Subacute combined degeneration of the spinal cord of toxic etiology (clinical case)

A. A. Kondratov, A. S. Kotov
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引用次数: 0

Abstract

For more than two hundred years after its discovery, nitric oxide (I) has been widely used in medicine as an anesthetic, in the car industry as an engine performance enhancer, in the food industry as a preservative, and, unfortunately, among young people as a mild narcotic substance. Despite the widespread opinion that there is no harm from the use of “laughing gas” for recreational purposes, in the literature and in practice, there are a lot of cases when patients suffer from various complications, including neurological ones, caused precisely by the use of nitric oxide (I). One of the main mechanisms of the pathological effects of nitrous oxide on the nervous tissue is the inactivation of vitamin B12. This has been proven by studying the physicochemical properties of the gas, the effect on the organisms of laboratory animals, the change in the concentration of certain substances in the human body, and also by the use of cyanocobalamin for the treatment of these patients. This article describes a clinical case of the development of myelopolyneuropathy caused by the toxic effects of nitric oxide (I).
中毒性脊髓亚急性联合变性(临床病例)
一氧化氮(I)被发现后的两百多年来,一直作为麻醉剂广泛应用于医学领域,作为发动机性能增强剂广泛应用于汽车工业,作为防腐剂广泛应用于食品工业,不幸的是,作为一种轻度麻醉物质也广泛应用于年轻人中间。尽管人们普遍认为出于娱乐目的使用 "笑气 "不会对人体造成伤害,但在文献和实践中,却有大量病例表明,病人正是因为使用了一氧化氮(I)而引发了各种并发症,包括神经系统并发症。一氧化氮对神经组织产生病理影响的主要机制之一是维生素 B12 失活。通过研究这种气体的物理化学特性、对实验动物机体的影响、人体内某些物质浓度的变化,以及使用氰钴胺治疗这些病人,都证明了这一点。本文描述了一个因一氧化氮(I)的毒性作用而导致骨髓多发性神经病的临床病例。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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