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The pharmacogenetic relevance of the tumour necrosis factor α (TNFα) gene has just begun to be investigated. There is only preliminary evidence that the –238 GG genotype is associated with unresponsiveness to conventional disease modifying antirheumatic drugs1 and that a combination of alleles (−308 TNF1/TNF1 and –1087 GG interleukin 10) is associated with good responsiveness to etanercept.2 In addition, Mugnier et al recently suggested that patients with rheumatoid arthritis (RA) with a TNFα −308 GG genotype might, in the short term, be better infliximab responders than patients with AA or AG genotypes.3
To evaluate the influence of the polymorphism at position −308 of the TNFα gene in the long term response to infliximab, we performed a prospective study of 22 consecutive patients with RA who were given infliximab treatment. …