title: Increased risk of developing atrophic gastritis in patients infected with CagA+ Helicobacter pylori.
abstract: BACKGROUND
  To clarify the possible role of CagA positive (CagA+) Helicobacter pylori strains in the development of atrophic gastritis, the prevalence of antibodies to H. pylori and CagA (120 kD protein) was studied among subjects with atrophic and non-atrophic gastritis.
  
  
  METHODS
  The study population was randomly selected among 12,252 Finnish men who were screened for atrophic corpus gastritis with serum pepsinogen I-assay (S-PGI). S-PGI level was used as a selection criterion. Group A consisted of 295 subjects with S-PGI <25 microg/l (low), group B of 320 subjects with S-PGI 25-100 microg/l (normal) and group C of 338 subjects with S-PGI >100 microg/l (high). Antibodies to H. pylori were measured with EIA and immunoblot analysis and antibodies to CagA with immunoblot analysis. Endoscopical and histological examinations were performed for 203 patients from group A.
  
  
  RESULTS
  The prevalence of antibodies to H. pylori was significantly lower in group B than in groups A or C (P < 0.0001, chi-squared test). There was a significant association between the prevalence of antibodies to CagA and the lowered level of S-PGI (P < 0.0001, Jonckheere-Terpstra trend test). There was also a linear decrease in the prevalence of antibodies to CagA as the atrophic corpus gastritis became more severe (P < 0.0001, linear-by-linear trend test).
  
  
  CONCLUSIONS
  The presence of antibodies to CagA seems to be associated with development of atrophic corpus gastritis.
authors.affiliation: Dept. of Clinical Chemistry, Helsinki University Central Hospital, Finland.
authors.forename: N
authors.initials: N
authors.lastname: Sande
authors.forename: M
authors.initials: M
authors.lastname: Nikulin
authors.forename: I
authors.initials: I
authors.lastname: Nilsson
authors.forename: T
authors.initials: T
authors.lastname: Wadström
authors.forename: F
authors.initials: F
authors.lastname: Laxén
authors.forename: M
authors.initials: M
authors.lastname: Härkönen
authors.forename: O
authors.initials: O
authors.lastname: Suovaniemi
authors.forename: P
authors.initials: P
authors.lastname: Sipponen
mesh_terms: D000907:Antibodies, Bacterial / Q000276:immunology; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000378:metabolism*; D005757:Gastritis, Atrophic / Q000453:epidemiology / Q000382:microbiology*; D016481:Helicobacter Infections / Q000453:epidemiology* / Q000276:immunology; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D020116:Pepsinogen A / Q000097:blood; D011897:Random Allocation; D012307:Risk Factors; D012680:Sensitivity and Specificity; D016036:Seroepidemiologic Studies
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori; D020116:Pepsinogen A