title: Effect of Helicobacter pylori infection and its eradication on cell proliferation, DNA status, and oncogene expression in patients with chronic gastritis.
abstract: BACKGROUND
  Helicobacter pylori, the main cause of chronic gastritis, is a class I gastric carcinogen. Chronic gastritis progresses to cancer through atrophy, metaplasia, and dysplasia. Precancerous phenotypic expression is generally associated with acquired genomic instability.
  
  
  OBJECTIVE
  To evaluate the effect of H pylori infection and its eradication on gastric histology, cell proliferation, DNA status, and oncogene expression.
  
  
  METHODS
  Morphometric and immunohistochemical techniques were used to examine gastric mucosal biopsy specimens from eight controls, 10 patients with H pylori negative chronic gastritis, 53 with H pylori positive chronic gastritis, and 11 with gastric cancer.
  
  
  RESULTS
  All patients with chronic gastritis were in a hyperproliferative state related to mucosal inflammation, regardless of H pylori infection. Atrophy was present in three of 10 patients with H pylori negative chronic gastritis and in 26 of 53 with H pylori positive chronic gastritis, associated in 18 with intestinal metaplasia. DNA content was abnormal in only 11 patients with atrophy and H pylori infection; eight of these also had c-Myc expression, associated in six cases with p53 expression. Fifty three patients with H pylori positive chronic gastritis were monitored for 12 months after antibiotic treatment: three dropped out; infection was eradicated in 45, in whom cell proliferation decreased in parallel with the reduction in gastritis activity; atrophy previously detected in 21/45 disappeared in five, regressed from moderate to mild in nine, and remained unchanged in seven; complete metaplasia disappeared in 4/14, and markers of genomic instability disappeared where previously present. In the five patients in whom H pylori persisted, atrophy, metaplasia, dysplasia, and markers of genomic instability remained unchanged.
  
  
  CONCLUSIONS
  Chronic H pylori infection seems to be responsible for genomic instability in a subset of cases of H pylori positive chronic atrophic gastritis; eradication of H pylori infection can reverse inflammation and the related atrophy, metaplasia, and genomic instability.
mesh_terms: D000328:Adult; D000368:Aged; D000782:Aneuploidy; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D001284:Atrophy; D002455:Cell Division; D002908:Chronic Disease; D004247:DNA / Q000235:genetics; D005260:Female; D005500:Follow-Up Studies; D005753:Gastric Mucosa / Q000737:chemistry / Q000382:microbiology* / Q000473:pathology; D005756:Gastritis / Q000150:complications* / Q000188:drug therapy* / Q000235:genetics / Q000382:microbiology / Q000473:pathology; D015870:Gene Expression; D019254:Genes, bcl-2; D016259:Genes, myc; D016158:Genes, p53; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis; D013274:Stomach Neoplasms / Q000382:microbiology / Q000473:pathology