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Macrophage migration inhibitory factor (MIF) polymorphisms do not predict therapeutic response to glucocorticoids or TNF-αneutralising therapies in rheumatoid arthritis.
  1. Timothy RDJ Radstake (t.radstake{at}reuma.umcn.nl)
  1. University Medical Center Nijmegen, Netherlands
    1. Jaap Fransen (j.fransen{at}reuma.umcn.nl)
    1. University Medical Centre Nijmegen, Netherlands
      1. Erik JM Toonen (e.toonen{at}antrg.umcn.nl)
      1. University Medical Centre Nijmegen, Netherlands
        1. Marieke JH Coenen (m.coenen{at}antrg.umcn.nl)
        1. University Medical Centre Nijmegen, Netherlands
          1. Agnes E Eijsbouts (a.eijsbouts{at}maartenskliniek.nl)
          1. St. Maartenskliniek, Netherlands
            1. Rachelle Donn (rachelle.donn{at}manchester.ac.uk)
            1. Arthritis Research Campaign Epidemiology Unit6, United Kingdom
              1. Frank HJ van den Hoogen (f.vandenhoogen{at}maartenskliniek.nl)
              1. St. Maartenskliniek, Netherlands
                1. Piet LCM van Riel (p.vanriel{at}reuma.umcn.nl)
                1. University Medical Center Nijmegen, Netherlands

                  Abstract

                  Introduction: Macrophage migration inhibiting factor (MIF) is an inflammatory mediator associated with RA severity. In various diseases MIF polymorphisms are associated with clinical response to glucocorticoid (GC) therapy. It is unclear whether MIF polymorphisms determine GC response in RA and to other RA therapies. Therefore, we studied whether two functional variants in MIF are associated with the response to GC and TNF-α neutralizing therapies in RA.

                  Methods: Data from two cohorts of an RA registry were used. For patients who started with GC or TNF-α neutralising (Infliximab) treatment, courses with a duration of at least three months were included and response to GC or TNF-α blockers was calculated according to the EULAR response criteria. MIF-173G>C genotyping was achieved using an Assay-on-Demand allelic discrimination assay and alleles of the CATT repeat element were identified using a fluorescently labeled PCR primer and capillary electrophoresis. Logistic regression modelling was used for the statistical analysis.

                  Results: 192 courses of oral prednisone or methylprednisolone injections in 98 RA patients, and 90 RA patients on TNF-α neutralising therapies were documented. 27% of the RA patients was found to be heterozygous for CATT7 whereas 31% of them were heterozygous for -173C. Four and six percent of the RA patients were homozygous for the MIF CATT7 repeat or MIF -173C allele. Neither carrier ship nor homozygosity for CATT7 repeat nor MIF -173C allele of MIF was associated with response to GC (Odds ratios close to 1) or TNFα neutralising therapy (OR's close to 2).

                  Conclusion: The MIF-CATT7 repeat and the MIF-173G>C functional variant are not strongly associated with a decreased clinical response to GC or TNF-α neutralising therapy in RA.

                  • anti-TNFα
                  • glucocorticoids
                  • macrophage migration inhibtory factor
                  • rheumatoid arthritis

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