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正己烷多发性神经病。一种鞋匠的职业病。

n-hexane polyneuropathy. An occupational disease of shoemakers.

作者信息

Rizzuto N, De Grandis D, Di Trapani G, Pasinato E

出版信息

Eur Neurol. 1980;19(5):308-15. doi: 10.1159/000115166.

DOI:10.1159/000115166
PMID:6249607
Abstract

The epidemiological, clinical, electrophysiological and nerve biopsy findings of 3 cases of n-hexane neuropathy in shoe industry are reported. The disease affects more than 1 person working in the same environment, regardless of their specific role, and occurs in factories where standards of hygiene are low. In the most severe cases the picture of peripheral neuropathy is associated with symptoms suggesting a concurrent involvement of the central nervous system such as dysarthria, disproportionate ataxia of the gait, blurred vision, and sometimes, after the recovery of the peripheral neuropathy, appearance of leg spasticity. Light- and electron microscopic study of peripheral nerve biopsies shows that the toxic produces a primary axonopathy characterized by segmental swellings of the fibers, due to accumulation of filaments. Retraction of the myelin from the node and segmental demyelination are secondary to the axonal changes. Experimental models of hexacarbon neurotoxicity may offer an explanation for the anatomical substrate underlying the symptoms related to the involvement of the central nervous system.

摘要

报告了3例制鞋行业正己烷中毒性神经病的流行病学、临床、电生理及神经活检结果。该病影响在同一环境中工作的不止一人,无论其具体工种如何,且发生在卫生标准较低的工厂。在最严重的病例中,周围神经病的表现伴有提示中枢神经系统同时受累的症状,如构音障碍、步态共济失调不成比例、视力模糊,有时在周围神经病恢复后出现腿部痉挛。周围神经活检的光镜和电镜研究表明,该毒物导致原发性轴索性神经病,其特征为纤维节段性肿胀,系细丝积聚所致。髓鞘从结处回缩及节段性脱髓鞘是轴突改变的继发表现。六碳化合物神经毒性的实验模型可能为与中枢神经系统受累相关症状的解剖学基础提供解释。

相似文献

1
n-hexane polyneuropathy. An occupational disease of shoemakers.正己烷多发性神经病。一种鞋匠的职业病。
Eur Neurol. 1980;19(5):308-15. doi: 10.1159/000115166.
2
Neurophysiological studies of n-hexane polyneuropathy in the sandal factory.凉鞋厂正己烷多发性神经病的神经生理学研究
Electroencephalogr Clin Neurophysiol Suppl. 1982;36:671-81.
3
Hexacarbon neurotoxicity.
Neurobehav Toxicol Teratol. 1981 Winter;3(4):437-44.
4
Patients with n-hexane induced polyneuropathy: a clinical follow up.正己烷所致多发性神经病患者:临床随访
Br J Ind Med. 1990 Jul;47(7):485-9. doi: 10.1136/oem.47.7.485.
5
Electrophysiological studies of shoemakers exposed to sub-TLV levels of n-hexane.制鞋工人在亚 TLV 水平的正己烷环境下的电生理学研究。
J Occup Health. 2012;54(5):376-82. doi: 10.1539/joh.12-0029-fs. Epub 2012 Aug 2.
6
Biphasic recovery in n-hexane polyneuropathy. A clinical and electrophysiological study.正己烷多发性神经病的双相恢复:一项临床和电生理研究
Acta Neurol Scand. 1989 Dec;80(6):610-5. doi: 10.1111/j.1600-0404.1989.tb03936.x.
7
Toxic polyneuropathy of shoe workers in Italy. A clinical, neurophysiological and follow-up study.意大利制鞋工人的中毒性多发性神经病。一项临床、神经生理学及随访研究。
Ital J Neurol Sci. 1983 Dec;4(4):463-72. doi: 10.1007/BF02125628.
8
Toxic polyneuropathy due to n-hexane.
J Neurol Sci. 1980 Jul;47(1):7-19. doi: 10.1016/0022-510x(80)90021-0.
9
Urinary excretion of 2,5-hexanedione and peripheral polyneuropathies workers exposed to hexane.接触己烷工人的2,5-己二酮尿排泄与周围神经病变
J Toxicol Environ Health. 1987;20(3):219-28. doi: 10.1080/15287398709530976.
10
N-hexane polyneuropathy--a case report with a review of the literature.
Med J Osaka Univ. 1977 Sep;28(1):77-85.

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Bone marrow mesenchymal stem cells promote remyelination in spinal cord by driving oligodendrocyte progenitor cell differentiation via TNFα/RelB-Hes1 pathway: a rat model study of 2,5-hexanedione-induced neurotoxicity.骨髓间充质干细胞通过 TNFα/RelB-Hes1 通路促进少突胶质前体细胞分化,从而促进脊髓髓鞘再生:2,5-己二酮诱导神经毒性的大鼠模型研究。
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Recovery from 2,5-hexanediol intoxication of the retinotectal tract of the rat. An ultrastructural study.大鼠视网膜顶盖束2,5 -己二醇中毒后的恢复。一项超微结构研究。
Acta Neuropathol. 1982;58(4):286-90. doi: 10.1007/BF00688611.
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The effects of 2,5-hexanedione on axonal regeneration after nerve crush in the rat.2,5 -己二酮对大鼠神经挤压伤后轴突再生的影响。
Acta Neuropathol. 1983;59(3):216-24. doi: 10.1007/BF00703206.
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Impairment of human polymorphonuclear leukocyte chemotaxis by 2,5-hexanedione.2,5 -己二酮对人多形核白细胞趋化性的损害
Cell Biol Toxicol. 1986 Mar;2(1):33-9. doi: 10.1007/BF00117705.