Taraneh Mehrani1, Michelle Petri. 1. Department of Medicine, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 7500, Baltimore, MD 21205, USA. mpetri@jhmi.edu
Abstract
OBJECTIVE: IgA isotypes of anticardiolipin and anti-ß(2) glycoprotein I (anti-ß(2)-GPI) are omitted from the revised antiphospholipid syndrome (APS) classification criteria. Multiple studies have found a high prevalence of IgA anti-ß(2)-GPI in systemic lupus erythematosus (SLE). We determined the frequency and associations of IgA anti-ß(2)-GPI in a cohort of patients with SLE. METHODS: anti-ß(2)-GPI was measured in 796 patients with SLE (93% women, 53% white, 38% African American, mean age 45 yrs). IgA anti-ß(2)-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-ß(2)-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-ß(2)-GPI has the strongest association with thrombosis in SLE. However, IgA anti-ß(2)-GPI was more strongly associated with deep venous thrombosis and with stroke than was IgM. These results indicate that assessment of IgA anti-ß(2)-GPI is associated with thrombosis in SLE, and that the classification criteria for APS should be revised to include IgA anti-ß(2)-GPI in patients with SLE.
OBJECTIVE: IgA isotypes of anticardiolipin and anti-ß(2) glycoprotein I (anti-ß(2)-GPI) are omitted from the revised antiphospholipid syndrome (APS) classification criteria. Multiple studies have found a high prevalence of IgA anti-ß(2)-GPI in systemic lupus erythematosus (SLE). We determined the frequency and associations of IgA anti-ß(2)-GPI in a cohort of patients with SLE. METHODS: anti-ß(2)-GPI was measured in 796 patients with SLE (93% women, 53% white, 38% African American, mean age 45 yrs). IgA anti-ß(2)-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-ß(2)-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-ß(2)-GPI has the strongest association with thrombosis in SLE. However, IgA anti-ß(2)-GPI was more strongly associated with deep venous thrombosis and with stroke than was IgM. These results indicate that assessment of IgA anti-ß(2)-GPI is associated with thrombosis in SLE, and that the classification criteria for APS should be revised to include IgA anti-ß(2)-GPI in patients with SLE.
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