Factor V Resistance To Activated Protein C (Apc)

Mutations of factor V make it resistant to the normal cleavage and inactivation by activated protein C, and promote the development of venous thrombosis.

Mutations of factor V make it resistant to the normal cleavage and inactivation by activated protein C, and promote the development of venous thrombosis.

(See also Thrombotic diseases at a glance.) Mutations of the factor V make it resistant to the normal cleavage and inactivation by activated protein C, and promote the development of venous thrombosis. Activated protein C (APC) neutralized in complex with Protein S, the coagulation factors Va and VIIIa thus inhibiting coagulation. To date, several mutations in the factor V gene have been described. Each of them results in resistance to inactivation by APC and consequently to an increased risk of thrombosis. Factor V Leiden is the most common mutation. Homozygous mutations increase the risk of thrombosis again significantly compared to the heterozygous mutations. Scheme of blood clotting. Factor V Leiden as Einzelgenmutation occurs in about 5% of the European population. In Asian or African populations of this gene defect occurs much less frequently. It is detectable in 20-60% of patients with spontaneous venous thrombosis. Diagnostic plasma clotting sample Diagnosis is by a functional plasma clotting assay (z. B. no extension of PTT with patient plasma in the presence of activated protein C with snake venom) and molecular analysis of the factor V gene found. Anticoagulation therapy with anticoagulation A parenteral heparin or low molecular weight heparin, followed by oral warfarin, is used for venous thrombosis or for the prophylaxis of patients at increased risk of thrombosis (for. Example, by immobilization, heavy injury, surgery). It is not yet known if the newer oral anticoagulants, either thrombin (dabigatran) or factor Xa (z. B. rivaroxaban, apixaban) inhibit can be used for this disorder instead of warfarin.

Health Life Media Team

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