Müting D, Perisoara A, Baum G, Flasshoff H J, Bucsis L
Hepatogastroenterology. 1986 Apr;33(2):66-70.
Toxic protein metabolites are assumed to play an important role in the multifactorial pathogenesis of hepatic encephalopathy (HE). To investigate this, we examined the serum levels of free amino acids, free phenols and indoles in 100 healthy adults, and in 124 liver cirrhotics with HE and 80 without HE. We found a significant increase in free serum phenols and indican already in liver cirrhosis without portal hypertension (PH) and HE. In stage III and IV HE large amounts of p-hydroxy-phenyl lactic acid were detected, which was not the case in cirrhotics without HE. In HE the increase in free serum phenols and indican was much higher than that of the mother substances tyrosine and tryptophan. The quotient BCAA/AAA was decreased significantly already in PH without HE. In addition to the increased formation by intestinal bacteria, a diminished oxidative capacity of the cirrhotic liver seems to be one of the main causes of the increased serum levels of toxic protein metabolites in HE.
毒性蛋白质代谢产物被认为在肝性脑病(HE)的多因素发病机制中起重要作用。为了对此进行研究,我们检测了100名健康成年人、124例患有HE的肝硬化患者以及80例未患HE的肝硬化患者血清中的游离氨基酸、游离酚和吲哚水平。我们发现,在无门静脉高压(PH)和HE的肝硬化患者中,血清游离酚和吲哚硫酸盐就已显著升高。在III期和IV期HE患者中检测到大量对羟基苯乳酸,而在未患HE的肝硬化患者中则未出现这种情况。在HE患者中,血清游离酚和吲哚硫酸盐的升高幅度远高于其母体物质酪氨酸和色氨酸。在无HE的PH患者中,支链氨基酸/芳香族氨基酸比值就已显著降低。除了肠道细菌产生增加外,肝硬化肝脏氧化能力下降似乎是HE患者血清毒性蛋白质代谢产物水平升高的主要原因之一。