ArticleArthritis & rheumatology (Hoboken, N.J.)2026
Association of Clonal Hematopoiesis With Incident, Late-Onset, Seropositive Rheumatoid Arthritis.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed.
- Reply.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Clarifying the clinical implications of clonal hematopoiesis in late-onset seropositive rheumatoid arthritis: comment on the article by Zhao et al.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- EULAR Rheumatology Open Special Issue titled 'VSI: ATT2026': the role of clonal haematopoiesis in immunological and rheumatological diseases.EULAR rheumatology open · 2026Review
- Clonal hematopoiesis is associated with distinct rheumatoid arthritis phenotypes.Science advances · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
objectiveClonal hematopoiesis (CH), defined by acquired driver mutations in hematopoietic stem cells, is associated with many inflammatory diseases of aging. We investigated whether CH and its subtypes, CH of indeterminate potential (CHIP) and mosaic chromosomal alteration (mCA), are associated with incident rheumatoid arthritis (RA) and whether complement modifies these associations.
methodsCHIP was detected in NIH All of Us, Vanderbilt BioVU, and UK Biobank; mCA was detected in UK Biobank. A harmonized, high-specificity phenotyping algorithm was applied across biobanks to identify participants with seropositive and seronegative RA (SPRA and SNRA). Age-scale survival models assessed the effect of CH on risk of incident RA. Effect modification was tested with interaction models with genetically predicted complement protein levels.
resultsAmong 612,989 participants, 30,840 had CHIP, 1,535 had incident SPRA, and 1,090 had incident SNRA. CHIP was associated with an increased risk of incident SPRA (pooled hazard ratio [HR] 1.26; confidence interval [CI] 1.03-1.52; P = 2.3 × 10
conclusionAge-related CH, including DNMT3A-CHIP, autosomal mCA, and mLOY, are risk factors for incident SPRA but not SNRA, supporting a genotype- and serostatus-specific link between somatic mutation and RA, with the classical complement pathway as a potential modifier.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.