Prothrombin consumption, serum prothrombic activity and prothrombin conversion accelerator in hemophilia and thrombocytopenia.

Attention has recently been focused on the consumption of prothrombin during blood coagulation. Studies of the velocity of prothrombin conversion to thrombin have yielded important information concerning the clotting defect in various hemorrhagic disorders. Thrombin evolution is retarded in the coagulation of hemophilic blood (1-5), thrombocytopenic blood (3, 4, 6, 7) and blood exposed to siliconized surfaces (8). This is reflected in the high residual prothrombic activity of the serum. Precisely how much prothrombin is consumed per unit of time is, however, not clear. Obviously, prothrombin consumption can be computed from the difference between the prothrombin concentration of serum and that of its parent plasma. The reliability of this computation rests upon the specificity of methods for measuring the concentration of prothrombin in both plasma and serum. The one-stage procedure measures the velocity of thrombin formation in the presence of optimal thromboplastin and calcium. In applying it to serum one must exclude the possibility that in the transition from plasma to serum substances arise which affect the velocity of prothrombin conversion. Convincing evidence exists, however, that during coagulation prothrombin conversion accelerators evolve which are demonstrable in serum (9, 10). Observations presented in this paper show that such an accelerator can be obtained from hemophilic, thrombocytopenic and silicone.8 sera and that it contributes toward their high one-stage