Stuart Clotting Defect. I. Segregation of an Hereditary Hemorrhagic State from the Heterogeneous Group Heretofore Called “Stable Factor” (SPCA, Proconvertin, Factor VII) Deficiency

In 1951, Alexander, Goldstein, Landwehr, and Cook (1) described a patient with a congenital hemorrhagic diathesis of an unusual type. There was a normal prothrombin concentration, but a prolonged prothrombin time which could be corrected by serum and serum fractions but not by BaSO4-adsorbed plasma or serum. The clotting factor deficient in the plasma of this patient dif- fered, therefore, from prothrombin, Factor V, ac- celerator globulin (Ac-G), and antihemophilic factor (AHF). The normal analogue of the factor deficient in this patient was relatively heat stable, adsorbable by barium sulphate and diminished in dicoumarol plasma. The patient was believed to lack the precursor of SPCA (serum prothrombin conversion accelerator) a factor which had been studied previously (2).