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慢性酒精滥用者维生素缺乏的机制及韦尼克-科尔萨科夫综合征的发展

Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke-Korsakoff syndrome.

作者信息

Thomson A D

机构信息

Department of Gastroenterology, Greenwich District Hospital, London, UK.

出版信息

Alcohol Alcohol Suppl. 2000 May-Jun;35(1):2-7. doi: 10.1093/alcalc/35.supplement_1.2.

Abstract

The classic signs of vitamin deficiency only occur in states of extreme depletion and are unreliable indicators for early treatment or prophylaxis of alcoholic patients at risk. Post-mortem findings demonstrate that thiamine (vitamin B1) deficiency sufficient to cause irreversible brain damage is not diagnosed ante mortem in 80-90% of these patients. The causes of vitamin deficiency are reviewed with special attention to the inhibition of oral thiamine hydrochloride absorption in man caused by malnutrition present in alcoholic patients or by the direct effects of ethanol on intestinal transport. As the condition of the patient misusing alcohol progresses, damage to brain, liver, gastrointestinal tract, and pancreas continue (with other factors discussed) to further compromise the patient. Decreased intake, malabsorption, reduced storage, and impaired utilization further reduce the chances of unaided recovery. Failure of large oral doses of thiamine hydrochloride to provide an effective treatment for Wernicke's encephalopathy emphasizes the need for adequate and rapid replacement of depleted brain thiamine levels by repeated parenteral therapy in adequate doses.

摘要

维生素缺乏的典型体征仅在极度缺乏的状态下出现,对于有风险的酒精性患者的早期治疗或预防而言,这些体征并不可靠。尸检结果表明,在这些患者中,80% - 90%生前未被诊断出足以导致不可逆脑损伤的硫胺素(维生素B1)缺乏。本文回顾了维生素缺乏的原因,特别关注酒精性患者存在的营养不良或乙醇对肠道转运的直接影响所导致的人体口服盐酸硫胺素吸收受抑制的情况。随着酗酒患者病情的发展,大脑、肝脏、胃肠道和胰腺的损害会持续(还涉及其他因素),进一步危及患者。摄入量减少、吸收不良、储存减少和利用受损进一步降低了患者自行康复的几率。大剂量口服盐酸硫胺素未能有效治疗韦尼克脑病,这凸显了通过重复给予足够剂量的肠外治疗来充分且快速补充大脑中缺乏的硫胺素水平的必要性。

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