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The Antiphospholipid Syndrome

The antiphospholipid syndrome (APS) is an autoimmune disorder in which vascular thrombosis or recurrent pregnancy losses occur in conjunction with a laboratory evidence of either a lupus anticoagulant antibodies (LAA) or anticardiolipin immunoglobulin G (IgG) or immunoglobulin M (IgM) antibodies (ACA) on 2 or more occasions at least 6 weeks apart. It is the most common of the hypercoagulability syndromes, accounting for about 28%. Other common causes of hypercoagulability include activated protein C resistance, elevated coagulation factor VIII levels, malignancy, sticky platelet syndrome, protein C deficiency, protein S deficiency, and homocystinemia. Antiphospholipid syndrome is classified as primary in the absence of another major autoimmune disorder such as systemic lupus erythematosus (SLE) and as secondary in the presence of such a disorder. The first serological clue of APS came with the observation of a biologically false-positive test for the Venereal Disease Research Laboratory (VDRL) test for syphilis in patients with SLE, but without clinical evidence of syphilis. It was further recognized that patients with SLE often exhibited an apparent anticoagulant activity and prolongation of the partial thromboplastin time, which used a phospholipid extract of animal brain (cephalin) as a platelet equivalent to accelerate coagulation. Paradoxically, this anticoagulant activity was associated with thrombosis, embolism, and recurrent pregnancy losses, rather than bleeding problems. In 1983, a quantitative immunologic test was developed for detection of antibodies against the anionic phospholipid cardiolipin. Cardiolipin is a mitochondrial phospholipid and is the primary antigen in the syphilis test. In the 1990s, it was discovered that some anticardiolipin antibodies require the plasma phospholipid-binding protein 2-glycoprotein I ( 2-GPI) to bind to cardiolipin and that this cofactor dependency is present in ACA from patients with APS or SLE, but generally not from patients with syphilis or other infections. Although LAA and ACA often coexist, they are not identical. To detect LAA, one must first document prolongation of coagulation in at least 1 phospholipid-dependent in vitro coagulation assay such as dilute prothrombin time, activated partial thromboplastin time, dilute activated par-