - Chorghade, Ginny
IR  - Chorghade G
FIR - Choy, Ernest
IR  - Choy E
FIR - Kelly, Stephen
IR  - Kelly S
FIR - Gogus, Feride
IR  - Gogus F
FIR - Tunc, Recep
IR  - Tunc R
FIR - Celic, Selda
IR  - Celic S
FIR - Skakic, Vlado
IR  - Skakic V
FIR - Dimic, Aleksander
IR  - Dimic A
FIR - Nedovic, Jovan
IR  - Nedovic J
FIR - Stankovic, Aleksandra
IR  - Stankovic A
FIR - Banja, Niska
IR  - Banja N
FIR - Pincus, Theodore
IR  - Pincus T
FIR - Swearingen, Christopher
IR  - Swearingen C
FIR - Yazici, Yusuf
IR  - Yazici Y
FIR - Bergman, Martin
IR  - Bergman M
FIR - Toloza, Sergio
IR  - Toloza S
FIR - Aguero, Santiago
IR  - Aguero S
FIR - Barrera, Sergio Orellana
IR  - Barrera SO
FIR - Retamozo, Soledad
IR  - Retamozo S
FIR - Alba, Paula
IR  - Alba P
FIR - Lascano, Cruz
IR  - Lascano C
FIR - Babini, Alejandra
IR  - Babini A
FIR - Albiero, Eduardo
IR  - Albiero E
FIR - Sokka, Tuulikki
IR  - Sokka T
EDAT- 2008/03/08 09:00
MHDA- 2008/09/24 09:00
PMCR- 2008/03/06
CRDT- 2008/03/08 09:00
PHST- 2007/04/01 00:00 [received]
PHST- 2008/03/06 00:00 [accepted]
PHST- 2008/03/08 09:00 [pubmed]
PHST- 2008/09/24 09:00 [medline]
PHST- 2008/03/08 09:00 [entrez]
PHST- 2008/03/06 00:00 [pmc-release]
AID - ar2383 [pii]
AID - 10.1186/ar2383 [doi]
PST - ppublish
SO  - Arthritis Res Ther. 2008;10(2):R30. doi: 10.1186/ar2383. Epub 2008 Mar 6.

PMID- 18177923
OWN - NLM
STAT- MEDLINE
DCOM- 20090203
LR  - 20131121
IS  - 1532-866X (Electronic)
IS  - 0049-0172 (Linking)
VI  - 38
IP  - 3
DP  - 2008 Dec
TI  - Characteristics and outcome of connective tissue diseases in patients with 
      sickle-cell disease: report of 30 cases.
PG  - 228-40
LID - 10.1016/j.semarthrit.2007.10.003 [doi]
AB  - OBJECTIVES: To analyze the main characteristics of adults with sickle cell 
      disease (SCD) and concurrent connective tissue disease (CTD). METHODS: A 
      retrospective investigational study was performed. CTD was diagnosed according to 
      standard international criteria. Severity of SCD was assessed by a clinical 
      severity score. RESULTS: Thirty patients, 23 women (76%) and 7 men, with 
      hemoglobin S/S (n = 25) or S/C (n = 5) SCD were included. The subtypes of CTD 
      were rheumatoid arthritis (RA) (n = 15), definite systemic lupus erythematosus or 
      "incomplete lupus" requiring treatment (n = 13), primary Sjögren's syndrome with 
      central nervous system involvement (n = 1), and systemic sclerosis (n = 1). 
      Twenty-five of the 30 patients (83%) received steroid treatment, and 15 (50%) 
      received at least 1 immunosuppressive agent (methotrexate in 14 cases) to control 
      CTD. Four RA patients were given antitumor necrosis factor (TNF)alpha and 1 was 
      treated with rituximab without SCD exacerbation. After a median follow-up of 4.5 
      years [range: 6 months to 30 years] from CTD diagnosis, 11 of the 25 (44%) 
      patients receiving steroids had at least 1 episode of severe infection (mostly 
      due to Staphylococcus aureus or Escherichia coli). SCD exacerbated in 13 of the 
      30 (43%) patients after CTD onset; 12 of these patients were receiving prednisone 
      and/or methotrexate. Six patients (20%) had died from sepsis (n = 2), stroke (n = 
      2), or acute chest syndrome (n = 2). CONCLUSIONS: CTD-related clinical 
      manifestations and outcome were not particularly severe in patients with SCD. 
      However, those with active CTD and undergoing steroid +/- methotrexate treatment 
      had more serious SCD-related manifestations, a higher rate of severe infections, 
      and an overall patient mortality rate of 20%. Thus, the management of patients 
      with CTD and underlying SCD should consider the risk/benefit ratio of each 
      treatment and steroid-sparing strategies should be implemented.
FAU - Michel, M
AU  - Michel M
AD  - Department of Internal Medicine, Henri-Mondor University Hospital, Créteil, 
      France. marc.michel@hmn.aphp.fr.
FAU - Habibi, A
AU  - Habibi A
FAU - Godeau, B
AU  - Godeau B
FAU - Bachir, D
AU  - Bachir D
FAU - Lahary, A
AU  - Lahary A
FAU - Galacteros, F
AU  - Galacteros F
FAU - Fifi-Mah, A
AU  - Fifi-Mah A
FAU - Arfi, S
AU  - Arfi S
LA  - eng
PT  - Journal Article
DEP - 20080104
PL  - United States
TA  - Semin Arthritis Rheum
JT  - Seminars in arthritis and rheumatism
JID - 1306053
RN  - 0 (Antisickling Agents)
RN  - 0 (Glucocorticoids)
RN  - 0 (Immunosuppressive Agents)
RN  - X6Q56QN5QC (Hydroxyurea)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Adult
MH  - Anemia, Sickle Cell/*complications/diagnosis/mortality/therapy
MH  - Antisickling Agents/therapeutic use
MH  - Arthritis, Rheumatoid/*complications/diagnosis/drug therapy/mortality
MH  - Blood Transfusion
MH  - Drug Therapy, Combination
MH  - Female
MH  - France/epidemiology
MH  - Glucocorticoids/therapeutic use
MH  - Humans
MH  - Hydroxyurea/therapeutic use
MH  - Immunosuppressive Agents/therapeutic use
MH  - Lupus Erythematosus, Systemic/*complications/diagnosis/drug therapy/mortality
MH  - Male
MH  - Methotrexate/therapeutic use
MH  - Retrospective Studies
MH  - Risk Assessment
MH  - Severity of Illness Index
MH  - Survival Rate
MH  - Treatment Outcome
EDAT- 2008/01/08 09:00
MHDA- 2009/02/04 09:00
CRDT- 2008/01/08 09:00
PHST- 2007/03/19 00:00 [received]
PHST- 2007/10/13 00:00 [revised]
PHST- 2007/10/21 00:00 [accepted]
PHST- 2008/01/08 09:00 [pubmed]
PHST- 2009/02/04 09:00 [medline]
PHST- 2008/01/08 09:00 [entrez]
AID - S0049-0172(07)00160-6 [pii]
AID - 10.1016/j.semarthrit.2007.10.003 [doi]
PST - ppublish
SO  - Semin Arthritis Rheum. 2008 Dec;38(3):228-40. doi: 
      10.1016/j.semarthrit.2007.10.003. Epub 2008 Jan 4.

PMID- 18026809
OWN - NLM
STAT- MEDLINE
DCOM- 20080114
LR  - 20211020
IS  - 1525-1497 (Electronic)
IS  - 0884-8734 (Print)
IS  - 0884-8734 (Linking)
VI  - 22 Suppl 3
IP  - Suppl 3
DP  - 2007 Dec
TI  - Mortality rate in veterans with multiple chronic conditions.
PG  - 403-7
AB  - BACKGROUND: Among patients with multiple chronic conditions, there is increasing 
      appreciation of the complex interrelatedness of diseases. Previous studies have 
      focused on the prevalence and economic burden associated with multiple chronic 
      conditions, much less is known about the mortality rate associated with specific 
      combinations of multiple diseases. OBJECTIVE: Measure the mortality rate in 
      combinations of 11 chronic conditions. DESIGN: Cohort study of veteran health 
      care users. PARTICIPANTS: Veterans between 55 and 64 years that used Veterans 
      Health Administration health care services between October 1999 and September 
      2000. MEASUREMENTS: Patients were identified as having one or more of the 
      following: COPD, diabetes, hypertension, rheumatoid arthritis, osteoarthritis, 
      asthma, depression, ischemic heart disease, dementia, stroke, and cancer. 
      Mutually exclusive combinations of disease based on these conditions were 
      created, and 5-year mortality rates were determined. RESULTS: There were 741,847 
      persons included. The number in each group by a count of conditions was: none = 
      217,944 (29.34%); 1 = 221,111 (29.8%); 2 = 175,228 (23.6%); 3 = 86,447 (11.7%); 
      and 4+ = 41,117 (5.5%). The 5-year mortality rate by the number of conditions 
      was: none = 4.1%; 1 = 6.0%; 2 = 7.8%; 3 = 11.2%; 4+ = 16.7%. Among combinations 
      with the same number of conditions, there was significant variability in 
      mortality rates. CONCLUSIONS: Patients with multiple chronic conditions have 
      higher mortality rates. Because there was significant variation in mortality 
      across clusters with the same number of conditions, when studying patients with 
      multiple coexisting illnesses, it is important to understand not only that 
      several conditions may be present but that specific conditions can differentially 
      impact the risk of mortality.
FAU - Lee, Todd A
AU  - Lee TA
AD  - Center for Management of Complex Chronic Care, Hines VA Hospital, P. O. Box 5000, 
      (151-H), Hines, IL, 60141, USA. todd.lee@va.gov
FAU - Shields, Alexandra E
AU  - Shields AE
FAU - Vogeli, Christine
AU  - Vogeli C
FAU - Gibson, Teresa B
AU  - Gibson TB
FAU - Woong-Sohn, Min
AU  - Woong-Sohn M
FAU - Marder, William D
AU  - Marder WD
FAU - Blumenthal, David
AU  - Blumenthal D
FAU - Weiss, Kevin B
AU  - Weiss KB
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Gen Intern Med
JT  - Journal of general internal medicine
JID - 8605834
SB  - IM
MH  - Chronic Disease/economics/epidemiology/*mortality
MH  - *Comorbidity
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - United States
MH  - United States Department of Veterans Affairs
MH  - Veterans/*statistics & numerical data
PMC - PMC2219704
EDAT- 2007/12/06 09:00
MHDA- 2008/01/15 09:00
PMCR- 2007/12/01
CRDT- 2007/12/06 09:00
PHST- 2007/12/06 09:00 [pubmed]
PHST- 2008/01/15 09:00 [medline]
PHST- 2007/12/06 09:00 [entrez]
PHST- 2007/12/01 00:00 [pmc-release]
AID - 277 [pii]
AID - 10.1007/s11606-007-0277-2 [doi]
PST - ppublish
SO  - J Gen Intern Med. 2007 Dec;22 Suppl 3(Suppl 3):403-7. doi: 
      10.1007/s11606-007-0277-2.

PMID- 17957709
OWN - NLM
STAT- MEDLINE
DCOM- 20080505
LR  - 20131121
IS  - 1053-8569 (Print)
IS  - 1053-8569 (Linking)
VI  - 16
IP  - 12
DP  - 2007 Dec
TI  - Hospitalization rates of generic metoprolol compared with the original 
      beta-blocker in an epidemiological database study.
PG  - 1298-307
AB  - PURPOSE: A less favourable galenic profile of generic formulations of the 
      beta-blocker metoprolol raised the concern of a higher risk for serious 
      cardiovascular (CV) events. We assessed hospital admission rates for CV diseases 
      and prescription prevalences of various drugs using claims data of statutory 
      health insurances (SHIs) to compare the incidence of serious CV events among 
      users of original and generic metoprolol. Index events included hospitalization 
      due to myocardial infarction, hypertensive crisis and stroke. METHODS: Data files 
      of three SHIs were linked with dispensing data of drug prescriptions from each 
      pharmacy's electronic data processing centre on an individual basis. Incidences 
      of hospital admissions among patients receiving original metoprolol and among 
      patients treated with the generic equivalent were compared by logistic 
      regression, stratified for Bremen and the rest of Northern Germany. Risk 
      estimates and confidence intervals were adjusted for confounders. RESULTS: A 
      total of 49,673 patients receiving metoprolol were identified within a cohort of 
      3,649,285 insurance members. While the crude analysis revealed a higher risk for 
      index events in patients receiving the generic drug (Bremen: RR 1.45; Northern 
      Germany: RR 1.14), no elevated risk remained after confounder adjustment (Bremen: 
      OR 1.06; Northern Germany: OR 1.04). Among co-morbid conditions considered as 
      confounders, a previous CV event and an elevated thromboembolic risk exerted the 
      strongest effect on index events. CONCLUSIONS: SHI data are a valuable source for 
      pharmacoepidemiology and health services research in Germany. Incidence rates of 
      serious CV events did not reveal any noticeable differences between the original 
      and the generic group after confounder adjustment.
CI  - Copyright 2007 John Wiley & Sons, Ltd.
FAU - Ahrens, Wolfgang
AU  - Ahrens W
AD  - Bremen Institute for Prevention Research and Social Medicine, Bremen, Germany. 
      ahrens@bips.uni-bremen.de
FAU - Hagemeier, Constantin
AU  - Hagemeier C
FAU - Mühlbauer, Bernd
AU  - Mühlbauer B
FAU - Pigeot, Iris
AU  - Pigeot I
FAU - Püntmann, Isabel
AU  - Püntmann I
FAU - Reineke, Achim
AU  - Reineke A
FAU - Steinbach, Monica
AU  - Steinbach M
FAU - Timm, Jürgen
AU  - Timm J
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Pharmacoepidemiol Drug Saf
JT  - Pharmacoepidemiology and drug safety
JID - 9208369
RN  - 0 (Adrenergic beta-Antagonists)
RN  - 0 (Drugs, Generic)
RN  - GEB06NHM23 (Metoprolol)
SB  - IM
MH  - Adrenergic beta-Antagonists/*adverse effects/therapeutic use
MH  - Aged
MH  - Arrhythmias, Cardiac/drug therapy/epidemiology
MH  - Arthritis, Rheumatoid/drug therapy/epidemiology
MH  - Databases, Factual/statistics & numerical data
MH  - Drug Prescriptions/statistics & numerical data
MH  - Drugs, Generic/*adverse effects/therapeutic use
MH  - Female
MH  - Germany/epidemiology
MH  - Hospitalization/*statistics & numerical data
MH  - Humans
MH  - Hypertension/diagnosis/drug therapy/epidemiology
MH  - Insurance Claim Review/statistics & numerical data
MH  - Logistic Models
MH  - Male
MH  - Metoprolol/*adverse effects/therapeutic use
MH  - Middle Aged
MH  - Myocardial Infarction/diagnosis/drug therapy/epidemiology
MH  - National Health Programs/statistics & numerical data
MH  - Pulmonary Disease, Chronic Obstructive/drug therapy/epidemiology
MH  - Risk Assessment/methods
MH  - Thromboembolism/drug therapy/epidemiology
EDAT- 2007/10/25 09:00
MHDA- 2008/05/06 09:00
CRDT- 2007/10/25 09:00
PHST- 2007/10/25 09:00 [pubmed]
PHST- 2008/05/06 09:00 [medline]
PHST- 2007/10/25 09:00 [entrez]
AID - 10.1002/pds.1494 [doi]
PST - ppublish
SO  - Pharmacoepidemiol Drug Saf. 2007 Dec;16(12):1298-307. doi: 10.1002/pds.1494.

PMID- 17538801
OWN - NLM
STAT- MEDLINE
DCOM- 20070724
LR  - 20131121
IS  - 0954-6634 (Print)
IS  - 0954-6634 (Linking)
VI  - 18
IP  - 3
DP  - 2007
TI  - Folic acid in general medicine and dermatology.
PG  - 138-46
AB  - Folic acid is a vitamin B essential for the integrity and function of DNA. 
      Relative deficiency of folic acid may occur in conditions such as pregnancy and 
      hyperproliferative or chronic inflammatory disorders. Folic acid supplementation 
      has been proven to be beneficial in the prevention of neural tube defects and in 
      limiting methotrexate side effects, and may reduce the risk of colorectal cancer. 
      Folate is a critical vitamin in determining plasma homocysteine levels, which in 
      turn is a major risk factor for cardiovascular diseases. The results of large 
      clinical trials with dietary supplementation of folic acid, vitamin B12 and 
      vitamin B6 have shown that this homocysteine-lowering therapy is effective in the 
      secondary prevention of non-fatal strokes, but had no effect in the prevention of 
      fatal cardiovascular diseases. Hyperhomocysteinemia has also been reported in 
      age-related neurological conditions with cognitive impairment (e.g. dementia), 
      and psychiatric disorders such as depression. Elevated homocysteine levels are 
      frequent in patients with chronic immune-mediated disorders including rheumatoid 
      arthritis, systemic lupus erythematosus, chronic plaque psoriasis and psoriatic 
      arthritis, which have in common a tendency to an accelerated atherosclerosis 
      leading to increased deaths from cardiovascular events. Folic acid 
      supplementation appears as a reasonable therapeutic option in patients affected 
      by chronic inflammatory skin diseases, such as moderate to severe psoriasis; in 
      particular, those with concomitant hyperhomocysteinemia, low plasma folate and 
      additional cardiovascular risk factors.
FAU - Gisondi, Paolo
AU  - Gisondi P
AD  - Department of Biomedical and Surgical Science, Section of Dermatology and 
      Venereology, University of Verona, Verona, Italy. paolo.gisondi@medicina.univr.it
FAU - Fantuzzi, Francesca
AU  - Fantuzzi F
FAU - Malerba, Mario
AU  - Malerba M
FAU - Girolomoni, Giampiero
AU  - Girolomoni G
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - J Dermatolog Treat
JT  - The Journal of dermatological treatment
JID - 8918133
RN  - 935E97BOY8 (Folic Acid)
SB  - IM
MH  - *Dietary Supplements
MH  - Folic Acid/*administration & dosage
MH  - Humans
MH  - Psoriasis/*prevention & control
RF  - 76
EDAT- 2007/06/01 09:00
MHDA- 2007/07/25 09:00
CRDT- 2007/06/01 09:00
PHST- 2007/06/01 09:00 [pubmed]
PHST- 2007/07/25 09:00 [medline]
PHST- 2007/06/01 09:00 [entrez]
AID - 779133821 [pii]
AID - 10.1080/09546630701247930 [doi]
PST - ppublish
SO  - J Dermatolog Treat. 2007;18(3):138-46. doi: 10.1080/09546630701247930.

PMID- 17476612
OWN - NLM
STAT- MEDLINE
DCOM- 20070628
LR  - 20070503
IS  - 0300-9742 (Print)
IS  - 0300-9742 (Linking)
VI  - 36
IP  - 2
DP  - 2007 Mar-Apr
TI  - Circulating endothelial progenitor cells as a link between synovial vascularity 
      and cardiovascular mortality in rheumatoid arthritis.
PG  - 83-90
AB  - Cardiovascular disease refers to the class of diseases that involve the heart 
      and/or blood vessels (arteries and veins). Most Western countries face high and 
      ever-increasing rates of cardiovascular disease. Each year, more Americans are 
      killed by heart disease than by cancer. Diseases of the heart alone cause 30% of 
      all deaths, with other diseases of the cardiovascular system causing substantial 
      further deaths and disability. Indeed, cardiovascular disease is the major cause 
      of death and disability in the USA and most European countries. The development 
      of the vascular systems requires an intricate interplay of molecules such as 
      vascular endothelial growth factor and endothelial progenitor cells. A defective 
      vascular repair/regeneration is thought to be responsible for propagation of 
      atherosclerosis, a key feature of cardiovascular disease. This is partly 
      attributed to a reduction in the circulating endothelial progenitor cells in 
      peripheral blood. Patients with rheumatoid arthritis (RA) have a higher than 
      average incidence of cardiovascular disease in comparison with the general 
      population, with an increased risk of stroke and myocardial infarction, and an 
      increased risk of fatality following myocardial infarction. This review focuses 
      on the current evidence linking the role played by endothelial progenitor cells 
      to the development of cardiovascular disease and why this might relate to the 
      increased risk observed in RA patients.
FAU - Akhavani, M A
AU  - Akhavani MA
AD  - Kennedy Institute of Rheumatology, Faculty of Medicine, Imperial College, London, 
      UK
FAU - Larsen, H
AU  - Larsen H
FAU - Paleolog, E
AU  - Paleolog E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Scand J Rheumatol
JT  - Scandinavian journal of rheumatology
JID - 0321213
RN  - 0 (VEGFA protein, human)
RN  - 0 (Vascular Endothelial Growth Factor A)
SB  - IM
MH  - Arthritis, Rheumatoid/*complications/mortality
MH  - Cardiovascular Diseases/*complications/mortality
MH  - Endothelial Cells/*physiology
MH  - Humans
MH  - Neovascularization, Pathologic/etiology
MH  - Stem Cells/*physiology
MH  - Synovial Membrane/blood supply
MH  - Vascular Endothelial Growth Factor A/physiology
RF  - 67
EDAT- 2007/05/04 09:00
MHDA- 2007/06/29 09:00
CRDT- 2007/05/04 09:00
PHST- 2007/05/04 09:00 [pubmed]
PHST- 2007/06/29 09:00 [medline]
PHST- 2007/05/04 09:00 [entrez]
AID - 778090473 [pii]
AID - 10.1080/03009740701305704 [doi]
PST - ppublish
SO  - Scand J Rheumatol. 2007 Mar-Apr;36(2):83-90. doi: 10.1080/03009740701305704.

PMID- 17385241
OWN - NLM
STAT- MEDLINE
DCOM- 20070327
LR  - 20131121
IS  - 2153-8387 (Print)
IS  - 2153-8387 (Linking)
VI  - 13
IP  - 3
DP  - 2007 Mar
TI  - Heart risks of RA drugs compared. Biologics confer same risk as old-fashioned 
      methotrexate; cytotoxic drugs increase cardiac risk.
PG  - 5
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Duke Med Health News
JT  - DukeMedicine healthnews
JID - 101510062
RN  - 0 (Immunosuppressive Agents)
RN  - YL5FZ2Y5U1 (Methotrexate)
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Humans
MH  - Immunosuppressive Agents/*adverse effects
MH  - Methotrexate/adverse effects
MH  - Myocardial Infarction/*chemically induced
MH  - Stroke/*chemically induced
EDAT- 2007/03/28 09:00
MHDA- 2007/03/28 09:01
CRDT- 2007/03/28 09:00
PHST- 2007/03/28 09:00 [pubmed]
PHST- 2007/03/28 09:01 [medline]
PHST- 2007/03/28 09:00 [entrez]
PST - ppublish
SO  - Duke Med Health News. 2007 Mar;13(3):5.

PMID- 17196469
OWN - NLM
STAT- MEDLINE
DCOM- 20070208
LR  - 20220330
IS  - 0002-9149 (Print)
IS  - 0002-9149 (Linking)
VI  - 99
IP  - 1
DP  - 2007 Jan 1
TI  - Risk of cardiovascular events in patients receiving celecoxib: a meta-analysis of 
      randomized clinical trials.
PG  - 91-8
AB  - Some nonsteroidal anti-inflammatory drugs (NSAIDs), including cyclooxygenase-2 
      selective inhibitors, have been associated with increased cardiovascular (CV) 
      events in recent clinical trials or observational studies. To determine whether 
      the cyclooxygenase-2 selective inhibitor celecoxib affects CV risk, the incidence 
      of CV events was analyzed in patients treated with celecoxib, placebo, or 
      nonselective NSAIDs in the clinical trial database for celecoxib using defined 
      Antiplatelet Trialists' Collaboration end points of nonfatal myocardial 
      infarction, nonfatal stroke, and CV death. Patient data were derived from studies 
      in osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, low back pain, 
      and Alzheimer's disease. This meta-analysis included (1) 7,462 patients exposed 
      to celecoxib 200 to 800 mg/day for 1,268 patient-years compared with 4,057 
      patients treated with placebo for 585 patient-years, and (2) 19,773 patients 
      treated with celecoxib 200 to 800 mg/day for 5,651 patient-years compared with 
      13,990 patients treated with nonselective NSAIDs (diclofenac, ibuprofen, 
      naproxen, ketoprofen, and loxoprofen) for 4,386 patient-years. CV events were 
      adjudicated by a 3-member expert end point committee (WBW, JSB, PBG) blinded to 
      treatment group and study. The incidence rates of the combined CV events were not 
      significantly different between patients treated with celecoxib and placebo or 
      between those treated with celecoxib and nonselective NSAIDs. Event rates were 
      similar for adjudicated and nonadjudicated data. Dose of celecoxib, the use of 
      aspirin, or the presence of CV risk factors did not alter these results. In 
      conclusion, these analyses failed to demonstrate an increased CV risk with 
      celecoxib relative to placebo and demonstrated a comparable rate of CV events 
      with celecoxib treatment compared with nonselective NSAIDs.
FAU - White, William B
AU  - White WB
AD  - Pat and Jim Calhoun Cardiology Center, University of Connecticut School of 
      Medicine, Farmington, CT, USA. wwhite@nso1.uchc.edu
FAU - West, Christine R
AU  - West CR
FAU - Borer, Jeffrey S
AU  - Borer JS
FAU - Gorelick, Philip B
AU  - Gorelick PB
FAU - Lavange, Lisa
AU  - Lavange L
FAU - Pan, Sharon X
AU  - Pan SX
FAU - Weiner, Ethan
AU  - Weiner E
FAU - Verburg, Kenneth M
AU  - Verburg KM
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
DEP - 20061110
PL  - United States
TA  - Am J Cardiol
JT  - The American journal of cardiology
JID - 0207277
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Pyrazoles)
RN  - 0 (Sulfonamides)
RN  - JCX84Q7J1L (Celecoxib)
SB  - IM
MH  - Administration, Oral
MH  - Aged
MH  - Anti-Inflammatory Agents, Non-Steroidal/administration & dosage/*adverse effects
MH  - Cardiovascular Diseases/*chemically induced
MH  - Celecoxib
MH  - Cyclooxygenase Inhibitors/administration & dosage/*adverse effects
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Pyrazoles/administration & dosage/*adverse effects
MH  - Randomized Controlled Trials as Topic
MH  - Risk
MH  - Sulfonamides/administration & dosage/*adverse effects
EDAT- 2007/01/02 09:00
MHDA- 2007/02/09 09:00
CRDT- 2007/01/02 09:00
PHST- 2006/04/24 00:00 [received]
PHST- 2006/07/12 00:00 [revised]
PHST- 2006/07/12 00:00 [accepted]
PHST- 2007/01/02 09:00 [pubmed]
PHST- 2007/02/09 09:00 [medline]
PHST- 2007/01/02 09:00 [entrez]
AID - S0002-9149(06)01823-6 [pii]
AID - 10.1016/j.amjcard.2006.07.069 [doi]
PST - ppublish
SO  - Am J Cardiol. 2007 Jan 1;99(1):91-8. doi: 10.1016/j.amjcard.2006.07.069. Epub 
      2006 Nov 10.

PMID- 21289940
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20110714
LR  - 20211020
IS  - 1861-8863 (Print)
IS  - 1861-8863 (Electronic)
IS  - 1861-8863 (Linking)
VI  - 3
DP  - 2007 Aug 10
TI  - Benefits and risks of hormonal contraception for women.
PG  - Doc06
LID - Doc06
AB  - SCIENTIFIC BACKGROUND: A large proportion of women of reproductive age in Germany 
      use various methods of pregnancy prevention (contraception), among them various 
      hormone-based methods. Hormonal contraceptives may be divided into combined 
      estrogen-progestogen contraceptives (pills, skin patches, vaginal rings), 
      progestogen-only contraceptives (pills, injections, implants, hormone spirals) 
      and emergency contraceptives. RESEARCH QUESTIONS: The evaluation addressed the 
      question of benefits and risks of hormonal contraceptives, their economic effects 
      as well as their ethical-social and legal implications. METHODS: A systematic 
      literature search was conducted in April 2006 starting from 2000. The evaluation 
      is primarily based on systematic reviews. RESULTS: In perfect use, all hormonal 
      contraceptives excluding emergency contraceptives proved to be the most effective 
      reversible contraceptive methods (rate of unintended pregnancies 0.05% to 0.3%). 
      However, the typical use of oral contraceptives, injections, skin patches, and 
      vaginal rings, which also considers possible application errors, showed a lower 
      contraceptive efficacy (rate of unintended pregnancies 3% to 8%). It was lower 
      than that of copper spirals. The risk of venous thromboembolism increased three 
      to six times in users of hormonal contraceptives, the risks of stroke and 
      myocardial infarction two to three times. The risk declined after discontinuation 
      of use. The effects were estrogen-dose and progestogen-type dependent. The use of 
      hormonal contraceptives showed a relative risk of ovarian and endometrial 
      carcinomas of approximately 0.5 or 0.7, of breast and cervical cancer of 
      approximately 1.2 or 1.6. The effect remained several years after discontinuation 
      of use. The results concerning hepatocellular carcinoma suggested a carcinogenic 
      effect. In women with acne, an improvement due to use of hormonal contraceptives 
      was proven. Cervical chlamydial infections were more frequent in users of 
      hormonal contraception. Headache appeared mostly only at the beginning of the use 
      of combined oral contraceptives. Progestogen-only contraceptives worsened the 
      results of the glucose tolerance test. A review of low evidence reported further 
      risks of hormonal contraceptives (concerning menstrual problems, ovarian cysts, 
      bone density, thyroid diseases and rheumatoid arthritis) as well as further 
      benefits (concerning blood pressure and Crohn's disease). Hormonal spirals were 
      shown to be more effective than spirals which do not release hormones. In 
      emergency contraception, Levonorgestrel was more effective than the Yuzpe method. 
      Most other proven differences between hormonal contraceptives were related to 
      menstrual problems. After spirals with or without hormone release, the other 
      hormonal contraceptives were shown in typical use to be the second most 
      cost-effective reversible methods of contraception. DISCUSSION: The addressed 
      questions could be answered only on relatively low evidence level, partly only 
      for applications with estrogen doses which are not used in Germany any more. The 
      transferability of the results of the analysed primary health-economics studies 
      on the current situation in Germany is limited (clinical assumptions from 
      out-dated information sources of low evidence levels, cost assumptions from the 
      American health system). CONCLUSIONS: In perfect use, hormonal contraceptives 
      have to be classified as the most effective reversible contraceptive methods. For 
      the individual decision concerning the use of hormonal contraception, benefits 
      should be related to the additional risks. Alternative methods such as spirals 
      should be prioritised if perfect use seems to be impossible. In this case, 
      spirals are also preferable from health-economics perspective. No ethical-social 
      or legal conclusions can be derived from the available data.
FAU - Gorenoi, Vitali
AU  - Gorenoi V
AD  - Medizinische Hochschule Hannover, Abteilung für Epidemiologie, Sozialmedizin und 
      Gesundheitssystemforschung, Hannover, Deutschland.
FAU - Schönermark, Matthias P
AU  - Schönermark MP
FAU - Hagen, Anja
AU  - Hagen A
LA  - eng
PT  - Journal Article
DEP - 20070810
PL  - Germany
TA  - GMS Health Technol Assess
JT  - GMS health technology assessment
JID - 101276045
PMC - PMC3011324
EDAT- 2007/01/01 00:00
MHDA- 2007/01/01 00:01
PMCR- 2007/08/10
CRDT- 2011/02/04 06:00
PHST- 2011/02/04 06:00 [entrez]
PHST- 2007/01/01 00:00 [pubmed]
PHST- 2007/01/01 00:01 [medline]
PHST- 2007/08/10 00:00 [pmc-release]
AID - hta000041 [pii]
PST - epublish
SO  - GMS Health Technol Assess. 2007 Aug 10;3:Doc06.

PMID- 17174586
OWN - NLM
STAT- MEDLINE
DCOM- 20070412
LR  - 20200205
IS  - 1778-7254 (Electronic)
IS  - 1297-319X (Linking)
VI  - 74
IP  - 1
DP  - 2007 Jan
TI  - Cardiovascular disease in rheumatoid arthritis: single-center hospital-based 
      cohort study in France.
PG  - 66-72
AB  - INTRODUCTION: Rheumatoid arthritis (RA) was independently associated with 
      cardiovascular events in several studies, most of which were conducted in the US. 
      OBJECTIVES: To estimate the risk of cardiovascular events in a cohort of RA 
      patients recruited at a hospital in France, to identify cardiovascular risk 
      factors, and to measure the severity of cardiovascular events. METHODS: Two 
      hundred and thirty-nine patients admitted between January 1, 1998, and March 31, 
      1999, for RA meeting American College of Rheumatology criteria, with a negative 
      history for cardiovascular events, were sent a questionnaire in 2004 to evaluate 
      the occurrence of myocardial infarction, stroke, or cardiovascular death. 
      RESULTS: During the mean follow-up of 5.4+/-1.8 years, there were 10 cases of 
      myocardial infarction (0.8%/year), 3 cases of stroke (0.2%/year), and 9 
      cardiovascular deaths (0.7%/year). Of the 10 patients who experienced myocardial 
      infarction, 5 had clinical symptoms of heart failure and 4 died from 
      cardiovascular causes. Independent risk factors for cardiovascular events were 
      older age (relative risk [RR], 2.5/10 years; 95% confidence interval [95%CI], 
      1.4-4.2), male gender (RR, 5.1; 95%CI, 1.8-14.6), treated hypertension (RR, 4.3; 
      95%CI, 1.4-13.2), and treated hypercholesterolemia (RR, 6.0; 95%CI, 1.8-20.7). 
      CONCLUSION: Our data suggest a higher risk of cardiovascular events in patients 
      with RA compared to the general population in France (0.1-0.5%/year for 
      myocardial infarction and 0.07%/year for stroke in the age group covered by our 
      cohort). Cardiovascular events in the patients with RA seemed unusually severe. 
      Patients with RA should be carefully screened for conventional cardiovascular 
      risk factors.
FAU - Assous, Noémie
AU  - Assous N
AD  - Rheumatology A Department, School of Medicine, René Descartes University, Cochin 
      Teaching Hospital, Paris, France.
FAU - Touzé, Emmanuel
AU  - Touzé E
FAU - Meune, Christophe
AU  - Meune C
FAU - Kahan, André
AU  - Kahan A
FAU - Allanore, Yannick
AU  - Allanore Y
LA  - eng
PT  - Journal Article
DEP - 20061117
PL  - France
TA  - Joint Bone Spine
JT  - Joint bone spine
JID - 100938016
SB  - IM
MH  - Age Distribution
MH  - Aged
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Cardiovascular Diseases/classification/*epidemiology
MH  - Cohort Studies
MH  - Comorbidity
MH  - Female
MH  - Follow-Up Studies
MH  - France/epidemiology
MH  - Hospitals, Teaching
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Proportional Hazards Models
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Sex Distribution
EDAT- 2006/12/19 09:00
MHDA- 2007/04/14 09:00
CRDT- 2006/12/19 09:00
PHST- 2005/12/20 00:00 [received]
PHST- 2006/10/19 00:00 [accepted]
PHST- 2006/12/19 09:00 [pubmed]
PHST- 2007/04/14 09:00 [medline]
PHST- 2006/12/19 09:00 [entrez]
AID - S1297-319X(06)00234-X [pii]
AID - 10.1016/j.jbspin.2006.10.001 [doi]
PST - ppublish
SO  - Joint Bone Spine. 2007 Jan;74(1):66-72. doi: 10.1016/j.jbspin.2006.10.001. Epub 
      2006 Nov 17.

