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Coagulation factor X, also known as Stuart-Prower factor, is a vitamin K-dependent serine protease synthesized in the liver and encoded by the F10 gene on chromosome 13q34. It plays a pivotal role in the coagulation cascade as the first enzyme of the common pathway, activated by either the extrinsic (factor VIIa-tissue factor) or intrinsic (factor IXa-VIIIa) pathways to form factor Xa. Factor Xa associates with factor Va, calcium, and phospholipids on platelet surfaces to form the prothrombinase complex, which efficiently converts prothrombin to thrombin, driving fibrin clot formation and thrombus generation. Deficiency in factor X, occurring at a frequency of 1 in 500,000 to 1 million individuals, is an autosomal recessive disorder leading to severe bleeding tendencies, including easy bruising, hemarthrosis, and prolonged bleeding after trauma or surgery, with severe cases showing less than 1% activity. Diagnosis involves prolonged PT and aPTT that correct with mixing studies, confirmed by specific factor X functional assays. Therapeutically, it is targeted with plasma-derived products like fresh frozen plasma or prothrombin complex concentrates for replacement during bleeding episodes, though challenges include risks of thrombosis if levels exceed 50% and lack of evidence-based dosing guidelines due to rarity. Recombinant factor X variants are under exploration to improve treatment safety and efficacy.
Replacement therapy to restore factor X levels for hemostasis, Prothrombinase complex formation to activate prothrombin
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