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双硫仑神经病变:一篇综述(1971 - 1988年)及一例病例报告

Disulfiram neuropathy: a review (1971-1988) and report of a case.

作者信息

Frisoni G B, Di Monda V

机构信息

Clinica Neurologica dell'Università di Brescia, Ospedale Civile, Italy.

出版信息

Alcohol Alcohol. 1989;24(5):429-37.

PMID:2554935
Abstract

Neuropathy is one of the most severe side effects of disulfiram therapy. We report the case of a young man who developed a neuropathy following disulfiram administration, with a virtually complete recovery in 14 months. We then discuss 37 cases of disulfiram neuropathy reported since 1971. Evidence is given that: (1) there is no numerical sex prevalence, although the incidence of the disease in women is probably disproportionately high; (2) symptom onset latency is dose-dependent, being longer at 250 mg/day or less; (3) neurological deficits are also dose-dependent, being milder at 250 mg/day or less; (4) the two previous findings and single observations suggest that disulfiram neuropathy is a dose-dependent phenomenon; (5) recovery probably follows a course which depends primarily on the initial degree of impairment; (6) the genetic mechanism probably involves carbon disulfide and a hypothesis as to the possible biochemical mechanism is proposed; (7) chloral hydrate can bear a potentiation effect on neuropathy, and the association with disulfiram is best avoided. Further, we give guidelines for the differentiation between alcoholic and disulfiram neuropathy, advise prescribing the drug at 250 mg daily or less, if possible, and stress the utmost importance of an early diagnosis.

摘要

神经病变是双硫仑治疗最严重的副作用之一。我们报告了一例年轻男性在服用双硫仑后出现神经病变的病例,该患者在14个月内几乎完全康复。然后我们讨论了自1971年以来报告的37例双硫仑所致神经病变病例。有证据表明:(1)虽然女性中该病的发病率可能不成比例地高,但在性别上没有数字上的流行差异;(2)症状发作潜伏期与剂量有关,每天250毫克或更低剂量时潜伏期更长;(3)神经功能缺损也与剂量有关,每天250毫克或更低剂量时缺损较轻;(4)前两个发现和单一观察结果表明双硫仑所致神经病变是一种剂量依赖性现象;(5)恢复过程可能主要取决于初始损伤程度;(6)遗传机制可能涉及二硫化碳,并提出了一种关于可能的生化机制的假设;(7)水合氯醛可对神经病变产生增强作用,最好避免与双硫仑联合使用。此外,我们给出了酒精性和双硫仑所致神经病变鉴别的指导原则,建议尽可能每天以250毫克或更低剂量开药,并强调早期诊断的至关重要性。

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