PMID- 17136752
OWN - NLM
STAT- MEDLINE
DCOM- 20070206
LR  - 20220317
IS  - 0004-3591 (Print)
IS  - 0004-3591 (Linking)
VI  - 54
IP  - 12
DP  - 2006 Dec
TI  - Immunosuppressive medications and hospitalization for cardiovascular events in 
      patients with rheumatoid arthritis.
PG  - 3790-8
AB  - OBJECTIVE: The risk of cardiovascular disease (CVD) is increased in patients with 
      rheumatoid arthritis (RA), most likely because of increased systemic 
      inflammation. Prior research suggests that immunosuppressive medications may 
      reduce the risk of CVD among RA patients. This study was undertaken to 
      investigate the effects of various immunosuppressive medications on the risk of 
      cardiovascular events among a group of older patients with RA. METHODS: In this 
      nested case-control study, the source cohort was derived from Medicare 
      beneficiaries receiving a drug benefit from the state of Pennsylvania. These 
      individuals were required to have been diagnosed as having RA on at least 2 
      visits and to have filled a prescription for an immunosuppressive agent. Cases 
      were defined as those patients who were hospitalized for a cardiovascular event 
      such as myocardial infarction or stroke, and 10 control subjects were matched to 
      each case by age, sex, and calendar year of the index date (the time of the first 
      cardiovascular event in each case). Current use of an immunosuppressive 
      medication was defined as having filled a prescription for these agents within 
      the 90 days prior to the index date. Multivariate logistic regression models that 
      included important covariates were assessed to determine the risk of 
      cardiovascular events associated with immunosuppressive agents and their 
      combinations. RESULTS: Among the study cohort, we identified 3,501 RA patients 
      who fulfilled our eligibility criteria. During followup of this cohort, 946 
      patients were hospitalized for a cardiovascular event. Although the 95% 
      confidence intervals (95% CIs) were wide in adjusted risk regression models with 
      methotrexate (MTX) monotherapy as the reference group, biologic immunosuppressive 
      agents showed neither protective nor deleterious effects (with biologics 
      monotherapy, odds ratio [OR] 1.0, 95% CI 0.5-1.9; with biologics plus MTX 
      combination therapy, OR 0.8, 95% CI 0.3-2.0; and with biologics plus other 
      immunosuppressive agents, OR 1.2, 95% CI 0.7-2.2). Monotherapy with oral 
      glucocorticoids was associated with an increased risk of cardiovascular events 
      (OR 1.5, 95% CI 1.1-2.1), and a similar trend in the direction of risk was seen 
      with glucocorticoid combination therapy (OR 1.3, 95% CI 0.8-2.0). Cytotoxic 
      immunosuppressive agents other than MTX (azathioprine, cyclosporine, and 
      leflunomide) were also associated with an increased risk of cardiovascular events 
      (with both monotherapy and combination treatment, OR 1.8, 95% CI 1.1-3.0). 
      CONCLUSION: When compared with RA patients receiving MTX monotherapy, those 
      receiving biologic immunosuppressive agents had neither an increased nor 
      decreased risk of experiencing a cardiovascular event, whereas use of oral 
      glucocorticoids and cytotoxic immunosuppressive agents was associated with 
      significant increases in the risk of cardiovascular events.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 
      02120, USA. dhsolomon@partners.org
FAU - Avorn, Jerry
AU  - Avorn J
FAU - Katz, Jeffrey N
AU  - Katz JN
FAU - Weinblatt, Michael E
AU  - Weinblatt ME
FAU - Setoguchi, Soko
AU  - Setoguchi S
FAU - Levin, Raisa
AU  - Levin R
FAU - Schneeweiss, Sebastian
AU  - Schneeweiss S
LA  - eng
GR  - K23-AR-48616/AR/NIAMS NIH HHS/United States
GR  - K24-02123/PHS HHS/United States
GR  - P60-AR-47782/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Immunosuppressive Agents)
SB  - IM
MH  - Aged, 80 and over
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/complications/*drug therapy/*epidemiology
MH  - Cardiovascular Diseases/*epidemiology/etiology/prevention & control
MH  - Cohort Studies
MH  - Comorbidity
MH  - Female
MH  - *Hospitalization/statistics & numerical data
MH  - Humans
MH  - Immunosuppressive Agents/*therapeutic use
MH  - Male
MH  - Medicare
MH  - Myocardial Infarction/epidemiology
MH  - Pennsylvania/epidemiology
MH  - Risk Factors
MH  - Stroke/epidemiology
EDAT- 2006/12/01 09:00
MHDA- 2007/02/07 09:00
CRDT- 2006/12/01 09:00
PHST- 2006/12/01 09:00 [pubmed]
PHST- 2007/02/07 09:00 [medline]
PHST- 2006/12/01 09:00 [entrez]
AID - 10.1002/art.22255 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2006 Dec;54(12):3790-8. doi: 10.1002/art.22255.

PMID- 17078593
OWN - NLM
STAT- MEDLINE
DCOM- 20061120
LR  - 20180417
IS  - 0755-4982 (Print)
IS  - 0755-4982 (Linking)
VI  - 35
IP  - 9 Spec No 1
DP  - 2006 Sep
TI  - [How to evaluate the cardiovascular and renal risk at the individual level?].
PG  - 1S35-40
AB  - The cardiovascular impact of the non-steroidal anti-inflammatory drugs and the 
      higher cardiovascular mortality during treatment of inflammatory rheumatism 
      impose a rigorous evaluation of the cardiovascular risk of rheumatic patients. 
      Large epidemiological studies have identified risk factors for cardiovascular 
      diseases such as the age, male gender, family history (infarct, stroke), tobacco 
      consumption, systolic arterial pressure, renal insufficiency, 
      hypercholesterolemia, diabetes mellitis, sedentariness, obesity and "electric" 
      ventricular hypertrophy. Some equations make it possible to evaluate the absolute 
      cardiovascular risk at the individual level, which corresponds to the onset risk 
      of a stroke in the 10 years to come in a subject according to the number and 
      importance of each of his risk factors. It has been demonstrated that the 
      correction of one or more risk factors reduce the overall cardiovascular risk 
      justifying the strategies for evaluating this risk to define therapeutic 
      intervention thresholds. The impact of a long-term anti-inflammatory treatment or 
      an inflammatory disease such as rheumatoid arthritis has not been the subject of 
      specific epidemiological study allowing these elements to be included in an 
      equation of the estimation of the cardiovascular risk. However, the introduction 
      of on anti-inflammatory treatment, likely to increase the cardiovascular risk of 
      a patient, certainly justifies an evaluation of the absolute cardiovascular risk.
FAU - Schaeverbeke, Thierry
AU  - Schaeverbeke T
AD  - Service de Rhumatologie, CHU Pellegrin, Bordeaux 33000. 
      thierry.schaeverbeke@chu-bordeaux.fr
FAU - Vicaut, Eric
AU  - Vicaut E
FAU - Cohen, Ariel
AU  - Cohen A
FAU - Ravaud, Philippe
AU  - Ravaud P
LA  - fre
PT  - Comparative Study
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - Comment evaluer le risque cardiovasculaire et rénal a l'echelon individuel?
PL  - France
TA  - Presse Med
JT  - Presse medicale (Paris, France : 1983)
JID - 8302490
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Hypolipidemic Agents)
SB  - IM
MH  - Adult
MH  - Age Factors
MH  - Aged
MH  - Aged, 80 and over
MH  - Anti-Inflammatory Agents, Non-Steroidal/*adverse effects/therapeutic use
MH  - Antihypertensive Agents/administration & dosage/therapeutic use
MH  - Cardiovascular Diseases/*chemically induced/*epidemiology/mortality/prevention & 
      control
MH  - Case-Control Studies
MH  - Cohort Studies
MH  - Female
MH  - Follow-Up Studies
MH  - France
MH  - Humans
MH  - Hypolipidemic Agents/administration & dosage/therapeutic use
MH  - Kidney Diseases/*chemically induced
MH  - Male
MH  - Middle Aged
MH  - Multicenter Studies as Topic
MH  - Randomized Controlled Trials as Topic
MH  - Rheumatic Diseases/drug therapy
MH  - Risk Assessment
MH  - Risk Factors
MH  - Time Factors
MH  - United States
RF  - 28
EDAT- 2006/11/03 09:00
MHDA- 2006/12/09 09:00
CRDT- 2006/11/03 09:00
PHST- 2006/11/03 09:00 [pubmed]
PHST- 2006/12/09 09:00 [medline]
PHST- 2006/11/03 09:00 [entrez]
AID - S0755-4982(06)74938-7 [pii]
PST - ppublish
SO  - Presse Med. 2006 Sep;35(9 Spec No 1):1S35-40.

PMID- 17054845
OWN - NLM
STAT- MEDLINE
DCOM- 20070717
LR  - 20071115
IS  - 0376-2491 (Print)
IS  - 0376-2491 (Linking)
VI  - 86
IP  - 25
DP  - 2006 Jul 4
TI  - [Risk factor assessment of cardiocerebrovascular diseases in patients with 
      rheumatoid arthritis].
PG  - 1769-73
AB  - OBJECTIVE: To assess the prevalence of cardiocerebrovascular diseases (CCVDs) in 
      the patients with rheumatoid arthritis (RA) and analyzed the risk factors. 
      METHODS: The clinical data of 568 RA patients hospitalized 1995 - 2005, were 
      analyzed retrospectively. RESULTS: (1) The total prevalence of CCVD was 16.2% 
      (92/568). The prevalence rate of coronary heart disease, cerebrovascular disease, 
      hypertensive heart disease together with coronary heart disease including 2 cases 
      of heart failure, atherogenesis in large and medium-size arteries proved by color 
      Doppler ultrasonic examination, and gangrene of extremities were 53.26% (49/92), 
      22.83% (21/92), 13.04% (12/92), 6.52% (6/92), and 4.34% (4/92) respectively. (2) 
      Complication of CCVD in RA patients was associated with age, DAS28 disease 
      activity score, number of involved extra-articular organs, platelet count, 
      hyperfibrinogenemia, and C-reactive protein; and was not associated with sex, 
      auto-antibody, hereditary factor, other traditional CCBVD risk factors, and the 
      number of risk factors. (3) The occurrence of CCVD in RA patients was 
      significantly correlated with poor therapeutic response, lack of persistent 
      effective prevention of the traditional risk factors, use of cyclooxygenase 
      (Cox)-2 specific inhibitors, and long-term medication of high-dosage 
      glucocorticoid. CONCLUSION: Activity of the disease of RA, high inflammatory 
      index, extra-articular involvement, poor response to treatment, lack of 
      persistent effective prevention of the traditional risk factors, use of Cox-2 
      specific inhibitor, and long-term medication of high-dosage glucocorticoid are 
      risk factors of CCVD-co-morbidities in RA pate.
FAU - Li, Hong-bin
AU  - Li HB
AD  - Department of Rheumatology, Peking Union Medical College Hospital, Peking Union 
      Medical College, Beijing 100730, China.
FAU - Bai, Li
AU  - Bai L
FAU - Wu, Qing-jun
AU  - Wu QJ
FAU - Zhang, Xuan
AU  - Zhang X
FAU - Zhang, Feng-chun
AU  - Zhang FC
LA  - chi
PT  - English Abstract
PT  - Journal Article
PL  - China
TA  - Zhonghua Yi Xue Za Zhi
JT  - Zhonghua yi xue za zhi
JID - 7511141
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Glucocorticoids)
SB  - IM
MH  - Aged
MH  - Arteriosclerosis/epidemiology
MH  - Arthritis, Rheumatoid/*complications/drug therapy
MH  - Coronary Disease/*epidemiology
MH  - Cyclooxygenase Inhibitors/adverse effects
MH  - Factor Analysis, Statistical
MH  - Female
MH  - Follow-Up Studies
MH  - Glucocorticoids/adverse effects
MH  - Humans
MH  - Incidence
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Retrospective Studies
MH  - Stroke/*epidemiology
EDAT- 2006/10/24 09:00
MHDA- 2007/07/18 09:00
CRDT- 2006/10/24 09:00
PHST- 2006/10/24 09:00 [pubmed]
PHST- 2007/07/18 09:00 [medline]
PHST- 2006/10/24 09:00 [entrez]
PST - ppublish
SO  - Zhonghua Yi Xue Za Zhi. 2006 Jul 4;86(25):1769-73.

PMID- 17003915
OWN - NLM
STAT- MEDLINE
DCOM- 20061113
LR  - 20151119
IS  - 0340-6245 (Print)
IS  - 0340-6245 (Linking)
VI  - 96
IP  - 4
DP  - 2006 Oct
TI  - Does a coxib-associated thrombotic risk limit the clinical use of the compounds 
      as analgesic anti-inflammatory drugs? Arguments in favor.
PG  - 407-12
AB  - Non-steroidal anti-inflammatory agents (NSAIDs) and selective cyclooxygenase 
      (COX-2) inhibitors (coxibs) are commonly used as analgesic and anti-inflammatory 
      agents. Selective COX-2 inhibitors or coxibs were primarily developed as a 
      response to the gastrointestinal toxicity of conventional NSAIDs but may have 
      other side effects. Currently available data suggests definite prothrombotic risk 
      with the coxibs, and the magnitude of risk may vary with individual agents. Based 
      on available data, coxibs should be restricted to use as 2nd-line, possibly as 
      3rd-line, agents for carefully chosen patients and randomized trials versus 
      placebo or an accepted comparator must be performed to define the overall safety 
      profile in diverse patient populations. The recently announced Prospective 
      Randomized Evaluation of Celecoxib Integrated Safety vs. Ibuprofen or Naproxen 
      (PRECISION) trial will assess the relative cardiovascular safety of three of the 
      most commonly used pain relievers in the treatment of arthritis patients, 
      ibuprofen, naproxen and celecoxib. The study will enroll patients with 
      osteoarthritis, the most common form of arthritis, who have known coronary heart 
      disease or who have multiple risk factors for heart disease and also some 
      patients with rheumatoid arthritis. Patients will be followed for an average of 
      two years to track the occurrence of serious cardiovascular events, including 
      death, heart attack and stroke. This study should provide some definitive 
      evidence of the relative cardiovascular safety of the available anti-inflammatory 
      agents but would be even more useful if it included an arm where patients were 
      treated with analgesics such as acetaminophen and/or moderate strength narcotics.
FAU - Mukherjee, Debabrata
AU  - Mukherjee D
AD  - Division of Cardiovascular Medicine, Gill Heart Institute, University of 
      Kentucky, Lexington, Kentucky 40536-0200, USA. Mukherjee@uky.edu
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Thromb Haemost
JT  - Thrombosis and haemostasis
JID - 7608063
RN  - 0 (Analgesics)
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
RN  - 0 (Lactones)
RN  - 0 (Pyrazoles)
RN  - 0 (Sulfonamides)
RN  - 0 (Sulfones)
RN  - 0QTW8Z7MCR (rofecoxib)
RN  - JCX84Q7J1L (Celecoxib)
SB  - IM
MH  - Analgesics/*adverse effects
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/*adverse effects
MH  - Arthritis/drug therapy
MH  - Celecoxib
MH  - Cyclooxygenase 2 Inhibitors/*adverse effects
MH  - Drug Evaluation, Preclinical
MH  - Humans
MH  - Lactones/adverse effects
MH  - Pyrazoles/adverse effects
MH  - Randomized Controlled Trials as Topic
MH  - Risk Assessment
MH  - Sulfonamides/adverse effects
MH  - Sulfones/adverse effects
MH  - Thrombosis/*chemically induced
RF  - 30
EDAT- 2006/09/28 09:00
MHDA- 2006/11/14 09:00
CRDT- 2006/09/28 09:00
PHST- 2006/09/28 09:00 [pubmed]
PHST- 2006/11/14 09:00 [medline]
PHST- 2006/09/28 09:00 [entrez]
AID - 06100407 [pii]
PST - ppublish
SO  - Thromb Haemost. 2006 Oct;96(4):407-12.

PMID- 16932466
OWN - NLM
STAT- MEDLINE
DCOM- 20061114
LR  - 20211203
IS  - 1745-8323 (Print)
IS  - 1745-8323 (Linking)
VI  - 2
IP  - 7
DP  - 2006 Jul
TI  - Drug insight: Immunomodulatory effects of statins--potential benefits for renal 
      patients?
PG  - 378-87
AB  - Statins inhibit 3-hydroxyl-3-methylglutaryl coenzyme A reductase, an enzyme 
      crucial to cholesterol synthesis. Drugs of this class reduce the risk of coronary 
      heart disease and stroke, in large part through lipid modulation. Emerging 
      evidence indicates that statins have additional modes of action. These actions, 
      which encompass modification of endothelial function, plaque stability, thrombus 
      formation and inflammatory pathways, are widely referred to as 'pleiotropic 
      effects'. These pleiotropic effects indicate that the therapeutic potential of 
      statins might extend beyond cholesterol lowering and cardiovascular disease to 
      other inflammatory disorders or conditions such as transplantation, multiple 
      sclerosis, rheumatoid arthritis and chronic kidney disease. Experimental and 
      clinical data provide evidence to support these broader applications of statins; 
      however, more large-scale trials are needed to clarify the therapeutic benefit.
FAU - Steffens, Sabine
AU  - Steffens S
AD  - Division of Cardiology, Department of Medicine, University Hospital, Foundation 
      for Medical Research, Geneva, Switzerland.
FAU - Mach, François
AU  - Mach F
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Nat Clin Pract Nephrol
JT  - Nature clinical practice. Nephrology
JID - 101261800
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
SB  - IM
MH  - Animals
MH  - Cardiovascular Diseases/*prevention & control
MH  - Chronic Disease
MH  - Disease Models, Animal
MH  - Humans
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/*therapeutic use
MH  - Immune System/*drug effects
MH  - Immunosuppression Therapy
MH  - Kidney Diseases/*prevention & control
RF  - 108
EDAT- 2006/08/26 09:00
MHDA- 2006/11/15 09:00
CRDT- 2006/08/26 09:00
PHST- 2005/10/31 00:00 [received]
PHST- 2006/03/17 00:00 [accepted]
PHST- 2006/08/26 09:00 [pubmed]
PHST- 2006/11/15 09:00 [medline]
PHST- 2006/08/26 09:00 [entrez]
AID - ncpneph0217 [pii]
AID - 10.1038/ncpneph0217 [doi]
PST - ppublish
SO  - Nat Clin Pract Nephrol. 2006 Jul;2(7):378-87. doi: 10.1038/ncpneph0217.

PMID- 16922642
OWN - NLM
STAT- MEDLINE
DCOM- 20060925
LR  - 20191110
IS  - 1742-5255 (Print)
IS  - 1742-5255 (Linking)
VI  - 1
IP  - 2
DP  - 2005 Aug
TI  - Clinical pharmacology of etoricoxib.
PG  - 269-82
AB  - Etoricoxib is a highly selective COX-2 inhibitor (coxib) approved in Europe for 
      the treatment of osteoarthritis (OA), rheumatoid arthritis and acute gouty 
      arthritis. Etoricoxib is an effective analgesic drug that has shown some improved 
      efficacy versus traditional NSAIDs and it is the only coxib approved for the 
      treatment of acute gouty arthritis. Moreover, recent studies evidence its 
      efficacy in patients with ankylosing spondylitis. In the Etoricoxib Diclofenac 
      Gastrointestinal Evaluation study performed in patients with OA, etoricoxib 
      significantly reduced the rate of discontinuation by 50% due to gastrointestinal 
      adverse events versus diclofenac. Comparable rates of thrombotic cardiovascular 
      events were detected. Rates of discontinuation due to hypertension-related 
      adverse effects were higher on etoricoxib than diclofenac. Similarly to other 
      selective COX-2 inhibitors, etoricoxib is contraindicated in patients with 
      ischaemic heart disease or stroke and it should be used with caution in patients 
      with risk factors for heart disease. The European Medicines Agency has 
      contraindicated the use of etoricoxib in patients with uncontrolled hypertension. 
      Selective COX-2 inhibitors remain an appropriate choice in patients at low 
      cardiovascular risk, but with increased risk of gastrointestinal complications.
FAU - Capone, Marta L
AU  - Capone ML
AD  - Department of Medicine and Center of Excellence on ageing, G.d' Annunzio' 
      University School of Medicine and Gabriele d'Annunzio University Foundation, c/o 
      Palazzina Se.B.I., Via dei Vestini 31, 66013 Chieti, Italy.
FAU - Tacconelli, Stefania
AU  - Tacconelli S
FAU - Patrignani, Paola
AU  - Patrignani P
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Expert Opin Drug Metab Toxicol
JT  - Expert opinion on drug metabolism & toxicology
JID - 101228422
RN  - 0 (Cyclooxygenase 2 Inhibitors)
RN  - 0 (Pyridines)
RN  - 0 (Sulfones)
RN  - WRX4NFY03R (Etoricoxib)
SB  - IM
MH  - Clinical Trials as Topic
MH  - Cyclooxygenase 2 Inhibitors/adverse effects/*pharmacology/therapeutic use
MH  - Etoricoxib
MH  - Humans
MH  - Pyridines/adverse effects/*pharmacology/therapeutic use
MH  - Sulfones/adverse effects/*pharmacology/therapeutic use
RF  - 70
EDAT- 2006/08/23 09:00
MHDA- 2006/09/26 09:00
CRDT- 2006/08/23 09:00
PHST- 2006/08/23 09:00 [pubmed]
PHST- 2006/09/26 09:00 [medline]
PHST- 2006/08/23 09:00 [entrez]
AID - 10.1517/17425255.1.2.269 [doi]
PST - ppublish
SO  - Expert Opin Drug Metab Toxicol. 2005 Aug;1(2):269-82. doi: 
      10.1517/17425255.1.2.269.

PMID- 16802340
OWN - NLM
STAT- MEDLINE
DCOM- 20060913
LR  - 20071115
IS  - 0004-3591 (Print)
IS  - 0004-3591 (Linking)
VI  - 54
IP  - 7
DP  - 2006 Jul
TI  - Increased case fatality rates following a first acute cardiovascular event in 
      patients with rheumatoid arthritis.
PG  - 2061-8
AB  - OBJECTIVE: Among patients with rheumatoid arthritis (RA), cardiovascular 
      mortality is increased compared with the rate among unaffected peers. In this 
      study, 30-day mortality rates following a first acute cardiovascular event 
      (myocardial infarction or stroke) were compared between RA patients and the 
      general population. METHODS: All cases of a first acute cardiovascular event 
      between July 1, 2001 and November 30, 2003 in Victoria, Australia were identified 
      from hospital discharge data. Individuals were classified as having RA when an 
      International Classification of Diseases, Ninth Revision, Clinical Modification 
      (ICD-9-CM) or an International Statistical Classification of Diseases and Related 
      Health Problems, Tenth Revision, Australian Modification code for RA was recorded 
      at the index admission or during the previous 5 years. Thirty-day mortality rates 
      were determined from linkage to the state death registry. RESULTS: A total of 
      29,924 patients experienced a first cardiovascular event during the study period, 
      359 (1.2%) of whom had RA. Thirty-day cardiovascular mortality was 17.6% in RA 
      patients versus 10.8% in non-RA patients. In fully adjusted models, the odds 
      ratio (OR) for cardiovascular death in RA patients following a first acute 
      cardiovascular event was 1.6 (95% confidence interval [95% CI] 1.2-2.2). Analysis 
      of index event subgroups revealed that this increased case fatality rate in 
      patients with RA was accounted for almost entirely by excess deaths following 
      myocardial infarction. The adjusted ORs for cardiovascular death in RA after 
      myocardial infarction and stroke were 1.9 (95% CI 1.3-2.7) and 1.2 (95% CI 
      0.7-2.0), respectively. CONCLUSION: RA patients have a substantially increased 
      risk of 30-day case fatality following myocardial infarction, but not stroke, 
      compared with non-RA patients. This higher case fatality rate is likely to 
      contribute to the observed overall excess of cardiovascular deaths in RA 
      populations.
FAU - Van Doornum, S
AU  - Van Doornum S
AD  - Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, 
      Post Office Royal Melbourne Hospital, Grattan Street, Parkville, Victoria 3050, 
      Australia. svd@unimelb.edu.au
FAU - Brand, C
AU  - Brand C
FAU - King, B
AU  - King B
FAU - Sundararajan, V
AU  - Sundararajan V
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/*complications/*mortality
MH  - Cohort Studies
MH  - Comorbidity
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Mortality/trends
MH  - Myocardial Infarction/*mortality
MH  - Odds Ratio
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Stroke/*mortality
MH  - Survival Rate
MH  - Victoria/epidemiology
EDAT- 2006/06/28 09:00
MHDA- 2006/09/14 09:00
CRDT- 2006/06/28 09:00
PHST- 2006/06/28 09:00 [pubmed]
PHST- 2006/09/14 09:00 [medline]
PHST- 2006/06/28 09:00 [entrez]
AID - 10.1002/art.21932 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2006 Jul;54(7):2061-8. doi: 10.1002/art.21932.

PMID- 16793844
OWN - NLM
STAT- MEDLINE
DCOM- 20061214
LR  - 20220318
IS  - 0003-4967 (Print)
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 65
IP  - 12
DP  - 2006 Dec
TI  - Patterns of cardiovascular risk in rheumatoid arthritis.
PG  - 1608-12
AB  - BACKGROUND: Although it is known that rheumatoid arthritis is associated with an 
      increased risk of cardiovascular disease (CVD), the pattern of this risk is not 
      clear. This study investigated the relative risk of myocardial infarction, stroke 
      and CVD mortality in adults with rheumatoid arthritis compared with adults 
      without rheumatoid arthritis across age groups, sex and prior CVD event status. 
      METHODS: We conducted a cohort study among all residents aged >or=18 years 
      residing in British Columbia between 1999 and 2003. Residents who had visited the 
      doctor at least thrice for rheumatoid arthritis (International Classification of 
      Disease = 714) were considered to have rheumatoid arthritis. A non-rheumatoid 
      arthritis cohort was matched to the rheumatoid arthritis cohort by age, sex and 
      start of follow-up. The primary composite end point was a hospital admission for 
      myocardial infarction, stroke or CVD mortality. RESULTS: 25 385 adults who had at 
      least three diagnoses for rheumatoid arthritis during the study period were 
      identified. During the 5-year study period, 375 patients with rheumatoid 
      arthritis had a hospital admission for myocardial infarction, 363 had a 
      hospitalisation for stroke, 437 died from cardiovascular causes and 1042 had one 
      of these outcomes. The rate ratio for a CVD event in patients with rheumatoid 
      arthritis was 1.6 (95% confidence interval (CI) 1.5 to 1.7), and the rate 
      difference was 5.7 (95% CI 4.9 to 6.4) per 1000 person-years. The rate ratio 
      decreased with age, from 3.3 in patients aged 18-39 years to 1.6 in those aged 
      >or=75 years. However, the rate difference was 1.2 per 1000 person-years in the 
      youngest age group and increased to 19.7 per 1000 person-years in those aged 
      >or=75 years. Among patients with a prior CVD event, the rate ratios and rate 
      differences were not increased in rheumatoid arthritis. CONCLUSIONS: This study 
      confirms that rheumatoid arthritis is a risk factor for CVD events and shows that 
      the rate ratio for CVD events among subjects with rheumatoid arthritis is highest 
      in young adults and those without known prior CVD events. However, in absolute 
      terms, the difference in event rates is highest in older adults.
FAU - Solomon, D H
AU  - Solomon DH
AD  - Division of Pharmacoepidemiology, Brigham and Women's Hospital, 1620 Tremont 
      Street, Suite 3030, Boston, MA 02120, USA. dhsolomon@partners.org
FAU - Goodson, N J
AU  - Goodson NJ
FAU - Katz, J N
AU  - Katz JN
FAU - Weinblatt, M E
AU  - Weinblatt ME
FAU - Avorn, J
AU  - Avorn J
FAU - Setoguchi, S
AU  - Setoguchi S
FAU - Canning, C
AU  - Canning C
FAU - Schneeweiss, S
AU  - Schneeweiss S
LA  - eng
PT  - Journal Article
DEP - 20060622
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
CIN - Nat Clin Pract Rheumatol. 2007 May;3(5):260-1. doi: 10.1038/ncprheum0476. PMID: 
      17389882
MH  - Adolescent
MH  - Adult
MH  - Age Distribution
MH  - Aged
MH  - Arthritis, Rheumatoid/*complications/epidemiology
MH  - British Columbia/epidemiology
MH  - Cardiovascular Diseases/epidemiology/*etiology
MH  - Epidemiologic Methods
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/epidemiology/etiology
MH  - Sex Distribution
MH  - Stroke/epidemiology/etiology
PMC - PMC1798453
COIS- Competing interests: None declared.
EDAT- 2006/06/24 09:00
MHDA- 2006/12/15 09:00
PMCR- 2009/12/01
CRDT- 2006/06/24 09:00
PHST- 2006/06/24 09:00 [pubmed]
PHST- 2006/12/15 09:00 [medline]
PHST- 2006/06/24 09:00 [entrez]
PHST- 2009/12/01 00:00 [pmc-release]
AID - ard.2005.050377 [pii]
AID - ar50377 [pii]
AID - 10.1136/ard.2005.050377 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2006 Dec;65(12):1608-12. doi: 10.1136/ard.2005.050377. Epub 2006 
      Jun 22.

PMID- 16786783
OWN - NLM
STAT- MEDLINE
DCOM- 20061106
LR  - 20061115
IS  - 0033-2240 (Print)
IS  - 0033-2240 (Linking)
VI  - 62
IP  - 12
DP  - 2005
TI  - [Atherosclerosis and rheumatoid arthritis].
PG  - 1506-9
AB  - There is growing evidence that patients with rheumatoid arthritis (RA) are at 
      higher risk of cardiovascular diseases (CVD) including myocardial infarction and 
      stroke. Recent analysis indicate that CVD is the most common cause of death in 
      RA; however research on traditional risk factors such as smoking, hypertension or 
      elevated cholesterol level has shown mixed results. There are many convincing 
      suggestions that RA-specific factors associated with systemic inflammation may 
      play a critical role in endothelial cell damage and accelerated development of 
      atherosclerosis. Since atherosclerosis is currently recognized as a chronic 
      inflammatory condition that can be converted into an acute clinical event by 
      plaque rupture and thrombosis--the interplay between inflammatory mediators 
      including cytokines (TNF-alpha, IL-1, IL-6), C-reactive protein, blood 
      coagulation factors and vessel wall cells attracts much attention. Their pivotal 
      role in the pathogenesis of both diseases, RA and atherosclerosis has been 
      presented and discussed in our review.
FAU - Löwenhoff, Tomasz
AU  - Löwenhoff T
AD  - Zakład Reumatologii i Balneologii, Collegium Medicum, Uniwersytetu 
      Jagiellońskiego, Kraków. zruj@mp.pl
FAU - Głuszko, Piotr
AU  - Głuszko P
LA  - pol
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - Miazdzyca naczyń w reumatoidalnym zapaleniu stawów.
PL  - Poland
TA  - Przegl Lek
JT  - Przeglad lekarski
JID - 19840720R
RN  - 0 (Cytokines)
SB  - IM
MH  - Arthritis, Rheumatoid/*immunology/therapy
MH  - Atherosclerosis/*immunology/therapy
MH  - Cytokines/immunology
MH  - Endothelium, Vascular/immunology
MH  - Humans
MH  - Inflammation/*complications/*immunology
RF  - 58
EDAT- 2006/06/22 09:00
MHDA- 2006/11/07 09:00
CRDT- 2006/06/22 09:00
PHST- 2006/06/22 09:00 [pubmed]
PHST- 2006/11/07 09:00 [medline]
PHST- 2006/06/22 09:00 [entrez]
PST - ppublish
SO  - Przegl Lek. 2005;62(12):1506-9.

PMID- 16778472
OWN - NLM
STAT- MEDLINE
DCOM- 20060929
LR  - 20201209
IS  - 1648-9144 (Electronic)
IS  - 1010-660X (Linking)
VI  - 42
IP  - 5
DP  - 2006
TI  - [Nonsteroidal anti-inflammatory agents--choice between disturbances of 
      gastrointestinal tract and cardiovascular toxicity].
PG  - 429-39
AB  - Nonsteroidal anti-inflammatory agents are used more than 100 years. Most of them 
      can cause undesirable effects on gastrointestinal tract: ulceration, bleeding and 
      perforation of stomach and duodenum. Gastrointestinal toxicity is diminished when 
      selective cyclooxygenase-2 inhibitors are used. However, recent clinical trials 
      have showed that the use of cyclooxygenase-2 inhibitors increases the risk of 
      cardiovascular event and cerebrovascular accident. According to the data such 
      risk may be high using also nonselective nonsteroidal anti-inflammatory agents, 
      however, it is lesser. Incidence rates of the cardiovascular events and 
      cerebrovascular accidents increase due to activated thrombotic activity. 
      Nonsteroidal anti-inflammatory agents are very useful in the management of 
      rheumatic diseases and as pain relievers. Choosing appropriate nonsteroidal 
      anti-inflammatory agent it is essential to consider the risk of gastrointestinal 
      as well cardiovascular damage.
FAU - Gumbrevicius, Gintautas
AU  - Gumbrevicius G
AD  - Department of Theoretical and Clinical Pharmacology, Kaunas University of 
      Medicine, Kaunas, Lithuania. gingum@takas.lt
FAU - Milasius, Arvydas
AU  - Milasius A
FAU - Sveikata, Audrius
AU  - Sveikata A
LA  - lit
PT  - Comparative Study
PT  - Journal Article
PT  - Review
TT  - Nesteroidiniai vaistai nuo uzdegimo--pasirinkimas tarp zalingo poveikio 
      virskinimo traktui bei galimo sirdies ir kraujagysliu pazeidimo.
PL  - Switzerland
TA  - Medicina (Kaunas)
JT  - Medicina (Kaunas, Lithuania)
JID - 9425208
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Anticoagulants)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
RN  - 0 (Glucocorticoids)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Age Factors
MH  - Aged
MH  - Aged, 80 and over
MH  - Anti-Inflammatory Agents, Non-Steroidal/*adverse effects
MH  - Anticoagulants/adverse effects
MH  - Arthritis, Rheumatoid/drug therapy
MH  - Cardiovascular Diseases/*chemically induced/mortality
MH  - Cerebrovascular Disorders/chemically induced/mortality
MH  - Controlled Clinical Trials as Topic
MH  - Cyclooxygenase 2 Inhibitors/adverse effects
MH  - Drug Interactions
MH  - Female
MH  - Gastrointestinal Diseases/*chemically induced
MH  - Gastrointestinal Hemorrhage/chemically induced
MH  - Glucocorticoids/adverse effects
MH  - Helicobacter Infections/complications
MH  - Helicobacter pylori
MH  - Humans
MH  - Kidney Diseases/chemically induced
MH  - Male
MH  - Middle Aged
MH  - Osteoarthritis/drug therapy
MH  - Peptic Ulcer/chemically induced/complications
MH  - Peptic Ulcer Hemorrhage/chemically induced
MH  - Peptic Ulcer Perforation/chemically induced
MH  - Risk Factors
MH  - Time Factors
RF  - 31
EDAT- 2006/06/17 09:00
MHDA- 2006/09/30 09:00
CRDT- 2006/06/17 09:00
PHST- 2006/06/17 09:00 [pubmed]
PHST- 2006/09/30 09:00 [medline]
PHST- 2006/06/17 09:00 [entrez]
AID - 0605-11l [pii]
PST - ppublish
SO  - Medicina (Kaunas). 2006;42(5):429-39.

PMID- 16633945
OWN - NLM
STAT- MEDLINE
DCOM- 20060523
LR  - 20221212
IS  - 1424-7860 (Print)
IS  - 0036-7672 (Linking)
VI  - 136
IP  - 3-4
DP  - 2006 Jan 21
TI  - The role of statins in clinical medicine--LDL--cholesterol lowering and beyond.
PG  - 41-9
AB  - In the past years, statins have emerged as the most important class of lipid 
      lowering agents. Through inhibition of HMG-CoA reductase, they restrict the 
      rate-limiting step of cholesterol synthesis, which leads to upregulation of LDL 
      receptors on the cell membrane and thus reduction of atherogenic LDLs. This 
      effect translates into clinical benefit by reducing cardiovascular events both in 
      primary and secondary prevention settings. As an approximate rule, statin therapy 
      leads to a relative risk reduction of 25-30% in most of the large randomised 
      controlled trials. Stroke risk is reduced to a similar degree. Despite initial 
      concerns, the currently available statins have a favourable safety profile; 
      however, potential interactions with other drugs must be considered. Recently, 
      characteristics unrelated to LDL lowering have been intensively studied. These 
      pleiotropic statin effects result from decreased levels of isoprenoid 
      intermediates of cholesterol synthesis. They include--among 
      others--anti-inflammatory, anti-proliferative, and immunomodulatory actions. 
      Pleiotropic effects favourably influence pathomechanisms of plaque formation. 
      Furthermore, they may prove beneficial in the prevention or treatment of diseases 
      unrelated to atherosclerosis, eg rheumatoid arthritis, multiple sclerosis, or 
      cancer.
FAU - Rutishauser, Jonas
AU  - Rutishauser J
AD  - Innere Medizin B, Universitätsspital, Basel, Switzerland. j.rutishauser@unibas.ch
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Switzerland
TA  - Swiss Med Wkly
JT  - Swiss medical weekly
JID - 100970884
RN  - 0 (Cholesterol, LDL)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
SB  - IM
MH  - Cardiovascular Diseases/prevention & control
MH  - Cholesterol, LDL/blood/*drug effects
MH  - *Clinical Medicine
MH  - Fractures, Bone
MH  - Homeostasis
MH  - Humans
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology/*therapeutic use
MH  - Hypercholesterolemia/*drug therapy
MH  - Neoplasms
MH  - Risk Assessment
MH  - Stroke/prevention & control
MH  - Switzerland
RF  - 101
EDAT- 2006/04/25 09:00
MHDA- 2006/05/24 09:00
CRDT- 2006/04/25 09:00
PHST- 2006/04/25 09:00 [pubmed]
PHST- 2006/05/24 09:00 [medline]
PHST- 2006/04/25 09:00 [entrez]
AID - smw-11170 [pii]
AID - 10.4414/smw.2006.11170 [doi]
PST - ppublish
SO  - Swiss Med Wkly. 2006 Jan 21;136(3-4):41-9. doi: 10.4414/smw.2006.11170.

