Abstract

The deficiency in the conversion of prothrombin to thrombin which develops after administration of dicumarol appears to be due largely to decreased cothromboplastin activity. Both the development of this deficiency and the recovery from it tend to precede the accompanying changes in prothrombin itself, as measured by the two-stage method. In terms of deviation from normal, the deficiency in conversion often exceeds in magnitude the deficiency of prothrombin itself.

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