Pathogenesis of Fibrinolysis in Defibrination Syndrome: Effect of Heparin Administration

Author:

MERSKEY CLARENCE12,JOHNSON ALAN J.13,PERT JAMES H.14,WOHL HERBERT15

Affiliation:

1. Department of Medicine and Unit for Research in Aging, Albert Einstein College of Medicine, and the Bronx Municipal Hospital Center, New York, N. Y.; the American National Red Cross Research Laboratories and the Department of Medicine, New York University-Bellevue Medical Center, New York, N. Y.; the American National Red Cross Research Laboratories and the Department of Medicine, George Washingt

2. Department of Medicine, Albert Einstein College of Medicine of Yeshiva University; Associate Visiting Physician in Medicine, Bronx Municipal Hospital Center, New York, N. Y.

3. Department of Medicine, New York University School of Medicine; Associate Director of American National Red Cross Research Laboratory, Eastern Division; Associate Attending in Medicine, New York University Hospital, New York, N. Y.

4. Blood Program, American National Red Cross, and Assistant Clinical Professor of Medicine, George Washington University School of Medicine, Washington, D. C.

5. Department of Medicine, Albert Einstein College of Medicine of Yeshiva University; Assistant Visiting Physician in Medicine, Bronx Municipal Hospital Center, New York, N. Y.

Abstract

Abstract 1. Spontaneous local fibrinolysis occurred with, and was probably a consequence of thrombosis, with defibrination in vivo. 2. The efficacy of heparin in the prevention of defibrination was clearly demonstrated; warfarin therapy seemed to be ineffective. 3. The efficacy of heparin in the prevention of the associated fibrinolysis was clearly inferred. 4. Serum immunoelectrophoresis against anti-fibrinogen sera demonstrated abnormal precipitin bands, during defibrination and fibrinolysis, which disappeared during heparin administration. 5. The serum bands showed immunologic identity with in vitro plasmin digests of fibrinogen and the intensity and position of these precipitin bands appeared to depend on the amount of fibrinogen and the duration of the in vivo digestion period. 6. In this hypofibrinogenemic state, defibrination was indicated by markedly reduced levels of anti-hemophilic factor and Factor V and a fall in blood platelets. The presence of fibrinolysis was shown by the lowered levels of plasminogen, streptokinase and urokinase inhibitors, prolonged thrombin clotting times and fibrinolytic breakdown products in the serum even though little or no lysis occurred on fibrin plates and the euglobulin lysis times were within normal limits. 7. The administration of fibrinolytic inhibitors is strongly contraindicated under these circumstances.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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2. Response to Heparin of Spontaneous Disseminated Intravascular Coagulation in the Dog;Zentralblatt für Veterinärmedizin Reihe A;2010-05-13

3. Reference;Acta Medica Scandinavica;2009-04-24

4. References;Acta Medica Scandinavica;2009-04-24

5. 10. TANNED RED CELL HEMAGGLUTINATION INHIBITION IMMUNOASSAY FOR FIBRINOGEN-FIBRIN-RELATED ANTIGEN (“Fibrinolytic Degradation Products”) IN HUMAN SERUM*;Scandinavian Journal of Haematology;2009-04-24

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