The Consumption of Prothrombin during Coagulation: The Defect in Haemophilia and Thrombo-Cytopenic Purpura.
نویسنده
چکیده
During the process of normal blood coagulation prothrombin is converted into thrombin. As a result serum contains considerably less prothrombin than the plasma from which it is derived, the prothrombin having been consumed during the coagulation of the blood. In certain conditions this conversion is incomplete and much prothrombin remains in the serum. Often this is not obvious from the usual tests of clotting function since only a small amount of thrombin is necessary for apparently normal coagulation of blood in glass tubes. This defect is unmasked by the prothrombin consumption test which offers another method for studying the efficacy of the blood clotting process. Bordet and Delange (1912) were the first to observe deficient prothrombin consumption in normal platelet-free plasma, and their findings were confirmed and elaborated by Quick (1947) and Quick, Shanberge, and Stefanini (1949a). A similar defect was reported in thrombocytopenic purpura (Soulier, 1948; Quick et al., 1949b, and Alexander and de Vries, 1949a), while at the same time Soulier (1948) pointed out that there were a number of haemorrhagic syndromes where, although the platelets were not numerically decreased, there was defective prothrombin consumption, and he postulated a qualitative platelet defect in these conditions. Brinkhous (1939) had pointed out a prothrombin consumption defect in haemophilia, and this observation was confirmed and extended by Quick (1947), Soulier (1948), and Alexander and de Vries (1949b). The observations of Quick (1947) and Soulier (1948) showed that thrombocytopenic plasma and haemophilic plasma consumed little prothrombin during coagulation. Onmixing and recalcifying these two types of plasma, a normal amount of prothrombin was used up in the clotting process. It was therefore argued that the defective consumption of prothrombin was due to a different deficiency in the two types of plasma, since each appeared to contain an excess of a factor lacking in the other. It is the purpose of this study to confirm and extend these observations.
منابع مشابه
The coagulation defect in hemophilia with particular reference to the conversion of prothrombin to thrombin and the evolution of the prothrombin conversion accelerator.
taneously increase prothrombin consumption. The latter author used this effect as a basis for assay of the antihemophilic activity of normal plasma. Recently, substances have been described which, arising in blood during its coagulation, accelerate the conversion of prothrombin to thrombin in the presence of thromboplastin plus calcium.3’ Their evolution and physiologic properties help cxplain ...
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ورودعنوان ژورنال:
- Journal of clinical pathology
دوره 3 2 شماره
صفحات -
تاریخ انتشار 1950