title: Tumor necrosis factor receptor II gene polymorphism and severity of rheumatoid arthritis.
abstract: OBJECTIVE
  The gene encoding tumor necrosis factor receptor type II (TNFRII) is a strong candidate in the pathogenesis of rheumatoid arthritis (RA). An association between a single-nucleotide polymorphism (196M/R) in exon 6 of the TNFRII gene and familial RA was recently reported. The present study was undertaken to test the hypothesis that there is an association between this polymorphism and the severity of RA.
  
  
  METHODS
  One hundred two white patients with early RA were included in this prospective study. The French version of the Health Assessment Questionnaire (F-HAQ) and a radiographic damage score (modified Sharp/van der Heijde method) were used to quantify the functional and structural severity of RA at baseline and after 4 years of followup. TNFRII 196M/R polymorphism genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism analysis.
  
  
  RESULTS
  Among the 102 patients with RA, 63 (61.8%) were homozygous for the 196M allele, 36 (35.3%) were heterozygous for alleles 196M and 196R, and 3 (2.9%) were homozygous for the 196R allele. At baseline, the median radiographic and F-HAQ scores did not differ between RA patients who carried the 196R allele and those who did not. After 4 years of followup, the F-HAQ score was higher in RA patients carrying the 196R allele (median 1 [interquartile range (IQR) 0.125, 1.375]) than in noncarriers (0.375 [IQR 0, 1]) (P = 0.02), while the median radiographic score did not differ between RA patients who carried the 196R allele and those who did not.
  
  
  CONCLUSIONS
  The results of the present study support the hypothesis that there is an association between the TNFRII 196 M/R gene polymorphism and the functional severity of early RA.
authors.affiliation: Centre Hospitalier Universitaire Rangueil, INSERM U558, and INSERM U563, Toulouse, France.
authors.forename: Arnaud
authors.initials: A
authors.lastname: Constantin
authors.forename: Philippe
authors.initials: P
authors.lastname: Dieudé
authors.forename: Valérie
authors.initials: V
authors.lastname: Lauwers-Cancès
authors.forename: Bénédicte
authors.initials: B
authors.lastname: Jamard
authors.forename: Bernard
authors.initials: B
authors.lastname: Mazières
authors.forename: Anne
authors.initials: A
authors.lastname: Cambon-Thomsen
authors.forename: François
authors.initials: F
authors.lastname: Cornélis
authors.forename: Alain
authors.initials: A
authors.lastname: Cantagrel
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D015703:Antigens, CD / Q000235:genetics*; D001120:Arginine / Q000235:genetics; D001172:Arthritis, Rheumatoid / Q000000981:diagnostic imaging / Q000235:genetics / Q000503:physiopathology*; D001175:Arthrography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D016015:Logistic Models; D008297:Male; D008715:Methionine / Q000235:genetics; D008875:Middle Aged; D011110:Polymorphism, Genetic; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics*; D047889:Receptors, Tumor Necrosis Factor, Type II; D012720:Severity of Illness Index
chemical_list: D015703:Antigens, CD; D018124:Receptors, Tumor Necrosis Factor; D047889:Receptors, Tumor Necrosis Factor, Type II; D001120:Arginine; D008715:Methionine