Ab0653 Impact of Tsdmard, Tofacitinib, on Endothelial Function in Ra and Its Association With Cellular Ratios

Background: Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in RA.¹ Endothelial dysfunction (ED), resulting from chronic inflammation and leading to accelerated atherosclerosis, is the key promoter of CVD². ED is the barometer of CV health. Objectives: In this study, we aimed to investigate the impact of tofacitinib on endothelial dysfunction in RA and association of endothelial dysfunction with NLR, PLR and LMR to determine whether these ratios could predict the impact of tofacitinib on CV risk. Methods: A total of 74 patients with RA patients (62 females, 12 males; mean age: 54.85 ± 8.39 years; range: 32 to 70 years) fulfilling the 2010 Rheumatoid Arthritis classification criteria with active disease (DAS28>3.2)were treated with Tofacitinib (5mg bd, n=20) for 12 weeks as an adjunct to existing stable antirheumatic drugs. Endothelial function was assessed by FMD using AngioDefender and serum lipids were also estimated at baseline and after 12 weeks of treatment. Neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte to monocyte (LMR) ratios and platelets were estimated. DAS28, ESR, CRP and HAQ-DI were also assessed at baseline and after 12 weeks of treatment. Results: After 12 weeks treatment with tofacitinib, FMD significantly improved (7.14± 2.48 to 8.22 ± 2.80, p=0.001). ESR, CRP, DAS-28, HAQ-DI and PLR improved significantly after 12 weeks of treatment (Table 1). However, there was no statistical significant improvent in NLR, LMR and platelets and serum lipids (Table 1). At baseline, a significant negative Pearson correlation was observed between FMD and Age and CRP (Table 2A). However, after 12 weeks treatment with tofacitinib, FMD corelated with age and platelets (Table 2A). DAS-28 significantly correlated with gender, ESR, CRP and FMD (Figure 1) at baseline (Table 2B). However, after 12 weeks treatment, DAS-28 significantly correlated with ESR and CRP level (Table 2B). Conclusion: Treatment with tofacitinib improves inflammatory disease activity and endothelial function. However, NLR, LMR and PLR did not significantly correlate with the FMD and disease activity score suggesting that these cellular ratios do not predict the response to tofacitinib therapy in RA. Platelets correlated with FMD after tofacitinib treatment. REFERENCES: [1] Gabriel SE. Cardiovascular morbidity and mortality in rheumatoid arthritis. Am J Med. 2008 Oct;121(10 Suppl 1):S9-14. doi: 10.1016/j.amjmed.2008.06.011. PMID: 18926169; PMCID: PMC2858687. [2] Naveed Sattar, David W. McCarey, Hilary Capell and Iain B. McInnes. Explaining How ''High-Grade'' Systemic Inflammation Accelerates Vascular Risk in Rheumatoid Arthritis. Circulation 2003; 108: 2957-63. Acknowledgements: NIL. Disclosure of Interests: None declared.