Holden Sean, Maksoud Rebekah, Eaton-Fitch Natalie, Cabanas Hélène, Staines Donald, Marshall-Gradisnik Sonya
National Centre for Neuroimmunology and Emerging Diseases (NCNED), Menzies Health Institute Queensland, Griffith University, Gold Coast, Australia.
School of Medicine, Griffith University, Gold Coast, Australia.
J Transl Med. 2020 Jul 29;18(1):290. doi: 10.1186/s12967-020-02452-3.
Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) or Systemic Exertion Intolerance Disease (SEID) present with a constellation of symptoms including debilitating fatigue that is unrelieved by rest. The pathomechanisms underlying this illness are not fully understood and the search for a biomarker continues, mitochondrial aberrations have been suggested as a possible candidate. The aim of this systematic review is to collate and appraise current literature on mitochondrial changes in ME/CFS/SEID patients compared to healthy controls.
Embase, PubMed, Scopus and Medline (EBSCO host) were systematically searched for articles assessing mitochondrial changes in ME/CFS/SEID patients compared to healthy controls published between January 1995 and February 2020. The list of articles was further refined using specific inclusion and exclusion criteria. Quality and bias were measured using the Joanna Briggs Institute Critical Appraisal Checklist for Case Control Studies.
Nineteen studies were included in this review. The included studies investigated mitochondrial structural and functional differences in ME/CFS/SEID patients compared with healthy controls. Outcomes addressed by the papers include changes in mitochondrial structure, deoxyribonucleic acid/ribonucleic acid, respiratory function, metabolites, and coenzymes.
Based on the included articles in the review it is difficult to establish the role of mitochondria in the pathomechanisms of ME/CFS/SEID due to inconsistencies across the studies. Future well-designed studies using the same ME/CFS/SEID diagnostic criteria and analysis methods are required to determine possible mitochondrial involvement in the pathomechanisms of ME/CFS/SEID.
肌痛性脑脊髓炎/慢性疲劳综合征（ME/CFS）或全身运动不耐受疾病（SEID）患者表现出一系列症状，包括休息后无法缓解的使人衰弱的疲劳。这种疾病的发病机制尚未完全明确，对生物标志物的探索仍在继续，线粒体异常被认为是一个可能的候选因素。本系统评价的目的是整理和评估当前关于ME/CFS/SEID患者与健康对照者线粒体变化的文献。
系统检索Embase、PubMed、Scopus和Medline（EBSCO主机），查找1995年1月至2020年2月发表的评估ME/CFS/SEID患者与健康对照者线粒体变化的文章。使用特定的纳入和排除标准进一步完善文章列表。使用乔安娜·布里格斯研究所病例对照研究关键评价清单测量质量和偏倚。
本评价纳入了19项研究。纳入的研究调查了ME/CFS/SEID患者与健康对照者线粒体结构和功能的差异。论文涉及的结果包括线粒体结构、脱氧核糖核酸/核糖核酸、呼吸功能、代谢物和辅酶的变化。
基于本评价中纳入的文章，由于各研究结果不一致，难以确定线粒体在ME/CFS/SEID发病机制中的作用。未来需要使用相同的ME/CFS/SEID诊断标准和分析方法进行精心设计的研究来确定线粒体是否可能参与ME/CFS/SEID的发病机制。
