Dubowitz Neuromuscular Centre, Institute of Child Health & Great Ormond Street Hospital, 30 Guilford Street, London WC1N 1EH, United Kingdom.
Neuromuscul Disord. 2010 Apr;20(4):241-50. doi: 10.1016/j.nmd.2010.02.001. Epub 2010 Mar 6.
Merosin deficient congenital muscular dystrophy 1A (MDC1A) results from mutations in the LAMA2 gene. We report 51 patients with MDC1A and examine the relationship between degree of merosin expression, genotype and clinical features. Thirty-three patients had absence of merosin and 13 showed some residual merosin. Compared to the residual merosin group, patients with absent merosin had an earlier presentation (<7days) (P=0.0073), were more likely to lack independent ambulation (P=0.0215), or require enteral feeding (P=0.0099) and ventilatory support (P=0.0354). We identified 33 novel LAMA2 mutations; these were distributed throughout the gene in patients with absent merosin, with minor clusters in exon 27, 14, 25 and 26 (55% of mutations). Patients with residual merosin often carried at least one splice site mutation and less frequently frameshift mutations. This large study identified novel LAMA2 mutations and highlights the role of immunohistochemical studies for merosin status in predicting clinical severity of MDC1A.
先天性肌营养不良症 1A(MDC1A)是由于 LAMA2 基因突变引起的。我们报告了 51 例 MDC1A 患者,并研究了不同程度的抗肌萎缩蛋白表达、基因型和临床特征之间的关系。33 例患者抗肌萎缩蛋白完全缺失,13 例患者存在部分抗肌萎缩蛋白。与存在部分抗肌萎缩蛋白的患者相比,完全缺失抗肌萎缩蛋白的患者起病更早(<7 天)(P=0.0073),更有可能无法独立行走(P=0.0215)、需要肠内喂养(P=0.0099)和呼吸机支持(P=0.0354)。我们发现了 33 种新的 LAMA2 突变;这些突变分布在完全缺失抗肌萎缩蛋白的患者的基因中,在第 27、14、25 和 26 外显子中存在小簇(55%的突变)。存在部分抗肌萎缩蛋白的患者通常携带至少一个剪接位点突变,而较少出现移码突变。这项大型研究确定了新的 LAMA2 突变,并强调了免疫组织化学研究对抗肌萎缩蛋白状态的重要性,它可以预测 MDC1A 的临床严重程度。