Hemophilioid Factors: Acquired Deficiencies in Several Hemorrhagic States

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.