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Kininogen deficiency in Fitzgerald trait: role of high molecular weight kininogen in clotting and fibrinolysis.

Abstract
Plasma from an asymptomatic person with defects in blood coagulation, release of kinin, and evolution of fibrinolytic activity upon contact with a foreign surface was deficient in kininogen. The coagulation defect was identified as "Fitzgerald trait." A preparation of high molecular weight kininogen repaired the defects in clotting, kinin release and fibrinolysis, but a preparation of low molecular weight kininogen did not. Therefore, Fitzgerald factor appears to be a high molecular weight kininogen. The site of action of the kininogen appears to be after that of activated Hageman factor and kallikrein in the generation of clot-promoting activity through activation of plasma thromboplastin antecedent (PTA).
AuthorsV H Donaldson, H I Glueck, M A Miller, H Z Movat, F Habal
JournalThe Journal of laboratory and clinical medicine (J Lab Clin Med) Vol. 87 Issue 2 Pg. 327-37 (Feb 1976) ISSN: 0022-2143 [Print] United States
PMID1245795 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Kininogens
  • Kinins
  • Factor VIII
  • Factor IX
  • Factor XII
  • Factor XI
  • Prekallikrein
Topics
  • Adult
  • Blood Coagulation
  • Blood Coagulation Disorders (blood, genetics, metabolism)
  • Blood Coagulation Tests
  • Factor IX (analysis)
  • Factor VIII (analysis)
  • Factor XI (analysis)
  • Factor XII (analysis)
  • Female
  • Fibrinolysis
  • Humans
  • Kininogens (blood)
  • Kinins (metabolism)
  • Male
  • Molecular Weight
  • Pedigree
  • Prekallikrein

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