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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.
Aliment Pharmacol Ther. 2001 Jan; 15(1):87-103.AP

Abstract

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 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.

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.

Authors+Show Affiliations

Division of Gastroenterology and Hepatology, The University of Alabama at Birmingham, 35294, USA. bhirschowitz@gihep.uab.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11136282

Citation

Hirschowitz, B I., and M M. Haber. "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." Alimentary Pharmacology & Therapeutics, vol. 15, no. 1, 2001, pp. 87-103.
Hirschowitz BI, Haber MM. 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. Aliment Pharmacol Ther. 2001;15(1):87-103.
Hirschowitz, B. I., & Haber, M. M. (2001). 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. Alimentary Pharmacology & Therapeutics, 15(1), 87-103.
Hirschowitz BI, Haber MM. 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. Aliment Pharmacol Ther. 2001;15(1):87-103. PubMed PMID: 11136282.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Hirschowitz,B I, AU - Haber,M M, PY - 2001/1/3/pubmed PY - 2001/3/3/medline PY - 2001/1/3/entrez SP - 87 EP - 103 JF - Alimentary pharmacology & therapeutics JO - Aliment Pharmacol Ther VL - 15 IS - 1 N2 - 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 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. 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. SN - 0269-2813 UR - https://www.unboundmedicine.com/medline/citation/11136282/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_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&amp;sid=nlm:pubmed&amp;issn=0269-2813&amp;date=2001&amp;volume=15&amp;issue=1&amp;spage=87 DB - PRIME DP - Unbound Medicine ER -