Cancer development based on chronic active gastritis and resulting gastric atrophy as assessed by serum levels of pepsinogen and Helicobacter pylori antibody titer.

摘要: Our study investigated the relationship between gastric cancer development and activity of Helicobacter pylori-associated chronic gastritis or resulting atrophic (CAG). A cohort 4,655 healthy asymptomatic subjects, in whom serum pepsinogen (PG) H. pylori antibody titer had been measured to assess stage gastritis, was followed for up 16 years, investigated. In subjects with a serologically diagnosed stomach (H. pylori-negative/CAG-negative), incidence rate low, at 16/100,000 person-years. With establishment infection progression significant stepwise risk elevations were seen from CAG-free pylori-positive/CAG-negative) [hazard ratio (HR) = 8.9, 95% confidence interval (CI) 2.7-54.7] CAG pylori-positive/CAG-positive) (HR 17.7, CI 5.4-108.6) finally metaplastic pylori-negative/CAG-positive) 69.7, 13.6-502.9). pylori-infected significantly elevated observed subgroup active inflammation-based high PG II level potent immune response-based titer; former associated particularly diffuse-type cancer, both subgroups showed rates around 250/100,000 person-years, comparable that CAG. No such elevation These results clearly indicate develops mainly gastritis-atrophy-metaplasia-cancer sequence partly direct carcinogenesis, levels provide indices subjects.