Abstract
Objective Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) have been associated with cardiovascular (CV) disease. The treatment of arthritis by tumour necrosis factor α (TNF- α) inhibitors may decrease the serum concentrations of vascular biomarkers. We determined circulating levels of oxidized LDL (oxLDL)/β2 glycoprotein I (β2GPI) complexes, antibodies to 60 kDa heat shock protein (anti-Hsp60), soluble urokinase plasminogen activator receptor (suPAR) and Brain type natriuretic peptide (BNP) fragment in sera of RA and AS patients undergoing anti-TNF treatment.
Methods Fifty-three RA/AS patients were treated with etanercept (ETN) or certolizumab pegol (CZP) for one year. Circulating oxLDL/β2GPI complex (AtherOx®), anti- Hsp60 IgG and BNP8-29 fragment levels were assessed by ELISA. suPAR levels were determined by suPARnostic® Quick Triage test. Flow-mediated vasodilation (FMD), carotid intima-media thickness (IMT) and arterial pulse-wave velocity (PWV) were determined by ultrasound.
Results One-year anti-TNF treatment significantly decreased oxLDL/β2GPI levels, as well as suPAR levels in patients with “critically” high suPAR levels at baseline. In RA, BNP levels were higher in seropositive vs seronegative patients. Serum levels of these vascular biomarkers variably correlated with lipids, ACPA, RF and CRP. IMT positively correlated with BNP, PWV with suPAR and anti-Hsp60, while FMD inversely associated with anti-Hsp60. In RM-ANOVA analysis, disease activity supported the effects of anti-TNF treatment on 12-month changes in oxLDL/β2GPI. IMT supported the effects of therapy on changes of anti-Hsp60 and suPAR.
Conclusion These biomarkers may be involved in the pathogenesis of atherosclerosis underlying RA/AS. TNF inhibition variably affect the serum levels of oxLDL/β2GPI, suPAR and BNP.
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