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先天性不对称远端肌病伴半侧颜面肌无力,由 nebulin 异质体大片从头缺失镶嵌突变所致。

Congenital asymmetric distal myopathy with hemifacial weakness caused by a heterozygous large de novo mosaic deletion in nebulin.

机构信息

Folkhälsan Research Center, Helsinki, Finland; Department of Medical Genetics, Medicum, University of Helsinki, Finland.

Folkhälsan Research Center, Helsinki, Finland; Department of Medical Genetics, Medicum, University of Helsinki, Finland.

出版信息

Neuromuscul Disord. 2021 Jun;31(6):539-545. doi: 10.1016/j.nmd.2021.03.006. Epub 2021 Mar 23.

Abstract

We report the first mosaic mutation, a deletion of exons 11-107, identified in the nebulin gene in a Finnish patient presenting with a predominantly distal congenital myopathy and asymmetric muscle weakness. The female patient is ambulant and currently 26 years old. Muscle biopsies showed myopathic features with type 1 fibre predominance, strikingly hypotrophic type 2 fibres and central nuclei, but no nemaline bodies. The deletion was detected in a copy number variation analysis based on next-generation sequencing data. The parents of the patient did not carry the deletion. Mosaicism was detected using a custom, targeted comparative genomic hybridisation array. Expression of the truncated allele, less than half the size of full-length nebulin, was confirmed by Western blotting. The clinical and histological picture resembled that of a family with a slightly smaller deletion, and that in patients with recessively inherited distal forms of nebulin-caused myopathy. Asymmetry, however, was a novel feature.

摘要

我们报告了首例镶嵌突变,即一个在 nebulin 基因中外显子 11-107 的缺失,该突变存在于一位芬兰患者中,其表现为主要为远端先天性肌病和非对称性肌无力。这位女性患者可自主行走,目前 26 岁。肌肉活检显示具有肌病特征,Ⅰ型纤维占优势,明显的小纤维型 2 纤维和中央核,但无杆状体。缺失是在基于下一代测序数据的拷贝数变异分析中发现的。患者的父母未携带缺失。使用定制的靶向比较基因组杂交阵列检测到镶嵌现象。通过 Western blot 证实截断等位基因的表达,其大小不到全长 nebulin 的一半。临床和组织学表现类似于携带略小缺失的家族,以及隐性遗传的 nebulin 引起的远端肌病的患者。然而,非对称性是一个新的特征。

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