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肌肉糖原贮积病0型中的心肌病与运动不耐受

Cardiomyopathy and exercise intolerance in muscle glycogen storage disease 0.

作者信息

Kollberg Gittan, Tulinius Már, Gilljam Thomas, Ostman-Smith Ingegerd, Forsander Gun, Jotorp Peter, Oldfors Anders, Holme Elisabeth

机构信息

Department of Pathology, Sahlgrenska University Hospital, Gothenburg, Sweden.

出版信息

N Engl J Med. 2007 Oct 11;357(15):1507-14. doi: 10.1056/NEJMoa066691.

Abstract

Storage of glycogen is essential for glucose homeostasis and for energy supply during bursts of activity and sustained muscle work. We describe three siblings with profound muscle and heart glycogen deficiency caused by a homozygous stop mutation (R462-->ter) in the muscle glycogen synthase gene. The oldest brother died from sudden cardiac arrest at the age of 10.5 years. Two years later, an 11-year-old brother showed muscle fatigability, hypertrophic cardiomyopathy, and an abnormal heart rate and blood pressure while exercising; a 2-year-old sister had no symptoms. In muscle-biopsy specimens obtained from the two younger siblings, there was lack of glycogen, predominance of oxidative fibers, and mitochondrial proliferation. Glucose tolerance was normal.

摘要

糖原的储存对于维持葡萄糖稳态以及在剧烈运动和持续肌肉工作期间提供能量供应至关重要。我们描述了三名兄弟姐妹,他们因肌肉糖原合酶基因中的纯合终止突变(R462→ter)而患有严重的肌肉和心脏糖原缺乏症。最大的哥哥在10.5岁时死于心脏骤停。两年后,一名11岁的哥哥在运动时出现肌肉疲劳、肥厚型心肌病以及异常的心率和血压;一名2岁的妹妹没有症状。在从两名年幼的兄弟姐妹身上获取的肌肉活检标本中,糖原缺乏,氧化纤维占优势,并且线粒体增殖。葡萄糖耐量正常。

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