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Helicobacter pylori effects on gastritis, gastrin and enterochromaffin‐like cells in Zollinger–Ellison syndrome and non‐Zollinger–Ellison syndrome acid hypersecretors treated long‐term with lansoprazole
Author(s) -
Hirschowitz B. I.,
Haber M. M.
Publication year - 2001
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2001.00876.x
Subject(s) - zollinger ellison syndrome , gastrinoma , medicine , gastroenterology , lansoprazole , gastrin , gastritis , helicobacter pylori , gastric acid , enterochromaffin like cell , hyperplasia , atrophic gastritis , stomach , secretion
Background: Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin‐like cell proliferation in gastro‐oesophageal reflux disease (GERD) patients treated long‐term with a proton pump inhibitor. Aims: To determine the effect of H. pylori infection on gastritis, enterochromaffin‐like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger–Ellison syndrome) or normal gastrin (non‐Zollinger–Ellison syndrome) before and during long‐term treatment with lansoprazole. Methods: Lansoprazole was individually titrated to reduce basal acid output to < 5 mmol/h (< 1 mmol/h in post‐surgical Zollinger–Ellison syndrome). Gastric corpus biopsies were obtained every 6 months before treatment and up to 8 years later. Results: H. pylori was present in corpus biopsies in ≈ 50%, causing active gastritis which resolved rapidly in 15 subjects after elimination of H. pylori . Patchy mild/moderate corpus atrophy was present at entry in two and at the end in four out of 60 patients, one being H. pylori ‐positive. Intestinal metaplasia (< 10%) was seen in six isolated biopsies (1% of total). H. pylori did not affect serum gastrin, enterochromaffin‐like cell density or hyperplasia. Enterochromaffin‐like cell density was twice as high in Zollinger–Ellison syndrome as in non‐Zollinger–Ellison syndrome patients (241 vs. 126 cells/mm 2 , P < 0.001). Enterochromaffin‐like cells remained normal in the non‐Zollinger–Ellison syndrome hypersecretors regardless of H. pylori status. Conclusion: Corpus enterochromaffin‐like cell increases were related to serum gastrin elevation, but neither H. pylori nor long‐term treatment with lansoprazole alone or together had any effect on enterochromaffin‐like cell density or hyperplasia. Corpus acute gastritis resulted from H. pylori infection, but did not result in mucosal atrophy despite long‐term proton pump inhibitor treatment and promptly resolved with loss of H. pylori .