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Factor X is a vitamin K-dependent serine protease that is synthesized in the liver. Its biological half-life is 24 to 48 hours. Factor X participates in both intrinsic and extrinsic pathways of coagulation (final common pathway) by serving as the enzyme (factor Xa) in the prothrombinase complex.
Congenital factor X deficiency is rare. Acquired deficiency associated with liver disease, warfarin therapy, vitamin K deficiency, systemic amyloidosis and inhibitors (rare). Deficiency may cause prolonged prothrombin time and activated partial thromboplastin time.
Diagnosing deficiency of coagulation factor X, congenital or acquired
Evaluating hemostatic function in liver disease
Investigation of prolonged prothrombin time or activated partial thromboplastin time
Acquired deficiency more common than congenital
Heterozygotes: 25% to 50%
Liver disease, warfarin therapy, or vitamin K deficiency may lower factor X levels.
Normal, full-term newborn infants or healthy premature infants may have decreased levels (> or =15-20%) which may not reach adult levels for > or =180 days postnatal.*
*See Pediatric Hemostasis References in Coagulation Studies in Special Instructions.
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2. Brenner B, Kuperman AA, Watzka M, Oldenburg J: Vitamin K-dependent coagulation factors deficiency. Semin Thromb Hemost 2009 Jun;35(4):439-446
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4. Girolami A, Ruzzon E, Tezza F, et al: Congenital FX deficiency combined with other clotting defects or with other abnormalities: a critical evaluation of the literature. Haemophilia 2008;14(2):323-328
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