肝性脑病的治疗。

K Grüngreiff
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引用次数: 0

摘要

肝性脑病(HE)的发病机制尽管在这一领域取得了实质性进展,但仍不清楚。本文讨论了四种主要的发病机制假说:氨作用假说、协同作用假说、假神经递质假说和正常神经递质及其受体改变假说。一个连接函数似乎与氨有关。减少口服蛋白质的摄入,选择某些蛋白质,口服不可吸收的抗生素和灌肠剂,以防止肠道吸收有毒的代谢产物。肠外营养使HE的治疗有了很大的改善。首先,患者接受支链氨基酸含量高、芳香酸含量低的特殊氨基酸混合物。通过脂肪交换碳水化合物在一定程度上改善了这些患者的肠外营养制度。不同的肝支持系统未能改善暴发性肝衰竭的预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Therapy of hepatic encephalopathy].

The pathogenesis of the hepatic encephalopathy (HE) in spite of substantial progresses in this field still rests unclear. Actually four main hypotheses of the pathogenesis are discussed: the ammonia-hypothesis, the synergism-hypothesis, the hypothesis of the false neurotransmitters and that one of the changes of the normal neurotransmitters and their receptors. A connecting function seems to come up to ammonia. --Reduction of oral protein intake, selection of certain proteins, oral administration of nonabsorbable antibiotics and enemas should be used in order to prevent the intestinal absorption of toxic metabolic products. The parenteral nutrition has the therapy of HE substantially improved. Primarily, the patients receive special amino acid mixtures with a high content of branched chain amino acids and a low content of aromatic acids. The exchange of carbohydrate to some extent through fat improves the parenteral nutrition regime for these patients. The different liver support systems have failed to improve the prognosis of fulminant hepatic failure.

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