PMID- 16546242
OWN - NLM
STAT- MEDLINE
DCOM- 20060908
LR  - 20060612
IS  - 0079-6107 (Print)
IS  - 0079-6107 (Linking)
VI  - 92
IP  - 1
DP  - 2006 Sep
TI  - Epidemiology of disease risks in relation to vitamin D insufficiency.
PG  - 65-79
AB  - Vitamin D from ultraviolet-B (UVB) irradiance, food, and supplements is receiving 
      increased attention lately for its role in maintaining optimal health. Although 
      the calcemic effects of vitamin D have been known for about a century, the 
      non-calcemic effects have been studied intently only during the past two-three 
      decades. The strongest links to the beneficial roles of UVB and vitamin D to date 
      are for bone and muscle conditions and diseases. There is also a preponderance of 
      evidence from a variety of studies that vitamin D reduces the risk of colon 
      cancer, with 1000 IU/day of vitamin D or serum 25-hydroxyvitamin D levels >33 
      ng/mL (82 nmol/L) associated with a 50% lower incidence of colorectal cancer. 
      There is also reasonable evidence that vitamin D reduces the risk of breast, 
      lung, ovarian, and prostate cancer and non-Hodgkin's lymphoma. There is weaker, 
      primarily ecologic, evidence for the role of vitamin D in reducing the risk of an 
      additional dozen types of cancer. There is reasonably strong ecologic and 
      case-control evidence that vitamin D reduces the risk of autoimmune diseases 
      including such as multiple sclerosis and type 1 diabetes mellitus, and weaker 
      evidence for rheumatoid arthritis, osteoarthritis, type 2 diabetes mellitus, 
      hypertension and stroke. It is noted that mechanisms whereby vitamin D exerts its 
      effect are generally well understood for the various conditions and diseases 
      discussed here.
FAU - Grant, William B
AU  - Grant WB
AD  - Sunlight, Nutrition and Health Research Center (SUNARC), 2107 Van Ness Avenue, 
      Suite 403B, San Francisco, CA 94109-2529, USA. wgrant@sunarc.org
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20060228
PL  - England
TA  - Prog Biophys Mol Biol
JT  - Progress in biophysics and molecular biology
JID - 0401233
RN  - 1406-16-2 (Vitamin D)
SB  - IM
MH  - Autoimmune Diseases/*mortality/prevention & control
MH  - Bone Diseases/*mortality/prevention & control
MH  - Causality
MH  - Comorbidity
MH  - Humans
MH  - Internationality
MH  - Muscular Diseases/*mortality/prevention & control
MH  - Neoplasms/*mortality/prevention & control
MH  - Prevalence
MH  - Risk Assessment/*methods
MH  - Risk Factors
MH  - Survival Rate
MH  - Vitamin D/therapeutic use
MH  - Vitamin D Deficiency/*mortality/prevention & control
RF  - 153
EDAT- 2006/03/21 09:00
MHDA- 2006/09/09 09:00
CRDT- 2006/03/21 09:00
PHST- 2006/03/21 09:00 [pubmed]
PHST- 2006/09/09 09:00 [medline]
PHST- 2006/03/21 09:00 [entrez]
AID - S0079-6107(06)00011-3 [pii]
AID - 10.1016/j.pbiomolbio.2006.02.013 [doi]
PST - ppublish
SO  - Prog Biophys Mol Biol. 2006 Sep;92(1):65-79. doi: 
      10.1016/j.pbiomolbio.2006.02.013. Epub 2006 Feb 28.

PMID- 16503422
OWN - NLM
STAT- MEDLINE
DCOM- 20060928
LR  - 20220330
IS  - 1567-5688 (Print)
IS  - 1567-5688 (Linking)
VI  - 7
IP  - 1
DP  - 2006 Apr
TI  - Statins: potential new indications in inflammatory conditions.
PG  - 31-5
AB  - Hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are 
      potent cholesterol-lowering drugs. In addition to their cholesterol-lowering 
      properties, statins exert a number of so-called 'pleiotropic', vasculoprotective 
      actions that include improvement of endothelial function, increased nitric oxide 
      (NO) bioavailability, antioxidant properties, stabilisation of atherosclerotic 
      plaques, regulation of progenitor cells, inhibition of inflammatory responses and 
      immunomodulatory actions. Pleiotropic actions of statins may have potential 
      clinical impact in vascular disease beyond cholesterol lowering. The ongoing 
      Justification for the Use of statins in Primary prevention: an Intervention Trial 
      Evaluating Rosuvastatin (JUPITER), for example, tests the effects of statins in 
      the primary prevention of cardiovascular disease among patients with low levels 
      of low-density lipoprotein cholesterol (LDL-C) and elevated high-sensitivity 
      C-reactive protein (hs-CRP). Additionally, previous studies have shown that 
      although cholesterol is not an established stroke risk factor, statin therapy is 
      associated with a reduction in the incidence of strokes. It is known that sudden 
      withdrawal of statin treatment may acutely impair vascular function and increase 
      morbidity and mortality in patients with vascular disease. Furthermore, the 
      anti-inflammatory effects of statins may have clinical impact in a number of 
      non-vascular conditions including multiple sclerosis and rheumatoid arthritis.
FAU - Endres, Matthias
AU  - Endres M
AD  - Klinik und Poliklinik für Neurologie, Charité-Universitätsmedizin Berlin, Campus 
      Mitte, Schumannstrasse 20/21, D-10117 Berlin, Germany. matthias.endres@charite.de
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20060228
PL  - Netherlands
TA  - Atheroscler Suppl
JT  - Atherosclerosis. Supplements
JID - 100973461
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Immunologic Factors)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Animals
MH  - C-Reactive Protein/analysis
MH  - Coronary Artery Disease/drug therapy
MH  - Heart Failure/drug therapy
MH  - Humans
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology/*therapeutic use
MH  - Immunologic Factors/pharmacology/therapeutic use
MH  - Inflammation/*drug therapy
MH  - Multiple Sclerosis/drug therapy
MH  - Stroke/drug therapy
RF  - 38
EDAT- 2006/03/01 09:00
MHDA- 2006/09/29 09:00
CRDT- 2006/03/01 09:00
PHST- 2005/01/13 00:00 [received]
PHST- 2006/03/01 09:00 [pubmed]
PHST- 2006/09/29 09:00 [medline]
PHST- 2006/03/01 09:00 [entrez]
AID - S1567-5688(06)80094-2 [pii]
AID - 10.1016/j.atherosclerosissup.2006.01.005 [doi]
PST - ppublish
SO  - Atheroscler Suppl. 2006 Apr;7(1):31-5. doi: 
      10.1016/j.atherosclerosissup.2006.01.005. Epub 2006 Feb 28.

PMID- 16393277
OWN - NLM
STAT- MEDLINE
DCOM- 20060503
LR  - 20181203
IS  - 0269-2813 (Print)
IS  - 0269-2813 (Linking)
VI  - 23
IP  - 1
DP  - 2006 Jan 1
TI  - Systematic review: coxibs, non-steroidal anti-inflammatory drugs or no 
      cyclooxygenase inhibitors in gastroenterological high-risk patients?
PG  - 27-33
AB  - Selective cyclooxygenase-2 inhibitors have been marketed as alternatives of 
      conventional, non-steroidal anti-inflammatory drugs with the purpose of 
      reducing/eliminating the risk of ulcer complications. Unexpectedly, 
      randomized-controlled trials revealed that long-term use of coxibs, such as 
      rofecoxib, significantly increased the risk of myocardial infarction and stroke, 
      while the use of valdecoxib was associated with potentially life-threatening skin 
      reactions. Subsequently, rofecoxib and valdecoxib were withdrawn from the market. 
      Although more strict precautions for other coxibs, such as celecoxib, etoricoxib, 
      lumiracoxib and parecoxib, may be accepted/recommended by regulatory agencies, a 
      critical review of published data suggests that their use may not be justified - 
      even in high-risk patients - taking benefits, costs and risks into consideration. 
      Clinicians should, therefore, never prescribe coxibs to patients with 
      cardiovascular risk factors, and should only reluctantly prescribe coxibs to 
      patients with a history of ulcer disease or dyspepsia to overcome persistent pain 
      due to, e.g. rheumatoid arthritis or osteoarthritis. Instead, they should 
      consider using conventional non-steroidal anti-inflammatory drugs in combination 
      with a proton pump inhibitor or a prostaglandin analogue, especially for patients 
      with increased cardiovascular risks, i.e. established ischaemic heart disease, 
      cerebrovascular disease and/or peripheral arterial disease, or alternatively 
      acetaminophen. An evidence-based algorithm for treatment of a chronic arthritis 
      patient with one or more gastrointestinal risk factors is presented.
FAU - Nielsen, O H
AU  - Nielsen OH
AD  - Department of Gastroenterology C, Herlev Hospital, University of Copenhagen, 
      Denmark. ohn@dadlnet.dk
FAU - Ainsworth, M
AU  - Ainsworth M
FAU - Csillag, C
AU  - Csillag C
FAU - Rask-Madsen, J
AU  - Rask-Madsen J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PT  - Systematic Review
PL  - England
TA  - Aliment Pharmacol Ther
JT  - Alimentary pharmacology & therapeutics
JID - 8707234
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal/*adverse effects
MH  - Cardiovascular Diseases/*chemically induced/prevention & control
MH  - Cyclooxygenase 2 Inhibitors/*adverse effects
MH  - Gastrointestinal Diseases/*drug therapy
MH  - Humans
MH  - Risk Factors
RF  - 31
EDAT- 2006/01/06 09:00
MHDA- 2006/05/04 09:00
CRDT- 2006/01/06 09:00
PHST- 2006/01/06 09:00 [pubmed]
PHST- 2006/05/04 09:00 [medline]
PHST- 2006/01/06 09:00 [entrez]
AID - APT2745 [pii]
AID - 10.1111/j.1365-2036.2006.02745.x [doi]
PST - ppublish
SO  - Aliment Pharmacol Ther. 2006 Jan 1;23(1):27-33. doi: 
      10.1111/j.1365-2036.2006.02745.x.

PMID- 16366138
OWN - NLM
STAT- MEDLINE
DCOM- 20060216
LR  - 20220408
IS  - 1220-4749 (Print)
IS  - 1220-4749 (Linking)
VI  - 42
IP  - 4
DP  - 2004
TI  - Cardiovascular risk and rheumatoid arthritis: from mechanisms of atherosclerosis 
      to therapeutic approach.
PG  - 659-69
AB  - Large epidemiological studies showed that one of the most important causes of 
      death in patients with rheumatoid arthritis (RA) is represented by cardiovascular 
      disease. Thus, the presence of RA is associated with an increased risk of the 
      occurrence of stable angina, myocardial infarction, heart failure and stroke. 
      However, studies performed during the last years failed to bring us clear 
      evidence regarding the role of traditional cardiovascular risk factors 
      (hyperlipidemia, diabetes mellitus, hypertension, smoking and obesity) in the 
      pathogenesis of cardiovascular disease in these patients. Recently, the role of 
      inflammation and its mediators not only in the atherosclerosis plaque development 
      but also in the mechanisms of vulnerable plaque was clearly demonstrated. From 
      this point of view, recent studies showed that inflammatory cells and mediators 
      of inflammation are both markers of an increased cardiovascular risk and 
      unfavorable cardiovascular outcome, and also cardiovascular risk factors that act 
      in an active manner in the processes that promote atherosclerosis. Taking into 
      account the fact that RA is a systemic inflammatory status, recent reports 
      demonstrated the involvement of inflammation mediators in connection with 
      prothrombotic factors and endothelial dysfunction in the development of 
      cardiovascular disease in RA patients. There are only scarce data in the 
      literature regarding the benefice of cardiovascular risk reduction therapies in 
      this group. Further studies are required for the refinement of the cardiovascular 
      risk stratification algorithms and for the improvement of the cardiovascular risk 
      management in rheumatoid arthritis.
FAU - Jurcuţ, Ciprian
AU  - Jurcuţ C
AD  - Internal Medicine I Department, Central Military Hospital, Bucharest, Romania.
FAU - Jurcuţ, Ruxandra
AU  - Jurcuţ R
FAU - Tănăsescu, Coman
AU  - Tănăsescu C
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Rom J Intern Med
JT  - Romanian journal of internal medicine = Revue roumaine de medecine interne
JID - 9304507
RN  - 0 (Cytokines)
SB  - IM
MH  - Arthritis, Rheumatoid/*complications/*immunology/therapy
MH  - Atherosclerosis/etiology/immunology/therapy
MH  - Cardiovascular Diseases/*etiology/*immunology/therapy
MH  - Cytokines/immunology
MH  - Endothelium, Vascular/immunology
MH  - Humans
MH  - Inflammation/*complications/*immunology
MH  - Risk Factors
RF  - 45
EDAT- 2005/12/22 09:00
MHDA- 2006/02/17 09:00
CRDT- 2005/12/22 09:00
PHST- 2005/12/22 09:00 [pubmed]
PHST- 2006/02/17 09:00 [medline]
PHST- 2005/12/22 09:00 [entrez]
PST - ppublish
SO  - Rom J Intern Med. 2004;42(4):659-69.

PMID- 16333011
OWN - NLM
STAT- MEDLINE
DCOM- 20051209
LR  - 20220408
IS  - 1538-3598 (Electronic)
IS  - 0098-7484 (Linking)
VI  - 294
IP  - 21
DP  - 2005 Dec 7
TI  - Manifestations of chronic disease during pregnancy.
PG  - 2751-7
AB  - CONTEXT: Physiologic changes of pregnancy include insulin resistance, 
      thrombophilia, immunosuppression, and hypervolemia. These changes may herald the 
      development of disease in later life. OBJECTIVE: To summarize current evidence on 
      how pregnancy reveals risk of chronic disease. EVIDENCE ACQUISITION: MEDLINE was 
      searched for articles published between 1990 and 2005 relating pregnancy 
      conditions to the development of chronic disease. Bibliographies and the Web 
      sites of the International Society of Obstetric Medicine and International 
      Society for the Study of Hypertension in Pregnancy were also reviewed. EVIDENCE 
      SYNTHESIS: Pregnancy exaggerates atherogeniclike responses, including insulin 
      resistance and dyslipidemia, manifesting as preeclampsia or gestational diabetes. 
      These complications herald an increased risk of postpartum cardiovascular 
      disease, with a 2-fold increased risk of coronary artery disease and stroke. 
      Women with gestational diabetes mellitus can progress to type 2 diabetes 
      mellitus. The rate of progression varies from 6% to 92% depending on diagnostic 
      criteria, race/ethnicity, and duration of surveillance (from 6 months to 28 
      years). Pregnancy increases risk of venous thrombosis by 7- to 10-fold. Heritable 
      thrombophilia is present in at least 15% of Western populations and underlies at 
      least 50% of gestational venous thromboses. Thus, the procoagulant changes during 
      pregnancy can unmask hereditary thrombophilia. An important adaptation leading to 
      immunotolerance of the fetoplacental unit is a switch from helper T-cell (T(H)) 1 
      dominance to T(H)2 dominance. Patients with a T(H)1-dominant immune disease, such 
      as rheumatoid arthritis or multiple sclerosis, improve during pregnancy. However, 
      rheumatoid arthritis is 5 times more likely to develop after delivery than at any 
      other time. During pregnancy, there is a 50% increase in plasma volume, which can 
      unmask glomerulopathies, peripartum cardiomyopathy, arterial aneurysms, or 
      arteriovenous malformations. Development of intrahepatic cholestasis of pregnancy 
      predicts increased risk of later cholelithiasis. CONCLUSIONS: The physiologic 
      changes of pregnancy can reveal risk of chronic diseases. Exaggerated responses 
      reflective of the metabolic syndrome are seen in preeclampsia and gestational 
      diabetes and can herald future cardiovascular and metabolic disease. Pregnancy is 
      therefore an important screening opportunity for cardiovascular and metabolic 
      disease risk factors, with the possibility of early intervention.
FAU - Kaaja, Risto J
AU  - Kaaja RJ
AD  - Department of Obstetrics and Gynecology, Helsinki University Hospital, Helsinki, 
      Finland. risto.kaaja@hus.fi
FAU - Greer, Ian A
AU  - Greer IA
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - JAMA
JT  - JAMA
JID - 7501160
SB  - IM
MH  - Autoimmune Diseases/physiopathology
MH  - Cardiovascular Diseases/epidemiology/prevention & control
MH  - Cholestasis, Intrahepatic/physiopathology
MH  - Chronic Disease
MH  - Diabetes, Gestational/physiopathology
MH  - Female
MH  - Humans
MH  - Metabolic Diseases/epidemiology/prevention & control
MH  - Pre-Eclampsia/physiopathology
MH  - Pregnancy/*physiology
MH  - Pregnancy Complications/*physiopathology
MH  - Risk Factors
MH  - Thrombophilia/physiopathology
RF  - 99
EDAT- 2005/12/08 09:00
MHDA- 2005/12/13 09:00
CRDT- 2005/12/08 09:00
PHST- 2005/12/08 09:00 [pubmed]
PHST- 2005/12/13 09:00 [medline]
PHST- 2005/12/08 09:00 [entrez]
AID - 294/21/2751 [pii]
AID - 10.1001/jama.294.21.2751 [doi]
PST - ppublish
SO  - JAMA. 2005 Dec 7;294(21):2751-7. doi: 10.1001/jama.294.21.2751.

PMID- 16313350
OWN - NLM
STAT- MEDLINE
DCOM- 20060104
LR  - 20061115
IS  - 0105-2896 (Print)
IS  - 0105-2896 (Linking)
VI  - 208
DP  - 2005 Dec
TI  - Immune responses and bone loss: the estrogen connection.
PG  - 194-206
AB  - In addition to its effects on sexual differentiation and reproduction, estrogen 
      has important impact on the immune system and on bone. It has also been evident 
      that the effects of estrogen on bone to a large extent are mediated via its 
      action on immune cells. Estrogen has a dichotomous impact on the immune system by 
      downregulation of inflammatory immune responses but simultaneous upregulation of 
      immunoglobulin production. Consequently, immune-mediated diseases in humans and 
      in animal models are modulated by estrogen. Estrogen deficiency after ovariectomy 
      in mice and after menopause in women is associated with significant bone loss. In 
      rheumatic diseases such as rheumatoid arthritis (RA), osteoporosis is frequent, 
      and in patients with postmenopausal RA, the degree of bone loss is dramatically 
      increased. Hormone replacement therapy (HRT) in murine and human arthritis has 
      beneficial effects on bone loss, as expected, but it also ameliorates 
      inflammation and inflammation-triggered joint destruction. Long-term use of HRT 
      has been associated with increased risk of breast cancer, thrombosis, and 
      possibly also stroke. Accordingly, there is great need for new activators of 
      estrogen receptors (ERs) selectively reproducing only the beneficial effects of 
      estrogen. To achieve this aim, better knowledge of the mechanisms of how 
      activation of ER-alpha and ER-beta modulates the immune system and bone at the 
      cellular and molecular levels is necessary.
FAU - Carlsten, Hans
AU  - Carlsten H
AD  - Department of Rheumatology and Inflammation Research, The Sahlgrenska Academy at 
      Göteborg University, Göteborg, Sweden. hans.carlsten@rheuma.gu.se
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Immunol Rev
JT  - Immunological reviews
JID - 7702118
RN  - 0 (Estrogen Receptor alpha)
RN  - 0 (Estrogen Receptor beta)
RN  - 0 (Estrogens)
RN  - 0 (Interleukin-6)
RN  - 0 (Selective Estrogen Receptor Modulators)
SB  - IM
MH  - Animals
MH  - Arthritis, Experimental/etiology
MH  - Estrogen Receptor alpha/physiology
MH  - Estrogen Receptor beta/physiology
MH  - Estrogen Replacement Therapy
MH  - Estrogens/*physiology
MH  - Humans
MH  - Immune System/*physiology
MH  - Interleukin-6/physiology
MH  - Lupus Erythematosus, Systemic/etiology
MH  - Lymphopoiesis
MH  - Osteoporosis/*etiology
MH  - Selective Estrogen Receptor Modulators/pharmacology
RF  - 95
EDAT- 2005/11/30 09:00
MHDA- 2006/01/05 09:00
CRDT- 2005/11/30 09:00
PHST- 2005/11/30 09:00 [pubmed]
PHST- 2006/01/05 09:00 [medline]
PHST- 2005/11/30 09:00 [entrez]
AID - IMR326 [pii]
AID - 10.1111/j.0105-2896.2005.00326.x [doi]
PST - ppublish
SO  - Immunol Rev. 2005 Dec;208:194-206. doi: 10.1111/j.0105-2896.2005.00326.x.

PMID- 16199245
OWN - NLM
STAT- MEDLINE
DCOM- 20060721
LR  - 20161124
IS  - 0149-2918 (Print)
IS  - 0149-2918 (Linking)
VI  - 27
IP  - 8
DP  - 2005 Aug
TI  - Cardiovascular safety of lumiracoxib: a meta-analysis of all randomized 
      controlled trials > or =1 week and up to 1 year in duration of patients with 
      osteoarthritis and rheumatoid arthritis.
PG  - 1196-214
AB  - BACKGROUND: The cardiovascular (CV) safety of non-steroidal anti-inflammatory 
      drugs (NSAIDs) and selective cyclooxygenase-2 inhibitors has been the subject of 
      considerable debate. OBJECTIVE: The objective of this study was to determine the 
      risk of CV events with lumiracoxib by meta-analysis of all completed, randomized 
      controlled trials (RCTs) of > or =1 week and up to 1 year in duration of patients 
      with osteoarthritis and rheumatoid arthritis. METHODS: The Novartis Lumiracoxib 
      Clinical Trial Database, which includes all clinical studies conducted to date 
      with lumiracoxib, was reviewed. Data were extracted from RCTs of > or =1 week and 
      up to 1 year in duration, the maximum study duration; 34,668 patients were 
      included in standard and cumulative meta-analyses. Twenty-two RCTs of lumiracoxib 
      100 to 1200 mg daily were identified; 22,781 patients were included in 1-year 
      trials. Mean age of the patients was 61.5 years and 74% were female. More than 
      50% of the patients in these studies had hypertension at baseline and 6% had 
      diabetes. Parameters analyzed were the Antiplatelet Trialists' Collaboration 
      (APTC) composite CV end point of myocardial infarction (MI), stroke (ischemic and 
      hemorrhagic), and CV death; MI alone; and stroke alone. Twenty-one of the 22 RCTs 
      have been published. RESULTS: For all 3 parameters, relative risk (RR) was 
      calculated versus non-naproxen NSAIDs, naproxen, and placebo. The results were as 
      follows: for the APTC end point versus non-naproxen NSAIDs: RR 0.83, 95% CI, 
      0.46-1.51; versus naproxen: RR 1.49, 95% CI, 0.94-2.36; versus placebo: RR 1.08, 
      95% CI, 0.41-2.86; for MI alone versus non-naproxen NSAIDs: RR 0.80, 95% CI, 
      0.28-2.25; versus naproxen: RR 1.69, 95% CI, 0.82-3.48; versus placebo: RR 1.27, 
      95% CI, 0.25-6.56; and for stroke alone versus non-naproxen NSAIDs: RR 0.91, 95% 
      CI, 0.35-2.35; versus naproxen: RR 1.42, 95% CI, 0.70-2.91; versus placebo: RR 
      0.59, 95% CI, 0.13-2.74. Cumulative meta-analyses of lumiracoxib versus all 
      comparators (placebo, diclofenac, ibuprofen, celecoxib, rofecoxib, and naproxen) 
      did not find any significant differences in APTC, MI alone, or stroke alone. 
      CONCLUSION: This meta-analysis of 34,668 patients receiving > or =1 week and up 
      to 1 year of treatment found no evidence that lumiracoxib was associated with a 
      significant increase in CV risk compared with naproxen, placebo, or all 
      comparators (placebo, diclofenac, ibuprofen, celecoxib, rofecoxib, and naproxen).
FAU - Matchaba, Patrice
AU  - Matchaba P
AD  - Novartis Pharmaceuticals Corporation, East Hanover, NJ 07936, USA. 
      patrice.matchaba@novartis.com
FAU - Gitton, Xavier
AU  - Gitton X
FAU - Krammer, Gerhard
AU  - Krammer G
FAU - Ehrsam, Elena
AU  - Ehrsam E
FAU - Sloan, Victor Schorr
AU  - Sloan VS
FAU - Olson, Melvin
AU  - Olson M
FAU - Mellein, Bernhard
AU  - Mellein B
FAU - Hoexter, Godehard
AU  - Hoexter G
FAU - Orloff, John
AU  - Orloff J
FAU - Garaud, Jean-Jacques
AU  - Garaud JJ
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Clin Ther
JT  - Clinical therapeutics
JID - 7706726
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
RN  - 0 (Organic Chemicals)
RN  - 144O8QL0L1 (Diclofenac)
RN  - V91T9204HU (lumiracoxib)
SB  - IM
MH  - *Anti-Inflammatory Agents, Non-Steroidal/adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Cardiovascular Diseases/*chemically induced
MH  - *Cyclooxygenase 2 Inhibitors/adverse effects/therapeutic use
MH  - Databases, Factual
MH  - Diclofenac/analogs & derivatives
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Organic Chemicals/adverse effects/therapeutic use
MH  - Osteoarthritis/*drug therapy
MH  - Randomized Controlled Trials as Topic/*statistics & numerical data
RF  - 54
EDAT- 2005/10/04 09:00
MHDA- 2006/07/22 09:00
CRDT- 2005/10/04 09:00
PHST- 2005/06/17 00:00 [accepted]
PHST- 2005/10/04 09:00 [pubmed]
PHST- 2006/07/22 09:00 [medline]
PHST- 2005/10/04 09:00 [entrez]
AID - S0149-2918(05)00142-6 [pii]
AID - 10.1016/j.clinthera.2005.07.019 [doi]
PST - ppublish
SO  - Clin Ther. 2005 Aug;27(8):1196-214. doi: 10.1016/j.clinthera.2005.07.019.

PMID- 16170682
OWN - NLM
STAT- MEDLINE
DCOM- 20060119
LR  - 20091103
IS  - 0340-9937 (Print)
IS  - 0340-9937 (Linking)
VI  - 30
IP  - 6
DP  - 2005 Sep
TI  - [Cardiovascular comorbidity in rheumatic disease. Does sex play a role?].
PG  - 512-21
AB  - The importance of sex- and gender-related features of various diseases regarding 
      the impact of different risk factors on the natural course of disease, the 
      response to therapy and outcome have only more recently been appreciated. Studies 
      investigating sex- and gender-related aspects in rheumatoid arthritis (RA) are 
      scarce. Unambiguous classification of factors of potential pathogenetic relevance 
      or with the capacity to influence clinical course and disease management into 
      sex- or gender- related aspects is difficult (Figure 1). The majority of RA 
      patients is female. As illustrated by Figure 2, available evidence indicates a 
      progressive decline in the incidence of this disease over the past 40 years in 
      both men and women. There appears to be a cyclical pattern in the annual 
      incidence rates with peaks and troughs occurring for both sexes, but at different 
      times, which suggests the changing exposure to environmental factors which may 
      promote or decrease RA. Current knowledge suggests that RA is characterized by 
      chronic local and systemic inflammation which may trigger accelerated 
      atherogenesis. Sex hormones may also play a pathogenetic role. Androgens and 
      estrogens may stimulate the production of inflammatory cytokines in the synovial 
      fluid. These cytokines then may influence sex hormone metabolism thus modifying 
      sex hormone levels (Figure 3). Compared to the general population (Figures 4 and 
      5), the risk of cardiovascular morbidity and mortality is significantly increased 
      in patients with rheumatic diseases and in particular in RA. This is evidenced by 
      a higher incidence of congestive heart failure (Figure 6), coronary artery 
      disease and (frequently silent) myocardial infarction, as well as sudden cardiac 
      death. Several studies have demonstrated a significantly increased standardized 
      mortality ratio in RA and identified cardiovascular events as the most frequent 
      cause. Compared with expected mortality rates in the normal population, women 
      with RA have a significantly more compromised life expectancy than men (Table 1). 
      Amongst factors with uneven distribution between sexes are traditional 
      cardiovascular risk factors (Table 2), but also more recently recognized 
      potential risk indicators or risk modifiers such as inflammatory markers and sex 
      hormones. Drugs directed against RA may influence the natural course of 
      cardiovascular disease, as, e. g., indicated by the increased rates of cardiac 
      events and stroke associated with cyclooxygenase-(COX-)2 inhibitor treatment. In 
      contrast, the effect of pharmacotherapy for cardiovascular diseases on the course 
      of RA is unexplored. Prospective cohort studies aiming at early detection of 
      cardiovascular morbidity and precise and detailed characterization of disease 
      manifestations will be required in order to more thoroughly understand the 
      interplay of factors and conditions determining an individuals' risk for 
      developing cardiovascular comorbidity in autoimmune diseases. This article 
      summarizes the available evidence for sex- and gender-related differences in the 
      disease manifestation of rheumatic disorders as well as in cardiovascular risk 
      factors with an emphasis on the cardiovascular comorbidity observed in RA.
FAU - Kung, Margret
AU  - Kung M
AD  - Medizinische Klinik und Poliklinik II, Herz- und Kreislaufzentrum der 
      Universität, Würzburg.
FAU - Störk, Stefan
AU  - Störk S
FAU - Angermann, Christiane E
AU  - Angermann CE
LA  - ger
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - Kardiovaskuläre komorbidität bei rheumatoider arthritis spielt das geschlecht 
      eine rolle?
PL  - Germany
TA  - Herz
JT  - Herz
JID - 7801231
SB  - IM
MH  - Age Distribution
MH  - Arthritis, Rheumatoid/*mortality
MH  - Cardiovascular Diseases/*mortality
MH  - Clinical Trials as Topic
MH  - Comorbidity
MH  - Humans
MH  - Incidence
MH  - Risk Assessment/*methods
MH  - Risk Factors
MH  - Sex Distribution
RF  - 56
EDAT- 2005/09/20 09:00
MHDA- 2006/01/20 09:00
CRDT- 2005/09/20 09:00
PHST- 2005/09/20 09:00 [pubmed]
PHST- 2006/01/20 09:00 [medline]
PHST- 2005/09/20 09:00 [entrez]
AID - 10.1007/s00059-005-2717-2 [doi]
PST - ppublish
SO  - Herz. 2005 Sep;30(6):512-21. doi: 10.1007/s00059-005-2717-2.

PMID- 16048553
OWN - NLM
STAT- MEDLINE
DCOM- 20051018
LR  - 20240109
IS  - 0105-2896 (Print)
IS  - 1600-065X (Electronic)
IS  - 0105-2896 (Linking)
VI  - 206
DP  - 2005 Aug
TI  - Oral tolerance.
PG  - 232-59
AB  - Multiple mechanisms of tolerance are induced by oral antigen. Low doses favor 
      active suppression, whereas higher doses favor clonal anergy/deletion. Oral 
      antigen induces T-helper 2 [interleukin (IL)-4/IL-10] and Th3 [transforming 
      growth factor (TGF)-beta] T cells plus CD4+CD25+ regulatory cells and 
      latency-associated peptide+ T cells. Induction of oral tolerance is enhanced by 
      IL-4, IL-10, anti-IL-12, TGF-beta, cholera toxin B subunit, Flt-3 ligand, and 
      anti-CD40 ligand. Oral (and nasal) antigen administration suppresses animal 
      models of autoimmune diseases including experimental autoimmune encephalitis, 
      uveitis, thyroiditis, myasthenia, arthritis, and diabetes in the non-obese 
      diabetic (NOD) mouse, plus non-autoimmune diseases such as asthma, 
      atherosclerosis, graft rejection, allergy, colitis, stroke, and models of 
      Alzheimer's disease. Oral tolerance has been tested in human autoimmune diseases 
      including multiple sclerosis (MS), arthritis, uveitis, and diabetes and in 
      allergy, contact sensitivity to dinitrochlorobenzene (DNCB), and nickel allergy. 
      Although positive results have been observed in phase II trials, no effect was 
      observed in phase III trials of CII in rheumatoid arthritis or oral myelin and 
      glatiramer acetate (GA) in MS. Large placebo effects were observed, and new 
      trials of oral GA are underway. Oral insulin has recently been shown to delay 
      onset of diabetes in at-risk populations, and confirmatory trials of oral insulin 
      are being planned. Mucosal tolerance is an attractive approach for treatment of 
      autoimmune and inflammatory diseases because of lack of toxicity, ease of 
      administration over time, and antigen-specific mechanisms of action. The 
      successful application of oral tolerance for the treatment of human diseases will 
      depend on dose, developing immune markers to assess immunologic effects, route 
      (nasal versus oral), formulation, mucosal adjuvants, combination therapy, and 
      early therapy.
FAU - Faria, Ana M C
AU  - Faria AM
AD  - Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical 
      School, Boston, MA 02115, USA.
FAU - Weiner, Howard L
AU  - Weiner HL
LA  - eng
GR  - R01 AI043458/AI/NIAID NIH HHS/United States
GR  - R01 AI043458-12/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - England
TA  - Immunol Rev
JT  - Immunological reviews
JID - 7702118
RN  - 0 (Antigens)
SB  - IM
MH  - Animals
MH  - Antigens/*administration & dosage/*immunology
MH  - Humans
MH  - *Immune Tolerance
MH  - Immunity, Mucosal
MH  - Intestinal Mucosa/*immunology
MH  - Mouth Mucosa/*immunology
PMC - PMC3076704
MID - NIHMS278192
EDAT- 2005/07/29 09:00
MHDA- 2005/10/19 09:00
PMCR- 2011/04/14
CRDT- 2005/07/29 09:00
PHST- 2005/07/29 09:00 [pubmed]
PHST- 2005/10/19 09:00 [medline]
PHST- 2005/07/29 09:00 [entrez]
PHST- 2011/04/14 00:00 [pmc-release]
AID - IMR280 [pii]
AID - 10.1111/j.0105-2896.2005.00280.x [doi]
PST - ppublish
SO  - Immunol Rev. 2005 Aug;206:232-59. doi: 10.1111/j.0105-2896.2005.00280.x.

PMID- 15909083
OWN - NLM
STAT- MEDLINE
DCOM- 20050922
LR  - 20181113
IS  - 0340-1855 (Print)
IS  - 0340-1855 (Linking)
VI  - 64
IP  - 4
DP  - 2005 May
TI  - [Accelerated atherosclerosis in rheumatic systemic diseases as an example of 
      systemic lupus erythematosus--what is the consequence?].
PG  - 229-38
AB  - Large increases in mortality related to premature atherosclerosis with coronary 
      artery disease and stroke have been reported during the last few years in 
      patients with systemic lupus erythematosus (SLE). Studies found relative risks of 
      5 to 7 for myocardial infarction in SLE patients. The traditional risk factors 
      fail to fully account for accelerated atherosclerosis in SLE and APS, in addition 
      prolonged glucocorticoid therapy and long duration of SLE seem to be of 
      importance. The disease SLE per se is an independent risk factor. The current 
      pathogenic hypothesis for atherosclerosis involves an inflammatory response, 
      autoantibodies, immune complexes (containing antibodies to phospholipids, to 
      oxidized LDLs, and to endothelial cells), CD40/CD40 ligand interactions, and 
      bacterial or viral infections responsible for an immune response. The 
      determination of classic and new risk factors, together with specific 
      autoantibody titers and the use of Doppler carotid ultrasound, are useful methods 
      to detect early atherosclerosis. Therapeutic strategies, including early risk 
      factor intervention and effective control of inflammation, are essential to 
      reduce morbidity and mortality and should be incorporated into the management of 
      connective tissue disease with the goal of protecting patients against 
      atherosclerosis.
FAU - Fischer-Betz, R
AU  - Fischer-Betz R
AD  - Rheumazentrum Düsseldorf, Heinrich-Heine-Universität, Moorenstrasse 5, 40225, 
      Düsseldorf, Germany.
FAU - Beer, S
AU  - Beer S
FAU - Schneider, M
AU  - Schneider M
LA  - ger
PT  - English Abstract
PT  - Journal Article
PT  - Review
TT  - Beschleunigte Arteriosklerose bei rheumatischen Systemerkrankungen am Beispiel 
      des systemischen Lupus erythematodes--was ist die Konsequenz?
PL  - Germany
TA  - Z Rheumatol
JT  - Zeitschrift fur Rheumatologie
JID - 0414162
SB  - IM
MH  - Arteriosclerosis/immunology/*mortality
MH  - Arthritis, Rheumatoid/immunology/*mortality
MH  - Clinical Trials as Topic
MH  - Comorbidity
MH  - Disease Progression
MH  - Humans
MH  - Internationality
MH  - Lupus Erythematosus, Systemic/immunology/*mortality
MH  - Prevalence
MH  - Rheumatic Diseases/immunology/*mortality
MH  - Risk Assessment/*methods
MH  - Risk Factors
MH  - Severity of Illness Index
RF  - 44
EDAT- 2005/05/24 09:00
MHDA- 2005/09/24 09:00
CRDT- 2005/05/24 09:00
PHST- 2005/02/09 00:00 [received]
PHST- 2005/03/08 00:00 [accepted]
PHST- 2005/05/24 09:00 [pubmed]
PHST- 2005/09/24 09:00 [medline]
PHST- 2005/05/24 09:00 [entrez]
AID - 10.1007/s00393-005-0733-5 [doi]
PST - ppublish
SO  - Z Rheumatol. 2005 May;64(4):229-38. doi: 10.1007/s00393-005-0733-5.

