Antibodies to β<sub>2</sub>‐glycoprotein I and clinical manifestations in patients with systemic lupus erythematosus

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<jats:title>Abstract</jats:title><jats:p><jats:italic>Objective</jats:italic>. To investigate whether anticardiolipin antibodies (aCL) in patients with systemic lupus erythematosus (SLE) bind to β<jats:sub>2</jats:sub>‐glycoprotein I (β<jats:sub>2</jats:sub>GPI), and to search for a relationship between the presence of IgG and/or IgM anti‐β<jats:sub>2</jats:sub>GPI antibody and clinical manifestations in SLE patients.</jats:p><jats:p><jats:italic>Methods</jats:italic>. IgG and IgM anti‐β<jats:sub>2</jats:sub>GPI in 308 Japanese SLE patients were measured using phospholipid‐independent enzyme immunoassays. Relationships to clinical histories and to various laboratory data were examined.</jats:p><jats:p><jats:italic>Results</jats:italic>. The values of anti‐β<jats:sub>2</jats:sub>GPI and aCL, as measured by conventional enzyme immunoassay, showed a strong correlation, but the anti‐β<jats:sub>2</jats:sub>GPI assay was more useful in distinguishing β<jats:sub>2</jats:sub>GPI‐dependent aCL from β<jats:sub>2</jats:sub>GPI‐independent aCL. The presence of IgG anti‐β<jats:sub>2</jats:sub>GPI was associated with an increased frequency of a history of thrombosis. Comparisons of various laboratory data suggested that the titer of anti‐β<jats:sub>2</jats:sub>GPI may fluctuate with disease activity.</jats:p><jats:p><jats:italic>Conclusion</jats:italic>. The results suggest that pathogenic aCL is directed against structurally altered β<jats:sub>2</jats:sub>GPI and that enzyme immunoassay for anti‐β<jats:sub>2</jats:sub>GPI may prove useful in evaluating the risk of thrombosis and monitoring the clinical course in patients with SLE.</jats:p>

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