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[一例先天性肌营养不良的独特病例]

[A unique case of congenital muscular dystrophy].

作者信息

Hermanová M, Vondrácek P, Lukás Z

机构信息

Patologicko-anatomický ústav FN, Brno.

出版信息

Cesk Patol. 2004 Apr;40(2):57-62.

Abstract

The congenital muscular dystrophies (CMD, MDC) represent a heterogeneous group of autosomal recessive disorders manifesting in infancy by muscle weakness and hypotonia. Approximately 40% of patients with CMD have a primary deficiency of the laminin alpha 3. chain of merosin (laminin-2) due to mutations in LAMA2 gene. Laminin-2 bound to alpha-dystroglycan forms a link between actin--associated cytoskeletal proteins and the components of extracellular matrix. Disruption of this axis is responsible for several forms of muscular dystrophy. A unique case of congenital muscular dystrophy simulating a juvenile polymyositis in a muscle biopsy is presented. A profound reduction of alpha-dystroglycan and less pronounced secondary deficiency of alpha 2-laminin were found. All known forms of CMD were excluded, and the disorder was diagnosed as so far undescribed form of CMD. The mutation in a gene encoding the protein, that seems to play a role in a glycosylation of alpha-dystroglycan, is presumed.

摘要

先天性肌营养不良症(CMD,MDC)是一组常染色体隐性疾病,在婴儿期表现为肌无力和肌张力减退。约40%的CMD患者因LAMA2基因突变导致merosin(层粘连蛋白-2)的层粘连蛋白α3链原发性缺乏。与α- dystroglycan结合的层粘连蛋白-2在肌动蛋白相关细胞骨架蛋白和细胞外基质成分之间形成联系。该轴的破坏是多种形式肌营养不良症的病因。本文介绍了一例在肌肉活检中模拟青少年型多发性肌炎的先天性肌营养不良症的独特病例。发现α- dystroglycan显著减少,α2-层粘连蛋白继发性缺乏程度较轻。排除了所有已知形式的CMD,该疾病被诊断为迄今未描述的CMD形式。推测在编码似乎在α- dystroglycan糖基化中起作用的蛋白质的基因中存在突变。

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