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

Ben Parker, Murray B. Urowitz, Dafna D. Gladman, Mark Lunt, Rachelle Donn, Sang Cheol Bae, Jorge Sanchez-Guerrero, Juanita Romero-Diaz, Caroline Gordon, Daniel J. Wallace, Ann E. Clarke, Sasha Bernatsky, Ellen M. Ginzler, David A. Isenberg, Anisur Rahman, Joan T. Merrill, Graciela S. Alarcón, Barri J. Fessler, Paul R. Fortin, John G. HanlyMichelle Petri, Kristjan Steinsson, Mary Anne Dooley, Susan Manzi, Munther A. Khamashta, Rosalind Ramsey-Goldman, Asad A. Zoma, Gunnar K. Sturfelt, Ola Nived, Cynthia Aranow, Meggan Mackay, Manuel Ramos-Casals, Ronald F. van Vollenhoven, Kenneth C. Kalunian, Guillermo Ruiz-Irastorza, S. Sam Lim, Diane L. Kamen, Christine A. Peschken, Murat Inanc, Ian N. Bruce

Research output: Contribution to journalArticlepeer-review

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 (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 persistent 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. © 2014 BMJ Publishing Group Ltd & European League Against Rheumatism.
Original languageEnglish
JournalAnnals of the rheumatic diseases
DOIs
Publication statusPublished - 1 Apr 2014

Keywords

  • Cardiovascular Disease
  • Inflammation
  • Systemic Lupus Erythematosus

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