Hemophilioid Factors: Acquired Deficiencies in Several Hemorrhagic States

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Abstract
Deficiencies of hemophilioid factors are not necessarily genetic in origin. Serum activities of plasma thromboplastin antecedent (PTA) and of plasma thromboplastin component (PTC) were depressed in 20 patients with a variety of hepatocellular disorders. PTA and PTC activities were also reduced in several patients who developed a deficiency of vitamin K subsequent to inability to adsorb fats. PTA and PTC were depressed in a number of patients following administration of 4-hydroxy coumarin compound. In these latter 2 groups, PTA and PTC activities rapidly increased toward normal following administration of vitamin K analogue. Significant deficiency of antihemophilic factor (AHF) was not found in any of the above conditions.

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