PMID- 15882125
OWN - NLM
STAT- MEDLINE
DCOM- 20061114
LR  - 20190917
IS  - 1744-7658 (Electronic)
IS  - 1354-3784 (Linking)
VI  - 14
IP  - 4
DP  - 2005 Apr
TI  - Clinical pharmacology of lumiracoxib, a second-generation cyclooxygenase 2 
      selective inhibitor.
PG  - 521-33
AB  - Although highly selective cyclooxygenase (COX)-2 inhibitors have been shown to be 
      less toxic to the gastrointestinal tract than conventional non-steroidal 
      anti-inflammatory drugs (NSAIDs), their overall safety profile is questioned. 
      Since different selective COX-2 inhibitors were found to be associated with 
      increased cardiovascular thrombotic events, the thrombotic hazard may be a class 
      effect. Furthermore, warnings have been issued regarding serious skin and 
      hypersensitivity reactions associated with valdecoxib. Lumiracoxib is a novel 
      COX-2 selective inhibitor (coxib) with improved biochemical selectivity over that 
      of currently available coxibs. It is structurally distinct from other drugs in 
      the class and has weakly acidic properties. Clinical studies support a once-daily 
      dosing regimen, despite its relatively short plasma elimination half-life (3 - 6 
      h). In randomised, controlled clinical trials, lumiracoxib 100 - 200 mg/day has 
      been shown to be superior to placebo in patients with symptomatic osteoarthritis, 
      with clinical efficacy similar to diclofenac 150 mg/day, celecoxib 200 mg/day or 
      rofecoxib 25 mg/day. Furthermore, lumiracoxib 200 - 400 mg/day appeared to be 
      effective in patients with rheumatoid arthritis. In patients with acute pain 
      related to primary dysmenorrhoea, dental or orthopaedic surgery, lumiracoxib 400 
      mg/day was found to be at least as effective as standard doses of traditional 
      NSAIDs and other coxibs. Endoscopic studies have indicated that lumiracoxib is 
      associated with a rate of gastroduodenal ulcer formation that is significantly 
      lower than with ibuprofen and does not differ from celecoxib. In the Therapeutic 
      Arthritis Research and Gastrointestinal Trial, which enrolled 18,325 patients 
      with osteoarthritis, the cumulative 1-year incidence of ulcer complications 
      (primary end point) was significantly reduced by approximately threefold on 
      lumiracoxib 400 mg/day compared with naproxen 1000 mg/day or ibuprofen 2400 
      mg/day (0.32 versus 0.91%). Reduction in ulcer complications was more pronounced 
      in the population not taking low-dose aspirin (0.2 versus 0.92%, respectively). 
      Conversely, the gastrointestinal advantage of lumiracoxib was abrogated in 
      patients receiving low-dose aspirin (0.69 versus 0.88%, respectively, p = 0.49). 
      Regarding cardiovascular events contributing to the trialists' composite end 
      point (myocardial infarction, stroke or cardiovascular death), there was no 
      significant difference between lumiracoxib (0.65%) versus combined comparator 
      NSAIDs (0.55%). Similarly, no significant difference was recorded in rates of 
      myocardial infarction (clinical and silent) between the lumiracoxib (0.25%) and 
      the combined NSAID (0.19%) treatment groups. Liver function test abnormalities 
      were more frequent with lumiracoxib (2.57%) than with the comparator NSAIDs 
      (0.63%). Whether or not this would result in an increased risk of clinical 
      hepatitis in the real world setting is unforeseeable.
FAU - Bannwarth, Bernard
AU  - Bannwarth B
AD  - Service de Rhumatologie, Groupe Hospitalier Pellegrin 3076, Bordeaux, Cedex, 
      France. bannwarth@u-bordeaux2.fr
FAU - Berenbaum, Francis
AU  - Berenbaum F
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Review
PL  - England
TA  - Expert Opin Investig Drugs
JT  - Expert opinion on investigational drugs
JID - 9434197
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
RN  - 144O8QL0L1 (Diclofenac)
RN  - V91T9204HU (lumiracoxib)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/adverse effects/pharmacology/therapeutic 
      use
MH  - Arthritis, Rheumatoid/drug therapy
MH  - Cyclooxygenase 2 Inhibitors/adverse effects/*pharmacology/*therapeutic use
MH  - Diclofenac/adverse effects/*analogs & derivatives/pharmacology/therapeutic use
MH  - Dysmenorrhea/prevention & control
MH  - Female
MH  - Gastrointestinal Hemorrhage/etiology
MH  - Humans
MH  - Osteoarthritis/drug therapy
MH  - Pain, Postoperative/prevention & control
MH  - Randomized Controlled Trials as Topic
RF  - 49
EDAT- 2005/05/11 09:00
MHDA- 2006/11/15 09:00
CRDT- 2005/05/11 09:00
PHST- 2005/05/11 09:00 [pubmed]
PHST- 2006/11/15 09:00 [medline]
PHST- 2005/05/11 09:00 [entrez]
AID - EID140413 [pii]
AID - 10.1517/13543784.14.4.521 [doi]
PST - ppublish
SO  - Expert Opin Investig Drugs. 2005 Apr;14(4):521-33. doi: 
      10.1517/13543784.14.4.521.

PMID- 15859024
OWN - NLM
STAT- MEDLINE
DCOM- 20050817
LR  - 20061115
IS  - 0036-5513 (Print)
IS  - 0036-5513 (Linking)
VI  - 65
IP  - 1
DP  - 2005
TI  - Serum C-reactive protein in elderly men and women: association with mortality, 
      morbidity and various biochemical values.
PG  - 23-31
AB  - OBJECTIVE: The primary aim of this study was to define the distribution and the 
      prognostic value of serum C-reactive protein (s-CRP) measured by a 
      high-sensitivity method in elderly subjects of both genders with special 
      reference to the distribution below 10 mg/l. As a secondary aim, a possible 
      gender difference of s-CRP was examined. MATERIAL AND METHODS: Baseline s-CRP was 
      described in a population-based sample of opposite-sex, twin-pairs (197 F, 189 M 
      available for blood-sampling) aged 71-80 years (mean age 74.5 years), considering 
      mortality through the next 4 years, morbidity (myocardial infarction, angina 
      pectoris, congestive heart failure, arterial hypertension, venous 
      thromboembolism, stroke, diabetes, gout, psoriasis, rheumatoid arthritis) before 
      and after blood sampling, biochemical values (serum levels of urate, urea, ApoA1, 
      ApoB, folate, FSH, LH, oestradiol, progesterone, testosterone, cortisol) and 
      anthropometric measurements (body mass index (BMI), circumference of waist, 
      buttocks and hips). RESULTS: The level of s-CRP did not deviate substantially 
      from what has been reported for younger subjects. Higher values indicated an 
      increased risk of cardiovascular morbidity and diabetes in women but not in men. 
      The s-CRP level was associated with serum levels of urate, progesterone, folate, 
      ApoA1, ApoB and the quotient ApoB/ApoA1 as well as with BMI and waist 
      circumference. CONCLUSIONS: For the 71-80 years age group, s-CRP below the 80th 
      percentile (4.3 mg/l) seems to have prognostic capacity mainly in women. The 
      highest association with mortality as well as with cardiovascular diseases, 
      diabetes and rheumatoid arthritis is found for s-CRP above 10 mg/l, which is the 
      arbitrary lower level for the earlier routine low-sensitivity s-CRP methods. The 
      association of s-CRP with serum urate, folate and the ApoB/ApoA1 quotient should 
      be considered.
FAU - Evrin, P E
AU  - Evrin PE
AD  - Department of Clinical Chemistry, Ryhov Hospital, Jönköping, Sweden.
FAU - Nilsson, S E
AU  - Nilsson SE
FAU - Oberg, T
AU  - Oberg T
FAU - Malmberg, B
AU  - Malmberg B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Scand J Clin Lab Invest
JT  - Scandinavian journal of clinical and laboratory investigation
JID - 0404375
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - C-Reactive Protein/analysis/*metabolism
MH  - Disease
MH  - Female
MH  - Humans
MH  - Male
MH  - *Morbidity
MH  - *Mortality
MH  - Sex Characteristics
EDAT- 2005/04/30 09:00
MHDA- 2005/08/18 09:00
CRDT- 2005/04/30 09:00
PHST- 2005/04/30 09:00 [pubmed]
PHST- 2005/08/18 09:00 [medline]
PHST- 2005/04/30 09:00 [entrez]
AID - 10.1080/00365510510013505 [doi]
PST - ppublish
SO  - Scand J Clin Lab Invest. 2005;65(1):23-31. doi: 10.1080/00365510510013505.

PMID- 15857301
OWN - NLM
STAT- MEDLINE
DCOM- 20050707
LR  - 20191109
IS  - 1568-007X (Print)
IS  - 1568-007X (Linking)
VI  - 4
IP  - 2
DP  - 2005 Apr
TI  - Therapeutic potential of TACE inhibitors in stroke.
PG  - 161-8
AB  - Stroke is the third leading cause of death and the leading cause of permanent 
      disability in western countries and the incidence of stroke is expected to 
      increase in the foreseeable future due to the ageing population. The effective 
      treatment of stroke remains challenging due to the complexity and heterogenicity 
      of the disease. Recombinant tissue plasminogen activator (rt-PA) is the only 
      FDA-approved therapy for stroke during the first 3 hr after the disease onset. 
      However the risk of hemorrhage and its narrow therapeutic window has limited its 
      use in clinic. Inflammation has been known to play a crucial role in the 
      induction and development of stroke and tumor necrosis factor-alpha (TNF-alpha) 
      is a central player in the initiation of multiple inflammatory cascades. The 
      recent success of three anti-TNF biologics in the clinic for the treatment of 
      rheumatoid arthritis as well as other inflammatory diseases has further validated 
      TNF159nflammation. TNF-alpha has also been shown to be associated with ischemic 
      stroke. Anti-TNF biologics have been shown to be effective in reducing the 
      disease symptoms in various pre-clinical stroke models. Small molecule TNF 
      inhibitors are highly desirable due to the limitations of protein therapeutics. 
      Tumor necrosis factor-alpha-converting enzyme (TACE) is the major sheddase of 
      TNF-alpha and is essential for the generation of soluble, mature TNF-alpha. Thus 
      TACE appears to be an attractive target for development of oral small molecule 
      TNF-alpha inhibitors. This review summarizes the role of TNF-alpha in stroke and 
      the effect of several TACE/MMP inhibitors in pre-clinical stroke models. The data 
      strongly suggest that TACE/MMP inhibitors have great therapeutic potential and 
      may be valuable alternatives in treating stroke in the clinic.
FAU - Lovering, F
AU  - Lovering F
AD  - Wyeth Research, Cambridge, MA 02140, USA.
FAU - Zhang, Y
AU  - Zhang Y
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Netherlands
TA  - Curr Drug Targets CNS Neurol Disord
JT  - Current drug targets. CNS and neurological disorders
JID - 101151150
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.24.- (ADAM Proteins)
RN  - EC 3.4.24.- (Metalloendopeptidases)
RN  - EC 3.4.24.86 (ADAM17 Protein)
RN  - EC 3.4.24.86 (ADAM17 protein, human)
SB  - IM
MH  - ADAM Proteins
MH  - ADAM17 Protein
MH  - Animals
MH  - Enzyme Inhibitors/*pharmacology/therapeutic use
MH  - Humans
MH  - Inflammation/complications/drug therapy/*enzymology
MH  - Metalloendopeptidases/*antagonists & inhibitors
MH  - Stroke/complications/*drug therapy/*enzymology
MH  - Tumor Necrosis Factor-alpha/*metabolism
RF  - 98
EDAT- 2005/04/29 09:00
MHDA- 2005/07/08 09:00
CRDT- 2005/04/29 09:00
PHST- 2005/04/29 09:00 [pubmed]
PHST- 2005/07/08 09:00 [medline]
PHST- 2005/04/29 09:00 [entrez]
AID - 10.2174/1568007053544147 [doi]
PST - ppublish
SO  - Curr Drug Targets CNS Neurol Disord. 2005 Apr;4(2):161-8. doi: 
      10.2174/1568007053544147.

PMID- 15852592
OWN - NLM
STAT- MEDLINE
DCOM- 20060821
LR  - 20141120
IS  - 0026-556X (Print)
IS  - 0026-556X (Linking)
VI  - 88
IP  - 3
DP  - 2005 Mar
TI  - The Vioxx fallout.
PG  - 26-30
FAU - Palmer, Kim
AU  - Palmer K
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Minn Med
JT  - Minnesota medicine
JID - 8000173
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
RN  - 0 (Lactones)
RN  - 0 (Sulfones)
RN  - 0QTW8Z7MCR (rofecoxib)
SB  - IM
MH  - Adverse Drug Reaction Reporting Systems
MH  - Anti-Inflammatory Agents, Non-Steroidal/*adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Cerebral Infarction/*chemically induced
MH  - Cyclooxygenase 2 Inhibitors/*adverse effects/therapeutic use
MH  - Humans
MH  - Lactones/*adverse effects/therapeutic use
MH  - Myocardial Infarction/*chemically induced
MH  - Patient Education as Topic
MH  - Product Surveillance, Postmarketing
MH  - Risk
MH  - Sulfones/*adverse effects/therapeutic use
EDAT- 2005/04/28 09:00
MHDA- 2006/08/22 09:00
CRDT- 2005/04/28 09:00
PHST- 2005/04/28 09:00 [pubmed]
PHST- 2006/08/22 09:00 [medline]
PHST- 2005/04/28 09:00 [entrez]
PST - ppublish
SO  - Minn Med. 2005 Mar;88(3):26-30.

PMID- 15823993
OWN - NLM
STAT- MEDLINE
DCOM- 20050726
LR  - 20111117
IS  - 0963-8288 (Print)
IS  - 0963-8288 (Linking)
VI  - 27
IP  - 3
DP  - 2005 Feb 4
TI  - Depression in adults with disabilities, in primary care.
PG  - 117-23
AB  - PURPOSE: This research was design to answer the question: Does the prevalence of 
      depression differ between adults with and without disability, in the same family 
      medicine practice? METHOD: A retrospective cohort design was used, to study 
      depression among adults, with and without primary disabling conditions, receiving 
      primary care in either a university based urban or rural family practice setting. 
      RESULTS: When we compared individuals with disability to those without 
      disability, and controlled for individual characteristics, the relative risk for 
      depression was significantly lower for individuals with autism (Relative Risk 
      (RR) 0.20: 95% Confidence Interval (CI) 0.05-0.55), cerebral palsy with mental 
      retardation (RR 0.40: 95% CI: 0.24-0.65), and MR (RR 0.56: 95% CI: 0.39-0.77). 
      The risk for depression was significantly higher for those with cerebral vascular 
      accidents/stroke (RR 2.18: 95% CI: 1.72-3.76) and traumatic brain injury (RR 
      2.55: 95% CI: 1.72-2.77). The earliest onset of depression was among individuals 
      with traumatic disabilities and milt mental retardation. Our estimate of 
      depression prevalence for the non-disabled and disabled primary care patients was 
      22.8% and 24.9% respectively, when patients with disabilities were grouped 
      together (p = 0.008). CONCLUSION: It is important for physicians to recognize the 
      higher prevalence of depression among patients with adult onset disabilities 
      (e.g. stroke, traumatic brain injury). In addition, they should be aware of lower 
      prevalence of depression among many individuals with lifelong disabilities, such 
      as mental retardation, cerebral palsy, and autism.
FAU - McDermott, Suzanne
AU  - McDermott S
AD  - Department of Family and Preventive Medicine, University of South Carolina School 
      of Medicine, Columbia, South Carolina, USA. Suzanne.mcdermott@palmettohealth.org
FAU - Moran, Robert
AU  - Moran R
FAU - Platt, Tan
AU  - Platt T
FAU - Issac, Terri
AU  - Issac T
FAU - Wood, Hope
AU  - Wood H
FAU - Dasari, Srikanth
AU  - Dasari S
LA  - eng
GR  - R04/CCR418776/CC/ODCDC CDC HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Disabil Rehabil
JT  - Disability and rehabilitation
JID - 9207179
SB  - IM
MH  - Adult
MH  - Arthritis, Rheumatoid/psychology
MH  - Autistic Disorder/psychology
MH  - Blindness/psychology
MH  - Brain Injuries/psychology
MH  - Cerebral Palsy/psychology
MH  - Cohort Studies
MH  - Deafness/psychology
MH  - Depression/*epidemiology
MH  - Disabled Persons/*psychology
MH  - Family Practice
MH  - Female
MH  - Humans
MH  - Intellectual Disability/psychology
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - *Primary Health Care
MH  - Retrospective Studies
MH  - Risk Assessment
MH  - Rural Population
MH  - Spinal Cord Injuries/psychology
MH  - Stroke/psychology
MH  - Urban Population
EDAT- 2005/04/13 09:00
MHDA- 2005/07/27 09:00
CRDT- 2005/04/13 09:00
PHST- 2005/04/13 09:00 [pubmed]
PHST- 2005/07/27 09:00 [medline]
PHST- 2005/04/13 09:00 [entrez]
AID - L3Q2QV57PF40V8JC [pii]
AID - 10.1080/09638280400007380 [doi]
PST - ppublish
SO  - Disabil Rehabil. 2005 Feb 4;27(3):117-23. doi: 10.1080/09638280400007380.

PMID- 15813652
OWN - NLM
STAT- MEDLINE
DCOM- 20050715
LR  - 20181113
IS  - 1170-229X (Print)
IS  - 1170-229X (Linking)
VI  - 22
IP  - 3
DP  - 2005
TI  - Cyclo-oxygenase-2 inhibitors: when should they be used in the elderly?
PG  - 185-200
AB  - Chronic pain in the elderly is frequently a result of arthritic disorders, 
      particularly osteoarthritis. The cyclo-oxygenase (COX)-2 inhibitors are as 
      effective as standard NSAIDs for the relief of pain and for improving function in 
      elderly patients with osteoarthritis and rheumatoid arthritis. COX-2 inhibitors 
      increase the risk of serious gastroduodenal adverse reactions but there is 
      evidence that they carry a lower risk for these adverse effects than standard 
      NSAIDs, except when there is concurrent aspirin use. Since gastroduodenal 
      disorders are the most frequently reported serious adverse effects of NSAIDs and 
      these disorders occur more frequently in the elderly, COX-2 inhibitors offer an 
      alternative to standard NSAIDs in this age group. However, they are not 
      appropriate for many patients with cardiovascular and renal disease. The adverse 
      reaction profile of the COX-2 inhibitors has confirmed the role of the COX-2 
      enzyme in renal function, salt and water homeostasis and the vascular 
      endothelium. Thus, like standard NSAIDs, COX-2 inhibitors can cause renal 
      failure, hypertension and exacerbation of cardiac failure. Of note is that these 
      disorders are dose related. Thus, there are good reasons to avoid high doses of 
      COX-2 inhibitors in the elderly. Clinical trials indicate that daily doses of 
      rofecoxib 12.5 mg, celecoxib 100-200 mg, valdecoxib 10mg and etoricoxib 60 mg are 
      the minimum effective doses of these agents. Data from the New Zealand Intensive 
      Medicines Monitoring Programme indicate that celecoxib 200 mg/day and rofecoxib 
      25 mg/day are/were the most commonly prescribed doses and that 6% of patients had 
      taken rofecoxib 50 mg/day for longer than recommended. Recent research indicates 
      that COX-2 inhibitors have a thrombotic potential, especially in high doses and 
      when use is prolonged, and this further limits the extent to which they can be 
      used in the elderly. Important interactions with COX-2 inhibitors in the elderly 
      include those with warfarin, which can result in loss of control of 
      anticoagulation, and those with ACE inhibitors, angiotensin II type 1 receptor 
      antagonists and diuretics, which can result in loss of control of blood pressure 
      and cardiac failure and, in hypovolaemic conditions, renal failure. The clinical 
      significance of an interaction between celecoxib and aspirin to reduce the 
      antiplatelet effect of the latter drug is unknown. Preliminary information from 
      spontaneous reporting systems indicates that there may be differences in the risk 
      of cardiac failure and hypertension between standard NSAIDs and COX-2 inhibitors 
      and between rofecoxib and celecoxib. More formal studies using equivalent doses 
      are needed to test this observation. Use of COX-2 inhibitors may be considered in 
      the elderly to reduce the risk of gastroduodenal complications associated with 
      standard NSAIDs but only when consideration has first been given to use of less 
      toxic medicines as alternatives or supplements, the appropriate dose of the COX-2 
      inhibitor or standard NSAID, the presence and possible impact of co-morbidities, 
      and the implications of taking COX-2 inhibitors with any concomitant medications. 
      Equally important is regular monitoring of the patient taking a COX-2 inhibitor 
      for efficacy and adverse effects, and ensuring that the patient has a continuing 
      need to keep taking the drug. Close attention also needs to be paid to 
      intercurrent illnesses and new prescriptions that may reduce the safety of the 
      COX-2 inhibitor. A standard NSAID plus a proton pump inhibitor may be equally 
      effective as a COX-2 inhibitor in reducing the risk of gastroduodenal toxicity 
      and if used the same prescribing advice applies. Current knowledge concerning the 
      thrombotic potential of COX-2 inhibitors suggests that this combination, if 
      tolerated, may be preferable to a COX-2 inhibitor, particularly where prolonged 
      use is required. This knowledge also indicates that for patients with or at high 
      risk of ischaemic heart disease or stroke, COX-2 inhibitors are contraindicated.
FAU - Savage, Ruth
AU  - Savage R
AD  - New Zealand Pharmacovigilance Centre, Department of Preventive and Social 
      Medicine, University of Otago, Dunedin, New Zealand. 
      ruth.savage@stonebow.otago.ac.nz
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - New Zealand
TA  - Drugs Aging
JT  - Drugs & aging
JID - 9102074
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase 2 Inhibitors)
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Membrane Proteins)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 1.14.99.1 (PTGS2 protein, human)
RN  - EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
SB  - IM
MH  - Aged
MH  - *Anti-Inflammatory Agents, Non-Steroidal/administration & dosage/adverse 
      effects/therapeutic use
MH  - Cyclooxygenase 2
MH  - Cyclooxygenase 2 Inhibitors
MH  - *Cyclooxygenase Inhibitors/administration & dosage/adverse effects/therapeutic 
      use
MH  - Humans
MH  - Membrane Proteins
MH  - Pain/*drug therapy
MH  - Prostaglandin-Endoperoxide Synthases/*metabolism
RF  - 82
EDAT- 2005/04/09 09:00
MHDA- 2005/07/16 09:00
CRDT- 2005/04/09 09:00
PHST- 2005/04/09 09:00 [pubmed]
PHST- 2005/07/16 09:00 [medline]
PHST- 2005/04/09 09:00 [entrez]
AID - 2231 [pii]
AID - 10.2165/00002512-200522030-00001 [doi]
PST - ppublish
SO  - Drugs Aging. 2005;22(3):185-200. doi: 10.2165/00002512-200522030-00001.

PMID- 15696570
OWN - NLM
STAT- MEDLINE
DCOM- 20050329
LR  - 20151119
IS  - 0004-3591 (Print)
IS  - 0004-3591 (Linking)
VI  - 53
IP  - 1
DP  - 2005 Feb 15
TI  - Effect of cardiovascular comorbidities and concomitant aspirin use on selection 
      of cyclooxygenase inhibitor among rheumatologists.
PG  - 12-7
AB  - OBJECTIVE: To evaluate the effects of cardiovascular comorbidities and aspirin 
      coprescription on cyclooxygenase (COX)-2 inhibitor (coxib) prescribing patterns 
      among rheumatologists. METHODS: A prospective cohort study was carried out with 
      rheumatoid arthritis and osteoarthritis patients in the Consortium of 
      Rheumatology Researchers of North America registry. Medication and comorbidity 
      data were obtained prospectively from physician and patient questionnaires 
      between March 2002 and September 2003. Multivariate adjusted associations between 
      coxib use and specific cardiovascular variables, including aspirin use, were 
      examined. RESULTS: A total of 3,522 arthritis patients were included. COX 
      inhibitors, including coxibs, nonselective nonsteroidal antiinflammatory drugs 
      (NSAIDs), and meloxicam, were prescribed to a larger proportion of osteoarthritis 
      patients (68.4%) than rheumatoid arthritis patients (47.1%) in our study (P < 
      0.001). COX inhibitors were prescribed to the majority of aspirin users (51.5%) 
      and a similar proportion of nonusers (49.8%). In multivariate analyses, 
      independent predictors of coxib use versus nonselective NSAID use included 
      diagnoses of osteoarthritis (odds ratio [OR] 2.52, 95% confidence interval [95% 
      CI] 1.81-3.52) and diabetes (OR 1.63, 95% CI 1.06-2.51). Conversely, aspirin use 
      independently predicted selection of a nonselective NSAID rather than a coxib (OR 
      0.73, 95% CI 0.55-0.98). Neither a history of myocardial infarction nor stroke 
      predicted utilization of a coxib. Similarly, cardiovascular variables did not 
      predict the use of rofecoxib versus celecoxib. CONCLUSION: Our data indicate that 
      COX inhibitor coprescription among aspirin users is frequent. Despite 
      cardiovascular concerns regarding the coxibs, our data suggest that aspirin use, 
      but not cardiovascular comorbidities, predicted the selection of nonselective 
      NSAIDs over coxibs.
FAU - Greenberg, Jeffrey D
AU  - Greenberg JD
AD  - New York University-Hospital for Joint Diseases, New York, New York, USA. 
      jeffrey.greenberg@nyumc.org
FAU - Bingham, Clifton O 3rd
AU  - Bingham CO 3rd
FAU - Abramson, Steven B
AU  - Abramson SB
FAU - Reed, George
AU  - Reed G
FAU - Sebaldt, Rolf J
AU  - Sebaldt RJ
FAU - Kremer, Joel
AU  - Kremer J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Aged
MH  - Anti-Inflammatory Agents, Non-Steroidal/administration & dosage/adverse effects
MH  - Arthritis, Rheumatoid/*drug therapy/*epidemiology
MH  - Aspirin/*administration & dosage/adverse effects
MH  - Cardiovascular Diseases/*drug therapy/*epidemiology
MH  - Comorbidity
MH  - Cyclooxygenase Inhibitors/*administration & dosage/adverse effects
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Osteoarthritis/drug therapy/epidemiology
MH  - Practice Patterns, Physicians'
MH  - Predictive Value of Tests
MH  - Prospective Studies
MH  - Registries
MH  - Risk Factors
MH  - Surveys and Questionnaires
EDAT- 2005/02/08 09:00
MHDA- 2005/03/30 09:00
CRDT- 2005/02/08 09:00
PHST- 2005/02/08 09:00 [pubmed]
PHST- 2005/03/30 09:00 [medline]
PHST- 2005/02/08 09:00 [entrez]
AID - 10.1002/art.20905 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2005 Feb 15;53(1):12-7. doi: 10.1002/art.20905.

PMID- 15674912
OWN - NLM
STAT- MEDLINE
DCOM- 20050527
LR  - 20240820
IS  - 1469-493X (Electronic)
IS  - 1361-6137 (Linking)
VI  - 2005
IP  - 1
DP  - 2005 Jan 25
TI  - Rofecoxib for rheumatoid arthritis.
PG  - CD003685
LID - CD003685
AB  - BACKGROUND: Editor's note: The anti-inflammatory drug rofecoxib (Vioxx) was 
      withdrawn from the market at the end of September 2004 after it was shown that 
      long-term use (greater than 18 months) could increase the risk of heart attack 
      and stroke. Further information is available at www.vioxx.com. Rheumatoid 
      arthritis (RA) is a systemic auto-immune disorder, in which the synovial lining 
      of many joints and tendon sheaths are persistently inflamed. OBJECTIVES: To 
      assess the efficacy and toxicity of rofecoxib for treating RA. SEARCH STRATEGY: 
      We searched the following electronic databases up to December 2000: MEDLINE, 
      EMBASE, Cochrane Database of Systematic Reviews, Cochrane Controlled Trials 
      Register, National Research Register, NHS Economic Evaluation Database, Health 
      Technology Assessment database. The bibliographies of retrieved papers were 
      scanned for additional references. The manufacturers of rofecoxib, MSD, were also 
      approached by the UK National Institute for Clinical Excellence to submit 
      additional evidence to inform it's appraisal on the use of cyclo-oxygenase 
      inhibitors for arthritis. SELECTION CRITERIA: We included randomised controlled 
      trials of parallel group design evaluating the efficacy and/or toxicity of 
      rofecoxib in RA, both placebo based and comparative trials were eligible. 
      Relevant outcome criteria had to be available to evaluate efficacy and/or 
      toxicity, such as the OMERACT outcomes. DATA COLLECTION AND ANALYSIS: Data were 
      abstracted independently by two reviewers and the results were compared for the 
      degree of agreement. A validated tool (Jadad 1996) was used to score the quality 
      of the randomised controlled trials. The planned analysis was to pool, where 
      appropriate, continuous outcome measures using mean or standardized mean 
      differences, and dichotomous outcome measures using relative risk ratios. MAIN 
      RESULTS: Two randomised controlled trials evaluating rofecoxib for the treatment 
      of RA were identified and met the inclusion criteria. One compared rofecoxib to 
      placebo and was designed to assess the safety and efficacy of several doses of 
      rofecoxib. The second trial compared rofecoxib to naproxen and was primarily 
      designed to assess the safety of rofecoxib so did not include all the recommended 
      RA efficacy measures. The overall number of ACR 20 responders who had received 
      25mg (82/ 171 = 48%) or 50mg (86/161 = 53%) was statistically significantly more 
      than those receiving placebo (58/168 = 35% ) (RR 1.39 CI: 1.07, 1.80 and RR 1.55 
      CI: 1.20, 1.99 respectively) with no statistically significant differences 
      between the 25 and 50 mg doses. The safety profile of rofecoxib was similar to 
      that of placebo. In the comparative trial, rofecoxib at a dosage of 50 mg/day 
      demonstrated similar efficacy to naproxen at a dosage of 500 mg twice daily. 
      However, the combined rate of clinically significant complicated 
      gastro-intestinal events (GI) (perforations, ulcers, bleeds, or obstructions) was 
      lower with rofecoxib than with naproxen (RR 0.46, 95% CI, 0.34 to 0.63) due to a 
      reduction in the number of ulcers and bleeds. Compared to patients taking 
      naproxen, patients taking rofecoxib had a greater risk of having any 
      cardiovascular event (45/4047 = 1.1% vs 19/4029 =0.47%) (RR 2.36 CI 1.38 to 4.02) 
      and had greater risk of having a non-fatal myocardial infarction (MI) (18/4047 =0 
      .44% and 4/4029 =0.1%) (RR 4.48, 95% CI, 1.52 to 13.23). AUTHORS' CONCLUSIONS: In 
      patients with RA, rofecoxib demonstrates a greater degree of efficacy than 
      placebo, while having a comparable safety profile. Rofecoxib demonstrates a 
      similar degree of efficacy as naproxen, but with a significantly lower rate of 
      ulceration and gastrointestinal bleeding. Rofecoxib was associated with a greater 
      risk for MI, but the exact significance and pathophysiology of this possible 
      relationship is unclear. Rofecoxib was voluntarily withdrawn from global markets 
      in October 2004. It cannot therefore be prescribed and therefore there are no 
      implications for practice concerning its use. None the less when considering 
      which NSAID to use, it must be borne in mind that the toxicity of NSAIDs is 
      variable amongst patients and drugs and it tends to be dose related and 
      associated with variation in the mode of action, absorption, distribution and 
      metabolism. There remains a number of questions over both the benefits and risks 
      associated with Cox II selective agents and further work is ongoing. It is likely 
      that this issue will not be resolved until research has enabled a fuller 
      understanding of the complex mechanism by which the Cox system operates.
FAU - Garner, S E
AU  - Garner SE
AD  - Department of Community Health Sciences, St George's Hospital Medical School, 
      Cranmer Terrace, Tooting, London, UK, SW17 0RE. SGarner@nice.nhs.uk
FAU - Fidan, D D
AU  - Fidan DD
FAU - Frankish, R R
AU  - Frankish RR
FAU - Judd, M G
AU  - Judd MG
FAU - Towheed, T E
AU  - Towheed TE
FAU - Wells, G
AU  - Wells G
FAU - Tugwell, P
AU  - Tugwell P
LA  - eng
PT  - Journal Article
PT  - Review
PT  - Systematic Review
DEP - 20050125
PL  - England
TA  - Cochrane Database Syst Rev
JT  - The Cochrane database of systematic reviews
JID - 100909747
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Lactones)
RN  - 0 (Sulfones)
RN  - 0QTW8Z7MCR (rofecoxib)
RN  - 57Y76R9ATQ (Naproxen)
SB  - IM
UOF - Cochrane Database Syst Rev. 2002;(3):CD003685. doi: 10.1002/14651858.CD003685. 
      PMID: 12137705
MH  - Anti-Inflammatory Agents, Non-Steroidal/adverse effects/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy
MH  - Cyclooxygenase Inhibitors/adverse effects/*therapeutic use
MH  - Drug Approval
MH  - Humans
MH  - Lactones/adverse effects/*therapeutic use
MH  - Naproxen/adverse effects/therapeutic use
MH  - Randomized Controlled Trials as Topic
MH  - Sulfones/adverse effects/*therapeutic use
PMC - PMC8725608
COIS- None known
EDAT- 2005/01/28 09:00
MHDA- 2005/05/28 09:00
PMCR- 2006/01/24
CRDT- 2005/01/28 09:00
PHST- 2005/01/28 09:00 [pubmed]
PHST- 2005/05/28 09:00 [medline]
PHST- 2005/01/28 09:00 [entrez]
PHST- 2006/01/24 00:00 [pmc-release]
AID - CD003685.pub2 [pii]
AID - 10.1002/14651858.CD003685.pub2 [doi]
PST - epublish
SO  - Cochrane Database Syst Rev. 2005 Jan 25;2005(1):CD003685. doi: 
      10.1002/14651858.CD003685.pub2.

PMID- 15608306
OWN - NLM
STAT- MEDLINE
DCOM- 20050217
LR  - 20220321
IS  - 0003-4967 (Print)
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 64
IP  - 1
DP  - 2005 Jan
TI  - Prevalence and determinants of one month hand pain and hand related disability in 
      the elderly (Rotterdam study).
PG  - 99-104
AB  - OBJECTIVE: To study the prevalence of hand pain and hand disability in an open 
      population, and the contribution of their potential determinants. METHODS: 
      Baseline data were used from 7983 participants in the Rotterdam study (a 
      population based study in people aged > or =55 years). A home interview was used 
      to determine the presence of hand pain during the previous month, rheumatoid 
      arthritis, osteoarthritis in any joint, diabetes, stroke, thyroid disease, 
      neck/shoulder pain, gout, history of fracture in the past five years, and 
      Parkinson's disease, as well as age, sex, and occupation. Hand disability was 
      defined as the mean score of eight questions related to hand function. Body mass 
      index was measured and hand x rays were taken. RESULTS: The one month period 
      prevalence of hand pain was 16.9%. The prevalence of hand disability was 13.6%. 
      In univariate analysis for hand pain, rheumatoid arthritis had the highest 
      explained variance (R(2)) and odds ratio. For hand disability, aging showed the 
      highest explained variance and Parkinson's disease had the highest odds ratio. 
      All determinants together showed an explained variance of 19.8% for hand pain and 
      25.2% for hand disability. In multivariate analysis, positive radiographic hand 
      osteoarthritis was a poor explanation for hand pain (R(2) = 0.5%) or hand 
      disability (R(2) = 0). CONCLUSIONS: The contribution of available potential 
      determinants in this study was about 20% for hand pain and 25% for hand 
      disability in an unselected population of elderly people. Thus a greater part of 
      hand pain/hand disability remains unexplained.
FAU - Dahaghin, S
AU  - Dahaghin S
AD  - Department of General Practice, Erasmus Medical Centre, PO Box 1738, 3000 DR 
      Rotterdam, Netherlands. s_dahaghin@yahoo.com
FAU - Bierma-Zeinstra, S M A
AU  - Bierma-Zeinstra SM
FAU - Reijman, M
AU  - Reijman M
FAU - Pols, H A P
AU  - Pols HA
FAU - Hazes, J M W
AU  - Hazes JM
FAU - Koes, B W
AU  - Koes BW
LA  - eng
PT  - Journal Article
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
SB  - IM
EIN - Ann Rheum Dis. 2005 Mar;64(3):516
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/complications/epidemiology
MH  - Disability Evaluation
MH  - Female
MH  - *Hand
MH  - Humans
MH  - Joint Deformities, Acquired/*epidemiology/etiology
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Netherlands/epidemiology
MH  - Osteoarthritis/complications/epidemiology
MH  - Pain/*epidemiology/etiology
MH  - Prevalence
MH  - Prospective Studies
MH  - Severity of Illness Index
PMC - PMC1755169
EDAT- 2004/12/21 09:00
MHDA- 2005/02/18 09:00
PMCR- 2008/01/01
CRDT- 2004/12/21 09:00
PHST- 2004/12/21 09:00 [pubmed]
PHST- 2005/02/18 09:00 [medline]
PHST- 2004/12/21 09:00 [entrez]
PHST- 2008/01/01 00:00 [pmc-release]
AID - 64/1/99 [pii]
AID - 10.1136/ard.2003.017087 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 2005 Jan;64(1):99-104. doi: 10.1136/ard.2003.017087.

