Acid suppression and gastric mucosal cell biology

G. Delle Fave, H. Helander, S. Holt, I. M. Modlin, R. Powers, E. Solcia, A. Soll, Y. Tielemans, N. A. Wright

Research output: Contribution to journalArticlepeer-review

Abstract

This review examines recent concepts of gastric mucosal cell biology in relation to acid inhibition. Powerful acid-inhibitory drugs have been associated with the production of enterochromaffin-like (ECL) cell proliferation and the induction of ECL-cell carcinoids in rats. The ECL-cell lineage and its renewal is discussed, and the factors that regulate ECL-cell proliferation are reviewed. Current methods in use for assessing genotoxicity in gastric mucosa are scrutinized; the much discussed claim that antisecretory drugs induce unscheduled DNA synthesis is examined, and the methodology that is the basis for these claims is found defective and wanting. The nature of ECL-cell proliferation in rats receiving lifelong treatment with H2-receptor antagonists or acid pump inhibitors is explored, and their relationship to ECL-cell proliferation and ECL-cell carcinoids discussed. It is concluded that aged rats are very prone to developing endocrine proliferations, and this may be related to the multiple endocrine neoplasia syndrome found in humans. There is no evidence at present that long-term antisecretory therapy causes significant ECL-cell proliferation in humans.

Original languageEnglish
Pages (from-to)1843-1852
Number of pages10
JournalDigestive Diseases and Sciences
Volume39
Issue number9
DOIs
Publication statusPublished - Sep 1994

Keywords

  • acid suppression
  • enterochromaffin-like cells
  • gastric carcinoids
  • gastric mucosa
  • intestinal metaplasia
  • multiple endocrine neoplasia syndrome
  • unscheduled DNA synthesis

ASJC Scopus subject areas

  • Gastroenterology

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