Volume 6 Supplement 1

24th European Workshop for Rheumatology Research

Open Access

Polymorphism at the position -308 of TNF-α gene influences outcome of infliximab therapy in rheumatoid arthritis

  • B Mugnier1,
  • D Reviron1,
  • A Darque2,
  • N Balandraud1,
  • C Roudier1 and
  • J Roudier1
Arthritis Res Ther20046(Suppl 1):72

https://doi.org/10.1186/ar1114

Received: 16 January 2004

Published: 24 February 2004

Background

Not all rheumatoid arthritis (RA) patients respond well to the standard infliximab regimen. No clinical or biological factor that would allow one to predict response has yet been identified.

Objective

The aim of the study was to test whether the -308 G/A polymorphism in the promoter of the TNF-α gene and the -1082 G/A polymorphism in the promoter of the IL-10 gene influence response to infliximab therapy in patients with RA.

Methods

We genotyped 85 RA patients for -308TNFalfa polymorphism by PCR and subdivided them into group A (A/A or A/G genotypes) and group B (G/G genotypes). We compared clinical response to infliximab treatment between the two groups after four infusions, using the DAS28 index.

Results

We found that 47.4% of patients in group A and 79.3% of patients in group B had DAS28 index improvement greater than 1.2 (P = 0.0075) and that the average DAS28 improvement was 1.12 in group A and 2.08 in group B (P = 0.05). IL-10 polymorphism did not allow us to discriminate between good and poor responders.

Conclusion

These data suggest that the -308 A/G and the -308 A/A TNF-α genotypes predict poor response to infliximab therapy in RA. -308TNFalfa genotyping might represent an easy tool with which to predict response to infliximab treatment. Conversely, the IL-10 polymorphism did not appear to be useful.

Authors’ Affiliations

(1)
Immuno-Rhumatologie, INSERM EMI
(2)
Pharmacologie, Hôpital de la Conception

Copyright

© The Author(s) 2004

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