Vol.23 No.3

Original Article

Association between tumor necrosis factor-a (TNF-a) promoter 2308 G/A and response to TNF-a blockers in rheumatoid arthritis: a meta-analysis

Authors

Zhen Zeng1 , Zhenhua Duan1 , Tianchen Zhang1 , Sheng Wang1 , Guixing Li1 , Jing Gao1 , Dongqing Ye1 , Shengqian Xu2 , Jianhua Xu2 , Li Zhang3 , Faming Pan1

  • Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui, 230032, China
  • Department of Rheumatism and Immunity, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, China
  • Anhui Medical Genetics Center in Anhui Medical College, Hefei, Anhui, 230061, China
Received:

24 April 2012

Accepted:

6 June 2012

Published online:

4 July 2012

Full Text

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Abstract

Objectives Tumor necrosis factor (TNF)-a promoter -308G/A polymorphism has been shown to be associated with high TNF-a production and poor response to anti- TNF-a treatment. However, not all patients show a good response to TNF-a antagonists, so this association remains controversial. This study was designed to investigate whether TNF-a promoter -308 G/A polymorphism is associated with responsiveness to anti-TNF therapy in rheumatoid arthritis (RA) patients. The 28-joint count
Disease Activity Score (DAS) 28 or the American College of Rheumatology (ACR) improvement criteria 20 were used to measure patient response.
Methods A meta-analysis was performed. Pooled ORs and 95 % CIs were calculated by both dominant and
recessive genetic models.
Results Fifteen studies with a total of 2127 patients were included in this meta-analysis. The results showed that patients with the G allele responded better to the treatment (OR = 1.87, 95 % CI 1.26?2.79). A subanalysis showed similar results.
Conclusions Based on the results of this meta-analysis, RA patients with the TNF-a promoter -308 G allele respond better to TNF-a antagonist treatment, suggesting that this allele plays a major role in anti-TNF-alpha treatment response.

Key words

Meta-analysis, Rheumatoid arthritis, Response, TNF-α inhibitors, TNF-α -308 polymorphism