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Association between ß2-adrenergic receptor polymorphisms and rheumatoid arthritis in conjunction with HLA-DRB1 shared epitope
  1. Olga Malysheva (olga.malysheva{at}medizin.uni-leipzig.de)
  1. Medical Clinic IV, University Hospital Leipzig, Germany
    1. Matthias Pierer
    1. Medical Clinic IV, University Hospital Leipzig, Germany
      1. Uta Wagner
      1. Medical Clinic IV, University Hospital Leipzig, Germany
        1. Matthias Wahle
        1. Medical Clinic IV, University Hospital Leipzig, Germany
          1. Ulf Wagner
          1. Medical Clinic IV, University Hospital Leipzig, Germany
            1. Christoph Baerwald
            1. Medical Clinic IV, University Hospital Leipzig, Germany

              Abstract

              Purpose: The frequency of inherited polymorphisms of the β2-adrenergic receptor (β2AR) gene and the association with rheumatoid arthritis (RA) as well as HLA-DRB1 alleles was examined.

              Methods: An allele-specific polymerase chain reaction was used to determine the common variants of the β2AR at position 16, 27, and 164 in patients with RA (n= 310) and ethnically matched healthy controls (n= 305) from Germany. HLA-DRB1 genotyping was performed by oligonucleotide hybridisation of enzymatically amplified DNA allowing low-resolution HLA-DRB1 genotyping comprising specificities DRB1*01 to DRB1*17.

              Results: Arginine (Arg) at codon 16 was present in 278 RA patients (89.7 %) compared to 202 controls (66.2%; OR 4.43, 95 % CI 2.81 to 7.02, p=0.00001). Homozygosity for Arg16 was found in 107 RA patients (34.5 %) compared to 14 controls (4.6 %; OR 10.9, CI 5.9 to 20.5, p=0.00001). Stratifying patients for their HLA-DR status revealed that homozygosity for Arg16 exhibited the greatest risk for RA in combination with HLA-DRB1*04 (OR 17.1, 95% CI 1.71 to 414.4, p=0.004). Interestingly, patients with the Arg16 allele have a younger age at disease onset compared to patients without Arg16 (46.1±2.0 versus 53.1±2.7 respectively, p<0.05). Furthermore, 93.3% patients with homozygosity for Arg16 are positive for anti-CCP antibodies versus 75% patients with homozygosity for Gly16 (p<0.05).

              Conclusion: Between RA patients and controls there was a highly significant distortion in the distribution of β2AR polymorphisms at codon 16 contributing together with the HLA-DR alleles to the genetic background of RA.

              • German population
              • HLA-DR
              • polymorphisms
              • rheumatoid arthritis
              • ß2-adrenergic receptor

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