title: Atrophic gastritis and intestinal metaplasia in Helicobacter pylori infection: the role of CagA status.
abstract: OBJECTIVE
  Helicobacter pylori (H. pylori) is a major factor in determining the risk for development of gastric adenocarcinoma through the intermediate steps of atrophic gastritis and intestinal metaplasia. Because H. pylori infection is highly prevalent in asymptomatic populations and only a few people develop cancer, additional factors may influence the risk for development of cancer, once infection is established. Some factors may pertain to differences among bacterial strains. Because infection by H. pylori strains possessing cagA (cytotoxin-associated gene A), a gene encoding a high-molecular-weight immunodominant antigen (CagA), is associated with enhanced induction of gastritis, the aim of our study was to evaluate potential differences in the prevalence and intensity of atrophy and intestinal metaplasia between CagA-positive and CagA-negative H. pylori-infected patients.
  
  
  METHODS
  Eighty H. pylori-infected patients among 120 consecutive dyspeptic patients referred for upper gastrointestinal endoscopy were studied. Six bioptic specimens were taken from the gastric antrum: five for histological examination, and one for urease test. The H. pylori status was determined by histology, CLO test, and serology (in a standardized ELISA) for serum IgG and IgA directed to H. pylori. The CagA status was determined by Western blotting to detect serum IgG antibodies to CagA. Gastritis was classified according to the Sydney System. A score from 0 to 3 was assigned to each of the following morphological variables: atrophy, intestinal metaplasia, and mononuclear and neutrophilic cell infiltration. The association between CagA status and histological features was assessed by means of the chi2 test for trend.
  
  
  RESULTS
  Among the 80 H. pylori-infected patients 53 (66%) were CagA seropositive and 27 (34%) were CagA seronegative. The mean age of the two groups was similar. CagA-positive patients had significantly higher scores for atrophy (p = 0.006), intestinal metaplasia (p = 0.01), and mononuclear (p < 0.001) and polymorphonuclear (p = 0.002) cell infiltration than did CagA-negative patients. No differences in contrast, were found for H. pylori density.
  
  
  CONCLUSIONS
  Infection with CagA-positive H. pylori strains is associated with an increased prevalence and intensity of antral atrophy and intestinal metaplasia, in addition to higher degrees of gastritis. Our results seem to suggest that the CagA status could be a helpful parameter to define a subgroup of H. pylori-infected patients at increased risk of developing gastric adenocarcinoma.
authors.affiliation: Division of Gastroenterology and Digestive Endoscopy, C.R.O. Istituto Nazionale Tumori Centroeuropeo, Aviano, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Sozzi
authors.forename: M
authors.initials: M
authors.lastname: Valentini
authors.forename: N
authors.initials: N
authors.lastname: Figura
authors.forename: P
authors.initials: P
authors.lastname: De Paoli
authors.forename: R M
authors.initials: RM
authors.lastname: Tedeschi
authors.forename: A
authors.initials: A
authors.lastname: Gloghini
authors.forename: D
authors.initials: D
authors.lastname: Serraino
authors.forename: M
authors.initials: M
authors.lastname: Poletti
authors.forename: A
authors.initials: A
authors.lastname: Carbone
mesh_terms: D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000097:blood*; D001426:Bacterial Proteins / Q000097:blood*; D001706:Biopsy; D005260:Female; D005753:Gastric Mucosa / Q000276:immunology / Q000382:microbiology / Q000473:pathology*; D005757:Gastritis, Atrophic / Q000097:blood* / Q000150:complications / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000097:blood* / Q000150:complications; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008679:Metaplasia; D008875:Middle Aged
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori