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Proton pump inhibitors, enterochromaffin‐like cell growth and Helicobacter pylori gastritis
Author(s) -
SOLCIA E.,
VILLANI L.,
LUINETT O.,
FIOCCA R.
Publication year - 1993
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 - 10.1111/j.1365-2036.1993.tb00584.x
Subject(s) - atrophic gastritis , medicine , gastroenterology , gastritis , helicobacter pylori , hyperplasia , enterochromaffin like cell , gastrin , zollinger ellison syndrome , helicobacter , enterochromaffin cell , multiple endocrine neoplasia , chronic gastritis , pathology , gastric mucosa , stomach , biology , serotonin , biochemistry , receptor , secretion , gene
SUMMARY In both rodents and humans the development of gastrin‐promoted gastric argyrophil enterochromaffin‐like cell carcinoids requires the involvement of a genetic factor inherent to multiple endocrine neoplasia syndrome or of type A autoimmune chronic atrophic gastritis. Prolonged severe hypergastrinaemia acting on non‐gastritic mucosa, as in Zollinger‐Ellison syndrome patients, results in diffuse argyrophil enterochromaffin‐like cell hyperplasia but, as a rule, does not produce tumours. Combination of chronic atrophic gastritis (mostly related to Helicobacter pylori infection) with hypergastrinaemia frequently causes linear and micronodular hyperplasia of argyrophil cells, whereas carcinoids are exceptional. No tumours or preneoplastic lesions have been observed in patients treated long‐term with proton pump inhibitors, apart from rare cases in patients with combined Zollinger‐Ellison and multiple endocrine neoplasia syndromes. A moderate increase in the incidence of argyrophil cell clustering, with or without hyperplasia, probably results from the parallel evolution of ulcer‐associated Helicobacter gastritis into chronic atrophic gastritis. Eradication of H. pylori with a combination of proton pump inhibitors and antibiotics suppresses gastritis and prevents ulcer recurrence.