Does polymorphysm of genes coding for pro-inflammatory mediators predict the clinical response to tnf alpha blocking agents? A review analysis of the literature

Tumor necrosis factor-α (TNF-α) has a key role in the pathogenesis of rheumatoid arthritis (RA) and the introduction of anti-TNFα biological therapies has dramatically altered the treatment of RA. Anti-TNFα agents display good clinical efficacy in patients resistant to traditional disease-modifying antirheumatic drugs and superior efficacy in the suppression of erosive joint damage, even if a significant non-response rate has been reported (30–40%). Because anti-TNFα therapy is associated with expensive treatment costs, leading to restrictions in the numbers of patients who may be treated, the identification of predictors of treatment outcome may improve the cost-effectiveness of anti-TNFα therapies. Several candidate gene studies have addressed this topic, but they have had limited success in identifying predictors. It is not clear whether the response to anti-TNFα treatment will be conferred through a number of genes, each with a small effect size, or whether genes may predict the outcome of the treatment.