Thromb Haemost 1957; 01(02): 169-194
DOI: 10.1055/s-0038-1656170
Originalarbeiten – Original Article – Travaux Originaux
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Differentiation of the Factor VII Complex

Studies on the Stuart-Prower factor
F Bachmann
1   Coagulation Laboratory (Prof. F. Koller) of the Department of Medicine (Prof. W. Löffler), University of Zurich, Switzerland
,
F Duckert
1   Coagulation Laboratory (Prof. F. Koller) of the Department of Medicine (Prof. W. Löffler), University of Zurich, Switzerland
,
M Geiger
1   Coagulation Laboratory (Prof. F. Koller) of the Department of Medicine (Prof. W. Löffler), University of Zurich, Switzerland
,
P Baer
1   Coagulation Laboratory (Prof. F. Koller) of the Department of Medicine (Prof. W. Löffler), University of Zurich, Switzerland
,
F Koller
1   Coagulation Laboratory (Prof. F. Koller) of the Department of Medicine (Prof. W. Löffler), University of Zurich, Switzerland
› Author Affiliations
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Publication History

Publication Date:
08 June 2018 (online)

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Summary

A factor recently described and for which the designation Stuart-Prower Factor is proposed, was investigated. It is detected by the usual Factor VII assay but differs from this factor (Matching experiments with plasma and serum of Owren’s Factor VII deficient patient). Stuart-Prower factor is necessary for the conversion prothrombin-thrombin with tissue thromboplastin as well as for the formation of blood thromboplastin. Therefore lack of Stuart-Prower factor produces abnormal Quick’s prothrombin time (not normalized with Russell’s viper venom [Stypven]), and also abnormal prothrombin consumption, abnormal recalcification time and abnormal thromboplastin generation with serum. Matching experiments with plasma and serum of the patients of Graham and Hougie, Telfer Denson and Wright, and Beaumont and Bernard show that we are dealing with the same defect. Physiological and physico-chemical properties are indicated. The possible relationship between Stuart-Prower factor and Factor X is discussed. A critical review with 59 cases of the so-called Factor VII deficiency is given. Investigation of the family of our patient Delia B. indicates that the mode of inheritance is an intermediate autosomal one.