title: Rugal hyperplastic gastritis increases the risk of gastric carcinoma, especially diffuse and p53-independent subtypes.
abstract: OBJECTIVE
  Infection with Helicobacter pylori has been linked to chronic gastritis with atrophy or hyperrugosity. The development of noncardia gastric carcinoma, especially the intestinal type in Lauren's classification, has been associated with severe atrophic gastritis and p53 mutations. The objective of this study was to determine the association between hyperrugosity and gastric carcinogenesis, including p53 mutations.
  
  
  METHODS
  Barium meal roentgenograms were performed in 395 control participants and 132 gastric carcinoma patients. The fold width was measured at the greater curvature of the middle portion of the gastric body. Serum pepsinogens I and II were determined along with gastrin levels. Complete coding sequences and splice junctions for exons 5-8 of p53 gene were screened for mutations by polymerase chain reaction-based single-strand conformational polymorphism analysis.
  
  
  RESULTS
  Rugal hyperplastic gastritis (gastric body fold width>or=5 mm) increased the risk of gastric carcinoma [odds ratio, 2.60; 95% confidence interval, 1.69-4.01] as compared with the control group, especially diffuse-type gastric carcinoma (odds ratio, 4.13; 95% confidence interval, 2.36-7.24). The p53 mutational rate was significantly lower in gastric carcinoma patients with rugal hyperplastic gastritis. In intestinal-type gastric carcinoma with hyperrugosity, the incidence of p53 gene mutations decreased, but no association was found in diffuse-type gastric carcinoma between p53 mutations and rugal hyperplastic gastritis.
  
  
  CONCLUSIONS
  Rugal hyperplastic gastritis was associated with an elevated risk of gastric carcinoma, especially diffuse-type, and a lower frequency of p53 mutations.
authors.affiliation: Department of Gastroenterology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
authors.forename: Akihiko
authors.initials: A
authors.lastname: Oguri
authors.forename: Naoki
authors.initials: N
authors.lastname: Ohmiya
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: Yasumasa
authors.initials: Y
authors.lastname: Niwa
authors.forename: Osamu
authors.initials: O
authors.lastname: Maeda
authors.forename: Takafumi
authors.initials: T
authors.lastname: Ando
authors.forename: Hidemi
authors.initials: H
authors.lastname: Goto
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001483:Base Sequence; D005260:Female; D005757:Gastritis, Atrophic / Q000150:complications* / Q000235:genetics / Q000473:pathology; D005773:Gastroscopy; D016158:Genes, p53 / Q000235:genetics*; D020022:Genetic Predisposition to Disease; D016481:Helicobacter Infections / Q000150:complications; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation; D013274:Stomach Neoplasms / Q000209:etiology* / Q000235:genetics