Severe acquired vitamin K deficiency: a hypothesis for rapid response to therapy

The potential mechanism underlying the rapid response to vitamin K replacem ent in acquired deficiency states is incompletely understood. To examine vi tamin K metabolism, a 10-year-old boy with autoimmune enteropathy on oral v itamin K supplementation, who presented with profuse nosebleeds and calf te nderness, was evaluated. Laboratory analyses were consistent with severe vi tamin K deficiency: vitamin K dependent protein (VKDP) levels < 5%, normal vitamin K epoxide level and depressed total prothrombin antigen (carboxylat ed and undercarboxyated forms). Intramuscular vitamin K (10 mg) was adminis tered. Nine hours following therapy, VKDP levels corrected completely. Tota l prothrombin antigen increased indicating new prothrombin synthesis. Howev er, the increase in the prothrombin-clotting assay far exceeded the increas e in total prothrombin, supporting storage of undercarboxylated prothrombin in vitamin K deficiency states, with carboxylation and secretion after vit amin K replacement. Although this mechanism is known to occur in rodents, i t has not been reported in humans. Our findings suggest a new potential mec hanism of prothrombin metabolism in humans. Blood Coagul Fibrinolysis 11:30 9-311 (C) 2000 Lippincott Williams & Wilkins.