Objective: The purpose of this study was to assess the effect of a functional polymorphism (676T>G, M196R) in the Tumor Necrosis Factor Receptor super family 1b (TNFSF1b) gene on disease activity, radiologic joint damage and response to infliximab and adalimumab therapy in patients with rheumatoid arthritis (RA).
Methods: Two RA patient cohorts 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 (DREAM) register with detailed information on their response to anti-TNF therapy (infliximab and adalimumab), the other concerned patients from a long-term observational early inception cohort at our center (n=248).
Results: The 676T>G polymorphism was not associated with anti-TNF response after three or six months of therapy. Linear regression analysis showed no significant difference in the progression of radiologic joint damage during the first three and six years of disease between the three genotype groups (TT, TG and GG). No difference in mean disease activity between genotypes was observed after three and six years of disease, either.
Conclusion: Despite its demonstrated functionality, the 676T>G polymorphism in the TNFSF1b gene does not play a major role in either the response to anti-TNF therapy or in the disease severity or radiologic progression in RA.
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