期刊
ANNALS OF THE RHEUMATIC DISEASES
卷 65, 期 9, 页码 1241-1243出版社
BMJ PUBLISHING GROUP
DOI: 10.1136/ard.2006.055137
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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 31 to 56)) 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.
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