An update on pharmacogenomics in rheumatoid arthritis with a focus on TNF-blocking agents

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Abstract

TNFα is a proinflammatory cytokine, which is crucial in the pathogenesis of rheumatoid arthritis (RA). In recent years, biological therapies which block the damaging effects of TNFα on synovium and cartilage have been developed. TNF antagonists, such as etanercept, infliximab and adalimumab, although highly effective in RA, are expensive, totaling several thousand US dollars in yearly costs. In addition, only approximately 60% of patients respond to these agents. This has led to the need to prospectively identify patients most likely to respond to these agents, which can be achieved by pharmacogenomics approaches. Polymorphisms in genes encoding for TNFα, the MHC region, and the Fcγ receptor IIIA, as well as their ability to predict disease progression in RA and response to anti-TNF therapies, have been the focus of a number of studies, which are discussed in this review. There is no consensus at present as to whether pharmacogenomics will allow prediction of anti-TNF therapy efficacy in RA. Large, prospective, multicenter studies are needed to replicate and validate the results of the studies outlined in this review.

Original languageEnglish
Pages (from-to)562-567
Number of pages6
JournalCurrent Opinion in Molecular Therapeutics
Volume10
Issue number6
StatePublished - Dec 1 2008

Keywords

  • FcγRIIIA
  • Pharmacogenetics
  • Pharmacogenomics
  • Rheumatoid arthritis
  • Single nucleotide polymorphism
  • TNF antagonists
  • TNFα

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