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Factor XI is synthesized in the liver. Its biological half-life is 60 to 80 hours. Factor XI is a component of intrinsic coagulation pathway which, when activated, activates factor IX to IXa.
Factor XI deficiency may cause prolonged partial thromboplastin time. Deficiency associated with mild bleeding diathesis, but there is poor correlation between activity level and clinical bleeding. A relatively high incidence of congenital deficiency occurs among Ashkenazi Jewish descent (hemophilia C).
Diagnosing deficiency of coagulation factor XI
Investigation of prolonged activated partial thromboplastin time
Acquired deficiency is associated with liver disease and rarely inhibitors.
Heterozygotes: 20% to 60%
Decreased plasma levels of factor XI do not correlate well with bleeding risk.
Normal, full-term newborn infants or healthy premature infants may have decreased levels (> or =10%) which may not reach adult levels for > or =180 days postnatal.*
*See Pediatric Hemostasis References in Coagulation Studies in Special Instructions.
1. He R, Chen D, He S: Factor XI: hemostasis, thrombosis, and antithrombosis. Thromb Res 2012 May;129(5):541-550
2. Martin-Salces M, Jimenez-Yuste V, Alvarez MT, et al: Review: Factor XI deficiency: review and management in pregnant women. Clin Appl Thromb Hemost 2010;16 (2):209-213
3. Seligsohn U. Factor XI in haemostasis and thrombosis: past, present and future. Thromb Haemost 2007;98(1):84-89
4. Santoro R, Prejano S, Iannaccaro P. Factor XI deficiency: a description of 34 cases and literature review. Blood Coagul Fibrinolysis 2011Jul;22(5):431-435