Vasculitis & polymyalgia rheumatica
Modifiable risk factors and inflammation-related proteins in polymyalgia rheumatica: genome-wide meta-analysis and Mendelian randomization
Authors' conclusion
Reducing smoking and visceral adiposity at a population level might reduce incidence of PMR. We identified proteins that may play causal roles in PMR, potentially suggesting new therapeutic opportunities.
Study context
- Population
- People of European ancestry from the UK Biobank and FinnGen
- Participants
- 8,156 vs 416,495
- Comparison
- PMR cases vs controls; genetically predicted modifiable risk factors and inflammation-related circulating proteins
- PMRn = 8,156
- Controlsn = 416,495reference
- Outcome
- PMR susceptibility: genome-wide significant loci and associations with eight modifiable risk factors and 65 inflammation-related circulating proteins
Methodological detailsinverse variance weighted and pleiotropy robust methods, UK Biobank and FinnGen, European ancestry
- Inverse variance weighted and pleiotropy robust methods
- UK Biobank and FinnGen
- European ancestry
Pooled result
As reported in the abstract
Smoking intensity, OR
1.32
95% CI 1.08–1.60P = 0.006
Visceral adiposity, OR
1.22
95% CI 1.10–1.37P = 3.10 × 10-4
Further pooled results
Inflammation-related circulating proteins and PMR (significant after correction for multiple testing)
- IL-1 receptor-like 2 (IL-36 receptor), OR (P = 1.89 × 10-32)
- 1.25
- Serum amyloid A2, OR (9.91 × 10-10)
- 1.06
- CXCL6, OR (P = 4.85 × 10-7)
- 1.09
- Multiple circulating proteins related to IL-1 family signalling were associated with PMR
Original publication
Modifiable risk factors and inflammation-related proteins in polymyalgia rheumatica: genome-wide meta-analysis and Mendelian randomization. Rheumatology (Oxford). Published 24 May 2024. doi:10.
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