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先天性IV型糖原贮积病的神经肌肉型与大片段缺失及复发性移码突变的关联。

Association of the congenital neuromuscular form of glycogen storage disease type IV with a large deletion and recurrent frameshift mutation.

作者信息

Li Sing-Chung, Hwu Wuh-Liang, Lin Ju-Li, Bali Deeksha S, Yang Chen, Chu Shih-Ming, Chien Yin-Hsiu, Chou Hung-Chieh, Chen Chien-Yi, Hsieh Wu-Shiun, Tsao Po-Nien, Chen Yuan-Tsong, Lee Ni-Chung

机构信息

School of Nutrition and Health Science, Taipei Medical University, Taipei, Taiwan.

出版信息

J Child Neurol. 2012 Feb;27(2):204-8. doi: 10.1177/0883073811415107. Epub 2011 Sep 13.

Abstract

Anderson disease, also known as glycogen storage disease type IV (MIM 232500), is a rare autosomal recessive disorder caused by a deficiency of glycogen branching enzyme. Glycogen storage disease type IV has a broad clinical spectrum ranging from a perinatal lethal form to a nonprogressive later-onset disease in adults. Here, we report 2 unrelated infants who were born small for their gestational age and who had profound hypotonia at birth and thus needed mechanical ventilation. Both of these patients shared the same frameshift mutation (c.288delA, pGly97GlufsX46) in the GBE1 gene. In addition, both of these patients were found to have 2 different large deletions in the GBE1 gene; exon 7 and exons 2 to 7, respectively, on the other alleles. This case report also highlights the need for a more comprehensive search for large deletion mutations associated with glycogen storage disease type IV, especially if routine GBE1 gene sequencing results are equivocal.

摘要

安德森病,也称为糖原贮积病IV型(MIM 232500),是一种罕见的常染色体隐性疾病,由糖原分支酶缺乏引起。糖原贮积病IV型具有广泛的临床谱,从围产期致死型到成人非进行性迟发型疾病。在此,我们报告2例与孕周不符、出生时严重肌张力减退因而需要机械通气的不相关婴儿。这两名患者在GBE1基因中具有相同的移码突变(c.288delA,pGly97GlufsX46)。此外,这两名患者在GBE1基因的其他等位基因上分别发现有2种不同的大片段缺失;分别为外显子7和外显子2至7。本病例报告还强调,需要更全面地搜索与糖原贮积病IV型相关的大片段缺失突变,特别是在常规GBE1基因测序结果不明确的情况下。

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