Evidence map›Paper›PMID 41779596›Full record

ArticleClinical and experimental rheumatology2026

Clonal haematopoiesis and risk of incident rheumatoid arthritis: results from the UK Biobank.

Jing Cui, Zhi Yu, Emily G Oakes, Buu Truong, Mesbah Uddin, Alexander Bick, Abhishek Niroula, Daniel H Solomon, Pradeep Natarajan, Karen H Costenbader

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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

10 authors.

Jing CuiDivision of Rheumatology, Inflammation and Immunity, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Zhi YuBroad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA; and Cardiovascular Research Center and Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA.
Emily G OakesDivision of Rheumatology, Inflammation and Immunity, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Buu TruongBroad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA.
Mesbah UddinBroad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA.
Alexander BickBroad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA; and Vanderbilt University Medical Center, Center for Precision Medicine, Nashville, TN, USA.
Abhishek NiroulaBroad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA; Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Sweden; and SciLifeLab, University of Gothenburg, Sweden.
Daniel H SolomonDivision of Rheumatology, Inflammation and Immunity, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Pradeep NatarajanBroad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA; and Cardiovascular Research Center and Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA.
Karen H CostenbaderDivision of Rheumatology, Inflammation and Immunity, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. kcostenbader@bwh.harvard.edu.

Funding

VERITY: Value and Evidence in Rheumatology using bioInformaTics, and advanced analYticsP30AR072577 · BRIGHAM AND WOMEN'S HOSPITAL · 2025 to 2025
$802k
Integrated omics analysis of clonal hematopoiesis and cardiovascular disease risk in TOPMedR01HL168894 · EMORY UNIVERSITY · 2025 to 2025
$646k
Multi-omic dissection of clonal hematopoiesis-associated diseasesR00HG012956 · MASSACHUSETTS GENERAL HOSPITAL · 2025 to 2025
$249k
NHGRI NIH HHS R00 HG012956NHLBI NIH HHS R01 HL148050NHLBI NIH HHS R01 HL168894NIAMS NIH HHS P30 AR072577
6 · The paper itself

Abstract

objectivesClonal haematopoiesis of indeterminate potential (CH), somatic genetic mutations conferring stem cells selective advantage, are associated with increased inflammatory cytokine production, cardiovascular disease (CVD), and malignancy. We investigated whether CH was related to risk of rheumatoid arthritis (RA), an inflammatory autoimmune disease.

methodsWithin the UK Biobank, we studied 186,577 unrelated individuals with baseline data collection, genome-wide genotyping, whole exome sequencing (WES) read for CHIP, and linked general practice (GP) data for identification of incident RA in follow-up. We excluded those with prevalent RA or taking RA medications at baseline. We tested for associations between variant allele fraction (VAF) >2% and >10% for the 8 most common CHIP mutations in the general population, and incident RA, identified by billing code algorithms. Cox regression models estimated hazard ratios (HR, 95% confidence interval) for incident RA.

results594 participants developed incident RA over median follow-up 7.1 years (IQR 6.4-8.0); median time to RA was 3.9 years (IQR 2.0-5.6). Incident RA cases were slightly older at enrolment, more likely to be female, have smoked, have higher body mass index (BMI), and have prevalent CVD, and hypercholesterolaemia at baseline. However, there was no difference in the presence of CHIP mutations at baseline; 6.3% vs. 6.4% of those who did and did not develop incident RA in follow-up had any CHIP mutation at >2% VAF.

conclusionsCommon CHIP mutations, including TET2, TP53, and SF3B1 mutations, were not associated with risk of incident RA when restricted to those with most complete general outpatient and hospital record follow-up in the UK Biobank.

Indexed as

Arthritis, RheumatoidClonal HematopoiesisAdultAgedBiological Specimen BanksDioxygenasesDNA-Binding ProteinsFemaleGenetic Predisposition to DiseaseHumansIncidenceMaleMiddle AgedMutationPhenotypeRisk AssessmentDioxygenasesDNA-Binding ProteinsTET2 protein, human

Identifiers

PMID41779596
PMCPMC12962563

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.