Division of Medical Genetics, Department of Pediatrics, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Pediatr Neurol. 2010 Oct;43(4):279-82. doi: 10.1016/j.pediatrneurol.2010.05.018.
Reported here is a novel presentation of late onset glutaric aciduria type 2 in two Thai siblings. A 9-year-old boy presented with gradual onset of proximal muscle weakness for 6 weeks. The initial diagnosis was postviral myositis, and then polymyositis. Electromyography and nerve conduction velocity testing indicated a myopathic pattern. Muscle biopsy revealed excessive accumulation of fat. Acylcarnitine profiling led to the diagnosis of glutaric aciduria type 2. Immunoblot analysis of electron-transferring-flavoprotein and its dehydrogenase electron-transferring-flavoprotein dehydrogenase led to mutation analysis of the ETFDH gene, which revealed two different pathogenic mutations in both alleles and confirmed the diagnosis of glutaric aciduria type 2 caused by electron-transferring-flavoprotein dehydrogenase deficiency. The boy recovered completely after treatment. Later, his younger sibling became symptomatic; the same diagnosis was confirmed, and treatment was similarly effective. Acylcarnitine profiling was a crucial investigation in making this diagnosis in the presence of normal urine organic acid findings. Late onset glutaric aciduria type 2, a rare cause of muscle weakness in children, should be included in the differential diagnosis of myopathy.
本研究报告了 2 例泰国家族性迟发性戊二酸血症 2 型患者。1 名 9 岁男孩,逐渐出现近端肌无力 6 周。初始诊断为病毒性肌炎,后为多发性肌炎。肌电图和神经传导速度检查提示肌病模式。肌肉活检显示脂肪过度堆积。酰基辅酶 A 谱分析导致诊断为戊二酸血症 2 型。电子转移黄素蛋白及其脱氢酶电子转移黄素蛋白脱氢酶的免疫印迹分析导致 ETFDH 基因突变分析,发现两个不同的致病突变均存在于两个等位基因中,从而确诊为电子转移黄素蛋白脱氢酶缺乏引起的戊二酸血症 2 型。男孩治疗后完全康复。后来,他的弟弟出现症状;同样的诊断得到确认,治疗同样有效。在正常尿有机酸检测结果的情况下,酰基辅酶 A 谱分析是做出这一诊断的关键检查。迟发性戊二酸血症 2 型是儿童肌无力的罕见病因,应纳入肌病的鉴别诊断。