ACID SUPPRESSION AND GASTRIC-MUCOSAL CELL BIOLOGY

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.