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Clinical and epidemiological research
Risk and protective factors for thrombosis in systemic lupus erythematosus: results from a large, multi-ethnic cohort
  1. R Kaiser,
  2. C M Cleveland,
  3. L A Criswell
  1. Rosalind Russell Medical Research Center for Arthritis, Department of Medicine, University of California, San Francisco, California, USA
  1. Lindsey A Criswell, UCSF Division of Rheumatology, 374 Parnassus, 1st Floor, Box 0500, San Francisco, CA 94143, USA; Lindsey.Criswell{at}ucsf.edu

Abstract

Objectives: Few studies have examined thrombosis in systemic lupus erythematosus (SLE), none have included Asian-Americans, and most have had small sample sizes. We analysed risk factors for thrombosis in a large, multi-ethnic SLE cohort.

Methods: We studied 1930 SLE subjects, including Caucasians, African-Americans, Asian-Americans and Hispanics. Data were derived from questionnaires and medical records. Documented history of thrombosis was the primary outcome. Explanatory variables included age at SLE diagnosis, gender, ethnicity, disease duration, smoking, antiphospholipid antibody (aPL) status, nephritis and specific medications.

Results: Smoking (OR 1.26, p = 0.011), longer disease duration (OR 1.26 per 5 years p = 0.027×10−7), nephritis (OR 1.35, p = 0.036), aPL positivity (OR 3.22, p<10−9) and immunomodulating medication use (OR 1.40, p = 0.011) were statistically significant risk factors for thrombosis. Younger age at SLE onset was protective (OR 0.52 for age ⩽20, p = 0.001). After adjusting for disease severity and incorporating propensity scores, hydroxychloroquine use remained significantly protective for thrombosis (OR 0.62, p = 4.91×10−4).

Conclusions: This study confirms that older age at onset, longer disease duration, smoking, aPL positivity, history of nephritis and immunomodulating medication use are risk factors for thrombosis in SLE. These data are the first to confirm in a large and ethnically diverse SLE cohort that hydroxychloroquine use is protective for thrombosis.

https://doi.org/10.1136/ard.2008.093013

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    Footnotes

    • Competing interests: None.

    • Funding: Sponsor details: Arthritis Foundation Post-Doctoral Fellowship Award, Kirkland Scholar Award, and NIH grants R01 AR22804, K24 AR02175 and P60 AR0533008. This study was performed in part in the General Clinical Research Center, Moffitt Hospital, University of California, San Francisco, California, USA, with funds provided by the National Center for Research Resources, 5 M01 RR-00079, US Public Health Service.