Severe acquired vitamin K deficiency: a hypothesis for rapid response to therapy.
The potential mechanism underlying the rapid response to vitamin K replacement in acquired deficiency states is incompletely understood. To examine vitamin K metabolism, a 10-year-old boy with autoimmune enteropathy on oral vitamin K supplementation, who presented with profuse nosebleeds and calf tenderness, was evaluated. Laboratory analyses were consistent with severe vitamin K deficiency: vitamin K dependent protein (VKDP) levels < 5%, normal vitamin K epoxide level and depressed total prothrombin antigen (carboxylated and undercarboxyated forms). Intramuscular vitamin K (10 mg) was administered. Nine hours following therapy, VKDP levels corrected completely. Total prothrombin antigen increased indicating new prothrombin synthesis. However, the increase in the prothrombin-clotting assay far exceeded the increase in total prothrombin, supporting storage of undercarboxylated prothrombin in vitamin K deficiency states, with carboxylation and secretion after vitamin K replacement. Although this mechanism is known to occur in rodents, it has not been reported in humans. Our findings suggest a new potential mechanism of prothrombin metabolism in humans.
Sakkinen
P A
PA
Department of Pathology, University of Vermont and Fletcher Allen Health Care, Burlington 05405, USA.
Dickerman
J D
JD
Colletti
R B
RB
Sadowski
J A
JA
Golden
E A
EA
Bovill
E G
EG
D001777:Blood Coagulation; D002648:Child; D006801:Humans; D008297:Male; D011516:Prothrombin; D014813:Vitamin K Deficiency / Q000097:blood
D011516:Prothrombin