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Subclinical atherosclerosis profiles in rheumatoid arthritis and primary Sjögren’s syndrome: The impact of BAFF genetic variations

Rheumatology (Oxford). 2022 Jun 11:keac337. doi: 10.1093/rheumatology/keac337. Online ahead of print.


OBJECTIVES: Rheumatoid Arthritis (RA) and primary Sjögren’s Syndrome (SS) carry increased atherosclerotic risk, while B cell activating factor holds a vital role in disease pathogenesis and atherosclerosis. We aimed to compare subclinical atherosclerosis profiles between the two clinical entities and define whether BAFF genetic variants alter atherosclerotic risk.

METHODS: DNA from 166 RA, 148 primary SS patients and 200 healthy controls of similar age and sex distribution was subjected to PCR-based assay for the detection of five single nucleotide polymorphisms of the BAFF gene (rs1224141, rs12583006, rs9514828, rs1041569, and rs9514827). Genotype and haplotype frequencies were determined by SNPStats software and statistical analysis was performed by SPSS and Graphpad Software. Subclinical atherosclerosis was defined by the presence of carotid/femoral plaque formation and arterial wall thickening.

RESULTS: Atherosclerotic plaque formation was more frequently detected in the RA vs primary SS group (80.7% vs 62.2%, p-value <0.001), along with higher rates of family CVD history, current steroid dose, and serum inflammatory markers. The TT genotype of the rs1224141 variant was more prevalent in RA but not primary SS patients with plaque and arterial wall thickening vs their counterparts without. Regarding the rs1014569 variant, among RA patients the TT genotype increased the risk for plaque formation while in primary SS patients the AT genotype conferred increased risk. Haplotype GTTTT was protective in the RA cohort, while TATTT and TTCTT haplotypes increased susceptibility for arterial wall thickening in the primary SS cohort.

CONCLUSIONS: 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.

PMID:35689637 | DOI:10.1093/rheumatology/keac337

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