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Author Notes:

Correspondence to Professor Ian N Bruce, Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal Research, Institute of Inflammation and Repair, Manchester Academic Health Science Centre, The University of Manchester, Oxford Road, Manchester M13 9PT, UK; ian.bruce@manchester.ac.uk

See publication for full list of authors.

Contributors: The study was conceived by INB, ML, MBU and DDG.

Data analysis and interpretation and manuscript preparation was performed by BP, MBU, DDG, ML and INB.

All authors contributed to data collection, critically reviewed and edited the manuscript and approved the final version.

The views expressed in this publication are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health.

Competing interests: None.

Subjects:

Research Funding:

his study was funded by the Canadian Institutes of Health Research (grant number 93695), Arthritis Research UK (Arthritis Research UK Epidemiology Unit Core Support Programme Grant) and independent research supported by the National Institute for Health Research (NIHR) Biomedical Research Unit Funding Scheme and the NIHR Manchester Biomedical Research Centre (BP, ML, INB, RD). INB is a NIHR Senior Investigator and is supported by Arthritis Research UK, the Manchester Academic Health Science Centre, the NIHR Biomedical Research Unit Funding Scheme, the NIHR Manchester Wellcome Trust Clinical Research Facility and the NIHR Manchester Biomedical Research Centre. Additional author support: BP (Arthritis Research Clinical Research Fellowship 18845); S-CB (Korea Healthcare Technology R&D project (A120404), Ministry for Health and Welfare, Republic of Korea); CG (Lupus UK, NIHR/Wellcome Trust Clinical Research Facility at University Hospital Birmingham NHS Foundation Trust and City Hospital, Sandwell and West Birmingham Hospitals NHS Trust, UK); RR-G (NIH grants UL1 RR025741, P60AR 30692, K24 AR 002138); MP (Hopkins Lupus Cohort NIH grant RD-1 43727); GR (Department of Education, Universities and Research, Basque Government); SB (Singer Family Fund for Lupus Research); MAD (NIH grant RR00046); PRF (tier 1 Canada Research Chair on Systemic Autoimmune Rheumatic Diseases, Université Laval); JGH (Canadian Institutes of Health Research, operating grant number 86526).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Rheumatology
  • CORONARY-HEART-DISEASE
  • TREATMENT PANEL-III
  • RISK-FACTORS
  • ACCELERATED ATHEROSCLEROSIS
  • DIABETES-FEDERATION
  • WOMEN
  • CHOLESTEROL
  • HYDROXYCHLOROQUINE
  • ASSOCIATION
  • PREVALENCE

Impact of early disease factors on metabolic syndrome in systemic lupus erythematosus: data from an international inception cohort

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Journal Title:

Annals of the Rheumatic Diseases

Volume:

Volume 74, Number 8

Publisher:

, Pages 1530-1536

Type of Work:

Article | Final Publisher PDF

Abstract:

Background The metabolic syndrome (MetS) may contribute to the increased cardiovascular risk in systemic lupus erythematosus (SLE). We examined the association between MetS and disease activity, disease phenotype and corticosteroid exposure over time in patients with SLE. Methods Recently diagnosed (>15 months) patients with SLE from 30 centres across 11 countries were enrolled into the Systemic Lupus International Collaborating Clinics (SLICC) Inception Cohort from 2000 onwards. Baseline and annual assessments recorded clinical, laboratory and therapeutic data. A longitudinal analysis of factors associated with MetS in the first 2 years of follow-up was performed using random effects logistic regression. Results We studied 1150 patients with a mean (SD) age of 34.9 (13.6) years and disease duration at enrolment of 24.2 (18.0) weeks. In those with complete data, MetS prevalence was 38.2% at enrolment, 34.8% at year 1 and 35.4% at year 2. In a multivariable random effects model that included data from all visits, prior MetS status, baseline renal disease, SLICC Damage Index <1, higher disease activity, increasing age and Hispanic or Black African race/ethnicity were independently associated with MetS over the first 2 years of follow-up in the cohort. Conclusions MetS is a persi stent phenotype in a significant proportion of patients with SLE. Renal lupus, active inflammatory disease and damage are SLE-related factors that drive MetS development while antimalarial agents appear to be protective from early in the disease course.

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Copyright Published by the BMJ Publishing Group Limited.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NoDerivs 3.0 Unported License (http://creativecommons.org/licenses/by-nd/3.0/).

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