Anticardiolipin Antibody, Thrombosis and Atherosclerosis

Abstract

This chapter discusses the current understanding of the role of anticardiolipin antibody, thrombosis, and atherosclerosis in the antiphospholipid syndrome (APS). During the late seventies, it became apparent that a subgroup of patients with systemic lupus erythematosus (SLE) had a clotting disorder, and a constellation of feature, which included strokes, venous thrombosis, recurrent abortion, and occasional thrombocytopenia. Later, these symptoms were called antiphospholipid syndrome (APS). If a patient has one or more of the triad—thrombosis, recurrent abortions, and thrombocytopenia—by positive tests for anticardiolipin antibodies (aCL) and/or lupus anticoagulant (LA), antiphospholipid antibodies (aPL), the patient is diagnosed to suffer from APS. The most frequently reported association with aPL is deep vein thrombosis (DVT). In clinical manifestations of arterial occlusion associated with aPL, strokes which are often preceded by transient ischemic attacks, were the most frequent arterial events encountered in these patients. Recurrent fetal losses occur in patients with the APS, whether in association with defined SLE, or lupus-like disease. These fetal losses are associated with thrombosis of the placental vessels and subsequent infarction resulting in placental insufficiency, fetal growth retardation, and ultimately fetal losses. There is a strong association between thrombocytopenia and the presence of aCL in patients with SLE. W/B F1 male mice that develop lupus nephritis, myocardial infarction, and thrombocytopenia in association with aCL, may be suitable animal model for use in elucidating the role of aCL and β2GPI in thrombus formation and aCL-associated thrombocytopenia frequently found in patients with APS.