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Factor IX is a vitamin K-dependent serine protease synthesized in the liver and participates in the intrinsic coagulation pathway. Its biological half-life is 18 to 24 hours.
Congenital deficiency inherited as an X-linked recessive bleeding disorder (hemophilia B). Severe deficiency (<1%) characterized by hemarthroses, deep tissue bleeding, excessive bleeding with trauma and ecchymoses.
Acquired deficiency associated with liver disease, vitamin K deficiency, warfarin therapy and inhibitors (rare).
Diagnosing deficiencies, particularly hemophilia B (Christmas disease)
Assessing the impact of liver disease on hemostasis
Investigation of a prolonged activated partial thromboplastin time
Acquired deficiency is more common than congenital.
Mild hemophilia B: 5% to 50%
Moderate hemophilia B: 1% to 5%
Severe hemophilia B: <1%
Liver disease, warfarin therapy, or vitamin K deficiency may lower factor IX levels.
Normal, full-term newborn infants or healthy premature infants may have decreased levels (> or =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. Franchini M, Lippi G, Favaloro EJ: Acquired inhibitors of coagulation factors: part II. Semin Thromb Hemost 2012 Jul;38(5):447-453
3. Carcao MD: The diagnosis and management of congenital hemophilia. Semin Thromb Hemost 2012 Oct;38(7):727-734