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Factor V Resistance to Activated Protein C (APC)

By Joel L. Moake, MD, Professor Emeritus of Medicine;Senior Research Scientist and Associate Director, Baylor College of Medicine;J. W. Cox Laboratory for Biomedical Engineering, Rice University

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Mutations of factor V make it resistant to its normal cleavage and inactivation by activated protein C and predispose to venous thrombosis.

Activated protein C (APC), in complex with protein S, degrades coagulation factors Va and VIIIa, thus inhibiting coagulation. Any of several mutations to factor V make it resistant to inactivation by APC, increasing the tendency for thrombosis.

Factor V Leiden is the most common of these mutations. Homozygous mutations increase the risk of thrombosis more than do heterozygous mutations.

Pathways in blood coagulation.

Factor V Leiden as a single gene defect is present in about 5% of European populations, but it rarely occurs in native Asian or African populations. It is present in 20 to 60% of patients with spontaneous venous thrombosis.


  • Plasma coagulation assay

Diagnosis is based on a functional plasma coagulation assay (eg, the failure of patient's plasma PTT to become prolonged in the presence of snake venom–activated patient protein C) and on molecular analysis of the factor V gene.


  • Anticoagulation

Anticoagulation with parenteral heparin or low molecular weight heparin, followed by oral warfarin, is used for venous thrombosis or for prophylaxis for patients at increased thrombotic risk (eg, by immobilization, severe injury, surgery).

It is not yet known if the newer oral anticoagulants that inhibit either thrombin (dabigatran) or factor Xa (eg, rivaroxaban, apixaban) can be used in place of warfarin for this disorder.

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