Genetics and Genome Biology, The Research Institute, The Hospital for Sick Children, Toronto, Canada.
Mol Genet Metab. 2009 Dec;98(4):378-82. doi: 10.1016/j.ymgme.2009.07.012. Epub 2009 Jul 26.
We report here the identification of a patient with muscle-specific glycogen synthase deficiency. The 8-year-old patient showed no prior signs of distress before collapsing during a bout of exercise, resulting in death. Initial post-mortem analysis of tissues suggested death was due to metabolic complications of mitochondrial myopathy, but upon further examination it was found that the anomalies were indicative of mitochondrial proliferation and oxidative compensation. A homozygous two base pair deletion was identified in exon 2 of GYS1, and the parents and sibling were confirmed as heterozygous carriers of the deletion. This case highlights the importance of differentiating between mitochondrial compensatory phenomena and true mitochondrial disease, and suggests that GYS1 deficiency could be a common cause of sudden cardiac death in children. Children with abnormal cardiac responses to increased workloads as well as those with defined myocardial disease should therefore be tested for GYS1 deficiency.
我们在此报告一名肌肉特异性糖原合酶缺乏症患者的鉴定。这名 8 岁的患者在一次运动中突然倒下之前没有任何不适的迹象,导致死亡。最初的死后组织分析表明死亡是由于线粒体肌病的代谢并发症引起的,但进一步检查发现,异常表明存在线粒体增殖和氧化补偿。在 GYS1 的外显子 2 中发现了一个纯合的两个碱基对缺失,父母和兄弟姐妹被确认为该缺失的杂合携带者。这个病例强调了区分线粒体代偿现象和真正的线粒体疾病的重要性,并表明 GYS1 缺乏可能是儿童心脏性猝死的常见原因。因此,对于那些对增加工作量有异常心脏反应的儿童以及那些有明确心肌疾病的儿童,应该进行 GYS1 缺乏症的检测。