title: Atrophic changes of gastric mucosa are caused by Helicobacter pylori infection rather than aging: studies in asymptomatic Japanese adults.
abstract: BACKGROUND
  The current study was designed to evaluate the effect of aging and Helicobacter pylori infection on the gastric mucosa in asymptomatic Japanese adults.
  
  
  METHODS
  Eighty-five asymptomatic healthy adults were recruited from a health-screening center in Sapporo. All subjects underwent endoscopy and gastric biopsy, and serum was obtained for IgG antibodies to H. pylori, serum gastrin, and pepsinogen levels.
  
  
  RESULTS
  The prevalence of atrophic change of the gastric mucosa assessed by pathological findings increased with age (49% in the 30- to 39-year-old group compared to 89% in those 60 years and older, p < .001). The frequency of intestinal metaplasia also increased with age (38% in the 30- to 39-year-old group compared to 82% in those 60 years and older, p < .001). In contrast, the frequency of atrophic gastritis and intestinal metaplasia was extremely low in the H. pylori seronegative group regardless of age. Mean serum gastrin level in H. pylori-positive adults was significantly greater than in those who were H. pylori-negative (114.3 +/- 11.2 compared to 65.8 +/- 6.5 pg/ml, p < .03). The serum pepsinogen I-II ratio was significantly lower in those with H. pylori infection than in those without (3.1 compared to 6.6, p < .0001).
  
  
  CONCLUSIONS
  These results suggest that the chronological changes in the gastric mucosa in Japanese individuals are either entirely related to H. pylori infection or the process is greatly accelerated by H. pylori infection.
authors.affiliation: Third Department of Internal Medicine, Hokkaido University School of Medicine, Sappora, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Asaka
authors.forename: M
authors.initials: M
authors.lastname: Kato
authors.forename: M
authors.initials: M
authors.lastname: Kudo
authors.forename: M
authors.initials: M
authors.lastname: Katagiri
authors.forename: K
authors.initials: K
authors.lastname: Nishikawa
authors.forename: H
authors.initials: H
authors.lastname: Koshiyama
authors.forename: H
authors.initials: H
authors.lastname: Takeda
authors.forename: J
authors.initials: J
authors.lastname: Yoshida
authors.forename: D Y
authors.initials: DY
authors.lastname: Graham
mesh_terms: D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000276:immunology; D001284:Atrophy; D004386:Duodenum / Q000473:pathology; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology*; D005755:Gastrins / Q000097:blood; D005756:Gastritis / Q000097:blood / Q000276:immunology / Q000473:pathology*; D016481:Helicobacter Infections / Q000097:blood / Q000276:immunology / Q000473:pathology*; D016480:Helicobacter pylori / Q000276:immunology / Q000472:pathogenicity*; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007564:Japan; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D010435:Pepsinogens / Q000097:blood
chemical_list: D000907:Antibodies, Bacterial; D005755:Gastrins; D007074:Immunoglobulin G; D010435:Pepsinogens