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Clinical response, pharmacokinetics, development of human anti-chimeric antibodies, and synovial tissue response to rituximab treatment in patients with rheumatoid arthritis
  1. Rogier M Thurlings (r.m.thurlings{at}amc.uva.nl)
  1. Division of Clinical Immunology and Rheumatology, Academic Medical Center, University of Amsterdam, Netherlands
    1. Onno Teng (y.k.o.teng{at}lumc.nl)
    1. Department of Rheumatology, Leiden University Medical Center, Netherlands
      1. Koen Vos (k.vos{at}amc.uva.nl)
      1. Jan van Breemen institute, Amsterdam, Netherlands
        1. Danielle M Gerlag (d.m.gerlag{at}amc.uva.nl)
        1. Division of Clinical Immunology and Rheumatology, Academic Medical Center, University of Amsterdam, Netherlands
          1. Lucien Aarden (l.aarden{at}sanquin.nl)
          1. Department of Immunopathology, Sanquin, Netherlands
            1. Steven O Stapel
            1. Sanquin Research, Netherlands
              1. Jacob M van Laar (j.m.van-laar{at}newcastle.ac.uk)
              1. Musculoskeletal Research Group, Institute of Cellular Medicine, Newcastle University, United Kingdom
                1. Paul P Tak (p.p.tak{at}amc.uva.nl)
                1. Division of Clinical Immunology and Rheumatology, Academic Medical Center, University of Amsterdam, Netherlands
                  1. Gerrit Jan Wolbink (wolbink{at}gmail.com)
                  1. Department of Immunopathology, Sanquin, Netherlands

                    Abstract

                    Objectives: To analyze whether persistence of synovial B lineage cells and lack of clinical response to rituximab treatment in rheumatoid arthritis (RA) patients are associated with low rituximab serum levels and anti-rituximab antibody (ARA) formation.

                    Methods: Fifty-eight RA patients were treated with rituximab. The clinical response was determined 24 weeks after each treatment course using the disease activity score evaluated in 28 joints (DAS28) and EULAR response criteria. Rituximab serum levels, ARAs and synovial B lineage cell numbers were determined before and after treatment.

                    Results: Four weeks after treatment rituximab serum levels were highly variable. Low rituximab levels were associated with ARA formation (in 5 patients [8.6%]) and high baseline erythrocyte sedimentation rate. Interestingly, serum rituximab levels were not related to persistence of synovial B lineage cells or clinical response. Furthermore, response to treatment and re-treatment was similar in ARA positive compared to ARA negative patients.

                    Conclusion: There is clear variability in serum levels after rituximab treatment, but rituximab levels are not lower in patients with persistence of synovial B lineage cells or lack of clinical response. The current treatment schedule suffices to induce and maintain a clinical response, even when ARAs are formed.

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