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Factor XII is synthesized in the liver. Its biological half-life is 40 to 50 hours. Factor XII is a component of the contact activation system and is involved in both intrinsic pathway and fibrinolytic system
Factor XII deficiency is often discovered when activated partial thromboplastin time is found to be unexpectedly long. The deficiency causes no known bleeding disorder.
An association between severe factor XII deficiency and thrombosis risk has been proposed, but not proven.
Diagnosing deficiency of coagulation factor XII
Determining cause of prolonged activated partial thromboplastin time
Acquired deficiency is associated with liver disease, nephritic syndrome, and chronic granulocytic leukemia.
Congenital homozygous deficiency: 20%
Congenital heterozygous deficiency: 20% to 50%
Deficiencies of other contact activator proteins (prekallikrein, high molecular weight kininogen) can also cause prolonged activated partial thromboplastin time but do not cause clinical bleeding.
Normal, full-term newborn infants or healthy premature infants may have decreased levels (> or =15% to 20%) which may not reach adult levels for > or =180 days postnatal.*
*See Pediatric Hemostasis References in Coagulation Studies in Special Instructions.
Renne T, Schmaier AH, Nickel KF, et al: In vivo roles of factor XII. Blood 2012 Nov 22;120(22):4296-4303