NT-PROBNP AND INFLAMMATION IN ACTIVE ANKYLOSING SPONDYLITIS RECEIVING TNF BLOCKERS: IS THERE A LINK?

Abstract

Introduction: Cardiovascular disease plays a central role in morbidity and mortality in rheumatic patients. N-terminal pro-brain natriuretic peptide (NT-proBNP) is a strong marker of cardiovascular risk with recent evidence that inflammation may also influence its levels. The discrimination of this confounding variable is of particular interest in rheumatic diseases. Aim: to evaluate NT-proBNP in ankylosing spondylitis (AS) patients pre- and post-TNF blockage therapy to determine the possible association between NT-proBNP levels and inflammatory parameters. Materials and Methods: Forty-five consecutive AS patients without previous/current cardiovascular disease or systolic myocardial dysfunction, who were eligible to anti-TNF therapy, were prospectively enrolled. All patients received TNF blockers (infliximab, adalimumab and etanercept in their regular schedule) and they were evaluated for circulating NT-proBNP levels, clinical and laboratory parameters of disease activity including BASDAI, ASDAS, ESR and CRP, traditional cardiovascular risk factors including blood pressure, body mass index, waist circumference and dyslipidemia; conventional and tissue Doppler imaging echocardiography and treatment data at baseline (BL) and six months after (6M). Results: At BL, all patients had active AS, NT-proBNP levels had a median of 36 (20-72)pg/ml and 11% were high in spite of no systolic alteration. Multiple linear regression analysis revealed that this peptide, at BL, was independently correlated with ESR (p<0.001), age (p=0.01) and pulse pressure (p=0.01). After 6M, all disease parameters improved and NT-proBNP levels were significantly reduced [24 (16-47) pg/mL, p=0.037] compared to BL. Changes in NT-proBNP were positively correlated with ESR changes (r=0.41, p=0.006). Cardiovascular risk factors remained stable during follow-up. Conclusions: Elevations of NT-proBNP should be interpreted with caution in active AS patients with no evidence of cardiovascular disease. The short-term reduction of NT-proBNP levels in these patients treated with anti-TNF therapy appears to reflect an improvement in inflammatory status.