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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
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.
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.
Acquired deficiency more common than congenital
Heterozygotes: 25% to 50%
Liver disease, warfarin therapy, or vitamin K deficiency may lower factor X levels.
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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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