Spiegel Ronen, Gomez Estela Area, Akman Hasan O, Krishna Sindu, Horovitz Yoseph, DiMauro Salvatore
Department of Pediatrics, HaEmek Medical Center, Rappaport School of Medicine, Afula, Israel.
Neuromuscul Disord. 2009 Mar;19(3):207-11. doi: 10.1016/j.nmd.2008.12.004. Epub 2009 Jan 20.
We describe an 18-year-old man with muscle cramps and recurrent exertional myoglobinuria, without hemolytic anemia or brain dysfunction. Phosphoglycerate kinase (PGK) deficiency was documented in muscle and erythrocytes and molecular analysis of the PGK1 gene identified a novel mutation, T378P. This is the ninth case presenting with isolated myopathy, whereas most other patients show hereditary non-spherocytic hemolytic anemia alone or associated with brain dysfunction, and a few patients have myopathy plus brain involvement. Although the diverse tissue involvement in PGK deficiency remains unclear, all mutations in myopathic patients tend to cluster in the C terminal domain, adjacent to the substrate-binding pocket. This may lead to a failure in the closure of the N terminal and C terminal domains and loss of stability due to lack of inter-domain communication during the catalytic process.
我们描述了一名18岁男性,患有肌肉痉挛和复发性运动性肌红蛋白尿,无溶血性贫血或脑功能障碍。肌肉和红细胞中证实存在磷酸甘油酸激酶(PGK)缺乏,对PGK1基因的分子分析鉴定出一种新的突变,T378P。这是第九例表现为孤立性肌病的病例,而大多数其他患者仅表现为遗传性非球形细胞溶血性贫血或伴有脑功能障碍,少数患者有肌病加脑部受累。尽管PGK缺乏症中不同组织受累的情况尚不清楚,但肌病患者的所有突变往往聚集在与底物结合口袋相邻的C末端结构域。这可能导致N末端和C末端结构域无法闭合,并由于催化过程中缺乏结构域间通讯而导致稳定性丧失。