Recombinant factor VIIa is indicated for bleeding in hemophilia patients with inhibitors but carries a risk of adverse thromboembolic events.
Answers are grounded in this paper and cite their sources.
Requires thrombotic risk monitoring with recombinant factor VIIa use; reinforces guideline emphasis on selective application in hemophilia with inhibitors.
Recombinant activated factor seven (VIIa) is a vitamin K-dependent glycoprotein that is structurally similar to human plasma-derived factor VIIa. It has received approval from the Food and Drug Administration (FDA) for the treatment of bleeding episodes in patients with hemophilia A or B who have developed inhibitors to factor VIII or factor IX, respectively.1 It promotes hemostasis by activating the coagulation cascade. Complexing with tissue factor at the site of vascular injury, recombinant factor VIIa cleaves factor X to the enzyme-activated factor X. Factor X promotes the conversion of prothrombin to thrombin and of fibrinogen to fibrin, leading to the formation of a hemostatic plug.2,3 Factor VIIa (recombinant) has been primarily used in the treatment of bleeding episodes in hemophiliac patients with inhibitors to factor VIII or IX and patients with acquired he-mophilia due to auto-antibodies. The current recommended dose of factor VIIa (recombinant) in the treatment of bleeding episodes in these patients is 90 μg/kg i.v.1 In this population, factor VIIa (recombinant) has been associated with adverse thromboembolic events, including myocardial infarction, cerebrovascular infarct, venous thrombosis, and disseminated intravascular coagulopathy (DIC).1,4
No takes yet. Share an insight, caveat, or question.
Rudisill et al. (2006) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: