Rheumatology International

, Volume 30, Issue 10, pp 1299–1303

The −283C/T polymorphism of the DNMT3B gene influences the progression of joint destruction in rheumatoid arthritis

Authors

  • Eon Jeong Nam
    • Division of Rheumatology, Department of Internal MedicineKyungpook National University Hospital
  • Kyung Hoon Kim
    • Division of Rheumatology, Department of Internal MedicineKyungpook National University Hospital
  • Seung Woo Han
    • Division of Rheumatology, Department of Internal MedicineKyungpook National University Hospital
  • Chang Min Cho
    • Division of Rheumatology, Department of Internal MedicineKyungpook National University Hospital
  • Jongmin Lee
    • Department of Diagnostic RadiologyKyungpook National University School of Medicine
  • Jae Yong Park
    • Division of Rheumatology, Department of Internal MedicineKyungpook National University Hospital
    • Division of Rheumatology, Department of Internal MedicineKyungpook National University Hospital
Original Article

DOI: 10.1007/s00296-009-1141-y

Cite this article as:
Nam, E.J., Kim, K.H., Han, S.W. et al. Rheumatol Int (2010) 30: 1299. doi:10.1007/s00296-009-1141-y

Abstract

The objective of this study is to investigate the association between the −283C/T polymorphism at the promotor of DNMT3B gene and susceptibility to rheumatoid arthritis (RA) and to evaluate the effect of the polymorphism on clinical features such as progression of joint destruction in RA. A total of 309 patients with RA were compared with 297 control subjects. Genotyping of the −283C/T polymorphism was performed by real-time sequencing using Pyrosequencer. The genotype frequencies of the polymorphism at position −283 were not significantly different between patients with RA and controls. There were significantly positive correlations between the modified Sharp score and the disease duration for carriers of each genotype (y = 9.546x + 19.998, p < 0.001, for T allele carriers, y = 6.185x + 34.424, p < 0.001 for CC homozygotes). The slope of regression line of the T allele carriers was significantly steeper than that of the CC homozygotes (p = 0.014). In conclusion, our results suggest that the −283C/T polymorphism of the DNMT3B gene is a genetic marker related to the joint destruction of RA.

Keywords

DNMT3BPolymorphismRheumatoid arthritisModified Sharp score

Copyright information

© Springer-Verlag 2009