葡萄牙一个家族的 SIGMAR1 基因突变导致远端遗传性运动神经病。

Q3 Medicine
Acta Myologica Pub Date : 2018-05-01
Luciano Almendra, Francisco Laranjeira, Ana Fernández-Marmiesse, Luís Negrão
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引用次数: 0

摘要

SIGMAR1 基因编码一种非阿片类内质网(ER)蛋白,该蛋白参与多种细胞功能,在中枢神经系统和周围神经系统中普遍表达。其正常功能的改变可能导致两种不同的表型:幼年肌萎缩性脊髓侧索硬化症(ALS 16)和远端遗传性运动神经病(dHMN)。我们介绍了一例 37 岁女性患者的病例,她自孩提时代起就患有远端肌无力和肌萎缩,在生命的头二十年里病情缓慢发展。神经系统检查显示,患者上下肢远端对称性重度肌肉萎缩和无力,伴有爪手、足下垂、等趾畸形和锤状趾、全身肌无力,感觉检查正常。电诊断研究显示,该患者纯属慢性运动性周围神经受累,无脱髓鞘迹象。分子研究发现,SIGMAR1 基因第 4 号外显子上有 c.561_576del 缺失,第 4 号外显子全部缺失。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

<i>SIGMAR1</i> gene mutation causing Distal Hereditary Motor Neuropathy in a Portuguese family.

SIGMAR1 gene mutation causing Distal Hereditary Motor Neuropathy in a Portuguese family.

SIGMAR1 gene encodes a non-opioid endoplasmic reticulum (ER) protein which is involved in a large diversity of cell functions and is expressed ubiquitously in both central and peripheral nervous systems. Alterations of its normal function may contribute to two different phenotypes: juvenile amyotrophic lateral sclerosis (ALS 16) and distal hereditary motor neuropathies (dHMN). We present the case of a female patient, of 37-years-old, with distal muscle weakness and atrophy beginning in childhood and slowly progressive in the first two decades of life. Neurological examination revealed a symmetrical severe muscle wasting and weakness in distal lower and upper limbs, with claw hands, footdrop with equinovarus deformity and hammer toes, generalized areflexia and normal sensory examination. The electrodiagnostic study revealed a pure chronic motor peripheral nerve involvement without signs of demyelination. The molecular study found the deletion c.561_576del on exon 4 and a deletion of all exon 4, in the SIGMAR1 gene.

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来源期刊
Acta Myologica
Acta Myologica Medicine-Cardiology and Cardiovascular Medicine
CiteScore
3.70
自引率
0.00%
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0
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