Department of Epidemiology, University of North Carolina at Chapel Hill Gillings School of Global Public Health, Chapel Hill, NC, United States; Department of Epidemiology, Emory University Rollins School of Public Health, Atlanta, GA, United States.
Department of Epidemiology, Emory University Rollins School of Public Health, Atlanta, GA, United States; Kaiser Permanente Northern California, Division of Research, Oakland, CA, United States.
Brain Behav Immun. 2017 May;62:230-244. doi: 10.1016/j.bbi.2017.01.007. Epub 2017 Jan 12.
Fatigue is one of the most common and distressing symptoms, leading to markedly decreased quality of life among a large subset of patients with a variety of disorders. Susceptibility to fatigue may be influenced by genetic factors including single nucleotide polymorphisms (SNPs), especially in the regulatory regions, of relevant genes. To further investigate the association of SNPs with fatigue in various patient populations, a systematic search was conducted on Pubmed, CINAHL, PsycINFO, and Sociological Abstracts Database for fatigue related-terms in combination with polymorphisms or genetic variation-related terms. Fifty papers in total met the inclusion and exclusion criteria for this analysis. These 50 papers were further classified into three subgroups for evaluation: chronic fatigue syndrome (CFS), cancer-related fatigue (CRF) and other disease-related fatigue. SNPs in regulatory pathways of immune and neurotransmitter systems were found to play important roles in the etiologies of CFS, CRF and other disease-related fatigue. Evidence for associations between elevated fatigue and specific polymorphisms in TNFα, IL1b, IL4 and IL6 genes was revealed for all three subgroups of fatigue. We also found CFS shared a series of polymorphisms in HLA, IFN-γ, 5-HT and NR3C1 genes with other disease-related fatigue, however these SNPs (excluding IFN-γ) were not found to be adequately investigated in CRF. Gaps in knowledge related to fatigue etiology and recommendations for future research are further discussed.
疲劳是最常见和最令人痛苦的症状之一，导致大量患有各种疾病的患者的生活质量显著下降。疲劳的易感性可能受到遗传因素的影响，包括单核苷酸多态性 (SNPs)，尤其是在相关基因的调控区域。为了进一步研究 SNPs 与各种患者群体疲劳之间的关联，我们在 Pubmed、CINAHL、PsycINFO 和 Sociological Abstracts Database 上进行了系统搜索，使用与多态性或遗传变异相关的术语结合疲劳相关术语。共有 50 篇论文符合本分析的纳入和排除标准。这 50 篇论文进一步分为三个亚组进行评估：慢性疲劳综合征 (CFS)、癌症相关疲劳 (CRF) 和其他疾病相关疲劳。免疫和神经递质系统调节途径中的 SNPs 被发现与 CFS、CRF 和其他疾病相关疲劳的病因学有关。TNFα、IL1b、IL4 和 IL6 基因中特定 SNPs 与所有三组疲劳患者的疲劳升高之间存在关联的证据。我们还发现，CFS 与其他疾病相关疲劳的 HLA、IFN-γ、5-HT 和 NR3C1 基因中的一系列 SNPs 共享，但这些 SNPs（IFN-γ 除外）在 CRF 中没有得到充分研究。进一步讨论了与疲劳病因相关的知识差距和未来研究的建议。
