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
- Authors
- Lee, Young Ho; Ji, Jong Dae; Bae, Sang-Cheol; Song, Gwan Gyu
- Issue Date
- 4월-2010
- Publisher
- J RHEUMATOL PUBL CO
- Keywords
- RHEUMATOID ARTHRITIS; TUMOR NECROSIS FACTOR-alpha INHIBITORS; TUMOR NECROSIS FACTOR-alpha POLYMORPHISM; RESPONSIVENESS; SHARED EPITOPE
- Citation
- JOURNAL OF RHEUMATOLOGY, v.37, no.4, pp.740 - 746
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF RHEUMATOLOGY
- Volume
- 37
- Number
- 4
- Start Page
- 740
- End Page
- 746
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/116740
- DOI
- 10.3899/jrheum.090707
- ISSN
- 0315-162X
- 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/C 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 (>= 100) found no association between the TNF-alpha +308 A/C polymorphism and responsiveness to TNF blockers. The overall metaanalysis showed that the TNF-alpha -238 A/C 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/C polymorphism, but no associations between treatment response and the TNF-alpha -308 A/G polymorphism or SE status. (First Release March 1 2010; J Rheumatol 2010;37:740-6; doi:10.3899/jrheum.090707)
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