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Ann Rheum Dis. 2015 Jun;74(6):979-84. doi: 10.1136/annrheumdis-2013-203993. Epub 2014 Jan 17.

Rituximab versus an alternative TNF inhibitor in patients with rheumatoid arthritis who failed to respond to a single previous TNF inhibitor: SWITCH-RA, a global, observational, comparative effectiveness study.

Author information

  • 1Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Chapel Allerton Hospital, Leeds, UK NIHR Leeds Musculoskeletal Biomedical Research Unit, Leeds Teaching Hospitals NHS Trust, Leeds, UK.
  • 2Department of Rheumatology, CHU Strasbourg, Strasbourg, France.
  • 3University of Cologne, Cologne, Germany.
  • 4L Sacco University Hospital, Milan, Italy.
  • 5University of Montreal, Montreal, Canada.
  • 6Facultad de Medicina, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, Santander, Spain.
  • 7Hospital de Especialidades Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, México City, Mexico.
  • 8Department of Rheumatology, University of Liverpool, Liverpool, UK.
  • 9Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK.
  • 10Hellenic Foundation for Rheumatological Research, Athens, Greece.
  • 11Quintiles, Rockville, Maryland, USA.
  • 12F Hoffmann-La Roche Ltd, Basel, Switzerland.
  • 13Genentech Inc, San Francisco, California, USA.
  • 14University Hospital of Geneva, Geneva, Switzerland.



To compare the effectiveness of rituximab versus an alternative tumour necrosis factor (TNF) inhibitor (TNFi) in patients with rheumatoid arthritis (RA) with an inadequate response to one previous TNFi.


SWITCH-RA was a prospective, global, observational, real-life study. Patients non-responsive or intolerant to a single TNFi were enrolled ≤4 weeks after starting rituximab or a second TNFi. Primary end point: change in Disease Activity Score in 28 joints excluding patient's global health component (DAS28-3)-erythrocyte sedimentation rate (ESR) over 6 months.


604 patients received rituximab, and 507 an alternative TNFi as second biological therapy. Reasons for discontinuing the first TNFi were inefficacy (n=827), intolerance (n=263) and other (n=21). A total of 728 patients were available for primary end point analysis (rituximab n=405; TNFi n=323). Baseline mean (SD) DAS28-3-ESR was higher in the rituximab than the TNFi group: 5.2 (1.2) vs 4.8 (1.3); p<0.0001. Least squares mean (SE) change in DAS28-3-ESR at 6 months was significantly greater in rituximab than TNFi patients: -1.5 (0.2) vs -1.1 (0.2); p=0.007. The difference remained significant among patients discontinuing the initial TNFi because of inefficacy (-1.7 vs -1.3; p=0.017) but not intolerance (-0.7 vs -0.7; p=0.894). Seropositive patients showed significantly greater improvements in DAS28-3-ESR with rituximab than with TNFi (-1.6 (0.3) vs -1.2 (0.3); p=0.011), particularly those switching because of inefficacy (-1.9 (0.3) vs -1.5 (0.4); p=0.021). The overall incidence of adverse events was similar between the rituximab and TNFi groups.


These real-life data indicate that, after discontinuation of an initial TNFi, switching to rituximab is associated with significantly improved clinical effectiveness compared with switching to a second TNFi. This difference was particularly evident in seropositive patients and in those switched because of inefficacy.


Anti-TNF; B cells; DMARDs (biologic); Rheumatoid Arthritis; Treatment

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