Ann Rheum Dis

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Published Online First: 2 April 2008. doi:10.1136/ard.2008.088138
Annals of the Rheumatic Diseases 2008;67:1174-1177
Copyright © 2008 BMJ Publishing Group Ltd & European League Against Rheumatism

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CONCISE REPORTS

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

E J M Toonen 1, M J H Coenen 1, W Kievit 2, J Fransen 2, A M Eijsbouts 3, H Scheffer 1, T R D J Radstake 2, M C W Creemers 2, D-J R A M de Rooij 3, P L C M van Riel 2, B Franke 1, P Barrera 2

1 Department of Human Genetics, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
2 Department of Rheumatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
3 Department of Rheumatology, St Maartenskliniek, Nijmegen, The Netherlands

Correspondence to:
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}antrg.umcn.nl


ABSTRACT
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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