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Association of RF and anti-CCP positivity, but not carriage of shared epitope or PTPN22 susceptibility variants, with anti-TNF response in RA
  1. Catherine Potter (kate.potter{at}newcastle.ac.uk)
  1. University of Newcastle, United Kingdom
    1. Kimme L Hyrich (kimme.hyrich{at}manchester.ac.uk)
    1. University of Manchester, United Kingdom
      1. Andrew Tracey (andrew.tracey{at}manchester.ac.uk)
      1. University of Manchester, United Kingdom
        1. Mark Lunt (mark.lunt{at}manchester.ac.uk)
        1. University of Manchester, United Kingdom
          1. Darren Plant (darren.plant{at}manchester.ac.uk)
          1. University of Manchester, United Kingdom
            1. Deborah PM Symmons (deborah.symmons{at}manchester.ac.uk)
            1. University of Manchester, United Kingdom
              1. Wendy Thomson (wendy.thomson{at}manchester.ac.uk)
              1. University of Manchester, United Kingdom
                1. Jane Worthington (jane.worthington{at}manchester.ac.uk)
                1. University of Manchester, United Kingdom
                  1. Paul Emery (p.emery{at}leeds.ac.uk)
                  1. Dept of Rheumatology, United Kingdom
                    1. Ann W Morgan (a.w.morgan{at}leeds.ac.uk)
                    1. Leeds Institute of Molecular Medicine, United Kingdom
                      1. Anthony G Wilson (a.g.wilson{at}sheffield.ac.uk)
                      1. University of Sheffield, United Kingdom
                        1. John D Isaacs (j.d.isaacs{at}ncl.ac.uk)
                        1. Newcastle University, United States
                          1. Anne Barton (anne.barton{at}manchester.ac.uk)
                          1. University of Manchester, United Kingdom

                            Abstract

                            Objective: To determine whether rheumatoid factor (RF), anti-CCP antibodies, or carriage of shared epitope (SE) and PTPN22 genetic susceptibility variants predict response to therapy in patients with rheumatoid arthritis (RA) treated with anti-TNF agents.

                            Methods: UK-wide multi-centre collaborations were established to recruit a large cohort of patients treated with anti-TNF drugs for RA. Serum RF, anti-CCP antibody and SE status were determined using commercially available kits. PTPN22 R620W genotyping was performed by Sequenom MassArray®. Linear regression analyses were performed to investigate the role of these 4 factors in predicting response to treatment by 6 months, defined as the absolute change in DAS28.

                            Results: Of the 642 patients analysed, 46% received infliximab, 43% etanercept and 11% adalimumab. 89% and 82% of patients were RF and anti-CCP positive, respectively. RF negative patients had a 0.48 (95% CI: 0.08, 0.87) greater mean improvement in DAS28 compared to RF positive patients. A better response was also seen among anti-CCP negative patients. No association was demonstrated between drug response and SE or PTPN22 620W carriage.

                            Conclusion: The presence of RF or anti-CCP antibodies was associated with a reduced response to anti-TNF drugs. However, these antibodies only account for a small proportion of the variance in treatment response. It is likely that genetic factors will contribute to treatment response, but these do not include the well-established RA susceptibility loci, SE and PTPN22.

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