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Factor II (prothrombin) is a vitamin K-dependent serine protease synthesized in liver. It participates in the final common pathway of coagulation, as the substrate for the prothrombinase enzyme complex. Prothrombin is the precursor of thrombin (IIa) which converts fibrinogen to fibrin. Plasma biological half-life is about 3 days.
Deficiency of factor II may cause prolonged prothrombin time and activated partial thromboplastin time. Deficiency may result in a bleeding diathesis.
Diagnosing a congenital deficiency (rare) of coagulation factor II
Evaluating acquired deficiencies associated with liver disease or vitamin K deficiency, oral anticoagulant therapy, and antibody-induced deficiencies (eg, in association with lupus-like anticoagulant)
Determining warfarin treatment stabilization in patients with nonspecific inhibitors (ie, lupus anticoagulant)
Determining degree of anticoagulation with warfarin to correlate with level of protein S
Investigation of prolonged prothrombin time or activated partial thromboplastin time
Liver disease, vitamin K deficiency, or warfarin anticoagulation can cause decreased factor II activity.
Homozygotes generally have levels of <25%
Heterozygotes generally have levels of <50%
Normal newborn infants may have levels of 25% to 50%
Factor II is 1 of the last vitamin K-dependent coagulation factors to decrease after starting warfarin therapy and 1 of the last to return to normal when anticoagulation is discontinued. It may take 10 to 14 days for a return to baseline levels.
Normal, full-term newborn infants or healthy premature infants may have decreased levels (> or =25%) which may remain below adult levels for > or =180 days postnatal.*
*See Pediatric Hemostasis References in Coagulation Studies in Special Instructions.
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4. Brenner B, Kuperman AA, Watzka M, Oldenburg J: Vitamin K-dependent coagulation factors deficiency. Semin Thromb Hemost 2009 Jun;35(4):439-446