Christodoulou J, McInnes R R, Jay V, Wilson G, Becker L E, Lehotay D C, Platt B A, Bridge P J, Robinson B H, Clarke J T
Department of Pediatrics and Genetics, Hospital for Sick Children, Toronto, Ontario, Canada.
Am J Med Genet. 1994 Apr 15;50(3):255-64. doi: 10.1002/ajmg.1320500309.
Barth syndrome is an X-linked recessive condition characterized by skeletal myopathy, cardiomyopathy, proportionate short stature, and recurrent neutropenia, but with normal cognitive function. Some, but not all patients, exhibit carnitine deficiency and/or the presence of 3-methylglutaconic and ethylhydracylic acids in urine. Recently the mutation causing Barth syndrome was localised to the Xq28 region by linkage analysis. We report 6 cases of Barth syndrome from 4 families and highlight the fact that neuromuscular and cardiovascular symptoms and the severity of infections tend to improve with age, while short stature persists. Also previously unreported was myopathic facies and nasal quality to speech in our cases. The urinary organic acid abnormalities and plasma carnitine deficiency were inconsistent findings. We propose that they may be epiphenomena rather than indicators of the primary metabolic defect, and that the primary defect or defects in this disorder may lie in the mitochondrial electron transport chain.
巴氏综合征是一种X连锁隐性疾病,其特征为骨骼肌病、心肌病、身材比例矮小和复发性中性粒细胞减少症,但认知功能正常。部分(而非全部)患者存在肉碱缺乏和/或尿中出现3-甲基戊二酸和乙基羟基戊二酸。最近,通过连锁分析将导致巴氏综合征的突变定位到Xq28区域。我们报告了来自4个家庭的6例巴氏综合征病例,并强调了以下事实:神经肌肉和心血管症状以及感染的严重程度往往会随着年龄增长而改善,而身材矮小仍然存在。此外,我们病例中的肌病面容和鼻音在之前未被报道过。尿有机酸异常和血浆肉碱缺乏的结果并不一致。我们认为它们可能是附带现象而非原发性代谢缺陷的指标,并且这种疾病的原发性缺陷可能存在于线粒体电子传递链中。