Background: Cardiovascular (CV) morbidity, mortality, and metabolic syndrome are associated
with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Here, lipids and other
metabolic markers in relation to vascular function and clinical markers were evaluated
in RA and AS patients undergoing one-year anti-TNF therapy. Patients and methods:
Fifty-three patients including 36 RA patients treated with either etanercept (ETN)
or certolizumab pegol (CZP) and 17 AS patients treated with ETN were included in a
12-month follow-up study. Various lipids, paraoxonase (PON) and arylesterase (ARE)
activities, myeloperoxidase (MPO) and adipokine levels were determined overtime. Ultrasonography
was performed to determine flow-mediated vasodilation (FMD), common carotid intima-media
thickness (ccIMT), and arterial pulse-wave velocity (PWV) in all patients. All assessments
were performed at baseline and 6 and 12 months after treatment initiation. Results:
Anti-TNF therapy decreased ARE activity, MPO, adiponectin, and chemerin levels after
12 months (p < 0.05). Lipids, PON activity, and leptin remained unchanged. Regression
analyses suggested variable associations of IMT, PWV, and FMD with ARE, MPO, leptin,
and lipids (p < 0.05). On the other hand, these metabolic parameters were significantly
associated with disease duration, CV history, CRP, obesity, PWV, and IMT (p < 0.05).
One-year anti-TNF treatment together with baseline leptin (p = 0.039) or CRP (p =
0.016) levels determined 12 months of lipid changes overtime. TNF inhibition together
with baseline disease activity determined ARE activity changes (p = 0.046). Anti TNF
therapy and baseline chemerin levels determined IMT changes overtime (p = 0.003).
Conclusions: Assessment of various metabolic parameters together with disease activity,
CRP, and ultrasound based techniques may exert additional value in determining CV
burden and in monitoring the effects of biologics on preclinical vascular pathophysiology.