Liver function in patients with vitamin K deficiency in infancy.

Abstract

Liver chemistry was studied in fifteen patients with vitamin K deficiency in infancy (VKDI). All except 2 were exclusively breast fed and 4 of the 15 infants had received intramuscular vitamin K prophylaxis. A high incidence of hepatic dysfunction was found during long term follow-up in patients with VKDI. Abnormal aminotransferase was noted either at the time of onset (n = 6) or during the ensuing few weeks (n = 6). Cholestasis was documented in six cases at onset and another two in a later period. Most cases had increased serum alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), or bile acid levels regardless of hepatic enzymes and bilirubin levels. The abnormal enzymes returned to normal after 5 weeks to 23 months. This study demonstrates a close relationship between hepatic dysfunction and VKDI. Liver function impairment other than cholestasis may play some role in the pathogenesis of VKDI, but the cause of hepatic dysfunction can not be defined. Follow-up of liver chemistry is recommended in patients with VKDI. Parenteral vitamin K prophylaxis at birth may not give sustained protection against VKDI, especially in those with underlying liver disease.