Thiamine deficiency in fulminant hepatic failure and effects of supplementation.
Nine out of 24 patients with acute hepatocellular necrosis leading to fulminant hepatic failure showed biochemical evidence of thiamine deficiency early in the course of their illness, probably as a result of inadequate intake of the vitamin. This was corrected by twice daily administration of intravenous vitamin supplements containing thiamine hydrochloride (100 mg b.d.). These studies indicate that conversion of thiamine hydrochloride to its biologically active co-enzyme form, thiamine pyrophosphate, is possible even in the presence of severe acute hepatocellular necrosis, and it is suggested that supplements of the vitamin should be included in the routine management of patients with acute hepatic failure.
D000208:Acute Disease; D004912:Erythrocytes / Q000201:enzymology; D006801:Humans; D007275:Injections, Intravenous; D008107:Liver Diseases / Q000150:complications* / Q000378:metabolism; D013831:Thiamine / Q000008:administration & dosage / Q000627:therapeutic use* / Q000652:urine; D013832:Thiamine Deficiency / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism; D014174:Transketolase / Q000097:blood
D014174:Transketolase; D013831:Thiamine