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

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Abstract
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 histological/serological evidence of H. pylori infection were treated. Before and 6 and 12 months after H. pylori eradication the patients were evaluated for fasting gastrinemia and pepsinogen I, basal and peak acid output, and detailed histological assessment including the ECL cell proliferative patterns. Results: Six months after treatment, 25 out of 32 patients were cured (78%). Cure of infection was associated with improvement in both basal (basal acid 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. 16.6 ± 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 < 0.005). In contrast, the eradication had no effect on body corporal atrophy and 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 after 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 regression 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.