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Ann Rheum Dis 2006;65:1241-1243 doi:10.1136/ard.2006.055137
  • Concise report

Polymorphism at position +896 of the toll-like receptor 4 gene interferes with rapid response to treatment in rheumatoid arthritis

  1. K Kuuliala1,
  2. A Orpana2,
  3. M Leirisalo-Repo3,
  4. H Kautiainen4,
  5. M Hurme5,
  6. P Hannonen6,
  7. M Korpela,
  8. T Möttönen7,
  9. L Paimela8,
  10. K Puolakka9,
  11. A Karjalainen10,
  12. H Repo11
  1. 1Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland
  2. 2Department of Clinical Chemistry and Medical Genetics, Laboratory Diagnostics, Helsinki University Central Hospital, Helsinki
  3. 3Department of Medicine, Division of Rheumatology, Helsinki University Central Hospital
  4. 4Rheumatism Foundation Hospital, Heinola, Finland
  5. 5Department of Microbiology and Immunology, University of Tampere Medical School, and Tampere University Hospital, Tampere, Finland
  6. 6Department of Medicine, Jyväskylä Central Hospital, Jyväskylä, Finland
  7. 7Department of Medicine, Division of Rheumatology, Turku University Central Hospital, Paimio Hospital, Paimio, Finland
  8. 8Orton Hospital, Invalid Foundation, Helsinki
  9. 9Department of Medicine, Lappeenranta Central Hospital, Lappeenranta, Finland
  10. 10Department of Internal Medicine, Oulu University Hospital, Oulu, Finland
  11. 11Department of Medicine, Division of Infectious Diseases, Helsinki University Central Hospital
  1. Correspondence to:
    K Kuuliala
    Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, PO Box 21 (Haartmaninkatu 3), FIN-00014 Helsinki, Finland;krista.anttonen{at}helsinki.fi
  • Accepted 28 March 2006
  • Published Online First 10 April 2006

Abstract

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.

Footnotes

  • 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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