title: The association between tumour necrosis factor-alpha gene polymorphism and the susceptibility to rugal hyperplastic gastritis and gastric carcinoma.
abstract: OBJECTIVE
  Some subjects infected by Helicobacter pylori have enlarged folds in the gastric body, the precise mechanism of which remains obscure. The aim of this study was to clarify the association of tumour necrosis factor-alpha (TNFA) gene polymorphism with susceptibility to hyper-rugosity. We also examined the association of TNFA polymorphism with gastric carcinoma.
  
  
  METHODS
  Four hundred and seventy-two subjects (male/female = 351/121, aged 26-81 years) without gastric carcinoma (control group), and 300 patients (male/female = 218/82, aged 32-91 years) with gastric carcinoma. Barium meal roentgenograms were performed in 396 subjects in the control group and fold width was measured at the greater curvature of the middle portion of the gastric body. Fasting plasma anti-H. pylori IgG titres, pepsinogens (PGs) I and II were analysed, and TNFA -857 promoter polymorphism was distinguished by the 5' nuclease polymerase chain reaction assay and polymerase chain reaction restriction fragment length polymorphism using HincII in both groups.
  
  
  RESULTS
  Adjusted odds ratios of TNFA -857 T/T genotype and H. pylori seropositivity for hyper-rugosity (fold width = 6.0 mm) were 6.7 (95% confidence interval (CI) 1.5-28, P < 0.01) and 18.2 (95% CI 4.2-78, P < 0.0001), respectively. There were no significant differences in any genotype or allele frequencies between the control and total gastric carcinoma group. In a subgroup of gastric carcinoma patients who were negative for the PG assay, however, the odds ratio of the T allele was 1.4 (95% CI 1.0-2.0, P < 0.05).
  
  
  CONCLUSIONS
  The TNFA -857 T/T genotype and H. pylori infection were strongly associated with rugal hyperplastic gastritis. The TNFA -857 T allele may promote gastric carcinoma without severe atrophy.
authors.affiliation: Department of Therapeutic Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Itaru
authors.initials: I
authors.lastname: Ohyama
authors.forename: Naoki
authors.initials: N
authors.lastname: Ohmiya
authors.forename: Yasumasa
authors.initials: Y
authors.lastname: Niwa
authors.forename: Kennosuke
authors.initials: K
authors.lastname: Shirai
authors.forename: Ayumu
authors.initials: A
authors.lastname: Taguchi
authors.forename: Akihiro
authors.initials: A
authors.lastname: Itoh
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Hirooka
authors.forename: Kenji
authors.initials: K
authors.lastname: Wakai
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Hamajima
authors.forename: Naoyoshi
authors.initials: N
authors.lastname: Mori
authors.forename: Hidemi
authors.initials: H
authors.lastname: Goto
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D005758:Gastritis, Hypertrophic / Q000000981:diagnostic imaging / Q000209:etiology / Q000235:genetics*; D005838:Genotype; D016481:Helicobacter Infections / Q000150:complications / Q000000981:diagnostic imaging; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D020116:Pepsinogen A / Q000097:blood; D011110:Polymorphism, Genetic; D020641:Polymorphism, Single Nucleotide; D011859:Radiography; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects; D013274:Stomach Neoplasms / Q000209:etiology / Q000235:genetics*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*
chemical_list: D014409:Tumor Necrosis Factor-alpha; D020116:Pepsinogen A