Fujii T, Ito M, Okuno T, Mutoh K, Nishikomori R, Mikawa H
Department of Pediatrics, Kyoto University, Faculty of Medicine, Kyoto, Japan.
J Pediatr. 1990 Jan;116(1):84-7. doi: 10.1016/s0022-3476(05)81650-6.
Two infants who had clinical and radiographic findings consistent with Leigh syndrome were found to have deficiency of complex I (reduced nicotinamide-adenine dinucleotide--coenzyme Q reductase) activity. Significant abnormalities were found on computed tomographic scans and magnetic resonance images of the brain. Lactate and pyruvate concentrations in blood and cerebrospinal fluid were elevated, and muscle biopsy specimens showed abnormal mitochondria. These data indicate that Leigh syndrome, as well as MELAS syndrome (mitochondrial encephalopathy, myopathy, lactic acidosis, and stroke-like episodes) may result from complex I deficiency.
两名有与Leigh综合征相符的临床和影像学表现的婴儿被发现存在复合体I(还原型烟酰胺腺嘌呤二核苷酸-辅酶Q还原酶)活性缺乏。脑部计算机断层扫描和磁共振成像发现了显著异常。血液和脑脊液中的乳酸和丙酮酸浓度升高,肌肉活检标本显示线粒体异常。这些数据表明,Leigh综合征以及MELAS综合征(线粒体脑病、肌病、乳酸性酸中毒和类卒中发作)可能由复合体I缺乏引起。