Association of IgA Anti-ß2 Glycoprotein I with Clinical and Laboratory Manifestations of Systemic Lupus Erythematosus

Journal of Rheumatology - Tập 38 Số 1 - Trang 64-68 - 2011
Taraneh Mehrani1, Michelle Petri2,3,4,5,6
1Department of Medicine, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 7500, Baltimore, MD 21205, USA.
2Department of Medicine and Director, Johns Hopkins Lupus Center, Johns Hopkins University School of Medicine.
3Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, and the
4Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 7500, Baltimore, MD 21205, USA.
5National Institutes of Arthritis and Musculoskeletal and Skin Diseases (RO1 AR043727) and the Johns Hopkins University Institute for Clinical and Translational Research, Clinical Research Units. T. Mehrani, MD, Rheumatology Fellow, University of California, Irvine;
6University of California, Irvine, California, USA.

Tóm tắt

Objective.IgA isotypes of anticardiolipin and anti-ß2 glycoprotein I (anti-ß2-GPI) are omitted from the revised antiphospholipid syndrome (APS) classification criteria. Multiple studies have found a high prevalence of IgA anti-ß2-GPI in systemic lupus erythematosus (SLE). We determined the frequency and associations of IgA anti-ß2-GPI in a cohort of patients with SLE.Methods.Anti-ß2-GPI was measured in 796 patients with SLE (93% women, 53% white, 38% African American, mean age 45 yrs). IgA anti-ß2-GPI (> 20 phospholipid units) was found in 20%. Using a cohort database, associations with cumulative thrombotic and other manifestations were determined.Results.Of patients with SLE who demonstrated IgA anti-ß2-GPI positivity, about 6% had transient ischemic attack (p = 0.070), 4% had superficial thrombophlebitis (p = 0.647), 20% had deep venous thrombosis (p = 0.003), 4% had other venous thrombosis (p = 0.827), 12% had stroke (p = 0.050), and 1% had myocardial infarction (p = 0.397).Conclusion.IgG anti-ß2-GPI has the strongest association with thrombosis in SLE. However, IgA anti-ß2-GPI was more strongly associated with deep venous thrombosis and with stroke than was IgM. These results indicate that assessment of IgA anti-ß2-GPI is associated with thrombosis in SLE, and that the classification criteria for APS should be revised to include IgA anti-ß2-GPI in patients with SLE.

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