Abstract
Severe hemorrhagic diatheses resulting from insufficient or delayed thromboplastin formation may have varied causes: (1) Antihemophilic globulin (A.H.G.) deficiency in classic hemophilia (hemophilia type A) in men or homozygote women (daughters of a hemophiliac type A and carrier of the antihemophilic gene type A). (2) Plasma thromboplastin component (P.T.C.) deficiency (Christmas disease or hemophilia type B). (3) Plasma thromboplastin antecedent (P.T.A.) deficiency (hemophilia type C). (4) Combined antihemophilic globulin and plasma thromboplastin component deficiency. (5) A circulating anticoagulant may complicate the A.H.G. or P.T.C. deficiency and aggravate these conditions. (6) Presence of a circulating anticoagulant in non-hemophilic men. (7) In women, the presence of a circulating anticoagulant which may or may not be related to a recent pregnancy. (8) Antihemophilic globulin deficiency in women not belonging to a hemophiliac family. This condition is usually associated with a vascular defect. Absolute decrease or deficit in functional activity of platelets also is a frequent cause of inadequate thromboplastin formation. The relative occurrence and characteristics, and the diagnostic tests which differentiate these conditions are described.
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