C Tajima1, Y Suzuki, Y Mizushima, Y Ichikawa. 1. Department of Internal Medicine and Laboratory Medicine, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki, Japan.
Abstract
OBJECTIVE: To clarify whether immunoglobulin A (IgA) antiphospholipid antibodies (aPL) are an independent risk factor for specific manifestations of collagen vascular diseases. METHODS: We determined IgG, IgM, and IgA anticardiolipin antibodies (aCL) and lupus anticoagulant (LAC) in 77 patients with various collagen diseases. Fifty-four patients who had positive results for either or both antibody classes were compared to 23 patients with systemic lupus erythematosus who had none of these antibodies. The association between the antibodies and clinical manifestations (thrombosis, fetal loss, thrombocytopenia, biological false positive test for syphilis, cutaneous manifestations, central nervous system involvement, and renal involvement) was analyzed. RESULTS: Of 54 patients with aPL, 33 showed significantly high levels of IgA aCL. Among them, IgA aCL coexisted with other aCL isotypes or LAC in 24 patients. The 9 patients with IgA aCL alone frequently had vasculitis associated manifestations, although thrombotic events and recurrent fetal loss were rare. Multivariate linear regression analysis showed that IgA aCL were independently associated with thrombocytopenia, skin ulcers, chilblain lupus, and vasculitis. There was also an association between IgM aCL and skin ulcers or chilblain lupus. CONCLUSION: Clinical manifestations of patients with IgA aCL differ from those of patients with IgG aCL. Determination of all 3 aCL isotypes and LAC is important to assess the risk of specific clinical manifestations in patients with aPL.
OBJECTIVE: To clarify whether immunoglobulin A (IgA) antiphospholipid antibodies (aPL) are an independent risk factor for specific manifestations of collagen vascular diseases. METHODS: We determined IgG, IgM, and IgA anticardiolipin antibodies (aCL) and lupus anticoagulant (LAC) in 77 patients with various collagen diseases. Fifty-four patients who had positive results for either or both antibody classes were compared to 23 patients with systemic lupus erythematosus who had none of these antibodies. The association between the antibodies and clinical manifestations (thrombosis, fetal loss, thrombocytopenia, biological false positive test for syphilis, cutaneous manifestations, central nervous system involvement, and renal involvement) was analyzed. RESULTS: Of 54 patients with aPL, 33 showed significantly high levels of IgA aCL. Among them, IgA aCL coexisted with other aCL isotypes or LAC in 24 patients. The 9 patients with IgA aCL alone frequently had vasculitis associated manifestations, although thrombotic events and recurrent fetal loss were rare. Multivariate linear regression analysis showed that IgA aCL were independently associated with thrombocytopenia, skin ulcers, chilblain lupus, and vasculitis. There was also an association between IgM aCL and skin ulcers or chilblain lupus. CONCLUSION: Clinical manifestations of patients with IgA aCL differ from those of patients with IgG aCL. Determination of all 3 aCL isotypes and LAC is important to assess the risk of specific clinical manifestations in patients with aPL.