APL may be idiopathic or secondary when associated with other disorders. The two main aPL are the LA and the anticardiolipin antibody (ACL) occurring together in most cases but also independently. The antibody specificity is actually to |32-glycoprotein 1 (|32GP1), a phospholipid membrane-associated protein. Rarely antibodies to prothrombin co-exist and can cause hypoprothrombinaemia and bleeding. The mechanism of thrombosis is not clear; APL may act against other vitamin K dependent proteins PC and PS, or possibly the autoimmune state may lead to endothelial 400 damage and/or platelet activation.

Acquired thrombophilia due to APL is a much commoner cause of thrombosis than the congenital defects; the incidence depends on the patient group-e.g. 18% in young stroke patients, 21% young patients with Ml. The LA occurs in 1-2% of the population; most patients will not develop thrombosis.

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