Plasma pyridoxal phosphate levels in fulminant hepatic failure and the effects of parenteral supplementation.
Plasma concentrations of pyridoxal-5'-phosphate (PLP), the active coenzyme form of vitamin B6, were found to be markedly raised in patients with fulminant hepatic failure, when estimated within one week of the onset of symptoms. In parallel with the rise in plasma PLP, there was an increase in serum aminotransferase activity, suggesting that as a result of the severe hepatocyte injury, vitamin is released from theliver in the form of transaminase holoenzymes. There was no correlation between plasma levels of PLP and the urinary excretion of 4-pyridoxic acid, its main metabolite, either in the patients or normal control subjects. There was a progressive decline in plasma PLP levels after the initial period, which was not prevented by administration of high doses of pyridoxine hydrochloride (100 mg intravenously daily), suggesting that thseepatients are either unable to convert pyridoxine to PLP, or that degradation of PLP occurs at a pathologically incrased rate in this condition.
D006501:Hepatic Encephalopathy / Q000201:enzymology*; D006801:Humans; D007275:Injections, Intravenous; D008099:Liver / Q000378:metabolism; D011732:Pyridoxal Phosphate / Q000097:blood* / Q000378:metabolism; D011735:Pyridoxic Acid / Q000652:urine; D011736:Pyridoxine / Q000008:administration & dosage / Q000494:pharmacology; D013997:Time Factors; D000637:Transaminases / Q000097:blood
D011735:Pyridoxic Acid; D011732:Pyridoxal Phosphate; D000637:Transaminases; D011736:Pyridoxine