Associations between tumor necrosis factor-alpha (TNF-alpha) -308 and -238 G/A polymorphisms and shared epitope status and responsiveness to TNF-alpha blockers in rheumatoid arthritis: a metaanalysis update

J Rheumatol. 2010 Apr;37(4):740-6. doi: 10.3899/jrheum.090707. Epub 2010 Mar 1.

Abstract

Objective: To investigate whether tumor necrosis factor-alpha (TNF-alpha) promoter -308 A/G and -238 A/G polymorphisms and shared epitope (SE) status are associated with responsiveness to anti-TNF therapy in patients with rheumatoid arthritis (RA).

Methods: A comparative metaanalysis was conducted on A allele carriers (genotypes A/A + A/G) of the TNF-alpha promoter -308 and -238 A/G polymorphisms and SE status in responders and nonresponders to anti-TNF therapy.

Results: A total of 13 studies were included in the metaanalysis. Metaanalysis showed that the TNF-alpha -308 A/G polymorphism is not associated with responsiveness to TNF blockers in RA patients. Studies with a small number of subjects (< 100) showed that the odds ratio for the A allele carrier state was significantly lower among responders (OR 0.344, 95% CI 0.152-0.779, p = 0.01). Studies with a higher number of subjects (>or= 100) found no association between the TNF-alpha -308 A/G polymorphism and responsiveness to TNF blockers. The overall metaanalysis showed that the TNF-alpha -238 A/G polymorphism was not associated with the responsiveness of RA patients to TNF blockers, and stratification by TNF blocker revealed that the TNF-alpha -238 A/G polymorphism was associated with response of infliximab (OR 0.441, 95% CI 0.203-0.609, p = 0.039). SE status was found not to be associated with response to TNF blockers.

Conclusion: Metaanalysis of available data revealed an association between treatment response to infliximab and the TNF-alpha -238 A/G polymorphism, but no associations between treatment response and the TNF-alpha -308 A/G polymorphism or SE status.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Antibodies, Monoclonal / therapeutic use*
  • Antirheumatic Agents / therapeutic use
  • Arthritis, Rheumatoid / genetics*
  • Arthritis, Rheumatoid / therapy*
  • Epitopes / genetics
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Infliximab
  • Polymorphism, Single Nucleotide
  • Treatment Outcome
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / genetics*

Substances

  • Antibodies, Monoclonal
  • Antirheumatic Agents
  • Epitopes
  • Tumor Necrosis Factor-alpha
  • Infliximab