Brief report: lack of replication of an association between anti-citrullinated fibrinogen and subclinical atherosclerosis in patients with rheumatoid arthritis.

Abstract

[EN] Objective. Results of a recent study suggested that the excess cardiovascular (CV) risk observed in patients with rheumatoid arthritis (RA) could be partially ex- plained by the presence of immune complexes of antibod- ies against citrullinated proteins that locally promote and perpetuate inflammation and progression of athero- sclerotic plaques. The present study was undertaken to attempt to replicate one of the observations supporting this hypothesis, i.e., association between anti–citrullin- ated fibrinogen (anti–Cit-fibrinogen) positivity and sub- clinical atherosclerosis. Methods. Three surrogate markers of atherosclero- sis were assessed in 124 RA patients with no previous his- tory of CV events: carotid intima-media thickness (CIMT) assessed by carotid ultrasonography, carotid plaques assessed by carotid ultrasonography, and Coronary Artery Calcification Score (CACS) determined by multidetector computed tomography (CT) scanning. We analyzed the relationship of these 3 subclinical atherosclerosis markers to the presence and levels of autoantibodies, including anti–Cit-fibrinogen, anti–cyclic citrullinated peptide 2 (anti–CCP-2), and rheumatoid factor (RF). Results. Carotid plaques and CIMT >0.90 mm were present in 69.4% and 15.3%, of the patients, respectively, and the CACS was moderate or high in 21.0%. None of these surrogate markers of atheroscle- rosis showed a significant association with positivity for or the level of anti–Cit-fibrinogen antibodies (either against the whole protein [present in 33.9% of the patients] or against an immunodominant peptide [pre- sent in 23.4%]), anti–CCP-2 (present in 60.7%), or RF (present in 58.1%) in this series of patients with RA. Conclusion. Our results do not support the notion that there is a relationship between anti–Cit-fibrinogen antibodies and subclinical atherosclerosis in RA, thus calling into question the claim that these antibodies have a role in the increased risk of CV disease observed in patients with RA.