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Many clinical studies have reported the excellent clinical efficacy of infliximab (IFX), an antitumour necrosis factor α (anti-TNFα) monoclonal antibody, in the treatment of rheumatoid arthritis (RA).1 IFX is also reported to induce a rapid and marked reduction in circulating interleukin 6 (IL-6) levels, suggesting that its efficacy may result from the suppression of IL-6 as well as TNF.2,–,5 In the RISING Study (NCT00691028),6 ,7 we observed patients who showed no response to IFX therapy, despite maintaining a serum IFX level higher than the threshold level for clinical response. Here, we examined data on clinical response to better understand the mechanism of action of IFX.
In this study, patients with methotrexate-refractory RA treated with 3 mg/kg of IFX at weeks 0, 2 and 6 were randomly assigned to receive 3, 6 or 10 mg/kg of IFX every 8 weeks from week 14 to 46 in …
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