- Meeting abstract
- Open Access
Polymorphism at the position -308 of TNF-α gene influences outcome of infliximab therapy in rheumatoid arthritis
© The Author(s) 2004
- Received: 16 January 2004
- Published: 24 February 2004
- Rheumatoid Arthritis
- Rheumatoid Arthritis Patient
- Poor Response
- Biological Factor
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.
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.
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.
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.
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.