Prothrombotic mechanisms based on the impairment of fibrinolysis in the antiphospholipid syndrome

Abstract

Antiphospholipid syndrome (APS) is a clinical autoimmune disorder characterised by thrombosis, venous or arterial, and recurrent pregnancy morbidity in association with the persistence of antiphospholipid antibodies (aPL). The clinical variety of aPL ranges from asymptomatic individuals to those with multiple organ thromboses and failure developing over a short period, also known as catastrophic APS. An increasing number of phospholipid-binding proteins with crucial functions in the regulation of blood coagulation and fibrinolysis are targeted by APS-related autoantibodies. Disruption of fibrinolysis is one of the proposed pathophysiological mechanisms for the APS. There are some experimental data for an association between impaired overall fibrinolytic activity and autoimmune aPL; however, evidence is still inconclusive and more studies are needed in this area. In this article, we review the evidence by which aPL may disturb fibrinolysis.