Coffee consumption and the risk of rheumatoid arthritis and systemic lupus erythematosus: a Mendelian randomization study
Coffee consumption and the risk of rheumatoid arthritis and systemic lupus erythematosus: a Mendelian randomization study
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DOI：
10.1007/s10067-018-4278-9
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发表时间：
2018-10-01
影响因子：
3.4
通讯作者：
Lee, Young Ho
中科院分区：
文献类型：
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作者：
Bae, Sang-Cheol;Lee, Young Ho
我们的目的是分析咖啡消费与类风湿性关节炎（RA）和系统性红斑狼疮（SLE）风险之间的因果关系。我们使用逆方差加权（IVW）、MR-Egger回归和加权中位数方法进行了双样本孟德尔随机化（MR）分析。我们使用咖啡消费全基因组关联研究（GWAS）的公开汇总统计数据集作为暴露变量，RA和SLE GWAS作为结果。从咖啡消费的GWAS中选择四个单核苷酸多态性（SNP）作为工具变量（IV）来改善推断：NCARD（rs 16868941），POR（rs 17685），CYP 1A 1（rs 2470893）和LAMB 4（rs382140）。IVW方法显示咖啡消费与RA之间存在因果关系（β = 0.770，SE = 0.279，p = 0.006）。MR-Egger回归显示，方向性多效性不太可能使结果产生偏倚（截距=-0.145，p = 0.451）。虽然MR-Egger分析显示咖啡消费与RA之间没有因果关系（β = 2.744，SE = 1.712，p = 0.355），但加权中位数方法显示咖啡消费与RA之间存在因果关系（β = 0.751，SE = 0.348，p = 0.031）。然而，基于Bonferroni校正后的加权中位数分析的相关性不显著（校正后的p值= 0.091）。IVW、MR-Egger分析和加权中位数方法显示咖啡摄入量与SLE风险之间无因果关系（β = 0.594，SE = 0.437，p = 0.209; β = 3.100，SE = 3.632，p = 0.550; β = 0.733，SE = 0.567，p = 0.196）。MR分析结果不支持咖啡消费与RA和SLE的发展之间的因果关系。
We aimed to analyze the causal association between coffee consumption and the risk of rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). We performed a two-sample Mendelian randomization (MR) analysis using the inverse-variance weighted (IVW), MR-Egger regression, and weighted median methods. We used publicly available summary statistics datasets of coffee consumption genome-wide association studies (GWASs) as an exposure variable and RA and SLE GWASs as outcomes. Four single-nucleotide polymorphisms (SNPs) from GWASs of coffee consumption were selected as instrumental variables (IVs) to improve inference: NCARD (rs16868941), POR (rs17685), CYP1A1 (rs2470893), and LAMB4 (rs382140). The IVW method showed a causal association between coffee consumption and RA (beta = 0.770, SE = 0.279, p = 0.006). MR-Egger regression revealed that directional pleiotropy was unlikely to be biasing the result (intercept = - 0.145, p = 0.451). While the MR-Egger analysis showed no causal association between coffee consumption and RA (beta = 2.744, SE = 1.712, p = 0.355), the weighted median approach demonstrated a causal association between coffee consumption and RA (beta = 0.751, SE = 0.348, p = 0.031). However, the associations based on the weighted median analyses after the Bonferroni correction were not significant (adjusted p values = 0.091). The IVW, MR-Egger analysis, and weighted median methods showed no causal association between coffee consumption and SLE risk (beta = 0.594, SE = 0.437, p = 0.209; beta = 3.100, SE = 3.632, p = 0.550; beta = 0.733, SE = 0.567, p = 0.196). MR analysis results do not support causal associations between coffee consumption and the development of RA and SLE.