ACID SUPPRESSION AND GASTRIC-MUCOSAL CELL BIOLOGY

Citation
G. Dellefave et al., ACID SUPPRESSION AND GASTRIC-MUCOSAL CELL BIOLOGY, Digestive diseases and sciences, 40(2), 1995, pp. 121-131
Citations number
90
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
01632116
Volume
40
Issue
2
Year of publication
1995
Supplement
S
Pages
121 - 131
Database
ISI
SICI code
0163-2116(1995)40:2<121:ASAGCB>2.0.ZU;2-J
Abstract
This review examines recent concepts of gastric mucosal cell biology i n relation to acid inhibition. Powerful acid-inhibitory drugs have bee n associated with the production of enterochromaffin-like (ECL) cell p roliferation and the induction of ECL cell carcinoids in rats. The ECL cell lineage and its renewal is discussed, and the factors that regul ate ECL-cell proliferation are reviewed. Current methods in use for as sessing genotoxicity in gastric mucosa are scrutinized; the much discu ssed claim that antisecretory drugs induce unscheduled DNA synthesis i s examined, and the methodology that is the basis for these claims is found defective and wanting. The nature of ECL cell proliferation in r ats receiving lifelong treatment with H-2-receptor antagonists or acid pump inhibitors is explored, and their relationship to ECL cell proli feration and ECL cell carcinoids discussed. It is concluded that aged rats are very prone to developing endocrine proliferations, and this m ay be related to the multiple endocrine neoplasia syndrome found in hu mans. There is no evidence at present that long-term antisecretory the rapy causes significant ECL cell proliferation in humans.