PMID- 15497064
OWN - NLM
STAT- MEDLINE
DCOM- 20050124
LR  - 20191210
IS  - 1306-696X (Print)
IS  - 1306-696X (Linking)
VI  - 10
IP  - 4
DP  - 2004 Oct
TI  - An evaluation of the underlying causes of fall-induced hip fractures in elderly 
      persons.
PG  - 250-2
AB  - BACKGROUND: Falls are the major cause of hip fractures in elderly patients. The 
      aim of this prospective study was to investigate the underlying causes of 
      fall-induced hip fractures in the elderly. METHODS: The study included 32 
      patients (18 males, 14 females; mean age 78 years; range 57 to 95 years) who had 
      proximal femoral fractures following an unexpected and sudden fall from about a 
      meter height at a moment of lying, sitting, or standing position. Underlying 
      causes of falls were sought, including previous falls, stroke, polyneuropathy, 
      motion disorders, dementia, vision problems, fainting, vestibular pathologies, 
      and cardiac diseases. RESULTS: Eight patients (25%) had a history of previous 
      falls and 12 patients (37.5%) had a history of stroke. Polyneuropathy, 
      Parkinson's Disease, and dementia were diagnosed in eight (25%), three (9.4%), 
      and five (15.6%) patients, respectively. Twenty-one patients (65.6%) had 
      neurologic diseases, 11 patients (34.4%) had cataract or other vision problems, 
      eight patients (25%) had osteoarthritis and rheumatoid arthritis, 10 patients 
      (31.3%) had vestibular pathologies, and 17 patients (53.1%) had cardiac diseases 
      such as heart failure, orthostatic hypotension, ischemic heart disease, and 
      arrhythmia. CONCLUSION: In order to prevent recurrent falls, risk factors 
      associated with falls should be determined and preventive treatment and measures 
      should be put into practice in elderly patients who have fall-induced injuries.
FAU - Aktaş, Seref
AU  - Aktaş S
AD  - Department of Orthopedics and Traumatology, Acibadem Hospital, Istanbul, Turkey. 
      saktas@tnn.net
FAU - Celik, Yahya
AU  - Celik Y
LA  - eng
PT  - Evaluation Study
PT  - Journal Article
PL  - Turkey
TA  - Ulus Travma Acil Cerrahi Derg
JT  - Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency 
      surgery : TJTES
JID - 101274231
SB  - IM
MH  - Accidental Falls/*statistics & numerical data
MH  - Aged
MH  - Aged, 80 and over
MH  - Female
MH  - Health Services for the Aged
MH  - Hip Fractures/*epidemiology/*etiology
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Risk Factors
MH  - Stroke
MH  - Turkey/epidemiology
EDAT- 2004/10/22 09:00
MHDA- 2005/01/26 09:00
CRDT- 2004/10/22 09:00
PHST- 2004/10/22 09:00 [pubmed]
PHST- 2005/01/26 09:00 [medline]
PHST- 2004/10/22 09:00 [entrez]
PST - ppublish
SO  - Ulus Travma Acil Cerrahi Derg. 2004 Oct;10(4):250-2.

PMID- 15470193
OWN - NLM
STAT- MEDLINE
DCOM- 20041025
LR  - 20191210
IS  - 1533-4406 (Electronic)
IS  - 0028-4793 (Linking)
VI  - 351
IP  - 17
DP  - 2004 Oct 21
TI  - Failing the public health--rofecoxib, Merck, and the FDA.
PG  - 1707-9
FAU - Topol, Eric J
AU  - Topol EJ
AD  - Cleveland Clinic Foundation, Cleveland, USA.
LA  - eng
PT  - Historical Article
PT  - Journal Article
DEP - 20041006
PL  - United States
TA  - N Engl J Med
JT  - The New England journal of medicine
JID - 0255562
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Lactones)
RN  - 0 (Sulfones)
RN  - 0QTW8Z7MCR (rofecoxib)
SB  - IM
CIN - N Engl J Med. 2004 Dec 30;351(27):2875-8; author reply 2875-8. doi: 
      10.1056/NEJM200412303512719. PMID: 15625342
CIN - N Engl J Med. 2004 Dec 30;351(27):2875-8; author reply 2875-8. PMID: 15625745
CIN - N Engl J Med. 2004 Dec 30;351(27):2875-8; author reply 2875-8. PMID: 15625749
MH  - Adverse Drug Reaction Reporting Systems
MH  - Advertising
MH  - Arthritis, Rheumatoid/drug therapy
MH  - Clinical Trials as Topic/history
MH  - Cyclooxygenase Inhibitors/*adverse effects/history
MH  - *Drug Approval/history
MH  - *Drug Industry/history/legislation & jurisprudence
MH  - History, 20th Century
MH  - History, 21st Century
MH  - Humans
MH  - Lactones/*adverse effects/history
MH  - Myocardial Infarction/*chemically induced
MH  - Risk
MH  - Stroke/chemically induced
MH  - Sulfones
MH  - United States
MH  - *United States Food and Drug Administration/history
EDAT- 2004/10/08 09:00
MHDA- 2004/10/27 09:00
CRDT- 2004/10/08 09:00
PHST- 2004/10/08 09:00 [pubmed]
PHST- 2004/10/27 09:00 [medline]
PHST- 2004/10/08 09:00 [entrez]
AID - NEJMp048286 [pii]
AID - 10.1056/NEJMp048286 [doi]
PST - ppublish
SO  - N Engl J Med. 2004 Oct 21;351(17):1707-9. doi: 10.1056/NEJMp048286. Epub 2004 Oct 
      6.

PMID- 28876734
STAT- Publisher
ISBN- 91-87890-96-8
PB  - Swedish Council on Health Technology Assessment (SBU)
CTI - SBU Systematic Review Summaries
DP  - 2004 Oct
BTI - Chronic Periodontitis – Prevention, Diagnosis and Treatment: A Systematic Review
AB  - This SBU report, "Chronic Periodontitis – Prevention, Diagnosis and Treatment", 
      is based on a systematic and critical review of the scientific literature. A 
      powered toothbrush is more effective than a manual toothbrush for reducing 
      gingivitis (Evidence Grade 3). Dentifrices containing stannous fluoride, amine 
      fluoride / stannous fluoride, chlorhexidine or triclosan / copolymer are more 
      effective than conventional fluoridated dentifrices for reducing gingivitis 
      (Evidence Grade 3). Mouth-rinsing with a chlorhexidine solution (0.12–0.2 
      percent) or essential oils as an adjunct to tooth brushing is more effective than 
      tooth brushing alone for reducing gingivitis (Evidence Grade 3). Repeated 
      instructions by dental professionals lead to increased knowledge about oral 
      hygiene. The findings are contradictory as to whether increased knowledge and 
      desired behavioral changes lead to reduction of gingivitis. Preventing Gingivitis 
      Diagnosing Chronic Periodontitis: Bleeding following probing of the periodontal 
      pocket is a sign of inflammation in the periodontal tissues (Evidence Grade 2). 
      Probing pocket depth overestimates the actual depth when periodontitis is present 
      and underestimates it when the periodontal tissues are healthy (Evidence Grade 
      2). The use of electronic pressure-sensitive probes does not improve the 
      reproducibility of periodontal pocket measurements compared to that of manual 
      probing (Evidence Grade 3). Radiographic measurements underestimate alveolar bone 
      loss. The degree of underestimation depends on the extent of bone loss and its 
      location in the dental arch (Evidence Grade 3). The accuracy of assessing 
      alveolar bone loss from direct digital radiography is comparable to that obtained 
      from film radiography (Evidence Grade 3). The number of periapical radiographs 
      can be considerably reduced when a clinical examination, along with bitewing 
      radiographs of the posterior teeth or a panoramic radiograph precedes a 
      full-mouth radiographic examination (Evidence Grade 3). The accuracy of bitewing 
      and periapical radiography is low for estimating small alveolar bone changes 
      (less than 1 mm) over time (Evidence Grade 3). Thus, performing radiographic 
      examinations at regular intervals for the purpose of assessing changes of the 
      periodontal support over time is not justified. Predicting Disease Progression: 
      The absence of “bleeding on probing” is a good predictor of periodontal stability 
      (Evidence Grade 3). Scientific evidence is insufficient for assessing the value 
      of pocket depth as a prognostic method. Treating Chronic Periodontitis: 
      Mechanical infection control (scaling and root planing) reduces probing pocket 
      depth and improves probing attachment level. Mechanical infection control 
      combined with flap surgery eliminates 10–15 percent more pockets deeper than 4 mm 
      than mechanical infection control alone (Evidence Grade 3). Local adjunctive 
      therapy with 25 percent metronidazole gel does not result in improved probing 
      pocket depth or probing attachment level compared to mechanical infection control 
      alone (Evidence Grade 3). Scientific evidence is insufficient for determining the 
      efficacy of other local antibiotics and antiseptics. Systemic antibiotic therapy 
      as an adjunct to mechanical infection control does not improve probing pocket 
      depth or probing attachment level compared to mechanical infection control alone 
      (Evidence Grade 1). Scientific evidence for the benefit derived from using 
      anti-inflammatory drugs is insufficient. Adjunctive therapy with guided tissue 
      regeneration (GTR) or with enamel matrix derivative (EMD) in individual angular 
      bone defects results in improved probing attachment level and bone level. An 
      improvement in probing attachment level by more than 4 mm can be expected twice 
      as often with GTR or EMD as with flap surgery alone (Evidence Grade 1). 
      Adjunctive therapy with coralline calcium carbonate in individual angular bone 
      defects improves bone level more effectively than flap surgery alone (Evidence 
      Grade 3). The outcomes are contradictory regarding probing attachment level. 
      Scientific evidence for the efficacy of using other filler materials is 
      insufficient. Adjunctive therapy with GTR and EMD appears to result in less 
      improvement in smokers than in non-smokers. Scientific evidence for assessing and 
      designing programs of supportive periodontal therapy is insufficient. Economic 
      Aspects: Scientific evidence is lacking for determining cost-effectiveness and 
      patient-perceived quality with regard to the various methods of prevention, 
      diagnosis and treatment of chronic periodontitis. The studies that were included 
      are too limited regarding quantity and assessed quality. Chronic Periodontitis as 
      a Risk for Other Diseases: Scientific evidence is contradictory as to whether 
      individuals with chronic periodontitis are at increased risk of developing 
      coronary heart disease or stroke. Scientific evidence is lacking as to whether 
      individuals with chronic periodontitis are at increased risk of developing 
      diabetes mellitus, chronic obstructive pulmonary disease or rheumatoid arthritis. 
      Scientific evidence is insufficient and contradictory as to whether women with 
      chronic periodontitis during pregnancy have an increased risk for preterm birth. 
      Scientific evidence of a relationship between chronic periodontitis and low birth 
      weight is also insufficient. Principles of Evidence Grading Quality refers to the 
      scientific quality of a particular study and its ability to reliably answer a 
      specific question. Evidence Grade refers to the total scientific evidence for a 
      conclusion, i.e., how many high-quality studies support the conclusion. Evidence 
      Grade 1 A conclusion assigned Evidence Grade 1 is supported by at least two 
      studies with high quality among the total scientific evidence. If some studies 
      are at variance with the conclusion, the evidence grade may be lower. Evidence 
      Grade 2 A conclusion assigned Evidence Grade 2 is supported by at least one study 
      with high quality and two studies with moderate quality among the total 
      scientific evidence. If some studies are at variance with the conclusion, the 
      evidence grade may be lower. Evidence Grade 3 A conclusion assigned Evidence 
      Grade 3 is supported by at least two studies with moderate quality among the 
      total scientific evidence. If some studies are at variance with the conclusion, 
      the evidence grade may be lower.
CI  - Copyright © 2004 by the Swedish Council on Health Technology Assessment.
CN  - Swedish Council on Health Technology Assessment
LA  - eng
PT  - Review
PT  - Book
PL  - Stockholm
EDAT- 2004/10/01 00:00
CRDT- 2004/10/01 00:00
AID - NBK447960 [bookaccession]

PMID- 15253953
OWN - NLM
STAT- MEDLINE
DCOM- 20040923
LR  - 20220409
IS  - 1468-201X (Electronic)
IS  - 1355-6037 (Print)
IS  - 1355-6037 (Linking)
VI  - 90
IP  - 8
DP  - 2004 Aug
TI  - Use of oral glucocorticoids and risk of cardiovascular and cerebrovascular 
      disease in a population based case-control study.
PG  - 859-65
AB  - OBJECTIVE: To assess whether use of oral glucocorticoids is associated with 
      cardiovascular and cerebrovascular morbidity. DESIGN AND SETTING: Nested 
      case-control study within a cohort of patients (> or = 50 years old) with at 
      least one prescription for oral or non-systemic glucocorticoids. Data were from 
      the general practice research database. PATIENTS: 50 656 patients were identified 
      with a first record for ischaemic heart disease (International classification of 
      diseases, ninth revision (ICD-9) codes 410, 411, 413, and 414), ischaemic stroke 
      or transient ischaemic attack (ICD-9 codes 430-436), or heart failure (ICD-9 code 
      428) between 1988 and 1998. One control was matched to each case by sex, age, 
      general practice, underlying disease, and calendar time. MAIN OUTCOME MEASURE: 
      Odds ratio (OR) of cardiovascular or cerebrovascular events in patients using 
      oral glucocorticoids compared with non-users. RESULTS: There was a significant 
      association between ever use of oral glucocorticoids and any cardiovascular or 
      cerebrovascular outcome (adjusted OR 1.25, 95% confidence interval (CI) 1.21 to 
      1.29). The association was stronger for current use of oral glucocorticoids than 
      for recent or past use. Among current users, the highest ORs were observed in the 
      group with the highest average daily dose, although the dose-response relation 
      was not continuous. Current use was associated with an increased risk of heart 
      failure (adjusted OR 2.66, 95% CI 2.46 to 2.87), which was consistent between 
      patients with rheumatoid arthritis, patients with chronic obstructive pulmonary 
      disease, and patients without either of the two conditions. Also, current use was 
      associated with a smaller increased risk of ischaemic heart disease (OR 1.20, 95% 
      CI 1.11 to 1.29). CONCLUSIONS: Oral glucocorticoid use was identified as a risk 
      factor for heart failure. However, the evidence remains observational and only a 
      randomised controlled trial of glucocorticoid treatment versus other disease 
      modifying agents is likely to distinguish the importance of the underlying 
      disease activity from its treatment in predicting cardiovascular outcomes.
FAU - Souverein, P C
AU  - Souverein PC
AD  - Department of Pharmacoepidemiology and Pharmacotherapy, Utrecht Institute for 
      Pharmaceutical Sciences, PO Box 80082, 3508 TB Utrecht, The Netherlands. 
      P.C.Souverein@pharm.uu.nl
FAU - Berard, A
AU  - Berard A
FAU - Van Staa, T P
AU  - Van Staa TP
FAU - Cooper, C
AU  - Cooper C
FAU - Egberts, A C G
AU  - Egberts AC
FAU - Leufkens, H G M
AU  - Leufkens HG
FAU - Walker, B R
AU  - Walker BR
LA  - eng
PT  - Journal Article
PL  - England
TA  - Heart
JT  - Heart (British Cardiac Society)
JID - 9602087
RN  - 0 (Glucocorticoids)
SB  - IM
CIN - Heart. 2004 Aug;90(8):829-30. doi: 10.1136/hrt.2003.031492. PMID: 15253942
MH  - Administration, Oral
MH  - Aged
MH  - Aged, 80 and over
MH  - Cardiovascular Diseases/chemically induced/*mortality
MH  - Case-Control Studies
MH  - Cerebrovascular Disorders/chemically induced/mortality
MH  - Cohort Studies
MH  - Dose-Response Relationship, Drug
MH  - Glucocorticoids/administration & dosage/*adverse effects
MH  - Humans
MH  - Middle Aged
MH  - Risk Factors
PMC - PMC1768386
EDAT- 2004/07/16 05:00
MHDA- 2004/09/24 05:00
PMCR- 2007/08/01
CRDT- 2004/07/16 05:00
PHST- 2004/07/16 05:00 [pubmed]
PHST- 2004/09/24 05:00 [medline]
PHST- 2004/07/16 05:00 [entrez]
PHST- 2007/08/01 00:00 [pmc-release]
AID - 90/8/859 [pii]
AID - 0900859 [pii]
AID - 10.1136/hrt.2003.020180 [doi]
PST - ppublish
SO  - Heart. 2004 Aug;90(8):859-65. doi: 10.1136/hrt.2003.020180.

PMID- 15142472
OWN - NLM
STAT- MEDLINE
DCOM- 20040803
LR  - 20191108
IS  - 1523-3812 (Print)
IS  - 1523-3812 (Linking)
VI  - 6
IP  - 3
DP  - 2004 Jun
TI  - Impact of medical comorbid disease on antidepressant treatment of major 
      depressive disorder.
PG  - 193-201
AB  - A major factor in evaluating and treating depression is the presence of comorbid 
      medical problems. In this paper, the authors will first evaluate studies showing 
      that medical illness is a risk factor for depression. The authors will review a 
      series of randomized, controlled studies of antidepressant treatment in subjects 
      with major depressive disorder (MDD) and comorbid medical illnesses (myocardial 
      infarction, stroke, diabetes, cancer, and rheumatoid arthritis). Most of these 
      studies report an advantage for an active antidepressant over placebo in 
      improvement of depressive symptoms. The authors also will review a series of 
      studies in which the outcome of antidepressant treatment is compared between 
      subjects with MDD with and without comorbid medical illness. In these studies, 
      subjects with medical illness tend to have lower improvement of depressive 
      symptoms and higher rates of depressive relapse with antidepressant treatment 
      compared with MDD subjects with no medical comorbidity. In addition, the authors 
      will review hypotheses on the mechanism of the interaction between medical 
      illness and clinical response in MDD. The paper will conclude that medical 
      comorbidity is a predictor of treatment resistance in MDD.
FAU - Iosifescu, Dan V
AU  - Iosifescu DV
AD  - Massachusetts General Hospital, 50 Staniford Street, Suite 401, Boston, MA 02114, 
      USA. diosifescu@partners.org
FAU - Bankier, Bettina
AU  - Bankier B
FAU - Fava, Maurizio
AU  - Fava M
LA  - eng
GR  - 1K23 MH 067111-01A1/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Curr Psychiatry Rep
JT  - Current psychiatry reports
JID - 100888960
RN  - 0 (Antidepressive Agents)
SB  - IM
MH  - Antidepressive Agents/*therapeutic use
MH  - Chronic Disease
MH  - Comorbidity
MH  - Controlled Clinical Trials as Topic
MH  - Depressive Disorder, Major/*drug therapy/epidemiology/*etiology/psychology
MH  - *Health Status
MH  - Humans
MH  - Randomized Controlled Trials as Topic
MH  - Risk Factors
MH  - Treatment Outcome
RF  - 98
EDAT- 2004/05/15 05:00
MHDA- 2004/08/04 05:00
CRDT- 2004/05/15 05:00
PHST- 2004/05/15 05:00 [pubmed]
PHST- 2004/08/04 05:00 [medline]
PHST- 2004/05/15 05:00 [entrez]
AID - 10.1007/s11920-004-0064-2 [doi]
PST - ppublish
SO  - Curr Psychiatry Rep. 2004 Jun;6(3):193-201. doi: 10.1007/s11920-004-0064-2.

PMID- 14626790
OWN - NLM
STAT- MEDLINE
DCOM- 20040312
LR  - 20200825
IS  - 0304-4602 (Print)
IS  - 0304-4602 (Linking)
VI  - 32
IP  - 5
DP  - 2003 Sep
TI  - The combined oral contraceptive pill in women over age forty.
PG  - 624-31
AB  - INTRODUCTION: By the age of 35 years, most women would have completed their 
      families and contraception then becomes an important consideration. In the next 
      one or two decades, other health concerns such as osteoporosis, dysfunctional 
      uterine bleeding, ovarian, endometrial, colorectal and breast cancers and 
      cardiovascular diseases will assume prominence in the lives of women. We review 
      the role of the combined oral contraceptive (OC) pill in the older woman in the 
      context of these important health concerns. METHODS: A Medline search was made 
      for possible interaction between OC use and the above conditions. An important 
      criteria for citation was publication in a high impact factor journal; 
      furthermore to represent the wider context from which there issues derive we 
      choose, whenever appropriate, general journal with wide readership including, but 
      not limited to the Lancet or New England Journal of Medicine; we also choose 
      studies published in journals of other medical disciplines instead of purely 
      gynaecological journals to reflect the multidisciplinary impact of the combined 
      OC pills. RESULTS: Combined OC retards bone demineralisation which could 
      translate clinically to a reduction in postmenopausal osteoporotic fractures; it 
      affords good menstrual cyclicity and alleviation of perimenopausal vasomotor 
      symptoms; it offers chemoporophylaxis against epithelial ovarian cancers and 
      endometrial cancers. There is evidence that it could be protective against 
      colorectal cancers. The combined OC may attenuate the disease progression of 
      rheumatoid arthritis and reduces the risk of ectopic pregnancy and pelvic 
      inflammatory disease. In an older woman who does not smoke and is in good health, 
      the excess risk of stroke, myocardial infarcts and venous thromboembolism is 
      minimal, if at all, as is the risk of breast neoplasm. In women with proven human 
      papilomavirus infection of the cervix who are using OCs, regular cervical 
      screening is especially important. CONCLUSION: The non-contraceptive health 
      benefits of the combined OCs justify its usage in the healthy older woman.
FAU - Wong, M T
AU  - Wong MT
AD  - Department of Obstetrics and Gynaecology, National University Hospital, National 
      University of Singapore, 5 Lower Kent Ridge Road, Singapore 119074.
FAU - Singh, K
AU  - Singh K
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Singapore
TA  - Ann Acad Med Singap
JT  - Annals of the Academy of Medicine, Singapore
JID - 7503289
RN  - 0 (Contraceptives, Oral, Combined)
RN  - 0 (Contraceptives, Oral, Hormonal)
SB  - IM
MH  - Adult
MH  - Age Factors
MH  - Breast Neoplasms/epidemiology/*etiology
MH  - Cohort Studies
MH  - Contraceptives, Oral, Combined/administration & dosage/*adverse effects
MH  - Contraceptives, Oral, Hormonal/administration & dosage/*adverse effects
MH  - Decision Making
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Intracranial Embolism/epidemiology/*etiology
MH  - Middle Aged
MH  - Prognosis
MH  - Risk Assessment
MH  - Singapore/epidemiology
MH  - Uterine Cervical Neoplasms/epidemiology/*etiology
RF  - 55
EDAT- 2003/11/25 05:00
MHDA- 2004/03/16 05:00
CRDT- 2003/11/25 05:00
PHST- 2003/11/25 05:00 [pubmed]
PHST- 2004/03/16 05:00 [medline]
PHST- 2003/11/25 05:00 [entrez]
PST - ppublish
SO  - Ann Acad Med Singap. 2003 Sep;32(5):624-31.

PMID- 12737445
OWN - NLM
STAT- MEDLINE
DCOM- 20031028
LR  - 20191210
IS  - 0036-5521 (Print)
IS  - 0036-5521 (Linking)
VI  - 38
IP  - 3
DP  - 2003 Mar
TI  - Early cancer of the stomach arising after successful treatment of gastric MALT 
      lymphoma in patients with autoimmune disease.
PG  - 294-7
AB  - BACKGROUND: Extranodal marginal zone B-cell lymphoma of the mucosa associated 
      lymphoid tissue (MALT lymphoma) arises in lymphoid tissue acquired through 
      chronic antigenic stimulation as exemplified by Helicobacter pylori. Secondary 
      development of gastric cancer, however, is thought to be a rare event. The 
      detection of a signet ring cell carcinoma during follow-up endoscopy after 
      successful therapy of MALT lymphoma in a patient with Sjögren's syndrome prompted 
      us to analyse the frequency of subsequent gastric cancer in patients with 
      underlying autoimmune disease (AD). METHODS: Patients with early stage MALT 
      lymphoma and an underlying AD were evaluated for the occurrence of a secondary 
      gastric cancer during the course of follow-up. Data analysed included the type of 
      AD, stage of MALT lymphoma, H. pylori status, treatment for MALT lymphoma and 
      response, follow-up, the presence of a secondary cancer, and time to development 
      of cancer. In all patients, histologic samples were reassessed for the extent of 
      gastritis, presence of intestinal metaplasia or focal atrophy at the time of 
      lymphoma diagnosis. RESULTS: A total of eight patients with overt AD at the time 
      of diagnosis of MALT lymphoma were identified. All patients were women aged 
      between 56 and 77 years; 5 had Sjögren's syndrome, 2 had autoimmune thyroiditis 
      (1 along with psoriasis) and 1 suffered from polymyalgia rheumatica. All patients 
      had early stage MALT lymphoma restricted to the mucosa and submucosa at the time 
      of diagnosis, and the presence of H. pylori was found in all cases. Two of these 
      patients achieved complete remission (CR) of the lymphoma following H. pylori 
      eradication, while six were judged unresponsive and underwent chemotherapy, 
      resulting in CR in all cases. One patient died from stroke while being in CR for 
      2 months following chemotherapy. Two patients (25%) developed early cancer 
      limited to the gastric mucosa while being in CR from lymphoma for 9 and 27 
      months, respectively, and underwent partial gastrectomy. Final staging of gastric 
      cancer revealed pT1pN0M0 in both cases. Of the remaining 5 cases, 1 patient had a 
      local lymphoma relapse 18 months after CR and was salvaged with radiotherapy. In 
      the remaining 4 patients, no evidence of lymphoma recurrence or a second 
      malignancy has been found so far by regular follow-up every 3 months for a 
      time-span between 52 and 63 months after initial diagnosis. CONCLUSION: Patients 
      with concurrent MALT lymphoma and an underlying autoimmune condition show not 
      only an impaired response to H. pylori eradication but might also be at increased 
      risk for the development of gastric cancer. In view of this, such patients should 
      be followed closely by regular endoscopies after remission of MALT lymphoma.
FAU - Raderer, M
AU  - Raderer M
AD  - Dept. of Internal Medicine I, Division of Oncology, University of Vienna, 
      Austria. markus.raderer@akh-wien.ac.at
FAU - Püspök, A
AU  - Püspök A
FAU - Stummvoll, G
AU  - Stummvoll G
FAU - Längle, F
AU  - Längle F
FAU - Chott, A
AU  - Chott A
LA  - eng
PT  - Evaluation Study
PT  - Journal Article
PL  - England
TA  - Scand J Gastroenterol
JT  - Scandinavian journal of gastroenterology
JID - 0060105
SB  - IM
MH  - Adenocarcinoma/diagnosis/therapy
MH  - Aged
MH  - Antineoplastic Combined Chemotherapy Protocols
MH  - Austria
MH  - Autoimmune Diseases/diagnosis/*therapy
MH  - Biopsy
MH  - Carcinoma, Signet Ring Cell/diagnosis/therapy
MH  - Endosonography
MH  - Female
MH  - Follow-Up Studies
MH  - Gastric Mucosa/*pathology
MH  - Humans
MH  - Lymphoma, B-Cell, Marginal Zone/diagnosis/*therapy
MH  - Metaplasia
MH  - Middle Aged
MH  - Neoplasm Staging
MH  - Polymyalgia Rheumatica/diagnosis/therapy
MH  - Pyloric Antrum/pathology
MH  - Remission Induction
MH  - Severity of Illness Index
MH  - Sjogren's Syndrome/diagnosis/therapy
MH  - Stomach Neoplasms/diagnosis/*therapy
MH  - Time Factors
MH  - Treatment Outcome
EDAT- 2003/05/10 05:00
MHDA- 2003/10/29 05:00
CRDT- 2003/05/10 05:00
PHST- 2003/05/10 05:00 [pubmed]
PHST- 2003/10/29 05:00 [medline]
PHST- 2003/05/10 05:00 [entrez]
AID - 10.1080/00365520310000582 [doi]
PST - ppublish
SO  - Scand J Gastroenterol. 2003 Mar;38(3):294-7. doi: 10.1080/00365520310000582.

PMID- 12707707
OWN - NLM
STAT- MEDLINE
DCOM- 20040105
LR  - 20221207
IS  - 0028-2804 (Print)
IS  - 0028-2804 (Linking)
VI  - 74
IP  - 4
DP  - 2003 Apr
TI  - [Dissection of four cerebral arteries after protracted birth].
PG  - 366-9
AB  - A 37-year-old woman suffered from middle cerebral artery infarction secondary to 
      dissection of the left internal carotid artery. Nine days before, a cesarean 
      section had been performed on her after 20 h of unsuccessful labor. Cerebral 
      angiography at admission revealed no further vascular abnormalities. A few days 
      later, however, the patient developed additional dissections of the right 
      internal carotid artery and both vertebral arteries. Pregnancy, childbirth, and a 
      history of rheumatoid arthritis in this patient may have contributed to the 
      dissections; however, due to the unknown etiology of cervical dissections, the 
      pathogenetic contribution of all of these factors is incompletely understood.
FAU - Oehler, J
AU  - Oehler J
AD  - Neurologische Klinik, Universitätsklinikum Heidelberg.
FAU - Lichy, Ch
AU  - Lichy Ch
FAU - Gandjour, J
AU  - Gandjour J
FAU - Fiebach, J
AU  - Fiebach J
FAU - Grau, A J
AU  - Grau AJ
LA  - ger
PT  - Case Reports
PT  - English Abstract
PT  - Journal Article
TT  - Vier-Gefäss-Dissektion nach protrahierter Geburt.
PL  - Germany
TA  - Nervenarzt
JT  - Der Nervenarzt
JID - 0400773
SB  - IM
MH  - Adult
MH  - Aortic Dissection/*diagnosis
MH  - Aphasia/diagnosis
MH  - Arthritis, Rheumatoid/diagnosis
MH  - Carotid Artery, Internal, Dissection/*diagnosis
MH  - *Cesarean Section
MH  - Diagnostic Imaging
MH  - Female
MH  - Follow-Up Studies
MH  - Hemiplegia/diagnosis
MH  - Humans
MH  - Infarction, Middle Cerebral Artery/diagnosis
MH  - Intracranial Aneurysm/*diagnosis
MH  - Obstetric Labor Complications/*diagnosis
MH  - Postoperative Complications/diagnosis
MH  - Pregnancy
MH  - Puerperal Disorders/*diagnosis
MH  - Recurrence
MH  - Risk Factors
MH  - Vertebral Artery Dissection/diagnosis
EDAT- 2003/04/23 05:00
MHDA- 2004/01/06 05:00
CRDT- 2003/04/23 05:00
PHST- 2003/04/23 05:00 [pubmed]
PHST- 2004/01/06 05:00 [medline]
PHST- 2003/04/23 05:00 [entrez]
AID - 10.1007/s00115-002-1471-4 [doi]
PST - ppublish
SO  - Nervenarzt. 2003 Apr;74(4):366-9. doi: 10.1007/s00115-002-1471-4.

PMID- 12672188
OWN - NLM
STAT- MEDLINE
DCOM- 20030718
LR  - 20061115
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 30
IP  - 4
DP  - 2003 Apr
TI  - Consequences of increased systolic blood pressure in patients with osteoarthritis 
      and rheumatoid arthritis.
PG  - 714-9
AB  - OBJECTIVE: To estimate the potential effect on cardiovascular event occurrence 
      and treatment costs associated with increases in systolic blood pressure (SBP) 
      among patients with osteoarthritis (OA) and rheumatoid arthritis (RA). METHODS: 
      We used cardiovascular risk prediction models from the Framingham Heart Study and 
      data on risk factors from the Third National Health and Nutrition Examination 
      Survey (NHANES III) to estimate occurrences of ischemic heart disease and stroke 
      over one year among US adults with OA/RA. Separate analyses were conducted for 
      treated hypertensive patients, and untreated hypertensive and normotensive 
      patients, respectively. Published estimates were used to assign costs to these 
      events and to follow care. The effect of incremental increases in SBP on events 
      and costs was then assessed. Monte Carlo simulation was undertaken to assess the 
      range of event occurrence and costs associated with alternative assumptions 
      regarding the distribution of increased SBP in the at-risk population. RESULTS: 
      Of the estimated 30 million adults in the US aged > or = 35 years with OA and RA, 
      roughly 11.8 million (39%) receive pharmacologic treatment for hypertension. 
      Increases in SBP of 1-5 mm Hg were associated with 7,100-35,700 additional 
      ischemic heart disease and stroke events over one year, with corresponding costs 
      (year 2000 USD) of 114-569 million year 2000 USD. A 20 mm Hg increase in SBP 
      experienced by 15% of the at-risk population (equivalent to a population-average 
      3 mm Hg increase) is associated with about 21,700 additional events (95% CI 
      19,120, 24,221) and 346 million year 2000 USD (95% CI 305 year 2000 USD, 387 
      million) in associated costs. CONCLUSION: Relatively small changes in SBP 
      associated with use of common arthritis medications can have a significant effect 
      on the cardiovascular risk profile. It is important that clinicians who treat 
      patients with OA/RA accurately weigh the potential risks of these medications 
      against their benefits.
FAU - Singh, Gurkirpal
AU  - Singh G
AD  - Medical Research International, Waltham, Massachusetts 02451-7341, USA.
FAU - Miller, Jeffrey D
AU  - Miller JD
FAU - Huse, Daniel M
AU  - Huse DM
FAU - Pettitt, Dan
AU  - Pettitt D
FAU - D'Agostino, Ralph B
AU  - D'Agostino RB
FAU - Russell, Mason W
AU  - Russell MW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
SB  - IM
CIN - J Rheumatol. 2003 Apr;30(4):642-5. PMID: 12672178
CIN - J Rheumatol. 2004 Apr;31(4):829. PMID: 15095747
MH  - Adult
MH  - Age Distribution
MH  - Aged
MH  - Arthritis, Rheumatoid/economics/*epidemiology
MH  - *Blood Pressure
MH  - Female
MH  - Health Care Costs
MH  - Humans
MH  - Hypertension/economics/*epidemiology/therapy
MH  - Male
MH  - Middle Aged
MH  - Monte Carlo Method
MH  - Osteoarthritis/economics/*epidemiology
MH  - Prevalence
MH  - Risk Factors
MH  - Sex Distribution
MH  - United States/epidemiology
EDAT- 2003/04/03 05:00
MHDA- 2003/07/19 05:00
CRDT- 2003/04/03 05:00
PHST- 2003/04/03 05:00 [pubmed]
PHST- 2003/07/19 05:00 [medline]
PHST- 2003/04/03 05:00 [entrez]
AID - 0315162X-30-714 [pii]
PST - ppublish
SO  - J Rheumatol. 2003 Apr;30(4):714-9.

