Prothrombin Utilization in Congenital Coagulation Deficiency States

Ch. A Owen Jr; J. H Thompson

doi:10.1055/s-0038-1654304

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1971; 25(02): 297-311
DOI: 10.1055/s-0038-1654304

Originalarbeiten – Original Articles – Travaux Originaux

Schattauer GmbH

Prothrombin Utilization in Congenital Coagulation Deficiency States

Authors

Ch. A Owen Jr M.D., Ph.D.

¹Rochester, Minnesota
J. H Thompson Ph.D.

¹Rochester, Minnesota

Abstract

Summary

The disappearance of plasma prothrombin was measured during the spontaneous clotting of whole blood from 15 normal adults, from patients lacking fibrinogen, factor V, VII, VIII, IX, X, XI, XII, or XIII, or Fletcher factor, from patients with von Willebrand’s disease or Glanzmann’s thrombasthenia, and from one patient with an unidentified prothromboplastic abnormality. Prothrombin utilization was normal in patients lacking fibrinogen or factor VII or XIII or who had Glanzmann’s thrombasthenia. Utilization was most abnormal in patients with the greatest deficiencies of factors V, VIII, IX, or XI. Patients lacking factor XII or Fletcher factor consumed prothrombin rapidly after an abnormal initial lag period. Within each group of patients with hemophilia A or von Willebrand’s disease, the lower the concentration of factor VIII the more slowly was prothrombin utilized, but with von Willebrand’s disease there was much more rapid prothrombin utilization than with hemophilia with higher levels of factor VIII. Patients with the most pronounced deficiencies of factor XI, factor XII, or Fletcher factor had abnormal platelet adhesiveness.

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References

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