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肌-管酸尿症中杂合子的表现:一个神话还是现实——他汀类药物的作用。

Manifesting heterozygotes in McArdle disease: a myth or a reality-role of statins.

机构信息

Grup de Recerca en Malalties Neuromusculars i Neuropediatriques, Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol, Campus Can Ruti, Universitat Autònoma de Barcelona, Badalona, Barcelona, Spain.

Centre for Biomedical Network Research on Rare Diseases (CIBERER), Instituto de Salud Carlos III, Madrid, Spain.

出版信息

J Inherit Metab Dis. 2018 Nov;41(6):1027-1035. doi: 10.1007/s10545-018-0203-2. Epub 2018 Jun 20.

Abstract

McArdle disease is an autosomal recessive condition caused by deficiency of the PYGM gene-encoded muscle isoform of glycogen phosphorylase. Some cases of "manifesting" heterozygotes or carriers (i.e., patients who show some McArdle-like symptoms or signs despite being carriers of only one mutated PYGM allele) have been reported in the literature but there is controversy, with misdiagnosis being a possibility. The purpose of our study was to determine if there are actually "manifesting" heterozygotes of McArdle disease and, if existing, whether statin treatment can trigger such condition. Eighty-one relatives of McArdle patients (among a total of 16 different families) were studied. We determined whether they were carriers of PYGM mutations and also collected information on exercise tests (second wind and modified Wingate anaerobic test) and statin intake. We found 50 carriers and 31 non-carriers of PYGM mutations. Although we found existence of heterozygotes manifesting some exercise-related muscle problems such as exacerbated myalgia or weakness, they only accounted for 14% of the carriers and muscle symptoms were milder than those commonly reported in patients. Further, no carrier (whether reporting symptoms or not) showed the second wind phenomenon or a flat blood lactate response to maximal-intensity exercise, both of which are hallmarks of McArdle disease. On the other hand, statin myotoxicity was not associated with muscle symptom onset.

摘要

肌磷酸化酶缺乏症是一种常染色体隐性遗传病,由编码肌肉同工型糖原磷酸化酶的 PYGM 基因突变引起。一些“表现型”杂合子或携带者(即尽管仅携带一个突变的 PYGM 等位基因,但表现出一些肌磷酸化酶缺乏症样症状或体征的患者)的病例已在文献中报道,但存在争议,误诊的可能性也存在。我们的研究目的是确定是否存在肌磷酸化酶缺乏症的“表现型”杂合子,如果存在,他汀类药物治疗是否会引发这种情况。我们研究了 81 名肌磷酸化酶缺乏症患者的亲属(共来自 16 个不同的家庭)。我们确定了他们是否为 PYGM 基因突变的携带者,并收集了有关运动试验(二次呼吸和改良的 Wingate 无氧试验)和他汀类药物摄入的信息。我们发现了 50 名 PYGM 基因突变的携带者和 31 名非携带者。尽管我们发现存在一些表现出与运动相关的肌肉问题的杂合子,如肌肉痛或无力加重,但这些杂合子仅占携带者的 14%,且肌肉症状比患者中常见的症状要轻。此外,没有携带者(无论是否报告症状)表现出二次呼吸现象或最大强度运动时血乳酸反应平坦,这两者都是肌磷酸化酶缺乏症的特征。另一方面,他汀类药物的肌肉毒性与肌肉症状的发作无关。

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