PMID- 12628952
OWN - NLM
STAT- MEDLINE
DCOM- 20030324
LR  - 20220410
IS  - 1524-4539 (Electronic)
IS  - 0009-7322 (Linking)
VI  - 107
IP  - 9
DP  - 2003 Mar 11
TI  - Cardiovascular morbidity and mortality in women diagnosed with rheumatoid 
      arthritis.
PG  - 1303-7
AB  - BACKGROUND: Rheumatoid arthritis may be associated with an increased risk of 
      cardiovascular disease. We compared the incidence rates of myocardial infarction 
      and stroke in subjects with and without rheumatoid arthritis. METHODS AND 
      RESULTS: A prospective cohort study was conducted among the 114 342 women 
      participating in the Nurses' Health Study who were free of cardiovascular disease 
      and rheumatoid arthritis at baseline in 1976. All self-reported cases of 
      rheumatoid arthritis were confirmed by medical record review. Fatal and nonfatal 
      myocardial infarctions and strokes were similarly confirmed. Multivariate pooled 
      logistic regression was used to adjust for potential cardiovascular risk factors. 
      Five hundred twenty-seven incident cases of rheumatoid arthritis and 3622 
      myocardial infarctions and strokes were confirmed during 2.4 million person-years 
      of follow-up. The adjusted relative risk of myocardial infarction in women with 
      rheumatoid arthritis compared with those without was 2.0 (95% confidence interval 
      [CI], 1.23 to 3.29). For stroke, the adjusted relative risk was 1.48 (95% CI, 
      0.70 to 3.12). Women who had rheumatoid arthritis for at least 10 years had a 
      risk for myocardial infarction of 3.10 (95% CI, 1.64 to 5.87). CONCLUSION: In 
      this large prospective cohort of women, participants with rheumatoid arthritis 
      had a significantly increased risk of myocardial infarction but not stroke 
      compared with those without rheumatoid arthritis. If these data are confirmed, 
      aggressive coronary heart disease prevention strategies should be tested for 
      persons with rheumatoid arthritis.
FAU - Solomon, Daniel H
AU  - Solomon DH
AD  - Division of Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's 
      Hospital, Harvard Medical School, Boston, Mass 02115, USA. dhsolomon@partners.org
FAU - Karlson, Elizabeth W
AU  - Karlson EW
FAU - Rimm, Eric B
AU  - Rimm EB
FAU - Cannuscio, Carolyn C
AU  - Cannuscio CC
FAU - Mandl, Lisa A
AU  - Mandl LA
FAU - Manson, JoAnn E
AU  - Manson JE
FAU - Stampfer, Meir J
AU  - Stampfer MJ
FAU - Curhan, Gary C
AU  - Curhan GC
LA  - eng
GR  - CA87969/CA/NCI NIH HHS/United States
GR  - HL34594/HL/NHLBI NIH HHS/United States
GR  - K23 AR48616-01/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
SB  - IM
CIN - ACP J Club. 2003 Sep-Oct;139(2):50. PMID: 12954042
MH  - Adult
MH  - Arthritis, Rheumatoid/*complications/diagnosis
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Middle Aged
MH  - Myocardial Infarction/*epidemiology/etiology/*mortality
MH  - Prospective Studies
MH  - Risk Factors
MH  - Stroke/*epidemiology/etiology/*mortality
EDAT- 2003/03/12 04:00
MHDA- 2003/03/26 04:00
CRDT- 2003/03/12 04:00
PHST- 2003/03/12 04:00 [pubmed]
PHST- 2003/03/26 04:00 [medline]
PHST- 2003/03/12 04:00 [entrez]
AID - 10.1161/01.cir.0000054612.26458.b2 [doi]
PST - ppublish
SO  - Circulation. 2003 Mar 11;107(9):1303-7. doi: 10.1161/01.cir.0000054612.26458.b2.

PMID- 12508387
OWN - NLM
STAT- MEDLINE
DCOM- 20030513
LR  - 20220331
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 30
IP  - 1
DP  - 2003 Jan
TI  - Increase in cardiovascular and cerebrovascular disease prevalence in rheumatoid 
      arthritis.
PG  - 36-40
AB  - OBJECTIVE: To determine whether the risk for cardiovascular and/or 
      cerebrovascular disease (CCVD) is increased in rheumatoid arthritis (RA) compared 
      to osteoarthritis (OA), a disease not known to be associated with increased CCVD. 
      METHODS: In July 1999, a survey was administered to a sample of 11,572 patients 
      (9,093 with RA, 2479 with OA) from the practices of 709 US community-based 
      rheumatologists. Patients reported past and current myocardial infarction (MI), 
      stroke (cerebrovascular accident, CVA), and lifetime congestive heart failure 
      (CHF), and also provided demographic and clinical information. To estimate the 
      impact of recall bias, medical records were obtained and reviewed for a 50% 
      random sample of the patients reporting CCVD events, with 95% of CCVD reported 
      events confirmed by record review. RESULTS: Patients with RA and OA differed 
      across all demographic variables. In addition, each variable was significantly 
      associated with MI, CHF, and CVA outcomes. Logistic regression was performed to 
      measure the associations of these outcomes with RA as compared to OA, adjusting 
      for age, sex, education level, smoking, income, hypertension, and body mass 
      index. Compared with OA, patients with RA had the following increased risks: for 
      current MI [odds ratio (OR), 95% confidence interval (95% CI)] 2.14, (1.48, 
      3.09), lifetime MI 1.28 (1.24, 1.33), CHF 1.43 (1.28, 1.59), current CVA 1.70 
      (1.29, 2.24), and lifetime CVA 1.005 (0.931, 1.196). The adjusted current and 
      lifetime prevalences of MI were 0.76 and 4.14% for RA versus 0.35 and 3.23% 
      respectively for OA; 0.86 and 3.02% (RA) versus 0.50 and 3.03% (OA) for CVA; and 
      for lifetime CHF, 2.34% (RA) versus 1.64% (OA), respectively. CONCLUSIONS: RA is 
      associated with an increased risk for CCVD morbidity due to MI, CHF, and probably 
      for CVA, and may be an independent risk factor for these events.
FAU - Wolfe, Frederick
AU  - Wolfe F
AD  - National Data Bank for Rheumatic Diseases, Wichita, Kansas, USA. 
      fwolfe@arthritis-research.org
FAU - Freundlich, Bruce
AU  - Freundlich B
FAU - Straus, Walter L
AU  - Straus WL
LA  - eng
PT  - Journal Article
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Female
MH  - Humans
MH  - Hypertension/epidemiology
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/*epidemiology
MH  - Osteoarthritis/epidemiology
MH  - Prevalence
MH  - Risk Factors
MH  - Severity of Illness Index
MH  - Stroke/*epidemiology
EDAT- 2003/01/01 04:00
MHDA- 2003/05/14 05:00
CRDT- 2003/01/01 04:00
PHST- 2003/01/01 04:00 [pubmed]
PHST- 2003/05/14 05:00 [medline]
PHST- 2003/01/01 04:00 [entrez]
AID - 0315162X-30-36 [pii]
PST - ppublish
SO  - J Rheumatol. 2003 Jan;30(1):36-40.

PMID- 12402411
OWN - NLM
STAT- MEDLINE
DCOM- 20030221
LR  - 20220317
IS  - 1080-0549 (Print)
IS  - 1080-0549 (Linking)
VI  - 23
IP  - 3
DP  - 2002 Dec
TI  - Cardiac involvement in systemic autoimmune diseases.
PG  - 247-61
AB  - The heart and the vascular system are frequent and characteristic targets of 
      several systemic autoimmune diseases, in particular Systemic Lupus Erythematosus 
      (SLE), Rheumatoid Arthritis (RA) and Systemic Sclerosis (SSc). In this chapter we 
      review the classic cardiac abnormalities and the more recent data about 
      cardiovascular involvement as part of a major disease complication determining a 
      substantial morbidity and mortality. In addition to the classic cardiac 
      abnormalities involving the heart structures, acute and chronic ischemic heart 
      disease and cerebrovascular accidents are threatening clinical manifestations of 
      SLE and RA associated to an early accelerated atherosclerosis. Immune-mediated 
      inflammation is now recognized as an important factor involved in the 
      pathogenesis of atherosclerosis. Ongoing clinical studies are being devised to 
      find specific risk factors associated with systemic autoimmune diseases and/or 
      treatment regimens. Hopefully, prophylactic measures should be available within 
      the next few years.
FAU - Riboldi, Piersandro
AU  - Riboldi P
AD  - Department of Internal Medicine, University of Milan, Allergy and Clinical 
      Immunology Unit, IRCCS Istituto Auxologico, Via Ariosto 13, 20145, Milan, Italy. 
      piersandro.riboldi@unimi.it
FAU - Gerosa, Maria
AU  - Gerosa M
FAU - Luzzana, Cristina
AU  - Luzzana C
FAU - Catelli, Luca
AU  - Catelli L
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Clin Rev Allergy Immunol
JT  - Clinical reviews in allergy & immunology
JID - 9504368
SB  - IM
MH  - Autoimmune Diseases/*complications/epidemiology/*immunology
MH  - Cardiovascular Abnormalities/epidemiology/*etiology
MH  - Clinical Trials as Topic
MH  - Evidence-Based Medicine
MH  - Heart Conduction System/pathology
MH  - Humans
MH  - Lupus Erythematosus, Systemic/complications/epidemiology/immunology
MH  - Prevalence
RF  - 86
EDAT- 2002/10/31 04:00
MHDA- 2003/02/22 04:00
CRDT- 2002/10/31 04:00
PHST- 2002/10/31 04:00 [pubmed]
PHST- 2003/02/22 04:00 [medline]
PHST- 2002/10/31 04:00 [entrez]
AID - CRIAI:23:3:247 [pii]
AID - 10.1385/CRIAI:23:3:247 [doi]
PST - ppublish
SO  - Clin Rev Allergy Immunol. 2002 Dec;23(3):247-61. doi: 10.1385/CRIAI:23:3:247.

PMID- 12167735
OWN - NLM
STAT- MEDLINE
DCOM- 20021104
LR  - 20161020
IS  - 1024-2708 (Print)
IS  - 1024-2708 (Linking)
VI  - 8
IP  - 4
DP  - 2002 Aug
TI  - Cerebral infarct mimicking glioma in Sjogren's syndrome.
PG  - 292-4
AB  - A 50-year-old Chinese woman with a chronic 20-year history of ataxic gait 
      associated with dry eyes and mouth, was admitted to hospital after a single 
      episode of syncope. Magnetic resonance imaging scans showed a large left frontal 
      hypodense lesion suggestive of a glioma. Craniotomy was performed and the lesion 
      excised, with histology showing only infarcted tissue and no malignant cells. 
      Further diagnostic evaluation revealed that the patient had primary Sjogren's 
      syndrome, with demyelinating polyneuropathy. In the absence of risk factors for 
      stroke, it was considered likely that the cerebral infarct was secondary to 
      autoimmune-related vasculitis. Functional neuroimaging, such as magnetic 
      resonance spectroscopy, should be considered in evaluating doubtful or unusual 
      brain lesions in patients with autoimmune disease.
FAU - Koh, M S
AU  - Koh MS
AD  - Department of Neurosurgery, Singapore General Hospital, Outram Road, Singapore.
FAU - Goh, K Y C
AU  - Goh KY
FAU - Chen, C
AU  - Chen C
FAU - Howe, H S
AU  - Howe HS
LA  - eng
PT  - Case Reports
PT  - Journal Article
PL  - China
TA  - Hong Kong Med J
JT  - Hong Kong medical journal = Xianggang yi xue za zhi
JID - 9512509
SB  - IM
MH  - Brain/pathology
MH  - Brain Neoplasms/*diagnosis
MH  - Cerebral Infarction/*diagnosis/pathology
MH  - Craniotomy
MH  - Diagnosis, Differential
MH  - Female
MH  - Glioma/*diagnosis
MH  - Humans
MH  - Magnetic Resonance Imaging
MH  - Middle Aged
MH  - Sjogren's Syndrome/*pathology
EDAT- 2002/08/09 10:00
MHDA- 2002/11/26 04:00
CRDT- 2002/08/09 10:00
PHST- 2002/08/09 10:00 [pubmed]
PHST- 2002/11/26 04:00 [medline]
PHST- 2002/08/09 10:00 [entrez]
PST - ppublish
SO  - Hong Kong Med J. 2002 Aug;8(4):292-4.

PMID- 12020179
OWN - NLM
STAT- MEDLINE
DCOM- 20020605
LR  - 20220311
IS  - 0003-9926 (Print)
IS  - 0003-9926 (Linking)
VI  - 162
IP  - 10
DP  - 2002 May 27
TI  - Lower risk of thromboembolic cardiovascular events with naproxen among patients 
      with rheumatoid arthritis.
PG  - 1105-10
AB  - BACKGROUND: Naproxen strongly inhibits platelet aggregation. OBJECTIVE: To 
      examine the risk of acute thromboembolic cardiovascular events (TCEs) (myocardial 
      infarction, sudden death, and stroke) with current naproxen use among patients 
      with rheumatoid arthritis. METHODS: We studied patients aged 40 to 79 years with 
      rheumatoid arthritis in the British General Practice Research Database, excluding 
      those with a prior TCE and potentially confounding conditions. We matched up to 4 
      controls by sex, age, and site of medical practice to cases with first incident 
      TCEs. The case diagnosis date was designated as the index date for each case and 
      his or her controls. We categorized naproxen according to the most recent 
      prescription prior to the index date as being current (< or =30 days), past (> 30 
      days but < 365 days), or none (> or =365 days before index date). Using 
      conditional logistic regression, we conducted a matched case-control analysis 
      with adjustment for potential confounders. RESULTS: We identified 809 cases. 
      Current naproxen use was more common among controls (5.7%) than cases (3.2%). 
      Adjusting for calendar year of treatment start, systemic corticosteroid use, 
      diabetes, and comorbidity, we found that the odds ratio (95% confidence interval) 
      for current naproxen use was 0.61 (0.39-0.94) while that for past use was 0.87 
      (0.65-1.16). Secondary and sensitivity analyses supported these results. 
      CONCLUSIONS: In this case-control study, patients with rheumatoid arthritis and a 
      current prescription for naproxen had a reduced risk of acute major TCEs relative 
      to those with no naproxen prescription in the past year. These results are 
      consistent with the ability of naproxen to inhibit platelet aggregation.
FAU - Watson, Douglas J
AU  - Watson DJ
AD  - Department of Epidemiology, Merck Research Laboratories, 10 Sentry Pkwy (BL1-7), 
      Blue Bell, PA 19422, USA. watsond@merck.com
FAU - Rhodes, Thomas
AU  - Rhodes T
FAU - Cai, Bing
AU  - Cai B
FAU - Guess, Harry A
AU  - Guess HA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Arch Intern Med
JT  - Archives of internal medicine
JID - 0372440
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - 57Y76R9ATQ (Naproxen)
SB  - IM
EIN - Arch Intern Med 2002 Aug 12-26;162(15):1779
CIN - Arch Intern Med. 2002 May 27;162(10):1091-2. doi: 10.1001/archinte.162.10.1091. 
      PMID: 12020175
CIN - Arch Intern Med. 2002 Dec 9-23;162(22):2639; author reply 2640-2. doi: 
      10.1001/archinte.162.22.2639. PMID: 12456258
CIN - Arch Intern Med. 2002 Dec 9-23;162(22):2639-40; author reply 2640-2. doi: 
      10.1001/archinte.162.22.2639-a. PMID: 12456259
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/complications/*drug therapy
MH  - Case-Control Studies
MH  - England/epidemiology
MH  - Humans
MH  - Matched-Pair Analysis
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Myocardial Infarction/*epidemiology/mortality/prevention & control
MH  - Naproxen/*therapeutic use
MH  - Platelet Aggregation Inhibitors/*therapeutic use
MH  - Regression Analysis
MH  - Risk
MH  - Survival Analysis
MH  - Thromboembolism/*epidemiology/mortality/prevention & control
MH  - Wales/epidemiology
EDAT- 2002/05/22 10:00
MHDA- 2002/06/06 10:01
CRDT- 2002/05/22 10:00
PHST- 2002/05/22 10:00 [pubmed]
PHST- 2002/06/06 10:01 [medline]
PHST- 2002/05/22 10:00 [entrez]
AID - ioi20014 [pii]
AID - 10.1001/archinte.162.10.1105 [doi]
PST - ppublish
SO  - Arch Intern Med. 2002 May 27;162(10):1105-10. doi: 10.1001/archinte.162.10.1105.

PMID- 11974948
OWN - NLM
STAT- MEDLINE
DCOM- 20020507
LR  - 20190901
IS  - 0300-9173 (Print)
IS  - 0300-9173 (Linking)
VI  - 39
IP  - 2
DP  - 2002 Mar
TI  - [Maintenance and improvement of quality of life among elderly patients using a 
      pet-type robot].
PG  - 214-8
AB  - There have been reports of cases in which quality of life and loneliness of 
      elderly people have been affected by interaction with the pet-type robot AIBO. In 
      the present comparison between first and 20th sessions of activity with the 
      pet-type robot, statistically significant improvements were observed in speech, 
      emotional words and satisfaction index. The AKO loneliness scale value was 3.33 
      at the first session, and was 1.00 at the 20th session (statistically significant 
      decrease). In a comparison of health-related QOL before and after interaction 
      with AIBO, using the SF-36 survey, role function (RP) was statistically higher at 
      the 20th session than at the first session. Evaluation by CgA, a mental stress 
      index, showed a statistically significant decrease as the number of AIBO sessions 
      increased. Case 1: The patient was a 68-year-old woman with chronic rheumatoid 
      arthritis. Her AKO loneliness scale value was 4 on the first session and 1 on the 
      20th session. She said, "I do not think about anything while playing with the 
      pet-type robot. It heals my mind." Case 2: The patient was a 74-year-old woman 
      with cervical osteochondrosis. Her AKO loneliness scale value was 5 on the first 
      session and 2 on the 20th session. She said, "The first time, I didn't like 
      playing with the robot because I was depressed. After I had played with the robot 
      several times, I felt good." Case 3: The patient was an 84-year-old man with 
      cerebral apoplexy sequelae. His AKO loneliness scale value was 6 on the first 
      session and 1 on the 20th session. He sang with the robot occasionally. The 
      amount of conversation between him and his children greatly increased. Unlike 
      animals, a pet robot does not carry the risk of bacterial infection. The present 
      results suggest the possibility of using robots as a substitute for 
      animal-assisted therapy and other psychosocial therapy in aseptic rooms, ICUs, 
      children's wards, and special care wards for patients with dementia.
FAU - Kanamori, Masao
AU  - Kanamori M
AD  - School of Medicine, Hamamatsu University.
FAU - Suzuki, Mizue
AU  - Suzuki M
FAU - Tanaka, Misao
AU  - Tanaka M
LA  - jpn
PT  - Case Reports
PT  - English Abstract
PT  - Journal Article
PL  - Japan
TA  - Nihon Ronen Igakkai Zasshi
JT  - Nihon Ronen Igakkai zasshi. Japanese journal of geriatrics
JID - 7507332
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Arthritis, Rheumatoid/psychology
MH  - Cerebral Infarction/psychology
MH  - Female
MH  - Humans
MH  - Loneliness/*psychology
MH  - Osteochondritis/psychology
MH  - *Patient Satisfaction
MH  - *Quality of Life
MH  - *Robotics
EDAT- 2002/04/27 10:00
MHDA- 2002/05/08 10:01
CRDT- 2002/04/27 10:00
PHST- 2002/04/27 10:00 [pubmed]
PHST- 2002/05/08 10:01 [medline]
PHST- 2002/04/27 10:00 [entrez]
AID - 10.3143/geriatrics.39.214 [doi]
PST - ppublish
SO  - Nihon Ronen Igakkai Zasshi. 2002 Mar;39(2):214-8. doi: 10.3143/geriatrics.39.214.

PMID- 11886466
OWN - NLM
STAT- MEDLINE
DCOM- 20030717
LR  - 20191105
IS  - 1351-8216 (Print)
IS  - 1351-8216 (Linking)
VI  - 8
IP  - 1
DP  - 2002 Jan
TI  - Thrombotic stroke associated with the use of porcine factor VIII in a patient 
      with acquired haemophilia.
PG  - 56-8
AB  - Porcine factor VIII (pFVIII), which is used to control bleeding in patients with 
      congenital or acquired haemophilia who have high-titre neutralizing antibodies to 
      human FVIII, is not known to increase the risk of arterial or venous thrombosis. 
      We have recently encountered a patient with acquired haemophilia who developed a 
      thrombotic left middle cerebral artery distribution stroke while being treated 
      with pFVIII. To our knowledge, this is the first such reported thrombotic event. 
      We speculate that platelet activation induced by pFVIII may have contributed to 
      thrombosis and suggest that pFVIII be used with caution in elderly patients with 
      pre-existing cardiovascular risk factors.
FAU - Ashrani, A A
AU  - Ashrani AA
AD  - Division of Hematology, Oncology and Transplantation, Department of Medicine, 
      University of Minnesota Medical School, Minneapolis 55455, USA.
FAU - Reding, M T
AU  - Reding MT
FAU - Greeno, E W
AU  - Greeno EW
FAU - Shet, A
AU  - Shet A
FAU - Key, N S
AU  - Key NS
LA  - eng
PT  - Case Reports
PT  - Journal Article
PL  - England
TA  - Haemophilia
JT  - Haemophilia : the official journal of the World Federation of Hemophilia
JID - 9442916
RN  - 0 (Autoantibodies)
RN  - 9001-27-8 (Factor VIII)
SB  - IM
MH  - Aged
MH  - Animals
MH  - Arthritis, Rheumatoid
MH  - Autoantibodies/blood
MH  - Autoimmune Diseases/complications/drug therapy/immunology
MH  - Factor VIII/administration & dosage/*adverse effects/immunology
MH  - Fatal Outcome
MH  - Hemophilia A/*complications/drug therapy/immunology/pathology
MH  - Humans
MH  - Intracranial Thrombosis/*chemically induced/etiology
MH  - Male
MH  - Swine
EDAT- 2002/03/12 10:00
MHDA- 2003/07/18 05:00
CRDT- 2002/03/12 10:00
PHST- 2002/03/12 10:00 [pubmed]
PHST- 2003/07/18 05:00 [medline]
PHST- 2002/03/12 10:00 [entrez]
AID - 573 [pii]
AID - 10.1046/j.1365-2516.2002.00573.x [doi]
PST - ppublish
SO  - Haemophilia. 2002 Jan;8(1):56-8. doi: 10.1046/j.1365-2516.2002.00573.x.

PMID- 11809000
OWN - NLM
STAT- MEDLINE
DCOM- 20020626
LR  - 20200205
IS  - 1297-319X (Print)
IS  - 1297-319X (Linking)
VI  - 68
IP  - 6
DP  - 2001 Dec
TI  - Atherosclerosis and connective tissue diseases.
PG  - 564-75
AB  - Large increases in mortality related to premature atherosclerosis with coronary 
      artery disease and stroke have been reported in patients with systemic lupus 
      erythematosus (SLE), antiphospholipid syndrome (APLS), or rheumatoid arthritis 
      (RA). Studies found relative risks of 5 for myocardial infarction, 6 to 10 for 
      stroke in SLE patients, and 3.6 for cardiovascular deaths in RA patients. The 
      main risk factors for atherosclerosis included not only the classic factors 
      identified in epidemiological studies such as the Framingham study (advanced age, 
      high cholesterol levels, hypertension, diabetes mellitus, and obesity), but also 
      prolonged glucocorticoid therapy, long duration of SLE, postmenopausal status, 
      and heart failure. SLE per se is an independent risk factor. The current 
      pathogenic hypothesis for atherosclerosis involves an inflammatory response 
      (erythrocyte sedimentation rate, C-reactive protein, and fibrin), autoantibodies, 
      immune complexes (containing antibodies to phospholipids, to oxidized LDLs, and 
      to endothelial cells), cytokine-producing activated T cells, and bacterial or 
      viral infections responsible for an immune response against heat shock proteins 
      (endogenous HSP60 and its equivalent, bacterial HSP65). Early risk factor 
      intervention and effective control of inflammation should be incorporated into 
      the management of connective tissue disease with the goal of protecting patients 
      against atherosclerosis.
FAU - Meyer, O
AU  - Meyer O
AD  - Rheumatology Department, Hôpital Bichat, Paris, France. 
      olivier.meyer@bch.ap-hop-paris.fr
LA  - eng
PT  - Journal Article
PT  - Review
PL  - France
TA  - Joint Bone Spine
JT  - Joint bone spine
JID - 100938016
SB  - IM
CIN - Joint Bone Spine. 2003 Aug;70(4):311-2. doi: 10.1016/s1297-319x(03)00053-8. PMID: 
      12951320
MH  - Animals
MH  - Antiphospholipid Syndrome/*complications
MH  - Arteriosclerosis/*etiology/mortality
MH  - Arthritis, Rheumatoid/*complications
MH  - Female
MH  - Humans
MH  - Lupus Erythematosus, Systemic/*complications/mortality
MH  - Male
MH  - Risk Factors
RF  - 96
EDAT- 2002/01/26 10:00
MHDA- 2002/06/27 10:01
CRDT- 2002/01/26 10:00
PHST- 2002/01/26 10:00 [pubmed]
PHST- 2002/06/27 10:01 [medline]
PHST- 2002/01/26 10:00 [entrez]
AID - 10.1016/s1297-319x(01)00330-x [doi]
PST - ppublish
SO  - Joint Bone Spine. 2001 Dec;68(6):564-75. doi: 10.1016/s1297-319x(01)00330-x.

PMID- 11771864
OWN - NLM
STAT- MEDLINE
DCOM- 20020611
LR  - 20190906
IS  - 0036-5599 (Print)
IS  - 0036-5599 (Linking)
VI  - 35
IP  - 5
DP  - 2001 Oct
TI  - Association of non-urological diseases with lower urinary tract symptoms.
PG  - 377-81
AB  - OBJECTIVE: Clinical observations indicate that many non-urological diseases seem 
      to be associated with lower urinary tract symptoms (LUTS). This has also been 
      shown in studies usually concerning single diseases. This study investigated the 
      impact of non-urological diseases on LUTS in the general population. MATERIAL AND 
      METHODS: A questionnaire on LUTS and medical history was mailed to all 50-, 60- 
      and 70 year-old men in Tampere and in 11 municipalities in the same county, in 
      total 3143 subjects. Day-time frequency, nocturia, urge, urge incontinence, 
      hesitancy and incomplete emptying were used to form an index for LUTS. The men 
      were asked to report any disease that they had. The number of the following 
      diseases reported by the participants was large enough for statistical analysis: 
      lower back pain, hypertension, arthritis, heart disease, pulmonary disease, 
      diabetes, constipation. stroke, transient ischaemic attack, cancer (other than 
      prostate or bladder), neurological disease, inguinal hernia, rheumatoid arthritis 
      and faecal incontinence. The association between LUTS and non-urological diseases 
      was estimated by logistic regression as a prevalence odds ratio (OR) with 95% 
      confidence intervals (CI). RESULTS: In the multivariate analysis a significant 
      association was found between LUTS and the following diseases: faecal 
      incontinence (OR 4.5, CI 2 .3-9.1), neurological disease (OR 2.4, CI 1.3-4.4), 
      constipation (OR 2.3, CI 1.5-3.3) and arthritis (OR 1.5, CI 1.2-2.0). 
      CONCLUSIONS: According to this population-based study LUTS is an important part 
      of the symptomatology of faecal incontinence, neurological disease, constipation 
      and arthritis. Thus, the patients with these diseases and presenting with LUTS 
      require careful investigation, at least in the cases in which the primary therapy 
      of LUTS has failed.
FAU - Koskimäki, J
AU  - Koskimäki J
AD  - Department of Urology, Tampere University Hospital, Finland. 
      jkoskimaki@koti.tpo.fi
FAU - Hakama, M
AU  - Hakama M
FAU - Huhtala, H
AU  - Huhtala H
FAU - Tammela, T L
AU  - Tammela TL
LA  - eng
PT  - Journal Article
PL  - England
TA  - Scand J Urol Nephrol
JT  - Scandinavian journal of urology and nephrology
JID - 0114501
SB  - IM
MH  - Aged
MH  - Comorbidity
MH  - Finland/epidemiology
MH  - Humans
MH  - Logistic Models
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Prevalence
MH  - Prostatic Hyperplasia/complications
MH  - Quality of Life
MH  - Risk Factors
MH  - Surveys and Questionnaires
MH  - Urban Population/statistics & numerical data
MH  - Urination Disorders/*epidemiology/*etiology
EDAT- 2002/01/05 10:00
MHDA- 2002/06/12 10:01
CRDT- 2002/01/05 10:00
PHST- 2002/01/05 10:00 [pubmed]
PHST- 2002/06/12 10:01 [medline]
PHST- 2002/01/05 10:00 [entrez]
AID - 10.1080/003655901753224431 [doi]
PST - ppublish
SO  - Scand J Urol Nephrol. 2001 Oct;35(5):377-81. doi: 10.1080/003655901753224431.

PMID- 11762933
OWN - NLM
STAT- MEDLINE
DCOM- 20020108
LR  - 20220409
IS  - 0004-3591 (Print)
IS  - 0004-3591 (Linking)
VI  - 44
IP  - 12
DP  - 2001 Dec
TI  - High incidence of cardiovascular events in a rheumatoid arthritis cohort not 
      explained by traditional cardiac risk factors.
PG  - 2737-45
AB  - OBJECTIVE: To compare the incidence of cardiovascular (CV) events in persons with 
      rheumatoid arthritis (RA) with that in people from the general population, 
      adjusting for traditional CV risk factors. METHODS: Two hundred thirty-six 
      consecutive patients with RA were assessed for the 1-year occurrence of 1) 
      CV-related hospitalizations, including myocardial infarction, stroke or other 
      arterial occlusive events, or arterial revascularization procedures, or 2) CV 
      deaths. Both outcomes were ascertained by medical records or death certificates. 
      For comparison, we used CV events that occurred during an 8-year period among 
      participants in an epidemiologic study of atherosclerosis and CV disease who were 
      ages 25-65 years at study entry. We calculated the age- and sex-stratified 
      incidence rate ratio (IRR) of CV events between the 2 cohorts and used Poisson 
      regression to adjust for age, sex, smoking status, diabetes mellitus, 
      hypercholesterolemia, systolic blood pressure, and body mass index. RESULTS: Of 
      the 236 RA patients, 234 were observed for 252 patient-years, during which 15 CV 
      events occurred. Of these, 7 incident events occurred during the 204 
      patient-years contributed by patients ages 25-65 years, for an incidence of 3.43 
      per 100 patient-years. In the comparison cohort, 4,635 community-dwelling persons 
      were followed up for 33,881 person-years, during which 200 new events occurred, 
      for an incidence of 0.59 per 100 person-years. The age- and sex-adjusted IRR of 
      incident CV events associated with RA was 3.96 (95% confidence interval [95% CI] 
      1.86-8.43). After adjusting for CV risk factors using Poisson regression, the IRR 
      decreased slightly, to 3.17 (95% CI 1.33-6.36). CONCLUSION: The increased 
      incidence of CV events in RA patients is independent of traditional CV risk 
      factors. This suggests that additional mechanisms are responsible for CV disease 
      in RA. Physicians who provide care to individuals with RA should be aware of 
      their increased risk of CV events and implement appropriate diagnostic and 
      therapeutic measures.
FAU - del Rincón, I D
AU  - del Rincón ID
AD  - University of Texas Health Science Center at San Antonio, 78229-3900, USA.
FAU - Williams, K
AU  - Williams K
FAU - Stern, M P
AU  - Stern MP
FAU - Freeman, G L
AU  - Freeman GL
FAU - Escalante, A
AU  - Escalante A
LA  - eng
GR  - K23-HL004481/HL/NHLBI NIH HHS/United States
GR  - K24-AR47530/AR/NIAMS NIH HHS/United States
GR  - M01-RR1346/RR/NCRR NIH HHS/United States
GR  - R01-HD37151/HD/NICHD NIH HHS/United States
GR  - R37-HL36820/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Cardiovascular Diseases/*epidemiology
MH  - Cohort Studies
MH  - Coronary Artery Disease/epidemiology
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Myocardial Infarction/epidemiology
MH  - Risk Factors
MH  - Stroke/epidemiology
EDAT- 2002/01/05 10:00
MHDA- 2002/01/10 10:01
CRDT- 2002/01/05 10:00
PHST- 2002/01/05 10:00 [pubmed]
PHST- 2002/01/10 10:01 [medline]
PHST- 2002/01/05 10:00 [entrez]
AID - 10.1002/1529-0131(200112)44:12<2737::AID-ART460>3.0.CO;2-%23 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2001 Dec;44(12):2737-45. doi: 
      10.1002/1529-0131(200112)44:12<2737::AID-ART460>3.0.CO;2-%23.

PMID- 11696466
OWN - NLM
STAT- MEDLINE
DCOM- 20011204
LR  - 20190623
IS  - 1524-4539 (Electronic)
IS  - 0009-7322 (Linking)
VI  - 104
IP  - 19
DP  - 2001 Nov 6
TI  - Cardiovascular thrombotic events in controlled, clinical trials of rofecoxib.
PG  - 2280-8
AB  - BACKGROUND: In comparing aspirin, nonselective nonsteroidal antiinflammatory 
      agents (NSAIDs), and cyclooxygenase (COX)-2 inhibitors, variation in platelet 
      inhibitory effects exists that may be associated with differential risks of 
      cardiovascular (CV) thrombotic events. Among the randomized, controlled trials 
      with the COX-2 inhibitor rofecoxib, one study demonstrated a significant 
      difference between rofecoxib and its NSAID comparator (naproxen) in the risk of 
      CV thrombotic events. A combined analysis of individual patient data was 
      undertaken to determine whether there was an excess of CV thrombotic events in 
      patients treated with rofecoxib compared with those treated with placebo or 
      nonselective NSAIDs. METHODS AND RESULTS: CV thrombotic events were assessed 
      across 23 phase IIb to V rofecoxib studies. Comparisons were made between 
      patients taking rofecoxib and those taking either placebo, naproxen (an NSAID 
      with near-complete inhibition of platelet function throughout its dosing 
      interval), or another nonselective NSAIDs used in the development program 
      (diclofenac, ibuprofen, and nabumetone). The major outcome measure was the 
      combined end point used by the Antiplatelet Trialists' Collaboration, which 
      includes CV, hemorrhagic, and unknown deaths; nonfatal myocardial infarctions; 
      and nonfatal strokes. More than 28 000 patients, representing >14 000 
      patient-years at risk, were analyzed. The relative risk for an end point was 0.84 
      (95% CI: 0.51, 1.38) when comparing rofecoxib with placebo; 0.79 (95% CI: 0.40, 
      1.55) when comparing rofecoxib with non-naproxen NSAIDs; and 1.69 (95% CI: 1.07, 
      2.69) when comparing rofecoxib with naproxen. CONCLUSIONS: This analysis provides 
      no evidence for an excess of CV events for rofecoxib relative to either placebo 
      or the non-naproxen NSAIDs that were studied. Differences observed between 
      rofecoxib and naproxen are likely the result of the antiplatelet effects of the 
      latter agent.
FAU - Konstam, M A
AU  - Konstam MA
AD  - Division of Cardiology, New England Medical Center, Boston, Massachusetts, USA. 
      MKonstam@Lifespan.org
FAU - Weir, M R
AU  - Weir MR
FAU - Reicin, A
AU  - Reicin A
FAU - Shapiro, D
AU  - Shapiro D
FAU - Sperling, R S
AU  - Sperling RS
FAU - Barr, E
AU  - Barr E
FAU - Gertz, B J
AU  - Gertz BJ
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Meta-Analysis
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Isoenzymes)
RN  - 0 (Lactones)
RN  - 0 (Membrane Proteins)
RN  - 0 (Sulfones)
RN  - 0QTW8Z7MCR (rofecoxib)
RN  - 57Y76R9ATQ (Naproxen)
RN  - EC 1.14.99.1 (Cyclooxygenase 1)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 1.14.99.1 (PTGS1 protein, human)
RN  - EC 1.14.99.1 (PTGS2 protein, human)
RN  - EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
SB  - IM
CIN - Circulation. 2002 Jul 30;106(5):e18. doi: 10.1161/01.cir.0000023454.92028.12. 
      PMID: 12147551
MH  - Aged
MH  - Alzheimer Disease/drug therapy/prevention & control
MH  - Anti-Inflammatory Agents, Non-Steroidal/adverse effects/therapeutic use
MH  - Arthritis, Rheumatoid/drug therapy
MH  - Cardiovascular Diseases/*epidemiology
MH  - Chronic Disease
MH  - Clinical Trials, Phase II as Topic/statistics & numerical data
MH  - Clinical Trials, Phase III as Topic/statistics & numerical data
MH  - Clinical Trials, Phase IV as Topic/statistics & numerical data
MH  - Comorbidity
MH  - Cyclooxygenase 1
MH  - Cyclooxygenase 2
MH  - Female
MH  - Humans
MH  - Isoenzymes/antagonists & inhibitors
MH  - Lactones/*adverse effects/therapeutic use
MH  - Low Back Pain/drug therapy
MH  - Male
MH  - Membrane Proteins
MH  - Middle Aged
MH  - Naproxen/adverse effects/therapeutic use
MH  - Osteoarthritis/drug therapy
MH  - Proportional Hazards Models
MH  - Prostaglandin-Endoperoxide Synthases
MH  - Randomized Controlled Trials as Topic/*statistics & numerical data
MH  - Risk
MH  - Sulfones
MH  - Thrombosis/*epidemiology
EDAT- 2001/11/07 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/11/07 10:00
PHST- 2001/11/07 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/11/07 10:00 [entrez]
AID - 10.1161/hc4401.100078 [doi]
PST - ppublish
SO  - Circulation. 2001 Nov 6;104(19):2280-8. doi: 10.1161/hc4401.100078.

