Until recently, male persons with a severe hemorrhagic diathesis characterized by (1) a prolonged clotting time, (2) normal Quick plasma prothrombin time, but (3) a poor prothrombin consumption were unhesitatingly diagnosed as suffering from classic hemophilia. This disease is still widely attributed to a deficiency of antihemophilic factor (AHF)1 essential for the formation of blood thromboplastin. However, it has been emphasized that the demonstrable decrease of AHF activity in these patients may be functional rather than real, owing to the presence of an inhibitor (antithromboplastin).2
In 1952, Aggeler and co-workers3 described a syndrome, clinically and genetically indistinguishable from classic hemophilia, which is apparently caused by the absence or marked diminution of a previously unrecognized plasma constituent. They named this factor plasma thromboplastin component (PTC). PTC is also essential for the formation of blood thromboplastin. The PTCdeficiency syndrome is now known under a variety of names, such as
RAMOT B, ANGELOPOULOS B, SINGER K. Plasma Thromboplastin Antecedent: Deficiency. AMA Arch Intern Med. 1955;95(5):705–712. doi:10.1001/archinte.1955.00250110075009
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