title: Fcgamma receptor type IIIA genotype and response to tumor necrosis factor alpha-blocking agents in patients with rheumatoid arthritis.
abstract: OBJECTIVE
  To determine whether a functional single-nucleotide polymorphism in the gene encoding Fcgamma receptor type IIIA (FcgammaRIIIA) correlates with the response to treatment with tumor necrosis factor alpha 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 FcgammaRIIIA 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.
  
  
  CONCLUSIONS
  Unlike the findings of a previous study, the results of the current study suggest that the 158V/F polymorphism of FcgammaRIIIA is very unlikely to influence the clinical efficacy of infliximab or etanercept in patients with RA.
authors.affiliation: Linköping University, Linköping, Sweden. alfka@imk.liu.se
authors.forename: Alf
authors.initials: A
authors.lastname: Kastbom
authors.forename: Johan
authors.initials: J
authors.lastname: Bratt
authors.forename: Sofia
authors.initials: S
authors.lastname: Ernestam
authors.forename: Jon
authors.initials: J
authors.lastname: Lampa
authors.forename: Leonid
authors.initials: L
authors.lastname: Padyukov
authors.forename: Peter
authors.initials: P
authors.lastname: Söderkvist
authors.forename: Thomas
authors.initials: T
authors.lastname: Skogh
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D015331:Cohort Studies; D000068800:Etanercept; D005260:Female; D005838:Genotype; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology / Q000627:therapeutic use*; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D017452:Receptors, IgG / Q000235:genetics* / Q000502:physiology; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; C496124:FCGR3A protein, human; D007074:Immunoglobulin G; D017452:Receptors, IgG; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068800:Etanercept