Elevated plasmin-α2-antiplasmin complex levels in hereditary angioedema: Evidence for the in vivo efficiency of the intrinsic fibrinolytic system

Torbjôrn Nilsson; Ove Back

doi:10.1016/0049-3848(85)90318-4

Paper| Volume 40, ISSUE 6, P817-821, December 15, 1985

Elevated plasmin-α₂-antiplasmin complex levels in hereditary angioedema: Evidence for the in vivo efficiency of the intrinsic fibrinolytic system

Torbjôrn Nilsson
Torbjôrn Nilsson
Affiliations
Departments of Clinical Chemistry and Dermatology, University Hospital, S-901 85, Umeå, Sweden
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Ove Back
Ove Back
Affiliations
Departments of Clinical Chemistry and Dermatology, University Hospital, S-901 85, Umeå, Sweden
Search for articles by this author

DOI:https://doi.org/10.1016/0049-3848(85)90318-4

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Abstract

The contact activation and fibrinolytic systems were assessed in 5 patients with hereditary angioedema (HAE). Reductions in F XII levels and increase in kallikrein-like activity in some patients indicated activation of the contact (intrinsic) system of coagulation. A great increase in plasmin-α₂-antiplasmin complex in all subjects indicated that in this disease, there is a constantly ongoing fibrinolysis.

Since C1-inhibitor, the deficient protein in HAE, is a poor inhibitor of the well-known extrinsic (tissue-type) plasminogen activator, but the major inhibitor of the contact activation system and a related Math Eq

phenomenon termed intrinsic fibrinolysis, our data show that this fibrinolytic system is also sometimes operating efficiently Math Eq

. Furthermore, the known clinical data on HAE are compatible with a role of intrinsic fibrinolysis in the pathophysiology of this disease.

Keywords

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Article info

Publication history

Accepted: September 11, 1985

Received: July 15, 1985

Identification

DOI: https://doi.org/10.1016/0049-3848(85)90318-4

Copyright

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