Abstract
The concept that prothrombin is a complex is further demonstrated by the discovery of 2 families in which several members have a congenital hypoprothrombinemia. In the first family, the affected members have a deficiency of component B. This factor is also diminished in dicumarol poisoning. In mixing plasma lacking in this component with an equal vol. of normal plasma, the prothrombin time is not completely restored to normal. In the 2d family, the hypoprothrombinemia is due to a lowered concn. of a new factor designated component A. Preliminary studies suggest that component A is also reduced in vit. K deficiency. When human plasma lacking this factor is mixed with normal plasma in a ratio of 1 to 1, the prothrombin time is completely restored to normal. A third essential factor which disappears when oxalated human plasma is stored was originally designated component A, but has now been renamed the labile factor. It is postulated that the formation of thrombin required the following factors: prothrombin (components A and B), a labile factor, thrombo-plastin, and Ca; and that these interact stoichiometrically.