TK2基因c.416C > T纯合子突变患者的轻度肌病表型

Q3 Medicine
George K Papadimas, Efthimia Vargiami, Pinelopi Dragoumi, Rudy Van Coster, Joel Smet, Sara Seneca, Constantinos Papadopoulos, Evangelia Kararizou, Dimitrios Zafeiriou
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引用次数: 1

摘要

线粒体DNA缺失综合征(MDDS)的特点是广泛的表型变异,是由于核基因突变导致mtDNA拷贝数减少。众所周知,胸苷激酶2 (TK2)突变与MDDS有关。到目前为止,还没有报道过携带TK2基因c.416C > T突变的严重病例。我们描述的情况下,14个月大的男孩与上述TK2基因致病性突变在纯合状态,表现出轻微的临床表型。除了在肌肉活检中发现严重的线粒体病理外,还发现组织化学证据表明腺苷酸脱氨酶缺乏。总的来说,本报告有助于进一步扩大与MDDS相关的TK2突变的临床谱。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Mild myopathic phenotype in a patient with homozygous c.416C > T mutation in <i>TK2</i> gene.

Mild myopathic phenotype in a patient with homozygous c.416C > T mutation in <i>TK2</i> gene.

Mild myopathic phenotype in a patient with homozygous c.416C > T mutation in TK2 gene.

The mitochondrial DNA depletion syndrome (MDDS) is characterized by extensive phenotypic variability and is due to nuclear gene mutations resulting in reduced mtDNA copy number. Thymidine kinase 2 (TK2) mutations are well known to be associated with MDDS. Few severely affected cases carrying the c.416C > T mutation in TK2 gene have been described so far. We describe the case of a 14months boy with the aforementioned TK2 gene pathogenic mutation at a homozygous state, presenting with a mild clinical phenotype. In addition to severe mitochondrial pathology on muscle biopsy, there was also histochemical evidence of adenylate deaminase deficiency. Overall, this report serves to further expand the clinical spectrum of TK2 mutations associated with MDDS.

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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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