Increased risk of developing atrophic gastritis in patients infected with CagA(+) Helicobacter pylori

Background: To clarify the possible role of CagA positive (CagA(+)) Helicob acter pylori strains in the development of atrophic gastritis, the prevalen ce of antibodies to H. pylori and CagA (120 kD protein) was studied among s ubjects with atrophic and non-atrophic gastritis. Methods: The study popula tion was randomly selected among 12,252 Finnish men who were screened for a trophic 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 <mu>g/l (low), group B of 320 subjects with S-PGI 25-100 mug/l (n ormal) and group C of 338 subjects with S-PGI > 100 mug/1 (high). Antibodie s to H. pylori were measured with EIA and immunoblot analysis and antibodie s to CagA with immunoblot analysis. Endoscopical and histological examinati ons were performed for 203 patients from group A. Results: The prevalence o f 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-PG I (P < 0.0001, Jonckheere-Terpstra trend test). There was also a linear dec rease in the prevalence of antibodies to CagA as the atrophic corpus gastri tis became more severe (P < 0.0001, linear-by-linear trend test). Conclusio n: The presence of antibodies to CagA seems to be associated with developme nt of atrophic corpus gastritis.