Yuanyuan Zeng, Xiaolan Yang, Shengda Tao, Ling Lei
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Two-sample MR analyses were performed separately for EA and the five CTDs.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>We found a negative causal relationship between EA and RA (OR<sub>IVW</sub> = 0.627, 95% CI = 0.537–0.732, <i>p</i> < .001), and SLE (OR<sub>IVW</sub> = 0.341, 95% CI = 0.123–0.944, <i>p</i> = .038). There were no genetic causal association between EA and SSc (OR<sub>IVW</sub> = 0.647, 95% CI = 0.351–1.195, <i>p</i> = .164), PM (OR<sub>IVW</sub> = 0.938, 95% CI = 0.320–2.746, <i>p</i> = .907), or DM (OR<sub>IVW</sub> = 0.754, 95% CI = 0.351–1.619, <i>p</i> = .468). None of the analyses revealed any horizontal pleiotropy or heterogeneity.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>Our findings indicated a potential causal association between EA and RA, SLE, emphasizing the need for further investigation and potential integration of EA into clinical practice to enhance treatment strategies.</p>\n </section>\n </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 7","pages":""},"PeriodicalIF":2.4000,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Association of education attainment and risk of connective tissue diseases\",\"authors\":\"Yuanyuan Zeng, Xiaolan Yang, Shengda Tao, Ling Lei\",\"doi\":\"10.1111/1756-185X.15264\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Objective</h3>\\n \\n <p>We employed two-sample Mendelian randomization (MR) to assess the genetic causal relationship between educational attainment (EA) and risk of five common connective tissue diseases (CTDs).</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methods</h3>\\n \\n <p>Educational attainment (self-reported at age ≥30 years) was obtained from a meta-analysis of years of schooling in 766 345 participants of European ancestry from genome-wide association studies (GWAS). A total of 1265 signals associated with EA were identified. Genetic data for five CTDs [rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), polymyositis (PM), and dermatomyositis (DM)] were obtained from the FinnGen consortium. Two-sample MR analyses were performed separately for EA and the five CTDs.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>We found a negative causal relationship between EA and RA (OR<sub>IVW</sub> = 0.627, 95% CI = 0.537–0.732, <i>p</i> < .001), and SLE (OR<sub>IVW</sub> = 0.341, 95% CI = 0.123–0.944, <i>p</i> = .038). There were no genetic causal association between EA and SSc (OR<sub>IVW</sub> = 0.647, 95% CI = 0.351–1.195, <i>p</i> = .164), PM (OR<sub>IVW</sub> = 0.938, 95% CI = 0.320–2.746, <i>p</i> = .907), or DM (OR<sub>IVW</sub> = 0.754, 95% CI = 0.351–1.619, <i>p</i> = .468). 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引用次数: 0
摘要
目的:我们采用双样本孟德尔随机法(MR)评估教育程度(EA)与五种常见结缔组织疾病(CTD)风险之间的遗传因果关系:我们采用双样本孟德尔随机法(MR)评估了受教育程度(EA)与五种常见结缔组织疾病(CTD)风险之间的遗传因果关系:教育程度(≥30 岁时的自我报告)是通过对全基因组关联研究(GWAS)中 766 345 名欧洲血统参与者的受教育年限进行荟萃分析获得的。共确定了 1265 个与 EA 相关的信号。五种 CTD [类风湿性关节炎(RA)、系统性红斑狼疮(SLE)、系统性硬化症(SSc)、多发性肌炎(PM)和皮肌炎(DM)]的基因数据来自芬兰基因联盟(FinnGen consortium)。对EA和五种CTD分别进行了双样本MR分析:我们发现 EA 与 RA 之间存在负因果关系(ORIVW = 0.627,95% CI = 0.537-0.732,p IVW = 0.341,95% CI = 0.123-0.944,p = .038)。EA与SSc(ORIVW = 0.647,95% CI = 0.351-1.195,p = .164)、PM(ORIVW = 0.938,95% CI = 0.320-2.746,p = .907)或DM(ORIVW = 0.754,95% CI = 0.351-1.619,p = .468)之间没有遗传因果关系。所有分析均未显示任何水平多向性或异质性:我们的研究结果表明,EA 与 RA 和系统性红斑狼疮之间存在潜在的因果关系,强调了进一步研究的必要性,以及将 EA 纳入临床实践以加强治疗策略的可能性。
Association of education attainment and risk of connective tissue diseases
Objective
We employed two-sample Mendelian randomization (MR) to assess the genetic causal relationship between educational attainment (EA) and risk of five common connective tissue diseases (CTDs).
Methods
Educational attainment (self-reported at age ≥30 years) was obtained from a meta-analysis of years of schooling in 766 345 participants of European ancestry from genome-wide association studies (GWAS). A total of 1265 signals associated with EA were identified. Genetic data for five CTDs [rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), polymyositis (PM), and dermatomyositis (DM)] were obtained from the FinnGen consortium. Two-sample MR analyses were performed separately for EA and the five CTDs.
Results
We found a negative causal relationship between EA and RA (ORIVW = 0.627, 95% CI = 0.537–0.732, p < .001), and SLE (ORIVW = 0.341, 95% CI = 0.123–0.944, p = .038). There were no genetic causal association between EA and SSc (ORIVW = 0.647, 95% CI = 0.351–1.195, p = .164), PM (ORIVW = 0.938, 95% CI = 0.320–2.746, p = .907), or DM (ORIVW = 0.754, 95% CI = 0.351–1.619, p = .468). None of the analyses revealed any horizontal pleiotropy or heterogeneity.
Conclusion
Our findings indicated a potential causal association between EA and RA, SLE, emphasizing the need for further investigation and potential integration of EA into clinical practice to enhance treatment strategies.
期刊介绍:
The International Journal of Rheumatic Diseases (formerly APLAR Journal of Rheumatology) is the official journal of the Asia Pacific League of Associations for Rheumatology. The Journal accepts original articles on clinical or experimental research pertinent to the rheumatic diseases, work on connective tissue diseases and other immune and allergic disorders. The acceptance criteria for all papers are the quality and originality of the research and its significance to our readership. Except where otherwise stated, manuscripts are peer reviewed by two anonymous reviewers and the Editor.