P Bohanec Grabar, 1 B Rozman, 2 D Logar, 2 S Praprotnik, 2 V Dolz ˇan 1 1 Institute of Biochemistry, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia; 2 Department of Rheumatology, University Medical Centre Ljubljana, Ljubljana, Slovenia Correspondence to: Dr V Dolz ˇan, Institute of Biochemistry, Faculty of Medicine, University of Ljubljana, Vrazov trg 2, 1000 Ljubljana, Slovenia, vita.dolzan@mf.uni-lj.si Funding: This work was financially supported by the Slovenian Research Agency, grant No PO-0503-0381. Competing interests: None. Ethics approval: Approval from the National Medical Ethics Committee, Republic of Slovenia. Accepted 12 October 2008 Ann Rheum Dis 2009;68:1367–1368. doi:10.1136/ard.2008.099093 REFERENCES 1. Mladenovic V, Domljan Z, Rozman B, Jajic I, Mihajlovic D, Dordevic J, et al. Safety and effec- tiveness of leflunomide in the treatment of patients with active rheumatoid arthritis. Results of a randomized, placebo-controlled, phase II study. 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Sevilla-Mantilla C, Ortega L, Agundez JA, Fernandez-Gutierrez B, Ladero JM, Diaz- Rubio M. Leflunomide-induced acute hepatitis. Dig Liver Dis 2004;36:82–4. A single course of rituximab does not abrogate anti-infliximab antibodies in patients with rheumatoid arthritis The development of anti-infliximab antibodies in 8% to 43% of infliximab-treated patients is associated with decreased effi- ciency and increased risk of adverse effects. 1–3 An intervention that can diminish anti-infliximab antibody formation is there- fore warranted. Rituximab, a chimeric monoclonal antibody that selectively depletes CD20-positive B lymphocytes, could potentially inhibit the human antibody response against inflix- imab. Therefore, we assessed the proportion of patients with rheumatoid arthritis (RA) in which treatment with rituximab resulted in the depletion of anti-infliximab antibodies. Consecutive patients with RA with detectable anti-infliximab antibodies, who were initiated on treatment with either rituximab or adalimumab, were included in this prospective controlled cohort study. There were no exclusion criteria other than the regular contraindications. Baseline assessment included measurement of disease activity, demographic and clinical data. Patients received rituximab (2 6 1000 mg intravenously, day 0 and 15) or adalimumab at a dosage of 40 mg subcutaneously every other week. Anti-infliximab antibody measurements before the first administration of rituximab and after 16 and 24 were compared with patients treated with adalimumab as control group. Serum anti-infliximab antibody levels were determined by a previously described radioimmunoassay. 3 The baseline characteristics of the included 32 patients (17 rituximab and 15 adalimumab) are depicted in table 1. Although the baseline anti-infliximab antibody levels tended to be higher in the adalimumab group (100 (interquartile range (IQR) 28 to 416 AU/ml) compared to the rituximab group (29 (IQR 19 to 127)), this difference did not reach statistical significance (p = 0.2). A negative trend was found between baseline anti- infliximab antibody levels and the interval between the last administration of infliximab and start of the present therapy (r = 20.32, p = 0.07). Table 1 Baseline characteristics of patients Rituximab group (n = 17) Adalimumab group (n = 15) Age (years) 56 (12) 53 (12) Women (n, %) 8 (47)* 13 (87)* Disease duration (years) 15.7 (9.1) 15.8 (7.8) Previous DMARDs (n) 6.5 (2.6)* 3.7 (2.1)* Previous biologicals (n) 2.5 (0.9)* 1.3 (0.5)* Rheumatoid factor positive (n, %) 17 (100) 13 (87) Disease activity (DAS28) at baseline 6.0 (1.6) 5.0 (1.4) Interval between last infliximab infusion (months) and present therapy (median (p25–p75)) 25 (7.2 to 36)* 5.8 (2.5 to 25)* Concomitant DMARD at baseline (n, %) 15 (88) 13 (87) Methotrexate (n, %) 11 (65) 13 (87) Dose (mg/week) 13.6 (6.3) 16.9 (9.4) Azathioprine (n, %) 2 (12) 0 Leflunomide (n, %) 1 (6) 0 Oral corticosteroids at baseline (n, %) 10 (59) 5 (33) Dose (mg/day) 9.3 (2.9)* 4.9 (1.9)* Variables are expressed as mean (SD) unless stated otherwise. *p,0.05. DAS28, 28-joint Disease Activity Score; DMARD, disease-modifying antirheumatic drug. 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