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The tumour necrosis factor receptor superfamily member 1b 676T>G polymorphism in relation to response to infliximab and adalimumab treatment and disease severity in rheumatoid arthritis
  1. E J M Toonen1,
  2. M J H Coenen1,
  3. W Kievit2,
  4. J Fransen2,
  5. A M Eijsbouts3,
  6. H Scheffer1,
  7. T R D J Radstake2,
  8. M C W Creemers2,
  9. D-J R A M de Rooij3,
  10. P L C M van Riel2,
  11. B Franke1,
  12. P Barrera2
  1. 1
    Department of Human Genetics, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
  2. 2
    Department of Rheumatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
  3. 3
    Department of Rheumatology, St Maartenskliniek, Nijmegen, The Netherlands
  1. Dr M J H Coenen, Department of Human Genetics (855), Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands; m.coenen{at}


Objective: To assess the effect of a functional polymorphism (676T>G, M196R) in the tumour necrosis factor receptor super family 1b (TNFSF1b) gene on disease activity, radiological joint damage and response to infliximab and adalimumab treatment in patients with rheumatoid arthritis (RA).

Methods: Two cohorts of patients with RA were genotyped for the 676T>G polymorphism (rs1061622) in exon 6 of the TNFSF1b gene by restriction fragment length polymorphism analysis. One cohort (n = 234) included patients from the Dutch Rheumatoid Arthritis Monitoring register with detailed information on their response to anti-TNF therapy (infliximab and adalimumab), the other cohort comprised patients from a long-term observational early inception cohort at our centre (n = 248).

Results: The 676T>G polymorphism was not associated with anti-TNF response after 3 or 6 months of treatment. Linear regression analysis showed no significant difference in the progression of radiological joint damage during the first 3 and 6 years of disease between the three genotype groups (TT, TG and GG). Additionally, no difference in mean disease activity between genotypes was seen after 3 and 6 years of disease.

Conclusion: Despite its demonstrated functionality, the 676T>G polymorphism in the TNFSF1b gene does not have a major role in either the response to anti-TNF therapy or in the disease severity or radiological progression in RA.

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  • Funding: This work was supported by a personal grant to MJHC from the Netherlands Organisation for Scientific Research (grant 916.76.020).

  • Competing interests: None declared.

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