Cure of Helicobacter pylori infection in atrophic body gastritis patients does not improve mucosal atrophy but reduces hypergastrinemia and its related effects on body ECL-cell hyperplasia

Background: The effects of H. pylori eradication on atrophic body gastritis are controversial. Aim: To investigate the effect of triple therapy on atrophic body gastritis in H. pylori-positive patients and its effect on morpho-functional gastric parameters. Methods: Thirty-five consecutive atrophic body gastritis patients with hist ological/serological evidence of H. pylori infection were treated. Before a nd 6 and 12 months after H. pylori eradication the patients were evaluated for fasting gastrinemia and pepsinogen I, basal and peak acid output, and d etailed histological assessment including the ECL cell proliferative patter ns. Results: Six months after treatment, 25 out of 32 patients were cured (78%) . Cure of infection was associated with improvement in both basal (basal ac id output mean 0.23 +/- 0.14 mmol/h vs. 1.75 +/- 0.7 mmol/h, P < 0.005) and stimulated acid secretion (peak acid output mean 3.0 +/- 1.06 mmol/h vs. 1 6.6 +/- 4.1 mmol/h, P=0.0017) as well as with reduction in hypergastrinemia (mean gastrin levels 444.1 +/- 110.7 pg/mL vs. 85.3. +/- 28 pg/mL; P < 0.0 05). In contrast, the eradication had no effect on body corporal atrophy an d intestinal metaplasia, or pepsinogen I levels (mean 16.6 +/- 2.9 ng/mL vs . 14.2 +/- 2.1 ng/mL, N.S.). These results were confirmed at 12 months afte r eradication. A statistical inverse correlation was obtained (r=-0.3635, P < 0.05) between the corporal chronic infiltrate score and peak acid output values. A total of 53% of atrophic body gastritis patients showed a regres sion in severity of body ECL cell hyperplastic change. Conclusion: Cure of H. pylori infection in patients with atrophic gastritis reverses some adverse effects on gastric function and ECL cell hyperplasia . H. pylori infection may be cured in atrophic body gastritis patients with partial reversion of its negative consequences on acid secretion and body ECL cell hyperplasia.