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辅酶 Q10 在患有线粒体肌病的患者的肌肉中经常减少。

Coenzyme Q10 is frequently reduced in muscle of patients with mitochondrial myopathy.

机构信息

Centre de référence des Maladies Neuromusculaires, Nice Hospital, CNRS, UMR 6543, Faculté de Médicine, Nice, France.

出版信息

Neuromuscul Disord. 2010 Jan;20(1):44-8. doi: 10.1016/j.nmd.2009.10.014. Epub 2009 Nov 27.

Abstract

Coenzyme Q(10) (CoQ(10)) deficiency has been associated with an increasing number of clinical phenotypes. Whereas primary CoQ(10) defects are related to mutations in ubiquinone biosynthetic genes, which are now being unraveled, and respond well to CoQ(10) supplementation, the etiologies, and clinical phenotypes related to secondary deficiencies are largely unknown. The purpose of this multicenter study was to evaluate the frequency of muscle CoQ(10) deficiency in a cohort of 76 patients presenting with clinically heterogeneous mitochondrial phenotypes which included myopathy among their clinical features. A reliable diagnostic tool based on HPLC quantification was employed to measure muscle CoQ(10) levels. A significant proportion of these patients (28 over 76) displayed CoQ(10) deficiency that was clearly secondary in nine patients, who harbored a pathogenic mutation of mitochondrial DNA. This study provides a rationale for future therapeutic trials on the effect of CoQ(10) supplementation in patients with mitochondrial diseases presenting with myopathy among clinical features.

摘要

辅酶 Q(10)(CoQ(10))缺乏与越来越多的临床表型有关。虽然原发性 CoQ(10)缺陷与泛醌生物合成基因的突变有关,这些基因现在正在被揭示,并且对 CoQ(10)补充反应良好,但与继发性缺乏相关的病因和临床表型在很大程度上尚不清楚。这项多中心研究的目的是评估在 76 名表现出临床异质性线粒体表型的患者队列中肌肉 CoQ(10)缺乏的频率,这些患者的临床特征包括肌病。采用基于 HPLC 定量的可靠诊断工具来测量肌肉 CoQ(10)水平。这些患者中有相当一部分(76 例中有 28 例)显示 CoQ(10)缺乏,其中 9 例明显是继发性的,这些患者携带有致病性的线粒体 DNA 突变。这项研究为未来在有肌病临床表现的线粒体疾病患者中进行 CoQ(10)补充治疗效果的临床试验提供了依据。

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