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重度甲醇中毒时无阴离子间隙代谢性酸中毒:一例病例报告及文献复习

Absence of anion gap metabolic acidosis in severe methanol poisoning: a case report and review of the literature.

作者信息

Palmisano J, Gruver C, Adams N D

出版信息

Am J Kidney Dis. 1987 May;9(5):441-4. doi: 10.1016/s0272-6386(87)80150-6.

Abstract

Methanol poisoning in humans is characterized by a latent period with subsequent development of anion gap metabolic acidosis and blindness. We describe a patient with potentially lethal methanol ingestion as evidenced by an admission serum methanol level of 403 mg/dL and sustained serum methanol levels greater than 50 mg/dL for more than 18 hours after ingestion, despite hemodialysis therapy. That anion gap metabolic acidosis or visual impairment did not develop in this patient was attributed to documented prior ethanol ingestion (admission serum ethanol level of 158 mg/dL) and continued ethanol administration during hospitalization (sustained serum ethanol levels greater than 100 mg/dL). This case demonstrates the ability of ethanol to inhibit the metabolism of methanol to formic acid in humans. This inhibition was achieved without induction of lactic acidosis. Thus this case documents the efficacy of ethanol therapy in patients with methanol poisoning.

摘要

人类甲醇中毒的特征是有一段潜伏期,随后会出现阴离子间隙代谢性酸中毒和失明。我们描述了一名甲醇摄入量可能致命的患者,摄入后入院时血清甲醇水平为403mg/dL,尽管进行了血液透析治疗,但摄入后18小时以上血清甲醇水平持续高于50mg/dL。该患者未出现阴离子间隙代谢性酸中毒或视力损害,这归因于有记录的既往乙醇摄入史(入院时血清乙醇水平为158mg/dL)以及住院期间持续给予乙醇(血清乙醇水平持续高于100mg/dL)。该病例证明了乙醇在人体内抑制甲醇代谢为甲酸的能力。这种抑制作用在未诱发乳酸性酸中毒的情况下实现。因此,该病例证明了乙醇疗法对甲醇中毒患者的有效性。

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