PMID- 11521117
OWN - NLM
STAT- MEDLINE
DCOM- 20010913
LR  - 20190616
IS  - 0002-9378 (Print)
IS  - 0002-9378 (Linking)
VI  - 185
IP  - 2 Suppl
DP  - 2001 Aug
TI  - Current perspectives on oral contraceptive use.
PG  - S4-12
AB  - Oral contraceptives are one of the most highly effective forms of contraception 
      and provide many short- and long-term noncontraceptive health benefits. They 
      control menstrual cycle irregularities, such as breakthrough bleeding and 
      amenorrhea, and are effective in treating dysfunctional uterine bleeding. In 
      addition, for decades after oral contraceptive use is discontinued they are 
      associated with substantial decreases in the risk of ovarian cancer (up to 80%) 
      and of endometrial cancer (40%-50%), and nearly eliminate benign functional 
      ovarian cysts. Long-term oral contraceptive use confers protection against benign 
      breast disease and colorectal cancer, may help prevent rheumatoid arthritis, 
      decreases ectopic pregnancy and hospitalizations for pelvic inflammatory disease, 
      and helps preserve bone mineral density to reduce risk of fractures. Large bodies 
      of evidence from extensive research have clarified the perceived association of 
      oral contraceptive use with cardiovascular disease and with breast cancer. 
      Findings indicate that there is no increased risk of myocardial infarction or 
      stroke associated with oral contraceptive use in healthy, nonsmoking, 
      normotensive women. Although there is a 3- to 4-fold increased risk of venous 
      thromboembolism with current oral contraceptive use, the absolute risk is very 
      small and is half that associated with pregnancy. Women of all reproductive ages, 
      including perimenopausal women, can realize many health benefits through oral 
      contraceptive use, including improved health status later in life.
FAU - Burkman, R T
AU  - Burkman RT
AD  - Department of Obstetrics and Gynecology, Tufts University School of Medicine, 
      Boston, MA USA.
FAU - Collins, J A
AU  - Collins JA
FAU - Shulman, L P
AU  - Shulman LP
FAU - Williams, J K
AU  - Williams JK
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Am J Obstet Gynecol
JT  - American journal of obstetrics and gynecology
JID - 0370476
RN  - 0 (Contraceptives, Oral)
SB  - IM
MH  - Contraceptives, Oral/*therapeutic use
MH  - Female
MH  - Humans
MH  - *Menopause
RF  - 72
EDAT- 2001/08/25 10:00
MHDA- 2001/09/14 10:01
CRDT- 2001/08/25 10:00
PHST- 2001/08/25 10:00 [pubmed]
PHST- 2001/09/14 10:01 [medline]
PHST- 2001/08/25 10:00 [entrez]
AID - a117416 [pii]
AID - 10.1067/mob.2001.117416 [doi]
PST - ppublish
SO  - Am J Obstet Gynecol. 2001 Aug;185(2 Suppl):S4-12. doi: 10.1067/mob.2001.117416.

PMID- 11451713
OWN - NLM
STAT- MEDLINE
DCOM- 20010802
LR  - 20220330
IS  - 0002-9165 (Print)
IS  - 0002-9165 (Linking)
VI  - 74
IP  - 1
DP  - 2001 Jul
TI  - Treatment of protein-energy malnutrition in chronic nonmalignant disorders.
PG  - 6-24
AB  - Protein-energy malnutrition (PEM) is common in connection with chronic disease 
      and is associated with increased morbidity and mortality. Because the risk of PEM 
      is related to the degree of illness, the causal connections between malnutrition 
      and a poorer prognosis are complex. It cannot automatically be inferred that 
      nutritional support will improve the clinical course of patients with wasting 
      disorders. We reviewed studies of the treatment of PEM in cases of chronic 
      obstructive pulmonary disease, chronic heart failure, stroke, dementia, 
      rehabilitation after hip fracture, chronic renal failure, rheumatoid arthritis, 
      and multiple disorders in the elderly. Several methodologic problems are 
      associated with nutrition treatment studies in chronically ill patients. These 
      problems include no generally accepted definition of PEM, uncertain patient 
      compliance with supplementation, and a wide range of outcome variables. 
      Avail-able treatment studies indicate that dietary supplements, either alone or 
      in combination with hormonal treatment, may have positive effects when given to 
      patients with manifest PEM or to patients at risk of developing PEM. In chronic 
      obstructive pulmonary disease, nutritional treatment may improve respiratory 
      function. Nutritional therapy of elderly women after hip fractures may speed up 
      the rehabilitation process. When administered to elderly patients with multiple 
      disorders, diet therapy may improve functional capacity. The data regarding 
      nutritional treatment of the conditions mentioned above is still inconclusive. 
      There is still a great need for randomized controlled long-term studies of the 
      effects of defined nutritional intervention programs in chronically ill and frail 
      elderly with a focus on determining clinically relevant outcomes.
FAU - Akner, G
AU  - Akner G
AD  - Departments of Geriatric Medicine at Karolinska Hospital and Huddinge University 
      Hospital, Stockholm, Sweden.
FAU - Cederholm, T
AU  - Cederholm T
LA  - eng
PT  - Journal Article
PT  - Meta-Analysis
PT  - Review
PL  - United States
TA  - Am J Clin Nutr
JT  - The American journal of clinical nutrition
JID - 0376027
SB  - IM
CIN - Age Ageing. 2003 May;32(3):241-3. doi: 10.1093/ageing/32.3.241. PMID: 12720605
MH  - Aged
MH  - Cachexia
MH  - Chronic Disease/*therapy
MH  - Dietary Supplements
MH  - Female
MH  - Humans
MH  - MEDLINE
MH  - Male
MH  - Mortality
MH  - Nutritional Requirements
MH  - Nutritional Support
MH  - Patient Compliance
MH  - Prognosis
MH  - Protein-Energy Malnutrition/etiology/prevention & control/*therapy
MH  - Randomized Controlled Trials as Topic
MH  - Severity of Illness Index
MH  - Wasting Syndrome/etiology/prevention & control/*therapy
RF  - 247
EDAT- 2001/07/14 10:00
MHDA- 2001/08/03 10:01
CRDT- 2001/07/14 10:00
PHST- 2001/07/14 10:00 [pubmed]
PHST- 2001/08/03 10:01 [medline]
PHST- 2001/07/14 10:00 [entrez]
AID - 10.1093/ajcn/74.1.6 [doi]
PST - ppublish
SO  - Am J Clin Nutr. 2001 Jul;74(1):6-24. doi: 10.1093/ajcn/74.1.6.

PMID- 11441986
OWN - NLM
STAT- MEDLINE
DCOM- 20011207
LR  - 20191105
IS  - 1076-0296 (Print)
IS  - 1076-0296 (Linking)
VI  - 7
IP  - 3
DP  - 2001 Jul
TI  - Factor V Leiden and prothrombin G20210A in relation to arterial and/or vein 
      rethrombosis: two cases.
PG  - 234-7
AB  - The factor V Leiden (FV Leiden) and prothrombin G20210A mutations, are the most 
      common established genetic risk factors for deep vein thrombosis (DVT). However, 
      the relationship between these mutations and arterial thrombotic syndromes 
      (coronary heart disease, myocardial infarction, stroke) has not been established. 
      Some studies have suggested a relationship between them, but other authors have 
      considered it unlikely that these anomalies are a major risk factor for arterial 
      thrombosis. From the clinical point of view, a question arises concerning the 
      risk of repeated thrombosis in patients carrying one of these two mutations. The 
      question is whether the recurrence is attributable to the mutations or to the 
      presence of additional circumstantial risk factors. As the risk of repeated 
      thrombosis varies considerably from one patient to another, decisions about 
      long-term treatment require weighing the persistence of risk factors for vascular 
      disease (venous and arterial), especially in selected cases such as young 
      patients or patients with thrombosis of unusual localization.
FAU - Mira, Y
AU  - Mira Y
AD  - Department of Clinical Pathology, La Fe University Hospital, Valencia, Spain.
FAU - Todolí, T
AU  - Todolí T
FAU - Alonso, R
AU  - Alonso R
FAU - Micó, T L
AU  - Micó TL
FAU - Vayá, A
AU  - Vayá A
FAU - Ferrando, F
AU  - Ferrando F
FAU - Estellés, A
AU  - Estellés A
FAU - Villa, P
AU  - Villa P
FAU - Aznar, J
AU  - Aznar J
LA  - eng
PT  - Case Reports
PT  - Journal Article
PL  - United States
TA  - Clin Appl Thromb Hemost
JT  - Clinical and applied thrombosis/hemostasis : official journal of the 
      International Academy of Clinical and Applied Thrombosis/Hemostasis
JID - 9508125
RN  - 0 (3' Untranslated Regions)
RN  - 0 (Anticoagulants)
RN  - 0 (factor V Leiden)
RN  - 9001-24-5 (Factor V)
RN  - 9001-26-7 (Prothrombin)
SB  - IM
MH  - 3' Untranslated Regions
MH  - Adult
MH  - Angina Pectoris/*etiology
MH  - Anticoagulants/therapeutic use
MH  - Arthritis, Rheumatoid/complications
MH  - Autoimmune Diseases/complications
MH  - Cardiomyopathy, Hypertrophic/complications
MH  - Colitis, Ischemic/etiology
MH  - Factor V/*genetics
MH  - Female
MH  - Fingers/blood supply
MH  - Genetic Predisposition to Disease
MH  - Humans
MH  - Intracranial Embolism/*etiology
MH  - Ischemia/etiology
MH  - Male
MH  - Middle Aged
MH  - Obesity/complications
MH  - Postoperative Complications/etiology
MH  - Prothrombin/*genetics
MH  - Pulmonary Embolism/*etiology
MH  - Recurrence
MH  - Smoking/adverse effects
MH  - Thrombophilia/complications/drug therapy/*genetics
MH  - Thrombophlebitis/*etiology
MH  - Varicose Veins/surgery
EDAT- 2001/07/10 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/07/10 10:00
PHST- 2001/07/10 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/07/10 10:00 [entrez]
AID - 10.1177/107602960100700310 [doi]
PST - ppublish
SO  - Clin Appl Thromb Hemost. 2001 Jul;7(3):234-7. doi: 10.1177/107602960100700310.

PMID- 11426020
OWN - NLM
STAT- MEDLINE
DCOM- 20010726
LR  - 20220321
IS  - 1462-0324 (Print)
IS  - 1462-0324 (Linking)
VI  - 40
IP  - 6
DP  - 2001 Jun
TI  - Cardiovascular risk factors, including thrombotic variables, in a population with 
      rheumatoid arthritis.
PG  - 640-4
AB  - OBJECTIVE: To compare prevalent cardiovascular disease, conventional 
      cardiovascular risk factors and thrombotic variables in a cohort with 
      well-controlled rheumatoid arthritis (RA) and in population controls. METHODS: 
      Seventy-six RA patients and 641 controls, randomly sampled from the local 
      population in the North Glasgow MONICA study. Conventional cardiovascular risk 
      factors (blood pressure, smoking, cholesterol) and thrombotic variables 
      [fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator antigen 
      (t-PA), fibrin D-dimer, plasminogen activator inhibitor (PAI-1), plasma 
      viscosity] were measured by standard procedures. RESULTS: RA patients had a 
      significantly higher prevalence of angina pectoris (P=0.03). Stroke also tended 
      to be more common in the RA group, but the difference did not reach statistical 
      significance (P=0.08). Diastolic blood pressure was significantly higher and 
      serum cholesterol significantly lower in the RA group than in controls. Current 
      smoking habits and exercise history were similar in the two groups, although RA 
      patients were more likely to have previously smoked. Significant elevations in 
      several thrombotic predictors of cardiovascular disease (fibrinogen, vWF, t-PA 
      antigen and fibrin D-dimer) were found in the RA group. CONCLUSIONS: In this RA 
      patient population, diastolic blood pressure was higher than in controls and 
      thrombotic variables were elevated compared with controls. These features are 
      identified as potential additional cardiovascular risk factors in the RA patients 
      studied. Prospective studies of risk modification may permit the identification 
      of factors which could lead to a reduction in the known increased cardiovascular 
      risk in RA.
FAU - McEntegart, A
AU  - McEntegart A
AD  - Centre for Rheumatic Diseases, Glasgow Royal Infirmary, 84 Castle Street, Glasgow 
      G4 0SF, UK.
FAU - Capell, H A
AU  - Capell HA
FAU - Creran, D
AU  - Creran D
FAU - Rumley, A
AU  - Rumley A
FAU - Woodward, M
AU  - Woodward M
FAU - Lowe, G D
AU  - Lowe GD
LA  - eng
PT  - Journal Article
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
RN  - 0 (von Willebrand Factor)
RN  - 9001-32-5 (Fibrinogen)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/blood/*complications
MH  - Cardiovascular Diseases/*epidemiology/etiology
MH  - Female
MH  - Fibrinogen/metabolism
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Prevalence
MH  - Risk Factors
MH  - von Willebrand Factor/metabolism
EDAT- 2001/06/27 10:00
MHDA- 2001/07/28 10:01
CRDT- 2001/06/27 10:00
PHST- 2001/06/27 10:00 [pubmed]
PHST- 2001/07/28 10:01 [medline]
PHST- 2001/06/27 10:00 [entrez]
AID - 10.1093/rheumatology/40.6.640 [doi]
PST - ppublish
SO  - Rheumatology (Oxford). 2001 Jun;40(6):640-4. doi: 10.1093/rheumatology/40.6.640.

PMID- 11219247
OWN - NLM
STAT- MEDLINE
DCOM- 20010426
LR  - 20190831
IS  - 0009-9201 (Print)
IS  - 0009-9201 (Linking)
VI  - 44
IP  - 1
DP  - 2001 Mar
TI  - Oral contraceptives: current status.
PG  - 62-72
AB  - During the past four decades, oral contraceptives have remained a safe and 
      effective method of birth control. Reductions in the estrogen and progestin 
      dosages have significantly decreased the incidence of cardiovascular 
      complications. The association between oral contraceptives and breast cancer 
      appears to be primarily because of detection bias or possibly a promotional 
      effect. Despite the changes in formulation, the problems related to side effects 
      have not been totally solved. Because compliance and successful use is strongly 
      affected by side effects, improvement in this area is probably the biggest 
      challenge faced by developers of oral contraceptives. It is also clear that there 
      are a growing number of significant noncontraceptive benefits that accrue in oral 
      contraceptive users. Unfortunately, many women do not know about these benefits. 
      Thus, one of the issues that providers need to continue to address is how to 
      provide better information about oral contraceptives and contraception in general 
      to patients.
FAU - Burkman, R T
AU  - Burkman RT
AD  - Baystate Medical Center, Springfield, Massachusetts, USA.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Clin Obstet Gynecol
JT  - Clinical obstetrics and gynecology
JID - 0070014
RN  - 0 (Contraceptives, Oral)
SB  - IM
MH  - Acne Vulgaris/prevention & control
MH  - Adult
MH  - Arthritis, Rheumatoid/prevention & control
MH  - Bone Density/drug effects
MH  - Breast Neoplasms/chemically induced/epidemiology
MH  - Colorectal Neoplasms/prevention & control
MH  - Contraception/adverse effects/*methods/psychology/*trends
MH  - *Contraceptives, Oral/adverse effects/supply & distribution
MH  - Endometrial Neoplasms/prevention & control
MH  - Female
MH  - Humans
MH  - Leiomyoma/prevention & control
MH  - Menstruation Disturbances/prevention & control
MH  - Myocardial Infarction/chemically induced/epidemiology
MH  - Ovarian Cysts/prevention & control
MH  - Ovarian Neoplasms/prevention & control
MH  - Patient Compliance/psychology/statistics & numerical data
MH  - Pelvic Inflammatory Disease/prevention & control
MH  - Pregnancy
MH  - Pregnancy, Ectopic/prevention & control
MH  - Risk Factors
MH  - Stroke/chemically induced/epidemiology
MH  - Thromboembolism/chemically induced/epidemiology
RF  - 29
EDAT- 2001/02/24 12:00
MHDA- 2001/05/01 10:01
CRDT- 2001/02/24 12:00
PHST- 2001/02/24 12:00 [pubmed]
PHST- 2001/05/01 10:01 [medline]
PHST- 2001/02/24 12:00 [entrez]
AID - 10.1097/00003081-200103000-00010 [doi]
PST - ppublish
SO  - Clin Obstet Gynecol. 2001 Mar;44(1):62-72. doi: 10.1097/00003081-200103000-00010.

PMID- 10687887
OWN - NLM
STAT- MEDLINE
DCOM- 20000320
LR  - 20181130
IS  - 0306-9877 (Print)
IS  - 0306-9877 (Linking)
VI  - 53
IP  - 6
DP  - 1999 Dec
TI  - Vegan proteins may reduce risk of cancer, obesity, and cardiovascular disease by 
      promoting increased glucagon activity.
PG  - 459-85
AB  - Amino acids modulate the secretion of both insulin and glucagon; the composition 
      of dietary protein therefore has the potential to influence the balance of 
      glucagon and insulin activity. Soy protein, as well as many other vegan proteins, 
      are higher in non-essential amino acids than most animal-derived food proteins, 
      and as a result should preferentially favor glucagon production. Acting on 
      hepatocytes, glucagon promotes (and insulin inhibits) cAMP-dependent mechanisms 
      that down-regulate lipogenic enzymes and cholesterol synthesis, while 
      up-regulating hepatic LDL receptors and production of the IGF-I antagonist 
      IGFBP-1. The insulin-sensitizing properties of many vegan diets--high in fiber, 
      low in saturated fat--should amplify these effects by down-regulating insulin 
      secretion. Additionally, the relatively low essential amino acid content of some 
      vegan diets may decrease hepatic IGF-I synthesis. Thus, diets featuring vegan 
      proteins can be expected to lower elevated serum lipid levels, promote weight 
      loss, and decrease circulating IGF-I activity. The latter effect should impede 
      cancer induction (as is seen in animal studies with soy protein), lessen 
      neutrophil-mediated inflammatory damage, and slow growth and maturation in 
      children. In fact, vegans tend to have low serum lipids, lean physiques, shorter 
      stature, later puberty, and decreased risk for certain prominent 'Western' 
      cancers; a vegan diet has documented clinical efficacy in rheumatoid arthritis. 
      Low-fat vegan diets may be especially protective in regard to cancers linked to 
      insulin resistance--namely, breast and colon cancer--as well as prostate cancer; 
      conversely, the high IGF-I activity associated with heavy ingestion of animal 
      products may be largely responsible for the epidemic of 'Western' cancers in 
      wealthy societies. Increased phytochemical intake is also likely to contribute to 
      the reduction of cancer risk in vegans. Regression of coronary stenoses has been 
      documented during low-fat vegan diets coupled with exercise training; such 
      regimens also tend to markedly improve diabetic control and lower elevated blood 
      pressure. Risk of many other degenerative disorders may be decreased in vegans, 
      although reduced growth factor activity may be responsible for an increased risk 
      of hemorrhagic stroke. By altering the glucagon/insulin balance, it is 
      conceivable that supplemental intakes of key non-essential amino acids could 
      enable omnivores to enjoy some of the health advantages of a vegan diet. An 
      unnecessarily high intake of essential amino acids--either in the absolute sense 
      or relative to total dietary protein--may prove to be as grave a risk factor for 
      'Western' degenerative diseases as is excessive fat intake.
FAU - McCarty, M F
AU  - McCarty MF
AD  - Nutrition 21/AMBI, San Diego, CA, USA.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (Insulin)
RN  - 0 (Lipids)
RN  - 0 (Plant Proteins, Dietary)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - 9007-92-5 (Glucagon)
SB  - IM
MH  - Animals
MH  - Cardiovascular Diseases/*prevention & control
MH  - China
MH  - *Diet, Vegetarian
MH  - Female
MH  - Glucagon/*metabolism
MH  - Humans
MH  - Insulin/metabolism
MH  - Insulin Resistance
MH  - Insulin-Like Growth Factor I/metabolism
MH  - Lipids/blood
MH  - Liver/metabolism
MH  - Male
MH  - Neoplasms/*prevention & control
MH  - Obesity/*prevention & control
MH  - Plant Proteins, Dietary/*administration & dosage
MH  - Puberty/physiology
MH  - Risk Factors
MH  - Weight Loss
EDAT- 2000/02/25 09:00
MHDA- 2000/03/25 09:00
CRDT- 2000/02/25 09:00
PHST- 2000/02/25 09:00 [pubmed]
PHST- 2000/03/25 09:00 [medline]
PHST- 2000/02/25 09:00 [entrez]
AID - S0306-9877(99)90784-3 [pii]
AID - 10.1054/mehy.1999.0784 [doi]
PST - ppublish
SO  - Med Hypotheses. 1999 Dec;53(6):459-85. doi: 10.1054/mehy.1999.0784.

PMID- 10614714
OWN - NLM
STAT- MEDLINE
DCOM- 20000113
LR  - 20190905
IS  - 0009-9120 (Print)
IS  - 0009-9120 (Linking)
VI  - 32
IP  - 7
DP  - 1999 Oct
TI  - Moderate alcohol consumption: the gentle face of Janus.
PG  - 505-18
AB  - OBJECTIVES: The regular consumption of alcohol in moderate amounts (defined in 
      North America as up to 2 drinks per day for men and 1 drink per day for females) 
      has been recognized in the last decade as a negative risk factor for 
      atherosclerosis and its clinical sequelae: coronary heart disease (CHD), ischemic 
      stroke, and peripheral vascular disease. Mortality and morbidity attributable to 
      CHD are 40-60% lower in moderate drinkers than among abstainers. Among the 
      mechanisms accounting for these reductions, increased circulating concentrations 
      of HDL-cholesterol and inhibition of blood coagulation appear to be paramount. 
      Additional benefits are, in certain beverages, conferred by the presence of 
      constituents other than alcohol (e.g., flavonoids and hydroxystilbenes), which 
      prevent oxidative damage, free radical formation, and elements of the 
      inflammatory response. CONCLUSIONS: A number of other diseases appear to be 
      beneficially modulated by moderate alcohol consumption based on epidemiologic 
      surveys and, in some instances, experimental evidence. These include duodenal 
      ulcer, gallstones, enteric infections, rheumatoid arthritis, osteoporosis, and 
      diabetes mellitus (type II). Compared with abstainers, moderate drinkers exhibit 
      improved mental status characterized by decreased stress and depression, lower 
      absenteeism from work, and decreased incidence of dementia (including Alzheimer's 
      disease). Although limits of safe drinking have been conservatively defined, it 
      is regrettable that political considerations are hampering the clinical 
      application of this knowledge and its dissemination to the lay public.
FAU - Goldberg, D M
AU  - Goldberg DM
AD  - Department of Laboratory Medicine and Pathobiology, University of Toronto, 
      Ontario, Canada. david.goldberg@utoronto.ca
FAU - Soleas, G J
AU  - Soleas GJ
FAU - Levesque, M
AU  - Levesque M
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Clin Biochem
JT  - Clinical biochemistry
JID - 0133660
SB  - IM
MH  - *Alcohol Drinking
MH  - Cardiovascular Diseases/prevention & control
MH  - Diabetes Mellitus, Type 2/physiopathology
MH  - Female
MH  - Gastrointestinal Diseases/prevention & control
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Mental Health
MH  - Musculoskeletal Diseases/epidemiology/prevention & control
RF  - 171
EDAT- 1999/12/30 00:00
MHDA- 1999/12/30 00:01
CRDT- 1999/12/30 00:00
PHST- 1999/12/30 00:00 [pubmed]
PHST- 1999/12/30 00:01 [medline]
PHST- 1999/12/30 00:00 [entrez]
AID - S0009-9120(99)00051-X [pii]
AID - 10.1016/s0009-9120(99)00051-x [doi]
PST - ppublish
SO  - Clin Biochem. 1999 Oct;32(7):505-18. doi: 10.1016/s0009-9120(99)00051-x.

PMID- 10606363
OWN - NLM
STAT- MEDLINE
DCOM- 20000224
LR  - 20220331
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 26
IP  - 12
DP  - 1999 Dec
TI  - Extent of inflammation predicts cardiovascular disease and overall mortality in 
      seropositive rheumatoid arthritis. A retrospective cohort study from disease 
      onset.
PG  - 2562-71
AB  - OBJECTIVE: To identify predictors for cardiovascular disease (CVD) and for 
      overall survival in patients with rheumatoid arthritis (RA) followed from disease 
      onset. METHODS: A retrospective cohort of patients with seropositive RA and 
      disease onset between 1974 and 1978 (n = 211) was followed up at the end of 1995. 
      Potential predictors for CVD, as measured by "the first cardiovascular event," 
      and for overall survival were registered. The predictors were identified by 
      extended Cox regression models. RESULTS: In simple Cox regression analysis, male 
      sex, higher age at disease onset, HLA-B27, high disease activity, corticosteroid 
      treatment early in disease, and hypertension significantly increased risk of 
      cardiovascular event. Higher educational level, extensive disease modifying 
      antirheumatic drug (DMARD) treatment, and corticosteroids > or =1 yr before event 
      decreased the risk. In multiple Cox regression analysis, male sex, high age at 
      disease onset, hypertension, higher haptoglobin level at disease onset, and 
      corticosteroid treatment early in disease increased risk of CVD. In a multiple 
      model comprising only patients with CVD, corticosteroids delayed the event. A 
      high last registered erythrocyte sedimentation rate (ESR) value before event 
      increased CVD risk, in particular when early in disease progression. Decreased 
      life span was predicted by higher age at disease onset, male sex, low education 
      level, high disease activity, hypertension, and CVD. HLA-B27 was associated with 
      decreased life span, as was early, but not extensive corticosteroid treatment. 
      DMARD treatment was associated with decreased mortality risk, as was the presence 
      of joint prosthesis. In multiple regression, male sex, higher age at disease 
      onset, atlantoaxial subluxation early in disease, hypertension, and 
      cardiovascular event increased mortality. A high last registered ESR value before 
      event or death added to that risk. CONCLUSION: The study emphasizes the 
      importance of inflammation as an important risk indicator for CVD and mortality 
      in RA. The positive impact of disease activity reducing treatment on CVD risk and 
      survival is suggested.
FAU - Wållberg-Jonsson, S
AU  - Wållberg-Jonsson S
AD  - Department of Rheumatology, University Hospital, Institution of Statistics, 
      University of Umeå, Sweden.
FAU - Johansson, H
AU  - Johansson H
FAU - Ohman, M L
AU  - Ohman ML
FAU - Rantapää-Dahlqvist, S
AU  - Rantapää-Dahlqvist S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Adrenal Cortex Hormones)
RN  - 0 (HLA-B27 Antigen)
SB  - IM
CIN - J Rheumatol. 2000 Sep;27(9):2282-3. PMID: 10990252
MH  - Adrenal Cortex Hormones/therapeutic use
MH  - Age Distribution
MH  - Age of Onset
MH  - Arthritis, Rheumatoid/drug therapy/immunology/*mortality
MH  - Cardiovascular Diseases/immunology/*mortality
MH  - Cohort Studies
MH  - Comorbidity
MH  - Female
MH  - Follow-Up Studies
MH  - HLA-B27 Antigen/blood
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Multivariate Analysis
MH  - Myocardial Infarction/immunology/mortality
MH  - Predictive Value of Tests
MH  - Proportional Hazards Models
MH  - Pulmonary Embolism/immunology/mortality
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Sex Distribution
MH  - Stroke/immunology/mortality
MH  - Survival Analysis
MH  - Venous Thrombosis/immunology/mortality
EDAT- 1999/12/22 09:00
MHDA- 2000/02/26 09:00
CRDT- 1999/12/22 09:00
PHST- 1999/12/22 09:00 [pubmed]
PHST- 2000/02/26 09:00 [medline]
PHST- 1999/12/22 09:00 [entrez]
PST - ppublish
SO  - J Rheumatol. 1999 Dec;26(12):2562-71.

PMID- 10471421
OWN - NLM
STAT- MEDLINE
DCOM- 19991008
LR  - 20190727
IS  - 0039-2499 (Print)
IS  - 0039-2499 (Linking)
VI  - 30
IP  - 9
DP  - 1999 Sep
TI  - Prospective study of aspirin use and risk of stroke in women.
PG  - 1764-71
AB  - BACKGROUND AND PURPOSE: In secondary prevention, aspirin reduces risk of ischemic 
      stroke. In primary prevention of stroke, however, the role of aspirin is 
      uncertain, especially in women. METHODS: In 1980, 79 319 women in the Nurses' 
      Health Study cohort, 34 to 59 years of age and free of diagnosed cardiovascular 
      disease, cancer, and rheumatoid arthritis, completed questionnaires that included 
      information on aspirin use. Data on aspirin use were updated in 1982, 1984, and 
      1988. By 1994, after 994 231 person-years of follow-up, 503 incident strokes (295 
      ischemic strokes, 100 subarachnoid hemorrhages, 52 intraparenchymal hemorrhages, 
      and 56 strokes of undetermined type) were documented. RESULTS: There was no clear 
      relationship between aspirin use and risk of total stroke; risk was slightly 
      reduced among women who took 1 to 6 aspirin per week and slightly increased among 
      women who took 7 or more aspirin per week. Women who took 1 to 6 aspirin per week 
      had a lower risk of large-artery occlusive infarction compared with women who 
      reported no aspirin use; after simultaneous adjustment for other cardiovascular 
      risk factors and selected nutrients, the multivariate relative risk was 0.50 (95% 
      CI 0.29 to 0.85, P=0.01). Women who took 15 or more aspirin per week had an 
      excess risk of subarachnoid hemorrhage; the multivariate relative risk was 2.02 
      (95% CI 1.04 to 3.91, P for trend=0.02). The reduction in large-artery occlusive 
      infarction with aspirin was of greater magnitude for older, hypertensive, or 
      smoking women than for younger, nonhypertensive, or nonsmoking women; the 
      elevation in subarachnoid hemorrhage with aspirin was also more apparent for 
      older or hypertensive women than for younger or nonhypertensive women. Aspirin 
      use was not associated with risk of other subtypes of stroke. CONCLUSIONS: These 
      prospective data indicate that women who take 1 to 6 aspirin per week have a 
      reduced risk of large-artery occlusive infarction, but those who use 15 or more 
      aspirin per week have an increased risk of subarachnoid hemorrhage. This 
      observational study suggests benefits of aspirin for ischemic stroke with low 
      frequency of use and hazards for hemorrhagic stroke with high frequency of use, 
      particularly among older or hypertensive women. Thus, the effect on total stroke 
      will depend on the dose of aspirin and the distribution of stroke subtypes and 
      risk factors in the population.
FAU - Iso, H
AU  - Iso H
AD  - Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and 
      Harvard Medical School, Boston, Mass 02115, USA.
FAU - Hennekens, C H
AU  - Hennekens CH
FAU - Stampfer, M J
AU  - Stampfer MJ
FAU - Rexrode, K M
AU  - Rexrode KM
FAU - Colditz, G A
AU  - Colditz GA
FAU - Speizer, F E
AU  - Speizer FE
FAU - Willett, W C
AU  - Willett WC
FAU - Manson, J E
AU  - Manson JE
LA  - eng
GR  - CA40356/CA/NCI NIH HHS/United States
GR  - HL34594/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Stroke
JT  - Stroke
JID - 0235266
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Adult
MH  - Aspirin/adverse effects/*therapeutic use
MH  - Cerebrovascular Disorders/chemically induced/epidemiology/etiology/*prevention & 
      control
MH  - Cohort Studies
MH  - Female
MH  - Humans
MH  - Incidence
MH  - Middle Aged
MH  - Platelet Aggregation Inhibitors/adverse effects/*therapeutic use
MH  - Prospective Studies
MH  - Risk Factors
MH  - Subarachnoid Hemorrhage/epidemiology/etiology
EDAT- 1999/09/02 00:00
MHDA- 1999/09/02 00:01
CRDT- 1999/09/02 00:00
PHST- 1999/09/02 00:00 [pubmed]
PHST- 1999/09/02 00:01 [medline]
PHST- 1999/09/02 00:00 [entrez]
AID - 10.1161/01.str.30.9.1764 [doi]
PST - ppublish
SO  - Stroke. 1999 Sep;30(9):1764-71. doi: 10.1161/01.str.30.9.1764.

PMID- 10368519
OWN - NLM
STAT- MEDLINE
DCOM- 19990720
LR  - 20190615
IS  - 0002-9378 (Print)
IS  - 0002-9378 (Linking)
VI  - 180
IP  - 6 Pt 2
DP  - 1999 Jun
TI  - Benefits and risks of oral contraceptives.
PG  - S343-8
AB  - The major benefits of modern low-dose oral contraceptives include relative safety 
      and a high degree of efficacy, decreasing the need for abortion or surgical 
      sterilization; reduced risks of bacterial (but not viral) pelvic inflammatory 
      disease and of endometrial and ovarian cancer; improved menstrual regularity, 
      with less dysmenorrhea and blood flow; and, when low-dose combination (not 
      progestogen-only) oral contraceptives are used, reduced acne and hirsutism. Major 
      risks are cardiovascular. Preliminary data from nonrandomized studies suggest 
      that oral contraceptives containing third-generation progestogens are associated 
      with increased risk of venous thromboembolism, particularly in carriers of the 
      coagulation factor V Leiden mutation. The risk of arterial thrombosis, such as 
      myocardial infarction or stroke, may be directly related to estrogen dose, 
      particularly in women who have hypertension, smoke, or are >35 years old. 
      Considering that only users aged >/=30 years who smoke >/=25 cigarettes/d have a 
      higher estimated mortality rate than that of pregnant women, the benefits of oral 
      contraceptives appear to outweigh their risks.
FAU - Sherif, K
AU  - Sherif K
AD  - Institute for Women's Health, MCP Hahnemann University, Philadelphia, 
      Pennsylvania, USA.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Am J Obstet Gynecol
JT  - American journal of obstetrics and gynecology
JID - 0370476
RN  - 0 (Contraceptives, Oral)
SB  - IM
MH  - Cardiovascular Diseases/chemically induced
MH  - Contraceptives, Oral/*adverse effects/*therapeutic use
MH  - Contraindications
MH  - Drug Interactions
MH  - Female
MH  - Genital Diseases, Female/prevention & control
MH  - Humans
MH  - Pregnancy
MH  - Risk Factors
MH  - Smoking/adverse effects
RF  - 22
OID - PIP: 143355
OID - POP: 00289142
OAB - This article presents the benefits and risks of low-dose oral contraceptives 
      (OCs). Most OCs contain a low-dose combination of ethinyl estradiol (or= 35 mcg) 
      and a progestogen (0.1-1.5 mg, depending on the product type). OCs are relatively 
      safe and effective when used for years; they control fertility in women and 
      facilitate spontaneous sexual activity. Other benefits include: 1) improvement in 
      the regularity of menses; 2) decrease in the incidence of dysmenorrhea; 3) 
      circulation of blood flow; 4) reduction of the risks of ovarian and endometrial 
      cancer; 5) inhibition of rheumatoid arthritis progression from mild to severe; 
      and 6) when using low-dose combination (not progestogen-only) OCs, acne and 
      hirsutism are reduced. However, there are also risks in using OCs. The risks 
      associated with OC use are mostly cardiovascular. OCs containing third-generation 
      progestogens are linked with an increased risk of venous thromboembolism. 
      Moreover, acute myocardial infarction risk is great among smokers with 
      hypertension, particularly among women older than 35 years; however, the risk 
      decreases as the dosage of ethinyl estradiol decreases.
OABL- eng
OTO - PIP
OT  - Americas
OT  - Biology
OT  - Contraception
OT  - Contraceptive Agents
OT  - Contraceptive Agents, Estrogen
OT  - Contraceptive Agents, Female
OT  - *Contraceptive Agents, Progestin
OT  - Contraceptive Methods--beneficial effects
OT  - Contraceptive Methods--side effects
OT  - Developed Countries
OT  - *Ethinyl Estradiol
OT  - Family Planning
OT  - *Literature Review
OT  - North America
OT  - Northern America
OT  - *Oral Contraceptives, Low-dose--beneficial effects
OT  - *Oral Contraceptives, Low-dose--side effects
OT  - Oral Contraceptives--beneficial effects
OT  - Oral Contraceptives--side effects
OT  - *Risk Factors
OT  - United States
GN  - PIP: TJ: AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY.
EDAT- 1999/06/16 00:00
MHDA- 1999/06/16 00:01
CRDT- 1999/06/16 00:00
PHST- 1999/06/16 00:00 [pubmed]
PHST- 1999/06/16 00:01 [medline]
PHST- 1999/06/16 00:00 [entrez]
AID - S0002-9378(99)70694-0 [pii]
AID - 10.1016/s0002-9378(99)70694-0 [doi]
PST - ppublish
SO  - Am J Obstet Gynecol. 1999 Jun;180(6 Pt 2):S343-8. doi: 
      10.1016/s0002-9378(99)70694-0.

