Cardiovascular (CV) morbidity and mortality have been associated with rheumatoid arthritis
(RA) and ankylosing spondylitis (AS). Natural autoantibodies (nAAb) are involved in
innate immunity, as well as autoimmunity, inflammation, and atherosclerosis. There
have not been any studies assessing the effects of biologics on nAAbs in RA and AS,
also in relation to vascular pathophysiology. Fifty-three anti-TNF-treated RA and
AS patients were included in a 12-month follow-up study. Anti-citrate synthase (CS)
and anti-topoisomerase I fragment 4 (TOPO-F4) IgM and IgG levels were determined by
ELISA. Ultrasonography was performed to assess brachial artery flow-mediated vasodilation
(FMD), common carotid intima-media thickness (ccIMT), and arterial pulse-wave velocity
(PWV). Other variables were also evaluated at baseline and 6 and 12 months after treatment
initiation. Anti-TNF therapy improved FMD in RA and PWV in AS and stabilized ccIMT.
TNF inhibition increased anti-CS IgM and IgG, and possibly also anti-TOPO-F4 IgG levels.
Various correlation analyses revealed that nAAbs might be independently involved in
autoimmunity as well as changes in inflammation and vascular pathology over time in
biologic-treated patients (p < 0.05). We also found associations between anti-TOPO-F4
IgG and anti-Hsp60 IgG (p < 0.05). Baseline nAAb levels or nAAb level changes might
determine changes in CRP, disease activity, FMD, PWV, and ccIMT over time (p < 0.05).
The interplay between arthritis and inflammatory atherosclerosis, as well as the effects
of anti-TNF biologics on these pathologies, might independently involve nAAbs.
