Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are caused by mutations in the dystrophin gene. We studied 106 patients with a diagnosis of probable DMD/BMD by analyzing 20 exons of the dystrophin gene in their blood and, in some of the cases, by immunohistochemical assays for dystrophin in muscle biopsies. In 71.7% of the patients, deletions were found in at least one of the exons; 68% of these deletions were in the hot-spot 3' region. Deletions were found in 81.5% of the DMD cases and in all the BMD cases. The cases without deletions, which included the only woman in the study with DMD, had dystrophin deficiency. The symptomatic female carriers had no deletions but had abnormal dystrophin distribution in the sarcolemma (discontinuous immunostains). The following diagnoses were made for the remaining cases without deletions with the aid of a muscle biopsy: spinal muscular atrophy, congenital myopathy; sarcoglycan deficiency and unclassified limb-girdle muscular dystrophy. Dystrophin analysis by immunohistochemistry continues to be the most specific method for diagnosis of DMD/BMD and should be used when no exon deletions are found in the dystrophin gene in the blood.

译文

:Duchenne肌营养不良症(DMD)和Becker肌营养不良症(BMD)由肌营养不良蛋白基因的突变引起。我们通过分析血液中的肌营养不良蛋白基因的20个外显子,对某些诊断为DMD / BMD的患者进行了研究,在某些情况下,还通过免疫组织化学方法对肌肉活检中的肌营养不良蛋白进行了分析。在71.7%的患者中,至少有一个外显子被发现缺失。这些缺失中的68%位于热点3'区域。在81.5%的DMD病例和所有BMD病例中均发现缺失。没有删除的病例,包括研究中仅有的一名患有DMD的女性,患有肌营养不良蛋白缺乏症。有症状的女性携带者没有缺失,但肌膜中的肌营养不良蛋白分布异常(不连续的免疫染色)。余下的病例在肌肉活检的帮助下对没有缺失的病例做出了以下诊断:脊髓性肌萎缩,先天性肌病;肌糖蛋白缺乏和未分类的肢带型肌营养不良症。通过免疫组织化学进行肌营养不良蛋白分析仍然是诊断DMD / BMD的最具体方法,当血液中肌营养不良蛋白基因中未发现外显子缺失时,应使用肌营养不良蛋白分析。

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