PMID- 9696080
OWN - NLM
STAT- MEDLINE
DCOM- 19981124
LR  - 20220408
IS  - 0148-396X (Print)
IS  - 0148-396X (Linking)
VI  - 43
IP  - 2
DP  - 1998 Aug
TI  - Posterior C1-C2 transarticular screw fixation for atlantoaxial arthrodesis.
PG  - 275-80; discussion 280-1
AB  - OBJECTIVE: To assess the outcomes associated with C1-C2 transarticular screw 
      fixation. METHODS: The clinical outcomes of 121 patients treated with posterior 
      C1-C2 transarticular screws and wired posterior C1-C2 autologous bone struts were 
      evaluated prospectively. Atlantoaxial instability was caused by rheumatoid 
      arthritis in 48 patients, C1 or C2 fractures in 45, transverse ligament 
      disruption in 11, os odontoideum in 9, tumors in 6, and infection in 2. RESULTS: 
      Altogether, 226 screws were placed under lateral fluoroscopic guidance. Bilateral 
      C1-C2 screws were placed in 105 patients; each of 16 patients had only one screw 
      placed because of an anomalous vertebral artery (n = 13) or other pathological 
      abnormality. Postoperatively, each patient underwent radiography and computed 
      tomography to assess the position of the screw and healing. Most screws (221 
      screws, 98%) were positioned satisfactorily. Five screws were malpositioned (2%), 
      but none were associated with clinical sequelae. Four malpositioned screws were 
      reoperated on (one was repositioned, and three were removed). No patients had 
      neurological complications, strokes, or transient ischemic attacks. Long-term 
      follow-up (mean, 22 mo) of 114 patients demonstrated a 98% fusion rate. Two 
      nonunions (2%) required occipitocervical fixation. In comparison, our C1-C2 
      fixations with wires and autograft (n = 74) had an 86% union rate. CONCLUSION: 
      Rigidly fixating C1-C2 instability with transarticular screws was associated with 
      a significantly higher fusion rate than that achieved using wired grafts alone. 
      The risk of screw malpositioning and catastrophic vascular or neural injury is 
      small and can be minimized by assessing the position of the foramen transversaria 
      on preoperative computed tomographic scans and by using intraoperative 
      fluoroscopy and frameless stereotaxy to guide the screw trajectory.
FAU - Dickman, C A
AU  - Dickman CA
AD  - Division of Neurological Surgery, Barrow Neurological Institute, Mercy Healthcare 
      Arizona, Phoenix 85013-4496, USA.
FAU - Sonntag, V K
AU  - Sonntag VK
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - Neurosurgery
JT  - Neurosurgery
JID - 7802914
SB  - IM
CIN - Neurosurgery. 1999 Mar;44(3):687-9. doi: 10.1097/00006123-199903000-00157. PMID: 
      10069612
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Atlanto-Axial Joint/diagnostic imaging/*surgery
MH  - *Bone Screws
MH  - Bone Transplantation/instrumentation
MH  - Bone Wires
MH  - Child
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Joint Instability/diagnostic imaging/etiology/*surgery
MH  - Male
MH  - Middle Aged
MH  - Neurologic Examination
MH  - Postoperative Complications/diagnostic imaging/surgery
MH  - Radiography
MH  - Reoperation
MH  - Spinal Fusion/*instrumentation
MH  - Treatment Outcome
EDAT- 1998/08/08 00:00
MHDA- 1998/08/08 00:01
CRDT- 1998/08/08 00:00
PHST- 1998/08/08 00:00 [pubmed]
PHST- 1998/08/08 00:01 [medline]
PHST- 1998/08/08 00:00 [entrez]
AID - 10.1097/00006123-199808000-00056 [doi]
PST - ppublish
SO  - Neurosurgery. 1998 Aug;43(2):275-80; discussion 280-1. doi: 
      10.1097/00006123-199808000-00056.

PMID- 7974556
OWN - NLM
STAT- MEDLINE
DCOM- 19941129
LR  - 20190727
IS  - 0039-2499 (Print)
IS  - 0039-2499 (Linking)
VI  - 25
IP  - 11
DP  - 1994 Nov
TI  - Sjögren's syndrome presenting as ischemic stroke.
PG  - 2276-9
AB  - BACKGROUND: We describe a young woman who presented with minor stroke as a first 
      clinical symptom of Sjögren's syndrome (SS) in the absence of well-known risk 
      factors for cerebrovascular disease. CASE DESCRIPTION: The medical history 
      included recurrent miscarriages and sun rashes, which directed the diagnosis 
      toward immunologic disorders such as systemic lupus erythematosus and 
      antiphospholipid antibody syndrome, which are often associated with stroke. Only 
      complete laboratory testing, including SSB antibody studies, and ophthalmologic 
      and salivary gland evaluation revealed the correct diagnosis. CONCLUSIONS: 
      Sjögren's syndrome should be considered among the causes of stroke, especially in 
      a young female patient.
FAU - Bragoni, M
AU  - Bragoni M
AD  - V Clinica Neurologica, Universita' di Roma La Sapienza, Italy.
FAU - Di Piero, V
AU  - Di Piero V
FAU - Priori, R
AU  - Priori R
FAU - Valesini, G
AU  - Valesini G
FAU - Lenzi, G L
AU  - Lenzi GL
LA  - eng
PT  - Case Reports
PT  - Journal Article
PL  - United States
TA  - Stroke
JT  - Stroke
JID - 0235266
SB  - IM
MH  - Adult
MH  - Brain Ischemia/*diagnosis
MH  - Cerebrovascular Disorders/*diagnosis
MH  - Diagnosis, Differential
MH  - Female
MH  - Humans
MH  - Magnetic Resonance Imaging
MH  - Sjogren's Syndrome/*diagnosis
EDAT- 1994/11/01 00:00
MHDA- 1994/11/01 00:01
CRDT- 1994/11/01 00:00
PHST- 1994/11/01 00:00 [pubmed]
PHST- 1994/11/01 00:01 [medline]
PHST- 1994/11/01 00:00 [entrez]
AID - 10.1161/01.str.25.11.2276 [doi]
PST - ppublish
SO  - Stroke. 1994 Nov;25(11):2276-9. doi: 10.1161/01.str.25.11.2276.

PMID- 1605284
OWN - NLM
STAT- MEDLINE
DCOM- 19920710
LR  - 20190615
IS  - 0002-9378 (Print)
IS  - 0002-9378 (Linking)
VI  - 166
IP  - 6 Pt 2
DP  - 1992 Jun
TI  - The safety of oral contraceptives: epidemiologic insights from the first 30 
      years.
PG  - 1950-4
AB  - Because oral contraceptives are used by tens of millions of healthy women, their 
      safety for short-term and long-term use is an important issue that has been 
      examined in a large number of epidemiologic studies. These studies have become 
      more rigorous and have increased in size and analytic sophistication over the 
      years. Although breast cancer remains the most important safety concern, the bulk 
      of recent data suggests that oral contraceptives have no overall impact on a 
      woman's risk of developing this disease. The results are less clear on the risk 
      of cervical cancer and its precursors because of methodologic problems. However, 
      the newer oral contraceptive formulations no longer appear to be associated with 
      an increased risk of myocardial infarction or stroke.
FAU - Grimes, D A
AU  - Grimes DA
AD  - Department of Obstetrics and Gynecology, University of Southern California School 
      of Medicine, Los Angeles.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Am J Obstet Gynecol
JT  - American journal of obstetrics and gynecology
JID - 0370476
RN  - 0 (Contraceptives, Oral)
SB  - IM
MH  - Cardiovascular Diseases/chemically induced/epidemiology
MH  - Contraceptives, Oral/*adverse effects/pharmacology
MH  - Female
MH  - Humans
MH  - Life Expectancy
MH  - Neoplasms/chemically induced/epidemiology
RF  - 34
OID - IND: 8021543
OID - PIP: 073925
OID - POP: 00211230
OAB - Studies show that OCs have several benefits besides prevention of pregnancy. They 
      protect against ovarian and endometrial cancer, pelvic inflammatory disease, and 
      ectopic pregnancy. OCs also prevent iron deficiency anemia, primary dysmenorrhea, 
      functional ovarian cysts, and benign breast disease. They may even protect 
      against some benign uterine tumors, osteoporosis, toxic shock syndrome, and 
      rheumatoid arthritis. Despite many concerns, some large studies have not 
      identified an overall effect of OCs on breast cancer, but subgroup analyses 
      showed increased risk in 30-34 year old women and in women with 1 child. A 
      reanalysis of a large US study indicated an increase risk of breast cancer in 
      nulliparous women with increasing use of OCs by young women. Cervical cancer is 
      the leading cancer of women in developing countries which emphasizes the need to 
      examine the link between OC use and cervical cancer. Several studies show an 
      increased risk of cervical cancer. Several studies show an increased risk of 
      cervical cancer in long term OC users. In 1 study, long term use meant 5 years. 
      Yet these studies did not adequately address confounding factors such as smoking 
      and sexual behavior. 3 case control studies in the US and the UK found an 
      increased risk of liver cancer among OC users, yet a large case control study in 
      developing countries did not find a link between OC use and liver cancer. Studies 
      of high dose OCs found considerable increased risks of cardiovascular disease in 
      OC users, but they did not take into account cigarette smoking which indeed 
      increases the risk. Further health practitioners today do a more thorough job of 
      identifying underlying medical problems before prescribing OCs. Moreover estrogen 
      doses have fallen 10 fold since the original OCs. Finally, despite a transient 
      delay, women who take OCs experience a return to fertility at the same rate as 
      those who use other contraceptives.
OABL- eng
OTO - PIP
OT  - Americas
OT  - Behavior
OT  - Biology
OT  - *Breast Cancer
OT  - Cancer
OT  - *Cardiovascular Effects
OT  - *Cervical Cancer
OT  - Contraception
OT  - Contraceptive Methods--beneficial effects
OT  - Contraceptive Methods--side effects
OT  - Developed Countries
OT  - *Developing Countries
OT  - Diseases
OT  - *Dysmenorrhea
OT  - *Epidemiologic Methods
OT  - Europe
OT  - Evaluation
OT  - Family Planning
OT  - Hemic System
OT  - *Hemoglobin Level
OT  - Infections
OT  - *Infertility
OT  - *Literature Review
OT  - *Liver Neoplasms
OT  - Menstruation Disorders
OT  - Neoplasms
OT  - *Neoplasms, Benign
OT  - North America
OT  - Northern America
OT  - Northern Europe
OT  - *Oral Contraceptives--beneficial effects
OT  - *Oral Contraceptives--side effects
OT  - *Ovarian Cancer
OT  - *Ovarian Cysts
OT  - *Pelvic Infections
OT  - Physiology
OT  - Pregnancy Complications
OT  - *Pregnancy, Ectopic
OT  - Reproduction
OT  - Research Methodology
OT  - *Risk Assessment
OT  - *Smoking
OT  - *United Kingdom
OT  - United States
GN  - PIP: TJ: AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY.
EDAT- 1992/06/01 00:00
MHDA- 1992/06/01 00:01
CRDT- 1992/06/01 00:00
PHST- 1992/06/01 00:00 [pubmed]
PHST- 1992/06/01 00:01 [medline]
PHST- 1992/06/01 00:00 [entrez]
AID - 0002-9378(92)91394-P [pii]
AID - 10.1016/0002-9378(92)91394-p [doi]
PST - ppublish
SO  - Am J Obstet Gynecol. 1992 Jun;166(6 Pt 2):1950-4. doi: 
      10.1016/0002-9378(92)91394-p.

PMID- 1836280
OWN - NLM
STAT- MEDLINE
DCOM- 19920121
LR  - 20191022
IS  - 0049-0172 (Print)
IS  - 0049-0172 (Linking)
VI  - 21
IP  - 2 Suppl 1
DP  - 1991 Oct
TI  - Worldwide trends in the socioeconomic impact and long-term prognosis of 
      rheumatoid arthritis.
PG  - 4-12
AB  - Rheumatoid arthritis (RA), once considered a benign and nonprogressive disease, 
      is a debilitating condition with serious physical, emotional, and economic 
      consequences. It afflicts approximately 1% of the adult population worldwide; 
      prevalence increases with age, with twice as many women as men affected. In the 
      United States, age, lack of formal education, and lower socioeconomic class 
      correlate with both the incidence and poor prognosis of RA. The patient with RA 
      faces increasing functional disability, the likelihood of work disability within 
      10 years after the onset of the disease, and a drastic reduction in earnings. 
      Compared with individuals without the disease, patients with RA incur higher 
      medical care costs, increased hospitalization, and a greater number of physician 
      visits. As in the general population, the leading cause of death among patients 
      with RA is cardiovascular disease, and deaths due to malignancy occur at a 
      comparable incidence; however, patients with RA are at greater risk of mortality 
      due to infection, renal disease, respiratory conditions, and gastrointestinal 
      disease. Life expectancy is shorter among patients with RA than in the general 
      population, and survival rates are comparable to those for Hodgkin's disease, 
      diabetes mellitus, stroke, and three-vessel coronary artery disease. Efforts must 
      be made to develop improved therapeutic strategies and rehabilitative programs to 
      improve the quality of life of patients with RA.
FAU - Markenson, J A
AU  - Markenson JA
AD  - Department of Medicine, Cornell University Medical College, New York, NY.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Semin Arthritis Rheum
JT  - Seminars in arthritis and rheumatism
JID - 1306053
SB  - IM
MH  - Arthritis, Rheumatoid/economics/epidemiology/*physiopathology
MH  - Disabled Persons
MH  - Employment
MH  - *Global Health
MH  - Health Care Costs
MH  - Humans
MH  - Morbidity
MH  - Mortality
MH  - Prevalence
MH  - Prognosis
MH  - Socioeconomic Factors
MH  - Time Factors
RF  - 58
EDAT- 1991/10/01 00:00
MHDA- 1991/10/01 00:01
CRDT- 1991/10/01 00:00
PHST- 1991/10/01 00:00 [pubmed]
PHST- 1991/10/01 00:01 [medline]
PHST- 1991/10/01 00:00 [entrez]
AID - 0049-0172(91)90046-3 [pii]
AID - 10.1016/0049-0172(91)90046-3 [doi]
PST - ppublish
SO  - Semin Arthritis Rheum. 1991 Oct;21(2 Suppl 1):4-12. doi: 
      10.1016/0049-0172(91)90046-3.

PMID- 2057974
OWN - NLM
STAT- MEDLINE
DCOM- 19910726
LR  - 20190727
IS  - 0039-2499 (Print)
IS  - 0039-2499 (Linking)
VI  - 22
IP  - 6
DP  - 1991 Jun
TI  - Antiphospholipid antibodies in cerebral ischemia.
PG  - 750-3
AB  - In a 2-year prospective study of 146 patients with cerebral ischemia, we compared 
      vascular risk factors for stroke with clinical and laboratory findings, 
      particularly antiphospholipid antibodies. Ten patients (6.8%) were positive for 
      at least one antiphospholipid antibody; one patient had systemic lupus 
      erythematosus, one had rheumatoid arthritis, and the remaining eight fulfilled 
      criteria for the diagnosis of primary antiphospholipid syndrome. These patients 
      were predominantly male, not necessarily young, and 50% of them did not have any 
      other vascular risk factors; there were no significant clinical or paraclinical 
      differences between these patients and those without antiphospholipid antibodies. 
      Outcome in the 10 patients was good, and platelet antiaggregating drugs proved to 
      be useful in preventing further cerebrovascular ischemic events in our patients.
FAU - Montalbán, J
AU  - Montalbán J
AD  - Servei de Neurologia, Hospital General Vall d'Hebron, Barcelona, Spain.
FAU - Codina, A
AU  - Codina A
FAU - Ordi, J
AU  - Ordi J
FAU - Vilardell, M
AU  - Vilardell M
FAU - Khamashta, M A
AU  - Khamashta MA
FAU - Hughes, G R
AU  - Hughes GR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Stroke
JT  - Stroke
JID - 0235266
RN  - 0 (Autoantibodies)
RN  - 0 (Phospholipids)
SB  - IM
MH  - Arthritis, Rheumatoid/complications/immunology
MH  - Autoantibodies/*analysis
MH  - Brain Ischemia/complications/*immunology
MH  - Cerebrovascular Disorders/*etiology
MH  - Female
MH  - Humans
MH  - Lupus Erythematosus, Systemic/complications/immunology
MH  - Male
MH  - Middle Aged
MH  - Phospholipids/*immunology
MH  - Prospective Studies
MH  - Reference Values
MH  - Risk Factors
MH  - Syndrome
EDAT- 1991/06/01 00:00
MHDA- 1991/06/01 00:01
CRDT- 1991/06/01 00:00
PHST- 1991/06/01 00:00 [pubmed]
PHST- 1991/06/01 00:01 [medline]
PHST- 1991/06/01 00:00 [entrez]
AID - 10.1161/01.str.22.6.750 [doi]
PST - ppublish
SO  - Stroke. 1991 Jun;22(6):750-3. doi: 10.1161/01.str.22.6.750.

PMID- 2018026
OWN - NLM
STAT- MEDLINE
DCOM- 19910521
LR  - 20190510
IS  - 0002-9262 (Print)
IS  - 0002-9262 (Linking)
VI  - 133
IP  - 7
DP  - 1991 Apr 1
TI  - A preliminary study of excess risk of cardiovascular disease in the mothers of 
      patients with rheumatoid arthritis.
PG  - 715-20
AB  - Family histories were obtained from 123 patients with rheumatoid arthritis and 
      152 patients with other musculoskeletal complaints. The subjects were female 
      patients aged 40 years or more seen at the Arthritis Clinic of the State 
      University of New York Health Science Center at Brooklyn between October 1985 and 
      February 1986. It was found that death due to heart disease or stroke was more 
      common (adjusted p less than 0.02) in the mothers of patients with rheumatoid 
      arthritis than in the mothers of control patients, and that heart disease was 
      also reported to be more common in these mothers (adjusted p less than 0.005). 
      Thus, it is possible that cardiovascular disease at least partially accounts for 
      the previously noted (J Rheumatol 1986; 13:903-6) shorter life expectancy of the 
      mothers of patients with rheumatoid arthritis.
FAU - Kaplan, D
AU  - Kaplan D
AD  - Department of Medicine, State University of New York, Brooklyn 11203.
FAU - Feldman, J
AU  - Feldman J
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am J Epidemiol
JT  - American journal of epidemiology
JID - 7910653
RN  - 9009-79-4 (Rheumatoid Factor)
SB  - IM
MH  - Adult
MH  - Arthritis, Rheumatoid/complications/*genetics
MH  - Cardiovascular Diseases/etiology/*genetics/mortality
MH  - Female
MH  - Humans
MH  - Middle Aged
MH  - Mothers
MH  - Rheumatoid Factor/genetics
MH  - Risk Factors
EDAT- 1991/04/01 00:00
MHDA- 1991/04/01 00:01
CRDT- 1991/04/01 00:00
PHST- 1991/04/01 00:00 [pubmed]
PHST- 1991/04/01 00:01 [medline]
PHST- 1991/04/01 00:00 [entrez]
AID - 10.1093/oxfordjournals.aje.a115946 [doi]
PST - ppublish
SO  - Am J Epidemiol. 1991 Apr 1;133(7):715-20. doi: 
      10.1093/oxfordjournals.aje.a115946.

PMID- 2087578
OWN - NLM
STAT- MEDLINE
DCOM- 19910520
LR  - 20051116
IS  - 0889-857X (Print)
IS  - 0889-857X (Linking)
VI  - 16
IP  - 4
DP  - 1990 Nov
TI  - Exercise and arthritis. The hematology of inactivity.
PG  - 815-25
AB  - Arthritis tends to promote inactivity, and inactivity tends to promote an 
      unhealthful constellation of blood abnormalities that increases the risk of heart 
      attack and stroke. The hematology of inactivity comprises the following: low 
      plasma volume, high hematocrit, high plasma fibrinogen, elevated blood viscosity, 
      increased platelet aggregability, and diminished fibrinolysis. Regular exercise 
      reverses all these adverse blood changes and, thereby, helps prevent heart attack 
      and stroke. Simply put, exercise "improves" the blood, making it flow more easily 
      and clot less readily. This "healthy hematology of exercisers" is one more reason 
      why prudent exercise is as vital for patients with arthritis as it is for the 
      rest of us.
FAU - Eichner, E R
AU  - Eichner ER
AD  - Section of Hematology, University of Oklahoma Health Sciences Center, Oklahoma 
      City 73190.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Rheum Dis Clin North Am
JT  - Rheumatic diseases clinics of North America
JID - 8708093
RN  - 9001-32-5 (Fibrinogen)
SB  - IM
MH  - Arthritis/*blood
MH  - Arthritis, Rheumatoid/blood/mortality
MH  - Blood Platelets/physiology
MH  - Exercise
MH  - Fibrinogen/physiology
MH  - Fibrinolysis
MH  - Hematocrit
MH  - Humans
MH  - Longevity
MH  - Myocardial Infarction/etiology
MH  - *Physical Fitness
RF  - 49
EDAT- 1990/11/01 00:00
MHDA- 1990/11/01 00:01
CRDT- 1990/11/01 00:00
PHST- 1990/11/01 00:00 [pubmed]
PHST- 1990/11/01 00:01 [medline]
PHST- 1990/11/01 00:00 [entrez]
PST - ppublish
SO  - Rheum Dis Clin North Am. 1990 Nov;16(4):815-25.

PMID- 2692147
OWN - NLM
STAT- MEDLINE
DCOM- 19900221
LR  - 20051116
IS  - 0036-7672 (Print)
IS  - 0036-7672 (Linking)
VI  - 119
IP  - 50
DP  - 1989 Dec 16
TI  - Risks and benefits of long-term treatment with estrogens.
PG  - 1811-20
AB  - The goal of contemporary hormone replacement is to minimize net predictable 
      lifetime risk; success therefore depends upon quantitative assessments of the net 
      quality of life, of net morbidity and of net mortality. Estrogens ameliorate 
      menopausal symptoms, maintain bone integrity, and produce endometrial cancer; 
      these facts and their quantitative aspects can be stimulated. Other links are 
      gradually becoming clear: estrogens increase biliary disease, but prevent heart 
      disease, and, it now seems, stroke. Conventional wisdom to the contrary 
      notwithstanding, a critical review suggests that breast cancer is probably 
      increased in frequency by long-term estrogen use; the increase is modest as a 
      risk factor but because breast cancer is a common disease, it is substantial in 
      absolute terms. The addition of progestin seems attractive as a method of 
      opposing undesirable estrogenic effects on the endometrium. In fact, there is 
      reason for concern about the effect of an added progestin upon the risks from 
      breast cancer, heart disease, and stroke; even the magnitude of the expected 
      reduction in endometrial cancer may not be great when the hormone is administered 
      sequentially. Using a simple deterministic model of post-menopausal life with 
      hormone replacement, we have inserted available estimates of the regimen-specific 
      relative risk for each outcome, and translated each net impact into common 
      denominators of morbidity and mortality. While estrogens probably increase net 
      morbidity, as measured by either the number of hospitalizations to be anticipated 
      or by the more arbitrary measure of expected days of disability, these negative 
      changes are mostly due to gallbladder disease and endometrial cancer, both 
      largely treatable conditions. Largely because of protection against heart 
      disease, estrogen replacement in modest dose is likely to reduce substantially 
      the number of deaths to be expected in women treated through age 75 and even into 
      more advanced age. Hormone replacement which includes systemic progestin 
      supplementation has not been empirically tested; it may be beneficial, but it is 
      at least as likely to be harmful. Either a modest increment in the number of 
      additional breast cancers produced by estrogens, a modest reduction in the number 
      of cardiac events prevented by estrogens, or a simultaneous minor shift in the 
      same direction for each condition, would have the effect of shifting the net 
      reduction in cumulative deaths into an increase in the number of deaths as a 
      result of treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
FAU - Mack, T M
AU  - Mack TM
AD  - University of Southern California, Department of Preventine Medicine, Los Angeles 
      90033.
FAU - Ross, R K
AU  - Ross RK
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Switzerland
TA  - Schweiz Med Wochenschr
JT  - Schweizerische medizinische Wochenschrift
JID - 0404401
RN  - 0 (Estrogens)
RN  - 0 (Progestins)
SB  - IM
MH  - Aged
MH  - Arthritis, Rheumatoid/prevention & control
MH  - Breast Neoplasms/chemically induced
MH  - Cerebrovascular Disorders/prevention & control
MH  - Climacteric/drug effects
MH  - Coronary Disease/prevention & control
MH  - Estrogens/adverse effects/*therapeutic use
MH  - Female
MH  - Gallbladder Diseases/chemically induced
MH  - Humans
MH  - Middle Aged
MH  - Osteoporosis, Postmenopausal/*prevention & control
MH  - Progestins/adverse effects
MH  - Risk Factors
MH  - Uterine Neoplasms/chemically induced
RF  - 117
EDAT- 1989/12/16 00:00
MHDA- 1989/12/16 00:01
CRDT- 1989/12/16 00:00
PHST- 1989/12/16 00:00 [pubmed]
PHST- 1989/12/16 00:01 [medline]
PHST- 1989/12/16 00:00 [entrez]
PST - ppublish
SO  - Schweiz Med Wochenschr. 1989 Dec 16;119(50):1811-20.

PMID- 3523849
OWN - NLM
STAT- MEDLINE
DCOM- 19860805
LR  - 20180429
IS  - 0039-3665 (Print)
IS  - 0039-3665 (Linking)
VI  - 17
IP  - 3
DP  - 1986 May-Jun
TI  - Oral contraceptives and life expectancy.
PG  - 117-25
AB  - Life expectancy for women in the United States is 77.34 years; women who take 
      oral contraceptives (OCs) for five years before the age of 30 can expect to live 
      about four days longer. This is due primarily to protection against ovarian and 
      endometrial cancers. For women taking pills for five years in their thirties 
      there is a maximum loss of 18 days on the average that is attributable to OC use, 
      and for women over 45 this rises to 80 days. The decreased life expectancy is due 
      mainly to the increased mortality from myocardial infarction and stroke. This is 
      substantially less than life lost due to use of a variety of other substances, 
      most notably tobacco.
FAU - Fortney, J A
AU  - Fortney JA
FAU - Harper, J M
AU  - Harper JM
FAU - Potts, M
AU  - Potts M
LA  - eng
GR  - 089701/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Review
PL  - United States
TA  - Stud Fam Plann
JT  - Studies in family planning
JID - 7810364
RN  - 0 (Contraceptives, Oral)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Age Factors
MH  - Aged
MH  - Cerebrovascular Disorders/chemically induced/epidemiology
MH  - *Contraceptives, Oral/administration & dosage/adverse effects
MH  - Female
MH  - Gallbladder Diseases/epidemiology
MH  - Humans
MH  - *Life Expectancy
MH  - Middle Aged
MH  - Myocardial Infarction/chemically induced/epidemiology
MH  - Ovarian Neoplasms/prevention & control
MH  - Pelvic Inflammatory Disease/epidemiology/prevention & control
MH  - Pregnancy
MH  - Pregnancy Complications/chemically induced
MH  - Risk
MH  - United States
MH  - Uterine Neoplasms/chemically induced/prevention & control
RF  - 99
OID - PIP: 037394
OID - POP: 00157965
OAB - This report combines early and late mortality effects of oral contraceptives into 
      a life table analysis based on epidemiological evidence using US data. An 
      association between oral contraceptives and disease is included only if 
      demonstrated by at least 2 previous independent studies; those included in the 
      study are: pregnancy complications, cancer (ovarian, endometrial, cervical), 
      cardiovascular disease, gallbladder disease, pelvic inflammatory disease, and 
      rheumatoid arthritis. The model assumes women who use oral contraceptives 
      continuously for 5 years and then stop, and compares this with a base population 
      of US women aged 15-49 who are not using oral contraceptives. Results drawn from 
      these data are that oral contraceptives taken for 5 years have no effect on life 
      expectancy of women under 30; 5 years of use during the 30's reduces average life 
      expectancy by 7-22 days; and among older women (over 40) life expectancy 
      decreases up to 88 days. Protective effects of oral contraceptives against 
      reproductive cancers cancels out risks due to myocardial infarction and stroke. 
      This model does not account for different risks of smokers and non-smokers, 
      therefore the small differences in longevity are probably exaggerated. The 
      decreased life expectancy is due mainly to the increased mortality from 
      myocardial infarction and stroke. This is substantially less than life lost due 
      to use of a variety of other substances, most notably tobacco.
OABL- eng
OTO - PIP
OT  - *Age Specific Death Rate
OT  - Americas
OT  - Cancer
OT  - Cardiovascular Effects
OT  - Cervical Cancer
OT  - *Comparative Studies
OT  - *Contraception
OT  - Contraceptive Agents
OT  - *Contraceptive Agents, Female
OT  - Contraceptive Methods
OT  - Death Rate
OT  - Demographic Analysis
OT  - Demographic Factors
OT  - Developed Countries
OT  - Developing Countries
OT  - Diseases
OT  - Endometrial Cancer
OT  - *Epidemiologic Methods
OT  - Family Planning
OT  - Heart Diseases
OT  - *Length Of Life
OT  - *Life Expectancy
OT  - *Life Table Method
OT  - *Measurement
OT  - *Mortality
OT  - Myocardial Infarction
OT  - Neoplasms
OT  - North America
OT  - *Northern America
OT  - *Oral Contraceptives
OT  - Ovarian Cancer
OT  - Population
OT  - Population Dynamics
OT  - Pregnancy Complications
OT  - Research Methodology
OT  - *Research Report
OT  - Studies
OT  - United States
GN  - PIP: TJ: STUDIES IN FAMILY PLANNING.
EDAT- 1986/05/01 00:00
MHDA- 1986/05/01 00:01
CRDT- 1986/05/01 00:00
PHST- 1986/05/01 00:00 [pubmed]
PHST- 1986/05/01 00:01 [medline]
PHST- 1986/05/01 00:00 [entrez]
PST - ppublish
SO  - Stud Fam Plann. 1986 May-Jun;17(3):117-25.

PMID- 12311809
OWN - PIP
STAT- MEDLINE
DCOM- 19830307
LR  - 20061115
IS  - 0301-861X (Print)
IS  - 0301-861X (Linking)
VI  - 10
IP  - 11
DP  - 1982 Nov
TI  - [Oral contraception in 1983 (author's transl)].
PG  - 753-7
FAU - Castadot, R G
AU  - Castadot RG
LA  - fre
PT  - English Abstract
PT  - Journal Article
TT  - Le point sur la contraception orale en 1983.
PL  - France
TA  - Contracept Fertil Sex (Paris)
JT  - Contraception, fertilite, sexualite
JID - 0411244
RN  - 0 (Contraceptives, Oral)
RN  - 0 (Reproductive Control Agents)
MH  - Cerebrovascular Circulation
MH  - *Contraception
MH  - *Contraceptives, Oral
MH  - Family Planning Services
MH  - Neoplasms
MH  - *Reproductive Control Agents
OID - PIP: 012003
OID - POP: 00115304
OAB - Recent studies have demonstrated new benefits of pill use, reduced risks 
      associated with the minipill, and the possibility of screening out high risk 
      women. The minipill is as effective as other formulations except in cases of 
      chronic malnutrition or concomitant use of antibiotics or anticonvulsives. Oral 
      contraceptives (OCs) frequently lessen menstrual problems. They prevent 
      functional cysts in the ovaries, and reduce the incidence of benign breast tumors 
      and the relative risk of developing ovarian cancer after 3 years of use. Combined 
      OCs reduce the risk of endometrial cancer although sequentials increase it. OCs 
      offer protection against salpingitis and other pelvic infections, against tubal 
      pregnancies, and against chronic rheumatoid arthritis. Minipills appear to be 
      less frequently associated with bothersome side effects than other OCs. The most 
      significant risk of OCs is of death due to thrombo emboli of venous origin, 
      myocardial ischemia, cerebrovascular accidents, and hypertension in women over 
      35, particularly those who smoke heavily. In 1981 the 2 British studies reported 
      a reduced risk from these causes compared to results published in 1977. Estrogens 
      are clearly responsible for some of the complications, apparently due to a 
      weakening of the fibrinolytic systems, but progestagens or estrogen-progestagen 
      combinations are also implicated. Arterial hypertension and cerebral and cardiac 
      accidents appear to be due to the effect of progestagens on arterial tension, 
      glucose metabolism, and the level of high density lipoprotein cholesterol. Risks 
      of some liver diseases are elevated in pill users, but the question of tumors of 
      the pituitary is not yet resolved. The incidence of uterine cancer appears to be 
      elevated in pill users although the association is obscured by other factors. 
      Some evidence exists of an association between estrogen-progestagen formulations 
      and melanoma. No increase in abortion or fetal malformations except possibly an 
      increase in twin pregnancies is noted after discontinuation of the pill. Pills 
      should not be prescribed for smokers over 35 or any women over 45. Pills are 
      possibly acceptable for women 35-44 in good health with no signs of diabetes, 
      hypertension, or hyperlipoproteinemia. They should be followed up more frequently 
      and should recognize the signs of complications.
OABL- eng
OTO - PIP
OT  - Cancer
OT  - Cerebrovascular Effects
OT  - *Contraception
OT  - Contraceptive Methods--contraindications
OT  - Contraceptive Methods--indications
OT  - Contraceptive Methods--side effects
OT  - Family Planning
OT  - *Oral Contraceptives, Low-dose
OT  - *Oral Contraceptives--contraindications
OT  - *Oral Contraceptives--indications
OT  - *Oral Contraceptives--side effects
OT  - *Reproductive Control Agents
GN  - PIP: TJ: CONTRACEPTION, FERTILITE, SEXUALITE
EDAT- 1982/11/01 00:00
MHDA- 2002/10/09 04:00
CRDT- 1982/11/01 00:00
PHST- 1982/11/01 00:00 [pubmed]
PHST- 2002/10/09 04:00 [medline]
PHST- 1982/11/01 00:00 [entrez]
PST - ppublish
SO  - Contracept Fertil Sex (Paris). 1982 Nov;10(11):753-7.

PMID- 7202690
OWN - NLM
STAT- MEDLINE
DCOM- 19810513
LR  - 20041117
IS  - 0014-7354 (Print)
IS  - 0014-7354 (Linking)
VI  - 12
IP  - 6
DP  - 1980 Nov-Dec
TI  - The pill at 20: an assessment.
PG  - 278-83
FAU - Ory, H W
AU  - Ory HW
FAU - Rosenfield, A
AU  - Rosenfield A
FAU - Landman, L C
AU  - Landman LC
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Fam Plann Perspect
JT  - Family planning perspectives
JID - 0241370
RN  - 0 (Contraceptives, Oral)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Age Factors
MH  - Cardiovascular Diseases/chemically induced
MH  - Child
MH  - Contraceptives, Oral/*adverse effects
MH  - Female
MH  - Fertility/drug effects
MH  - Humans
MH  - Neoplasms/chemically induced
MH  - Prospective Studies
MH  - Risk
MH  - Smoking
OID - PIP: 802952
OID - POP: 00081818
OAB - During the 20 years since the oral contraceptive was introduced, it has been used 
      by some 150 million women around the world, and is perhaps the most carefully 
      monitored medication in history. This vast body of research shows that for the 
      overwhelming majority of healthy women under 30, the benefits of the pill 
      continue to outweigh the risks. The most serious life threatening risks are those 
      involving the cardiovascular system: heart attack, stroke, and throboembolism. 
      However, deaths from these causes would be reduced by 1/2 if women using the pill 
      did not smoke; further reductions would result if women with high blood pressure, 
      high chloresterol levels and diabetes millitus did not use the pill. There is no 
      evidence thus far to justify fears that the pill might be associated with an 
      increased risk of cancer. Most studies show that not only is there no association 
      between pill use and cancer of the ovaries, uterus and breast, but pill use may 
      protect against ovarian and endometrial cancer. Women taking the pill are 1/4 as 
      likely to develop benign breast lumps as nonusers, 1/14 as likely to develop 
      ovarian cysts, 2/3 as likely to develop iron deficiency anemia, and 1/2 as likely 
      to develop rheumatoid arthritis -- all relatively common conditions. In addition, 
      pelvic inflammatory disease, a major cause of infertility, appears to occur only 
      1/2 as often among pill users as among nonusers. The risk to life among pill 
      users younger than 30 who do not smoke is very small (virtually the same as that 
      of users of the IUD, diaphragm, or condom) and is much lower than the risk of 
      birth-related deaths among women who use no birth control.
OABL- eng
OTO - PIP
OT  - Cardiovascular Effects
OT  - Contraception
OT  - Contraceptive Methods--side effects
OT  - Family Planning
OT  - Fecundity
OT  - Fertility
OT  - Mortality
OT  - *Oral Contraceptives--side effects
OT  - Pregnancy Outcomes
OT  - Smoking
OT  - *Summary Report
GN  - PIP: Also in International Family Planning Perspectives 6(4):125-30, Dec 1980
GN  - PIP: TJ: FAMILY PLANNING PERSPECTIVES.
EDAT- 1980/11/01 00:00
MHDA- 1980/11/01 00:01
CRDT- 1980/11/01 00:00
PHST- 1980/11/01 00:00 [pubmed]
PHST- 1980/11/01 00:01 [medline]
PHST- 1980/11/01 00:00 [entrez]
PST - ppublish
SO  - Fam Plann Perspect. 1980 Nov-Dec;12(6):278-83.
