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从病理学角度看人类有机汞中毒与无机汞中毒的鉴别诊断

Differential diagnosis between organic and inorganic mercury poisoning in human cases--the pathologic point of view.

作者信息

Eto K, Takizawa Y, Akagi H, Haraguchi K, Asano S, Takahata N, Tokunaga H

机构信息

National Institute for Minamata Disease, Environment Agency, Minamata City, Kumamoto, Japan.

出版信息

Toxicol Pathol. 1999 Nov-Dec;27(6):664-71. doi: 10.1177/019262339902700608.

Abstract

Differences in pathology were found between acute and chronic exposure to methylmercury, mercury vapor, and inorganic mercury. Characteristic pathologic changes produced by organic mercury in the brain have previously been described in patients with Minamata disease. The brains of patients who presented with acute onset of symptoms and died within 2-mo showed loss of neurons with reactive proliferation of glial cells, microcavitation, vascular congestion, petechial hemorrhage, and edema in the cerebral cortices, predominantly in the calcarine, pre- and postcentral, and transverse temporal cortices and in the cerebellar cortex. The neuropathologic changes in the patients with acute onset of symptoms who survived for a long period (>10 yr) were also included neuronal loss with reactive proliferation of glial cells in similar anatomic locations. The neuropathologic changes in patients with inorganic mercury poisoning are quite different. Autopsies performed on 3 individuals with fatal cases of acute inorganic mercury poisoning who were exposed to mercury vapor for about 2 wk revealed diffuse organized pneumonia, renal cortical necrosis, disseminated intravascular coagulopathy, and infarctions in the brain and kidneys. In 2 other patients who worked in mercury mines for about 10 yr and who suffered from chronic inorganic poisoning, no specific lesions were demonstrated in the brain. However, the assay and the histochemistry of mercury revealed that inorganic mercury was present in the brain in all 3 groups irrespective of the brain lesions and the duration of clinical signs.

摘要

甲基汞、汞蒸气和无机汞的急性和慢性暴露在病理学上存在差异。水俣病患者先前已描述过有机汞在大脑中产生的特征性病理变化。症状急性发作且在2个月内死亡的患者大脑显示,神经元丢失,胶质细胞反应性增生,微空洞形成,血管充血,点状出血,大脑皮质水肿,主要发生在距状皮质、中央前回和中央后回以及颞横回和小脑皮质。症状急性发作且存活较长时间(>10年)的患者神经病理学变化也包括在类似解剖位置的神经元丢失和胶质细胞反应性增生。无机汞中毒患者的神经病理学变化则大不相同。对3例急性无机汞中毒致死病例进行尸检,这些病例接触汞蒸气约2周,结果显示弥漫性机化性肺炎、肾皮质坏死、弥散性血管内凝血以及脑和肾梗死。另外2例在汞矿工作约10年且患有慢性无机汞中毒的患者,大脑未显示出特异性病变。然而,汞的检测和组织化学显示,所有3组患者的大脑中均存在无机汞,无论有无脑部病变以及临床症状持续时间长短。

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