Gene-respiratory disease interactions for rheumatoid arthritis risk
Authors' conclusion
ILD-HLA GRS and asthma-MUC5B promoter variant showed synergistic interactions for RA risk.
Study context
- Population
- Mass General Brigham Biobank (mean 54 years, 76% female)matched case-control
- Participants
- 653 vs 2,607
- Comparison
- Genetic (overall genetic risk score (GRS), Human Leukocyte Antigen (HLA) GRS, MUC5B promoter variant) and preceding respiratory tract disease exposures, alone and combined, for RA risk
- RA casesn = 653
- Controlsn = 2,607reference
- Outcome
- RA risk: gene by respiratory tract disease interactions (attributable proportions and multiplicative ORs)
Methodological detailsmatched to four controls on age, sex, and electronic health record history, conditional logistic regression
- Matched to four controls on age, sex, and electronic health record history
- Conditional logistic regression
Main finding
As reported in the abstract
RA risk, interactions of genetic and respiratory exposures
Odds ratio (95% CI)
ILD and HLA GRS (both exposures)AP 0.51, 95% CI −0.16,1.18; synergistic
4.30(1.28,14.38)
Asthma and MUC5B promoter variant (both exposures), seropositive RAAP 0.62, 95% CI 0.24,1.00; synergistic
2.58(1.10,6.07)
Observational data: associations, not effects.
Further findings
RA risk, highest tertile of genetic risk scores
| OR (95% CI) | ||
|---|---|---|
| Overall GRS, highest tertile | 2.28 (1.89,2.74) | |
| HLA GRS, highest tertile | 2.02 (1.67–2.45) | |
| 0.20.5125Odds ratio (log scale) |
Original publication
Gene-respiratory disease interactions for rheumatoid arthritis risk. Semin Arthritis Rheum. Published 12 August 2023. doi:10.
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