The interaction between platelets and factor VII/VIIa

Abstract

Blood coagulation normally occurs when factor VII interacts with its specific cellular receptor, tissue factor, which is exposed when a blood vessel is severed. The factor VII/tissue factor complex then initiates a cascade of proteolytic reactions involving factors IX, X, prothrombin and fibrinogen, culminating in the formation of a fibrin clot. The role of platelets in the initiation phase of blood coagulation is still unclear. It has been postulated that platelets bind activated factor VIIa independently of tissue factor, and that this interaction forms the basis of the usefulness of high-dose recombinant factor VIIa in treating hemophiliacs with inhibitory antibodies, and other thrombocytopenia-like syndromes. In this review, we will examine the evidence for and against such an hypothesis, as well as discuss an alternative mechanism for the efficacy of high-dose factor VIIa in treating hemophilic patients with inhibitors.