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两步法铊中毒时迟发性加速性神经功能恶化

Tardily accelerated neurologic deterioration in two-step thallium intoxication.

作者信息

Kuroda Hiroshi, Mukai Yoshiyuki, Nishiyama Shuhei, Takeshita Takayuki, Tateyama Maki, Takeda Atsushi, Aoki Masashi

机构信息

Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.

Department of Neurology, Izumi Hospital, Sendai, Japan.

出版信息

J Clin Neurosci. 2016 Dec;34:234-236. doi: 10.1016/j.jocn.2016.09.003. Epub 2016 Sep 28.

Abstract

Thallium intoxication was reported in cases with accidental ingestion, suicide attempt, and criminal adulteration. Reported cases were mostly one-time ingestion, therefore, the clinical course of divisional ingestion has not been fully known. Here, we report a case with two-step thallium intoxication manifesting as tardily accelerated neurologic deterioration. A 16-year-old adolescent was cryptically poisoned with thallium sulfate twice at an interval of 52days. After the first ingestion, neurologic symptoms including visual loss, myalgia, and weakness in legs developed about 40days after the development of acute gastrointestinal symptoms and alopecia. After the second ingestion, neurologic symptoms deteriorated rapidly and severely without gastrointestinal or cutaneous symptoms. Brain magnetic resonance imaging exhibited bilateral optic nerve atrophy. Nerve conduction studies revealed severe peripheral neuropathies in legs. Thallium intoxication was confirmed by an increase in urine thallium egestion. Most of the neurologic manifestations ameliorated in two years, but the visual loss persisted. The source of thallium ingestion was unraveled afterward because a murder suspect in another homicidal assault confessed the forepast adulteration. This discriminating clinical course may be attributable to the cumulative neurotoxicity due to the longer washout-time of thallium in the nervous system than other organs. It is noteworthy that the divisional thallium intoxication may manifest as progressive optic and peripheral neuropathy without gastrointestinal or cutaneous symptoms.

摘要

铊中毒见于意外摄入、自杀未遂及投毒犯罪等案例。已报道的病例大多为一次性摄入,因此,分次摄入铊的临床病程尚未完全明确。在此,我们报告一例分两次摄入铊导致中毒的病例,其表现为迟发性神经功能加速恶化。一名16岁青少年被硫酸铊隐匿性中毒两次,间隔52天。首次摄入后,在急性胃肠道症状和脱发出现约40天后,出现包括视力丧失、肌痛和腿部无力等神经症状。第二次摄入后,神经症状迅速且严重恶化,无胃肠道或皮肤症状。脑磁共振成像显示双侧视神经萎缩。神经传导研究显示腿部严重的周围神经病变。尿铊排出量增加证实为铊中毒。大多数神经症状在两年内有所改善,但视力丧失仍持续存在。后来铊摄入的源头被查明,因为另一起杀人袭击案中的一名谋杀嫌疑人供认了之前的投毒行为。这种独特的临床病程可能归因于铊在神经系统中的清除时间比其他器官更长,从而导致累积神经毒性。值得注意的是,分次铊中毒可能表现为进行性视神经和周围神经病变,而无胃肠道或皮肤症状。

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