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Fcγ receptor type IIIA genotype and response to tumor necrosis factor alpha-blocking agents in patients with rheumatoid arthritis

Kastbom, Alf (author)
Östergötlands Läns Landsting,Linköpings universitet,Reumatologi,Hälsouniversitetet,Länskliniken för Reumatologi i Östergötland
Bratt, Johan (author)
Karolinska Institutet
Ernestam, Sofia (author)
Karolinska University Hospital Huddinge and Karolinska Institutet, Stockholm, Sweden
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Lampa, Jon (author)
Karolinska Institutet
Padyukov, Leonid (author)
Karolinska Institutet
Söderkvist, Peter (author)
Linköpings universitet,Cellbiologi,Hälsouniversitetet
Skogh, Thomas (author)
Östergötlands Läns Landsting,Linköpings universitet,Reumatologi,Hälsouniversitetet,Länskliniken för Reumatologi i Östergötland
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 (creator_code:org_t)
2007
2007
English.
In: Arthritis and Rheumatism. - : Wiley. - 0004-3591 .- 1529-0131. ; 56:2, s. 448-452
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Objective: To determine whether a functional single-nucleotide polymorphism in the gene encoding Fc receptor type IIIA (FcRIIIA) correlates with the response to treatment with tumor necrosis factor inhibitors in rheumatoid arthritis (RA). Methods: The study population comprised 282 Swedish patients with RA in whom the therapeutic efficacy of conventional disease-modifying antirheumatic drugs had been insufficient. Infliximab or etanercept treatment was initiated, and patients were evaluated after 3 months, using the American College of Rheumatology 20% improvement criteria (ACR20), the ACR50, and the ACR70 or the European League Against Rheumatism (EULAR) criteria. The chi-square test was used to compare response rates across FcRIIIA genotypes. Results: No differences in genotype distribution were observed among nonresponders compared with ACR20 responders (P = 0.80), ACR50 responders (P = 0.56), or ACR70 responders (P = 0.91). Similar results were observed when analyzing infliximab and etanercept separately or when using the EULAR response criteria. Conclusion: Unlike the findings of a previous study, the results of the current study suggest that the 158V/F polymorphism of FcRIIIA is very unlikely to influence the clinical efficacy of infliximab or etanercept in patients with RA.

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