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

Background: Helicobacter pylori is said to cause atrophy of the gastric cor pus and enterochromaffin-like cell proliferation in gastro-oesophageal refl ux disease (GERD) patients treated long-term with a proton pump inhibitor. Aims: To determine the effect of H. pylori infection on gastritis, enteroch romaffin-like cell density and hyperplasia, mucosal atrophy and serum gastr in in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h ) with either hypergastrinemia (Zollinger-Ellison syndrome) or normal gastr in (non-Zollinger-Ellison syndrome) before and during long-term treatment w ith lansoprazole. Methods: Lansoprazole was individually titrated to reduce basal acid output to < 5 mmol/h (< 1 mmol/h in post-surgical Zollinger-Ellison syndrome). Ga stric corpus biopsies were obtained every 6 months before treatment and up to 8 years later. Results: H. pylori was present in corpus biopsies in approximate to 50%, ca using active gastritis which resolved rapidly in 15 subjects after eliminat ion 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-posit ive. 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 hi gh in Zollinger-Ellison syndrome as in non-Zollinger-Ellison syndrome patie nts (241 vs. 126 cells/mm(2), P < 0.001). Enterochromaffin-like cells remai ned normal in the non-Zollinger-Ellison syndrome hypersecretors regardless of H. pylori status. Conclusions: Corpus enterochromaffin-like cell increases were related to se rum gastrin elevation, but neither H. pylori nor long-term treatment with l ansoprazole alone or together had any effect on enterochromaffin-like cell density or hyperplasia. Corpus acute gastritis resulted from H. pylori infe ction, but did not result in mucosal atrophy despite long-term proton pump inhibitor treatment and promptly resolved with loss of H. pylori.