Provias J P, Ackerley C A, Smith C, Becker L E
Department of Pathology (Division of Neuropathology), Hospital for Sick Children, Toronto, Ontario, Canada.
Acta Neuropathol. 1994;88(6):583-6. doi: 10.1007/BF00296497.
We report a boy of East Indian origin, aged 2 years and 10 months, who died suddenly and unexpectedly. Autopsy findings showed marked cerebral swelling with herniation and histological evidence of marked cerebral edema with perivascular protein leakage, indicating blood-brain barrier disruption. Energy dispersive X-ray microprobe analysis of the brain demonstrated the presence of cadmium and a marked increase in sulfur, predominantly intracellular, both within neuroglial, and to a lesser degree endothelial, cells. Localization was predominantly in the nucleus. Analysis of the kidney showed cadmium deposition in renal tubules and in the basal lamina of podocytes within the glomerulus. Although the environmental source of cadmium remains unknown, we speculate that acute cadmium toxicity led to brain intracellular accumulation with resultant cellular dysfunction, blood-brain barrier disruption, and lethal cerebral edema.
我们报告了一名2岁10个月大的东印度裔男孩,他突然意外死亡。尸检结果显示大脑明显肿胀并伴有脑疝形成,组织学证据表明存在明显的脑水肿,伴有血管周围蛋白渗漏,提示血脑屏障破坏。对大脑进行的能量色散X射线微探针分析显示存在镉,且硫含量显著增加,主要位于神经胶质细胞内,内皮细胞内的硫含量增加程度较小,且主要定位于细胞核。对肾脏的分析显示镉沉积在肾小管以及肾小球内足细胞的基膜中。尽管镉的环境来源尚不清楚,但我们推测急性镉中毒导致大脑细胞内镉蓄积,进而引起细胞功能障碍、血脑屏障破坏及致命性脑水肿。