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Abstract
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.