新型复合杂合子 FKRP 基因突变导致轻度肢腰肌营养不良症 R9 表型。

Ikhlass Belhassen, Rita Menassa, Salma Sakka, Laurence Michel-Calemard, Nathalie Streichenberger, Dorra Ben Ayed, Nadia Bouattour, Mariem Dammak, Chokri Mhiri
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摘要

福丁相关蛋白(FKRP)突变可导致多种肌肉萎缩症,从相对轻微的肢腰肌营养不良症9型(LGMDR9)到严重的先天性肌肉萎缩症(CMD)。本研究旨在报告一个突尼斯非血缘家族中的两对兄弟姐妹,他们携带一种新型复合杂合FKRP变异体,表现为轻度LGDMR9表型。为了筛选变异,研究人员进行了大规模平行测序,随后又进行了桑格测序和多重连接依赖性探针扩增(MLPA),以验证所发现变异的存在。通过免疫组化确定了α-肌张力蛋白的缺失。大脑和大腿磁共振成像(MRI)检测了大腿和大脑的异常。两兄妹的发病年龄较晚,临床检查显示,骨盆腰部的无力主要呈近端对称分布,没有心脏或呼吸系统受累。DNA测序结果显示,一个等位基因的第2和第3外显子发生了新的缺失,而第二个等位基因则发生了c.1364C > A的错义突变,据报道这种突变可导致先天性肌营养不良和智力低下。两个病例中同时出现这两种变异,表明变异与病理生理学存在分离。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mild limb girdle muscular dystrophy R9 phenotype caused by novel compound heterozygous FKRP gene mutation.

Fukutin-related protein (FKRP) mutations cause a broad spectrum of muscular dystrophies, from a relatively mild limb-girdle muscular dystrophy type 9 (LGMDR9) to severe congenital muscular dystrophy (CMD). This study aims to report two siblings belonging to a non-consanguineous Tunisian family harboring a novel compound heterozygous FKRP variant and presenting a mild LGDMR9 phenotype. For mutation screening, massive parallel sequencing was performed, followed by Sanger sequencing and multiplex ligation-dependent probe amplification (MLPA) to validate the existence of the discovered variants. The absence of alpha-dystroglycan was determined by immunohistochemistry. Brain and thigh magnetic resonance imaging (MRI) were performed to detect thigh and brain abnormalities. The two siblings had a late age at onset and clinical examination showed that the pelvic girdles had a predominantly proximal and symmetrical distribution of weakness without cardiac or respiratory involvement. They both had a modified Gardner-Medwin Walton Scale mGMWS grade of 4 and a modified Rankin Scale (mRS) score of 1. The DNA sequencing revealed a novel deletion of exons 2 and 3 in one allele and a missense mutation c.1364C > A, which has been reported to be responsible for congenital muscular dystrophy and mental retardation on the second allele. The simultaneous presence of the two variations in the two cases suggests that the variants segregate with the pathophysiology.

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