BACKGROUND: Atrophic body gastritis is considered the first important step in the histogenesis of gastric carcinoma, a multistep process starting from chronic gastritis and progressing through chronic atrophic gastritis, intestinal metaplasia, and dysplasia. Helicobacter pylori is involved in the induction of atrophic body gastritis, but documentation of H. pylori infection is difficult because of the progressive disappearance of the bacterium. Our study aimed to detect past H. pylori infection in patients with atrophic body gastritis. METHODS: We used Western blot analyses of whole bacterial protein lysate of 2 different strains to probe sera from 143 patients. All sera were analyzed by ELISA (Bio-Rad), and results of gastric histology were available for all patients. RESULTS: Among 111 patient sera previously classified as negative for H. pylori infection by ELISA, 106 (95.5%) were positive when assayed by immunoblotting. CONCLUSIONS: Commercial diagnostic reagent sets may fail to detect H. pylori infection. Western blotting of whole bacterial protein extracts could provide the basis of a noninvasive serology tool able to assess previous infection with H. pylori in patients with atrophic body gastritis.
BACKGROUND:Atrophic body gastritis is considered the first important step in the histogenesis of gastric carcinoma, a multistep process starting from chronic gastritis and progressing through chronic atrophic gastritis, intestinal metaplasia, and dysplasia. Helicobacter pylori is involved in the induction of atrophic body gastritis, but documentation of H. pyloriinfection is difficult because of the progressive disappearance of the bacterium. Our study aimed to detect past H. pyloriinfection in patients with atrophic body gastritis. METHODS: We used Western blot analyses of whole bacterial protein lysate of 2 different strains to probe sera from 143 patients. All sera were analyzed by ELISA (Bio-Rad), and results of gastric histology were available for all patients. RESULTS: Among 111 patient sera previously classified as negative for H. pyloriinfection by ELISA, 106 (95.5%) were positive when assayed by immunoblotting. CONCLUSIONS: Commercial diagnostic reagent sets may fail to detect H. pyloriinfection. Western blotting of whole bacterial protein extracts could provide the basis of a noninvasive serology tool able to assess previous infection with H. pylori in patients with atrophic body gastritis.