Association Between Rheumatoid Arthritis and Clonal Hematopoiesis: A Mendelian Randomization Study

被引:1
作者
Zhang, Jie [1 ]
Zhou, Chun [2 ]
Guan, Shaoxing [3 ,4 ,5 ]
机构
[1] Guangzhou Univ Chinese Med, Guangdong Prov Hosp Chinese Med, Affiliated Hosp 2, Dept Pharm, Guangzhou, Peoples R China
[2] Southern Med Univ, Sch Pharmaceut Sci, Guangdong Prov Key Lab Shock & Microcirculat, Guangzhou, Peoples R China
[3] Southern Med Univ, NMPA Key Lab Res & Evaluat Drug Metab, Guangzhou, Peoples R China
[4] Southern Med Univ, Guangdong Prov Key Lab New Drug Screening, Guangzhou, Peoples R China
[5] Southern Med Univ, Sch Pharmaceut Sci, Guangdong Hongkong Macao Joint Lab New Drug Screen, Guangzhou, Guangdong, Peoples R China
关键词
Rheumatoid arthritis; Clonal hematopoiesis; Mendelian randomization; INSTRUMENTS; AGE;
D O I
10.1017/thg.2024.24
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Immunity activation and inflammation are the main characteristics of rheumatoid arthritis and clonal hematopoiesis. However, it remains unclear whether rheumatoid arthritis increase the risk of clonal hematopoiesis. Here, a Mendelian randomization (MR) analysis was conduct to explore the causal effects of rheumatoid arthritis on clonal hematopoiesis. Summary statistics data of rheumatoid arthritis (13,838 cases and 33,742 controls) and clonal hematopoiesis (10,203 cases and 173,918 controls) derived from a genomewide association study were selected to analyze. We selected inverse-variance weighted, MR-Egger, weighted median, simple mode, and weighted mode to evaluate the causal effect of rheumatoid arthritis on clonal hematopoiesis. The two-sample MR analysis suggested a strong causal relationship between rheumatoid arthritis and clonal hematopoiesis by inverse-variance weighted (OR = 1.002311673, 95% CI [1.000110757, 1.004517433], p = .039706) and weighted median (OR = 1.002311673, 95% CI [1.000110757, 1.004517433], p = .039518447) methods. No significant pleiotropy or heterogeneity was found in the sensitivity analysis. These results supported a potentially causal relationship between rheumatoid arthritis and clonal hematopoiesis, and the exposure of rheumatoid arthritis increased the risks of clonal hematopoiesis. Our findings highlight the importance of how chronic inflammation and immune activation induced rheumatoid arthritis enhances the risks of clonal hematopoiesis, and that early intervention with rheumatoid arthritis patients might reduce the clonal hematopoiesis risks in rheumatoid arthritis patients. Moreover, our study provides clues for prediction of risk factors and potential mechanisms of clonal hematopoiesis.
引用
收藏
页码:169 / 173
页数:5
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