The aim of this study was to determine whether the +896 A→G substitution of the Toll-like receptor 4 (TLR4) gene, causing the Asp299→Gly change in the extracellular domain of TLR4, influences treatment response in recent-onset rheumatoid arthritis. 169 patients with rheumatoid arthritis were genotyped from the Finnish Rheumatoid Arthritis Combination Therapy trial, in which they were treated either with only one disease-modifying antirheumatic drug (DMARD) with or without prednisolone (single group), or with three DMARDs and prednisolone (combination group). Patients homozygotic for the wild-type +896A allele were compared with those having the polymorphic G allele in terms of early clinical response (at 6 months) by the 28-joint Disease Activity Score (DAS28). 1 of 20 (5%; (95% (confidence interval (CI) 1 to 5)) patients of the single group with TLR4 +896AG or GG and 29 of 67 (43%; (95% CI 31 to 56)) patients with AA were in remission (p = 0.001). DAS28 of the single group with TLR4 +896AG or GG was higher than with AA (p = 0.019). In the combination group, remission rates and DAS28 values were comparable between the genotypes. The polymorphic TLR4 +896G allele may impair treatment response to single DMARD treatment in recent-onset rheumatoid arthritis.
- DAS28, 28-joint Disease Activity Score
- DMARD, disease-modifying antirheumatic drug
- FIN-RACo, Finnish Rheumatoid Arthritis Combination Therapy
- TLR4, toll-like receptor 4
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Published Online First 10 April 2006
Funding: This study was supported by grants from Finska Läkaresällskapet to Krista Kuuliala and Helsinki University Hospital Research funds to HR.
Competing interests: None.
Ethics approval: The ethics committees in all 18 participating hospitals approved the study protocol.
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