Publications

Patients with active RA and little or no prior DMARD treatment, who achieved sustained clinical responses, were less likely to show structural damage progression, irrespective of treatment.RA-BEGIN was a 52-week double-blind, multicentre Phase 3 trial, which assessed the safety and efficacy of BARI as monotherapy or in combination with MTX versus MTX monotherapy, in RA patients with no or limited prior DMARDs use.1-4 This post-hoc analysis evaluated the structural damage progression in patients enrolled into RA-BEGIN. Patients were randomised to receive either BARI 4 mg or MTX monotherapy, or BARI 4 mg in combination with MTX. Radiographic data were analysed from 545 patients in the modified-intent-to-treat population of RA-BEGIN. Patients were stratified into two groups based on their DAS28-CRP and SDAI indexes. At Wk52, structural damage progression was evaluated based on response to treatment for the observed and adjusted proportion of patients achieving either a sustained DAS28-CRP≤3.2 vs DAS28-CRP>3.2 or a sustained SDAI score≤11 vs SDAI score>11. Patients achieving sustained DAS28-CRP or SDAI scores were less likely to show structural damage progression at Wk52, irrespective of treatment. For these patients, structural damage was less likely if patients were receiving BARI 4 mg mono- or combination therapy with MTX compared to MTX monotherapy. For patients who did not achieve sustained clinical responses, structural damage progression was less likely if patients were receiving BARI 4 mg plus MTX compared with either monotherapy. The authors concluded, patients who achieved a sustained clinical response were less likely to show structural damage progression when receiving BARI alone or in combination with MTX, compared to MTX monotherapy. Overall, patients achieving sustained responses were less likely to experience structural damage progression than patients who did not, independent of treatment.1. Fleischmann R, et al. Arthritis Rheumatol 2017;69:506–17.2. Taylor PC, et al. et al. N Engl J Med 2017;376:652–62. 3. Dougados M, et al. Ann Rheum Dis 2017;76:88–95. 4. Mark C, et al. N Engl H Med 2016;374:1243–1252.