Evidence map›Paper›PMID 39743524›Full record

ArticleBMC rheumatology2025

Association between red blood cell distribution width and genetic risk in patients with rheumatoid arthritis: a prospective cohort study and Mendelian randomization analysis.

Mingyang Chen, Jing Lei, Zhenqiu Liu, Renjia Zhao, Yanfeng Jiang, Kelin Xu, Tiejun Zhang, Chen Suo, Xingdong Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC rheumatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Mingyang Chen *State Key Laboratory of Genetic Engineering, Human Phenome Institute, Zhangjiang Fudan International Innovation Center, and School of Life Science, Fudan University, Shanghai, 200120, China.
Jing Lei *Department of Epidemiology, School of Public Health, Fudan University, Shanghai, 200032, China.
Zhenqiu LiuState Key Laboratory of Genetic Engineering, Human Phenome Institute, Zhangjiang Fudan International Innovation Center, and School of Life Science, Fudan University, Shanghai, 200120, China.
Renjia ZhaoState Key Laboratory of Genetic Engineering, Human Phenome Institute, Zhangjiang Fudan International Innovation Center, and School of Life Science, Fudan University, Shanghai, 200120, China.
Yanfeng JiangState Key Laboratory of Genetic Engineering, Human Phenome Institute, Zhangjiang Fudan International Innovation Center, and School of Life Science, Fudan University, Shanghai, 200120, China.
Kelin XuDepartment of Epidemiology, School of Public Health, Fudan University, Shanghai, 200032, China.
Tiejun ZhangDepartment of Epidemiology, School of Public Health, Fudan University, Shanghai, 200032, China.
Chen SuoDepartment of Epidemiology, School of Public Health, Fudan University, Shanghai, 200032, China. iamsuochen@gmail.com.
Xingdong ChenState Key Laboratory of Genetic Engineering, Human Phenome Institute, Zhangjiang Fudan International Innovation Center, and School of Life Science, Fudan University, Shanghai, 200120, China. xingdongchen@fudan.edu.cn.

Funding

Innovation Grant from Science and Technology Commission of Shanghai Municipality 20ZR1405600National Natural Science Foundation of China 91846302Shanghai Municipal Science and Technology Major Project 2017SHZDZX01Three-Year Action Plan for Strengthening Public Health System in Shanghai GWV-10.2-YQ32
6 · The paper itself

Abstract

objectiveElevated red blood cell distribution width (RDW) is associated with increased risk of rheumatoid arthritis (RA), but the potential interactions of RDW with genetic risk of incident RA remain unclear. This study aimed to investigate the associations between RDW, genetics, and the risk of developing RA.

methodsWe analysed data from 145,025 healthy participants at baseline in the UK Biobank. The endpoint was diagnosed rheumatoid arthritis (ICD-10 codes M05 and M06). Using previously reported results, we constructed a polygenic risk score for RA to evaluate the joint effects of RDW and RA-related genetic risk. Two-sample mendelian randomization and bayesian colocalization were used to infer the causal relation between them.

resultsA total of 675 patients with RA were enrolled and had a median followed up of 5.1 years, with an incidence rate of 0.57/1000 person-years. The hazard ratio of RA was 1.89 (95% CI: 1.45, 2.47) in highest RDW quartile group compared with the lowest RDW quartile group. Individuals within the top quintile of PRS showed a significantly high risk of RA. Moreover, Participants with high genetic risk and those in highest RDW group exhibited a significantly elevated hazard ratio (7.67, 95% CI: 3.98, 14.81), as opposed to participants with low genetic risk and those in lowest RDW group. Interactions between PRS and RDW on the multiplicative and additive scale were observed. Mendelian randomization provided suggestive evidence of a bi-directional causal relationship between RDW and RA. Loci near IL6R, IL1RN, FADS1/FADS2, UBE2L3 and HELZ2 showed colocalization.

conclusionIncreased RDW is associated with elevated risk of incident RA especially in the high genetic risk populations, but only suggestive evidence supports a causal relationship between them.

Indexed as

ColocalizationGenetic riskMendelian randomizationRed blood cell distribution widthRheumatoid arthritis

Identifiers

PMID39743524
PMCPMC11694378

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