Rossouw J E, Labadarios D, McConnell J B, Davis M, Williams R
Scand J Gastroenterol. 1977;12(1):123-7.
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.
在暴发性肝衰竭患者症状出现后一周内进行评估时,发现维生素B6的活性辅酶形式——磷酸吡哆醛(PLP)的血浆浓度显著升高。与血浆PLP升高同时出现的是血清转氨酶活性增加,这表明由于严重的肝细胞损伤,维生素以转氨酶全酶的形式从肝脏释放出来。无论是在患者还是正常对照受试者中,血浆PLP水平与4-吡哆酸(其主要代谢产物)的尿排泄之间均无相关性。在最初阶段之后,血浆PLP水平逐渐下降,给予大剂量盐酸吡哆醇(每日100mg静脉注射)并不能阻止这种下降,这表明这些患者要么无法将吡哆醇转化为PLP,要么在这种情况下PLP的降解以病理增加的速率发生。