Kamijo M, Yagihashi S, Kida K, Narita S, Nakata F
Third Department of Internal Medicine, Hirosaki University School of Medicine.
Rinsho Shinkeigaku. 1991 Feb;31(2):191-6.
We report here an autopsy case of chronic germanium intoxication with major pathological changes in the central and peripheral sensory nervous systems. The patient was a 4-year-old girl who had suffered from gait disturbance and generalized muscle weakness for 22 months. She had been given orally germanium compounds (containing germanium dioxide, 225-450 mg/day) for the previous 28 months. In addition to the findings of chronic renal failure and anemia, she presented characteristic neurological symptoms exemplified by diffuse muscle atrophy, tongue fasciculation, sensory impairment and truncal ataxia as well as areflexia. Median and ulnar sensory nerve conduction velocities were also reduced. On the 17th hospital day, she died of renal failure. In addition to conspicuous degeneration of renal tubular cells, pathological studies revealed marked nerve fiber loss, degeneration and gliosis in the dorsal column of the spinal cord, which were most conspicuous in the thoracic and cervical cord. Axonal degenerative changes were also conspicuous in the sural and sciatic nerves. High concentration of germanium was detected in the brain, cerebellum, spinal cord, sciatic nerve, liver and kidney. It was suggested that the neural involvement in the current case was caused by chronic toxicity of germanium.
我们在此报告一例慢性锗中毒的尸检病例,其在中枢和外周感觉神经系统有主要病理变化。患者为一名4岁女孩,有22个月的步态障碍和全身肌肉无力病史。在之前的28个月里,她一直口服锗化合物(含二氧化锗,每天225 - 450毫克)。除了慢性肾衰竭和贫血的表现外,她还出现了特征性神经症状,如弥漫性肌肉萎缩、舌肌束颤、感觉障碍、躯干共济失调以及反射消失。正中神经和尺神经感觉神经传导速度也降低。住院第17天,她死于肾衰竭。除了肾小管细胞明显变性外,病理研究显示脊髓后索有明显的神经纤维丢失、变性和胶质细胞增生,在胸段和颈段脊髓最为明显。腓肠神经和坐骨神经也有明显的轴突退行性改变。在脑、小脑、脊髓、坐骨神经、肝脏和肾脏中检测到高浓度的锗。提示本例中的神经受累是由锗的慢性毒性所致。