Reviewer: Jeremy Parsons, M.D. (see Reviewers page)
Revised: 8 June 2012, last major update June 2012
Copyright: (c) 2002-2012, PathologyOutlines.com, Inc.
● Consists of coagulation factors unknown in the 1950ís
● Includes factor XII (Hageman factor), prekallikrein (PK; Fletcher factor), high molecular weight kininogen (Williams, Flaujeac or Fitzgerald factor); some authors include factor XI
● Made in the liver
● Decreased activity is associated with liver disease, hepatic immaturity in newborns, antiphospholipid syndrome, Asian descent (for factor XII)
● Homozygous deficiencies are rare, autosomal recessive; cause very long PTT but no bleeding disorders and no definite association with hypercoagulability
● Contact pathway may play a large role in inflammation, as patients with factor XI deficiency often have repeated infections
● Recommended to not measure their activity in routine evaluation of patients with arterial or venous thromboembolism or acute coronary syndromes (Arch Pathol Lab Med 2002;126:1382)
● Homozygous deficiencies cause prolonged PTT
● Heterozygous deficiencies have near normal PTT
● The test for a particular contact factor is based on the ability of the patientís plasma to correct a prolonged PTT in plasma that is deficient in the factor being tested
● Even though the PTT may be decreased by deficiencies of contact factors, this does not necessarily correlate with increased bleeding risk
● Roberts H, Escobar M (2007). Less common congenital disorders of hemostasis. In C Kitchens, B Alving, C Kessler (Eds). Consultative hemostasis and thrombosis (pp 71-73). Saunders Elsevier
End of Coagulation > General > Contact System
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