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 corpus and enterochromaffin-like cell proliferation in gastro-oesophageal reflux disease (GERD) patients treated long-term with a proton pump inhibitor.


OBJECTIVE
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 approximately 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/mm2, P < 0.001). Enterochromaffin-like cells remained normal in the non-Zollinger-Ellison syndrome hypersecretors regardless of H. pylori status.


CONCLUSIONS
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.
Hirschowitz
B I
BI
Division of Gastroenterology and Hepatology, The University of Alabama at Birmingham, 35294, USA. bhirschowitz@gihep.uab.edu
Haber
M M
MM
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000328:Adult; D019861:Enterochromaffin-like Cells / Q000473:pathology*; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005755:Gastrins / Q000097:blood*; D005756:Gastritis / Q000209:etiology*; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D006965:Hyperplasia; D007413:Intestinal Mucosa / Q000473:pathology; D064747:Lansoprazole; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D009853:Omeprazole / Q000031:analogs & derivatives* / Q000627:therapeutic use; D015043:Zollinger-Ellison Syndrome / Q000188:drug therapy* / Q000382:microbiology / Q000473:pathology
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D004791:Enzyme Inhibitors; D005755:Gastrins; D064747:Lansoprazole; D009853:Omeprazole