Abstract
Aim To investigate the serum nitrite levels in patients with active rheumatoid arthritis (RA) after treatment with tocilizumab, an IL-6 antagonist, and to correlate between inflammatory disease activity measures and endothelial dysfunction. Materials and methods Eleven anti-IL-6-naive RA patients with high disease activity (DAS28 >5.1) were investigated. Inflammatory disease activity (DAS28 and HAQ-DI scores, ESR and CRP), serum nitrite concentration and flow mediated dilation (FMD) of the brachial artery were measured before and after 12 weeks of therapy with tocilizumab 8mg/kg intravenous infusion every 4 weeks. Serum nitrite levels and FMD were also estimated in 10 age- and sex- matched healthy controls. Results Serum nitrite levels in RA patients at baseline were significantly higher when compared to healthy volunteers (P <0.01). Level of serum nitrite significantly decreased (P <0.001), inflammatory disease activity measures and FMD significantly improved (P <0.001) after treatment. There was a significant correlation of serum nitrite with FMD, CRP, and DAS 28 both at baseline (P <0.05) and after 12 weeks therapy (P <0.05). Conclusion Nitrite production is enhanced to a greater extent in patients with RA compared to controls. Reduction in nitrite level after treatment is associated with the improvement in disease activity and endothelial dysfunction. Serum nitrite level may serve as a good predictor of both inflammatory disease activity and response to therapy in RA.
Highlights
Association between rheumatoid arthritis (RA) and atherosclerotic vascular disease is well recognized and these patients have 4-fold increased risk of cardiovascular disease (CVD).[1]
Nitrite production is enhanced to a greater extent in patients with RA compared to controls
Reduction in nitrite level after treatment is associated with the improvement in disease activity and endothelial dysfunction
Summary
Association between rheumatoid arthritis (RA) and atherosclerotic vascular disease is well recognized and these patients have 4-fold increased risk of cardiovascular disease (CVD).[1]. Inflammatory cytokines (TNF-α, IL-1, and IL-6) released from the synovium in RA patients generate a spectrum of proatherogenic changes such as insulin resistance, dyslipidemia, oxidation, upregulation of cellular adhesion molecule expression on endothelial cells, thrombin generation and platelet activation. These in turn contribute to an accelerated atherosclerosis.[4] In addition, patients with RA have a dual abnormality in nitric oxide (NO)-dependent vascular function, characterized by blunted endothelial nitric oxide synthase (eNOS) and enhanced inducible nitric oxide synthase (iNOS) by leukocytes and vascular smooth muscle cells (VSMCs).[1] Endothelial cells (ECs) serve as major targets for these
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