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Thromb Haemost 1971; 26(02): 325-331
DOI: 10.1055/s-0038-1653680
Originalarbeiten – Original Articles – Travaux Originaux
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The Role of Hageman Factor in Disseminated Intravascular Coagulation Induced by Septicemia, Neoplasia, or Liver Disease[*]

J. W Mason
1   Department of Pathology, Massachusetts General Hospital, Boston, Mass.
2   Pathology Service, Berkshire Medical Center, Pittsfield, Mass.
3   Department of Medicine of the Massachusetts General Hospital and Harvard Medical School, Boston, Mass.
,
R. W Colman
1   Department of Pathology, Massachusetts General Hospital, Boston, Mass.
2   Pathology Service, Berkshire Medical Center, Pittsfield, Mass.
3   Department of Medicine of the Massachusetts General Hospital and Harvard Medical School, Boston, Mass.
› Author AffiliationsThis investigation was supported by Grant HE-11519 from the National Institutes of Health.
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Publication Date:
24 July 2018 (online)

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Summary

The human plasma kallikrein system was assayed in patients with disseminated intravascular coagulation (DIC) induced by gram negative bacteremia, neoplasia and severe liver disease. Only the patients with gram negative septicemia showed activation of plasma kallikrein with concomitant depletion of kallikreinogen and kallikrein inhibition. Since the activation of kallikrein is a function of activated Hageman factor, it is suggested that in DIC associated with gram negative septicemia, Hageman factor activation may be involved in the DIC. In DIC associated with neoplasia or liver disease lack of Hageman factor activation should be considered.

* This study was presented in part at the Annual Meeting of the American Society of Clinical Pathologists, Sept. 17, 1969.


 

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