Subclinical atherosclerosis profiles in rheumatoid arthritis and primary Sjögren’s syndrome: the impact of BAFF genetic variations
Authors' conclusion
Increased inflammatory burden, higher steroid doses and distinct BAFF gene variations imply chronic inflammation and B-cell hyperactivity as key contributors for the augmented atherosclerotic risk among autoimmune patients.
Study context
- Population
- Patients with RA or primary SS and healthy controls of similar age and sex distribution
- Participants
- 166 / 148 / 200
- Exposure
- RA vs primary SS
- RAn = 166
- Primary SSn = 148reference
- Healthy controlsn = 200
- Outcome
- Subclinical atherosclerosis: carotid/femoral plaque formation and arterial wall thickening; association with BAFF gene variants
Methodological detailsgenetic association study, PCR-based genotyping of five BAFF SNPs
- Genetic association study
- PCR-based genotyping of five BAFF SNPs
Main finding
As reported in the abstract
Atherosclerotic plaque formation
P < 0.001
Observational data: associations, not effects.
Further findings
Clinical features, RA vs primary SS
- Higher rates of family CVD history, current steroid dose and serum inflammatory markers in RA
BAFF rs1224141 TT genotype
- More prevalent in RA (but not primary SS) patients with plaque and arterial wall thickening vs those without
BAFF rs1014569 variant and plaque formation
- TT genotype increased plaque risk in RA; AT genotype conferred increased risk in primary SS
BAFF haplotypes
- GTTTT protective in RA; TATTT and TTCTT increased susceptibility for arterial wall thickening in primary SS
Original publication
Subclinical atherosclerosis profiles in rheumatoid arthritis and primary Sjögren’s syndrome: the impact of BAFF genetic variations. Rheumatology (Oxford). Published 11 June 2022. doi:10.
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