Mechanisms of thrombosis in the antiphospholipid syndrome

Abstract

Patients with antiphospholipid syndrome (APS) have an increased risk of venous and arterial thrombosis, recurrent pregnancy loss, and/or thrombocytopenia. These clinical manifestations are associated with the presence of antiphospholipid antibodies (aPL), including anticardiolipin antibodies (aCL) and lupus anticoagulant (LA). Despite the strong association between aPL and thrombosis, the pathogenic role of aPL in the development of thrombosis has not been fully elucidated. It is known that aPL are directed against phospholipid-binding proteins expressed on, or bound to, the surface of vascular endothelial cells or platelets. The involvement of aPL in clinically important normal procoagulant and anticoagulant reactions and on certain cells altering the expression and secretion of various molecules may offer a basis for definitive investigations of possible mechanisms by which aPL may develop thrombotic events in patients with APS. In this article, we review the mechanisms by which aPL may develop thrombotic events in patients with APS.