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婴儿期起病的脑肌病、视网膜病变、视神经萎缩和线粒体 DNA 耗竭与一种新的致病性 DHX16 变异相关。

Infantile onset encephalomyopathy, retinopathy, optic atrophy, and mitochondrial DNA depletion associated with a novel pathogenic DHX16 variant.

机构信息

Research Unit of Clinical Medicine, Medical Research Center, University of Oulu, Oulu, Finland.

Oulu University Hospital, Oulu, Finland.

出版信息

Clin Genet. 2023 Dec;104(6):686-693. doi: 10.1111/cge.14416. Epub 2023 Aug 13.

Abstract

We studied a patient with mitochondrial DNA depletion in skeletal muscle and a multiorgan phenotype, including fatal encephalomyopathy, retinopathy, optic atrophy, and sensorineural hearing loss. Instead of pathogenic variants in the mitochondrial maintenance genes, we identified previously unpublished variant in DHX16 gene, a de novo heterozygous c.1360C>T (p. Arg454Trp). Variants in DHX16 encoding for DEAH-box RNA helicase have previously been reported only in five patients with a phenotype called as neuromuscular oculoauditory syndrome including developmental delay, neuromuscular symptoms, and ocular or auditory defects with or without seizures. We performed functional studies on patient-derived fibroblasts and skeletal muscle revealing, that the DHX16 expression was decreased. Clinical features together with functional data suggest, that our patient's disease is associated with a novel pathogenic DHX16 variant, and mtDNA depletion could be a secondary manifestation of the disease.

摘要

我们研究了一位患有骨骼肌中线粒体 DNA 耗竭和多器官表型的患者,包括致命性脑肌病、视网膜病变、视神经萎缩和感觉神经性听力损失。除了线粒体维持基因中的致病性变异外,我们还发现了先前未发表的 DHX16 基因中的变异,即从头杂合 c.1360C>T(p.Arg454Trp)。DHX16 编码 DEAH 盒 RNA 解旋酶的变异以前仅在五名患有称为神经肌肉眼耳综合征的患者中报道过,其特征包括发育迟缓、神经肌肉症状、眼部或耳部缺陷伴或不伴癫痫。我们对患者来源的成纤维细胞和骨骼肌进行了功能研究,发现 DHX16 的表达降低。临床特征和功能数据表明,我们患者的疾病与一种新的致病性 DHX16 变异有关,而 mtDNA 耗竭可能是该疾病的继发表现。

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