BackgroundAlthough a number of studies have reported that hyperuricemia and gout are independent risk factors for the development of cardiovascular disease (CVD), little is known about the relationship between hyperuricemia or gout and arterial stiffness.ObjectivesThis study sought to compare carotid arterial stiffness in gout patients and healthy controls, and evaluate the predictive factors for arterial stiffness in male patients with gout using carotid ultrasonography.MethodsIn this cross-sectional study, 69 male gout patients and 64 male healthy controls without any known CVD were prospectively analyzed. Carotid artery stiffness index β (β-index) and the intima-media thickness (IMT) were measured as surrogate markers of preclinical atherosclerosis. We also measured serum uric acid, high sensitivity C-reactive protein (hsCRP), erythrocyte sedimentation rate (ESR), lipid profiles, and renal function. Adjusted comparison of the β-index and cIMT in both groups and their associations with clinical parameters were investigated.ResultsThe gout group showed higher ESR, Cr, prevalence of HT and DM than the control group (p<0.05). However, HDL was higher in the control group (p<0.05). β-index and cIMT were higher in the gout group, but only β-index showed a statistically significant difference (11.12 ± 5.19 vs 8.68 ± 3.67, p=0.002). Multiple regression analyses showed that duration of gout was significantly associated with increased β-index and cIMT in the gout group (Table 1).ConclusionsPatients with gout had increased carotid arterial stiffness, which was significantly related to gout duration rather than serum uric acid level or status of inflammation.ReferencesRichette P, Perez-Ruiz F, Doherty M, Jansen TL, Nuki G, Pascual E, Punzi L, So AK, Bardin T. (2014) Improving cardiovascular and renal outcomes in gout: what should we target? Nat Rev Rheumatol. 10(11):654–61.Perez-Ruiz F, Becker MA. (2015) Inflammation: a possible mechanism for a causative role of hyperuricemia/gout in cardiovascular disease. Curr Med Res Opin. 31 Suppl 2:9–14.Disclosure of InterestNone declared

BackgroundRheumatoid arthritis (RA) is characterised by persistent synovitis and structural joint damage with T cell-driven inflammation. Tacrolimus suppress activation of T cells through the inhibition of calcineurin.ObjectivesWe evaluated the efficacy and safety of tacrolimus in Korean active RA patient who had inadequate response to disease-modifying anti-rheumatic drugs (DMARDs) including Methotrexate (MTX).MethodsDuring the study period from Aug. 2012 to Jan. 2016 in this open labelled, multicenter study, 115 patients were enrolled with DAS28 ≥3.2. Patients received tacrolimus during 24 weeks. The initial dose was 1 mg once daily and was increased to 3 mg by every 4 weeks. The disease activity and safety was assessed.ResultsData from 97 patients were evaluated in full set analysis. At week-24, EULAR response rate were 83.5% (81 of 97) with improvements from week-16 in 74.2% (72 of 97). Mean DAS28-ESR was continuously decreased of 5.64 at baseline, 4.14 (±1.22, p<0.001) at week-16 and 3.66 (±1.39, p<0.001) at week-24. Efficacy rates according to SDAI were 89.7% (87 of 97) and KHAQ-20 score decreased −2.42 (±4.37, p<0.001) from baseline 7.27 (±4.59) at week-24. Mean ESR was decreased −10.97 (±24.16, p<0.001) at week-16,–14.77 (±24.57, p<0.001) at week-24 from baseline 46.05 (±23.22). Mean CRP was decreased from 2.86 (±7.85, p=0.0578) at baseline to 1.34 (±3.02, p=0.0367) at week-24. In serious adverse events (6 of 108, 5.56%), two cases (pneumonia, high glucose level) were related with tacrolimus and recovered with treatment.ConclusionsThis study demonstrated the efficacy of add on tacrolimus therapy to MTX in patients with active RA patients.Disclosure of InterestNone declared