treatment difference for DAS28 (ESR) scores, ACR response rates, HAQ-DI responses and HRQoL improvements over- lapped. However, by day 365, the 95% CIs for the treatment difference between abatacept and infliximab for the reduction in DAS28 (ESR), good EULAR responses, LDAS, the ACR 20 response rate and the HRQoL physical summary measure did not include zero, suggesting a difference favouring abatacept for these specific endpoints. While the onset of response (as assessed by ACR 20 responses), initially appeared more rapid with infliximab, similar response rates were noted with abatacept and infliximab by day 85. Between 6 months and 1 year, abatacept responses were maintained, while those with infliximab were not. The sustained efficacy observed at 1 year compared with 6 months in abatacept-treated patients is consistent with results from other abatacept trials.2 3 Similarly, the finding that patients treated with infliximab did not sustain response rates over 1 year is also consistent with previous trials.11 When the impact of adding additional therapies was assessed using a sensitivity analysis according to the last score prior to addition, reductions in disease activity tended to be consistently higher with abatacept than with infliximab. Overall, abatacept had a relatively more acceptable safety and tolerability profile than infliximab. Over 1 year, fewer SAEs, AEs, infections, and discontinuations due to AEs or SAEs were observed with abatacept relative to infliximab. Generally, opportunistic infections appeared to be relatively uncommon in this study and were mainly observed in the infliximab group, including two events of TB, an event of P jiroveci pneumonia, an event of pseudomonal lung infection and an event of herpes encephalitis. No opportunistic infections were reported in the abatacept group. Autoimmune symptoms or disorders were uncommon (,1%) with abatacept and infliximab. All of the malignancies were reported during the first 6 months, including one in the abatacept group, one in the placebo group and two in the infliximab group. The data presented here should be interpreted within the context of several limitations. Although collectively the data support a relatively more acceptable risk-to-benefit profile of abatacept compared with infliximab, the design of this study utilised the infliximab dose of 3 mg/kg, without dose adjust- ment. At the time of the study, the recommended dose of infliximab (approved labelled starting dose for RA) was 3 mg/ kg; however, today regulatory agencies recognise the use of higher doses of infliximab, and physicians use them in a proportion of patients to maintain a durable response. In fact, the dose may be increased in up to 30% of patients.12 Although higher doses have been associated with an increased risk of AEs in clinical trials.5 13 Finally, this study was not designed to evaluate the effect of abatacept or infliximab vs placebo on radiographic progression. In conclusion, these two biologic therapies with two distinct mechanisms of action have different safety and efficacy profiles; however, abatacept and infliximab both offer clinical improve- ments to patients with an inadequate response to MTX. Over 1 year, abatacept exhibited a durable response, and had a E x t e n d e d r e p o r t relatively more acceptable safety and tolerability profile than infliximab, as evidenced by fewer SAEs, serious infections, acute infusional events and discontinuations due to AEs. Acknowledgements: This study was funded and sponsored by Bristol-Myers Squibb, Princeton, New Jersey, USA. The authors would like to thank Laura Gardiner, Medicus International, for her editorial assistance. Editorial support was funded by Bristol-Myers Squibb, Princeton, New Jersey, USA. All authors were involved in the drafting and critical revision of the article; in addition, all authors have seen and approved the final article for submission Funding: This study is based upon clinical trial results from a study sponsored by Bristol-Myers Squibb, Princeton, New Jersey, USA. The authors actively participated in the conduct of these trials, and had full access to the raw data and responsibility for the analysis and interpretation. Competing interests: RA is an employee of Bristol-Myers Squibb and owns stocks. JCB is an employee of Bristol-Myers Squibb, with stock options and restricted shares. PLNC is an employee of Bristol-Myers Squibb and owns shares. MD has received research grants, consulting fees and been on the speakers’ bureau for Bristol-Myers Squibb, Abbott and Wyeth, and has also received research grants and consulting fees from Centocor and Schering Plough. MK has received research grants and consulting fees from, and is an Advisory Board Member for, Bristol-Myers Squibb. TL is an employee of Bristol-Myers Squibb and owns stocks and shares. CL is an employee of Bristol-Myers Squibb and owns stocks and shares. MS has received research grants and consulting fees from Amgen, Bristol-Myers Squibb, Centocor and Wyeth. REFERENCES 1. 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