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酒精性谵妄的发病机制与治疗新进展(作者译)

[New aspects of the pathogenesis and therapy of alcoholic delirium (author's transl)].

作者信息

Müting D, Reikowski J

出版信息

MMW Munch Med Wochenschr. 1977 Feb 18;119(7):209-12.

PMID:403444
Abstract

Clinically, and especially biochemically, alcoholic delirium corresponds closely to an incipient but reversible exogenous hepatic coma. The blood levels of ammonia in particular, free phenols and lactate are greatly increased. These same metabolites increase slightly in the blood of persons with healthy livers after a single alcohol loading. The treatment of alcoholic delirium consists of optimal sedation with Distraneurin, which appears to have no side effects on the liver. There is even a lowering of the raised lactate level in the blood after a single administration of Distraneurin. Ammonia and phenols are reduced by ammonia-lowering aminoacids, lactulose and bifidum milk. Most important, however, is strict abstention from alcohol, which alone brings about a rapid improvement of pathological biochemical and morphological liver findings.

摘要

临床上,尤其是生化方面,酒精性谵妄与初期但可逆的外源性肝昏迷密切相关。特别是血液中的氨、游离酚和乳酸水平大幅升高。健康肝脏的人在单次饮酒后,这些相同的代谢产物在血液中的含量也会略有增加。酒精性谵妄的治疗包括使用地西泮进行最佳镇静,地西泮似乎对肝脏没有副作用。单次服用地西泮后,血液中升高的乳酸水平甚至会降低。降低氨的氨基酸、乳果糖和双歧牛奶可降低氨和酚的水平。然而,最重要的是严格戒酒,仅戒酒就能使肝脏病理生化和形态学表现迅速改善。

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