The antiphospholipid syndrome is now well recognized and is separable from SLE, but better quantitation of both the clinical elements and the serologic definitions is still needed. It is likely for autoimmune but not for infection-induced aPL that the antigen is not phospholipid itself but a complex formed by phospholipid and beta 2 glycoprotein I. There are few treatment trials yet published. Those that are available suggest that antiplatelet therapy or anticoagulant therapy are more valuable than is immunosuppression.
