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Review article: the use of gastric acid‐inhibitory drugs—physiological and pathophysiological considerations
Author(s) -
WALDUM H. L.,
BRENNA E.,
KLEVELAND P. M.,
SANDVIK A. K.,
SYVERSEN U.
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.tb00139.x
Subject(s) - gastric acid , secretion , gastrin , medicine , histamine , peptic , disease , gastroenterology , pathophysiology , stomach , peptic ulcer , helicobacter pylori , histamine antagonists , enterochromaffin like cell , enterochromaffin cell , gastric mucosa , receptor , serotonin
SUMMARY All vertebrates secrete gastric acid. Acid denatures the proteins in the food and thus makes them more accessible to proteolytic enzymes, and it kills swallowed micro‐organisms. Gastric acid plays an important pathogenetic role in peptic ulcer disease and reflux oesophagitis. In these diseases, drugs that inhibit secretion of gastric acid will heal the lesions and suppress the symptoms. However, both reflux oesophagitis and peptic ulcer tend to recur when the acid‐inhibitory treatment is stopped. Therefore, these patients often require long‐term treatment with acid‐inhibitors. In this overview the potential risks of long‐term profound inhibition of acid secretion, raising the pH above 4 for a considerable time, resulting in reduced killing of micro‐organisms and secondary hypergastrinaemia, are discussed. Gastrin regulates both the function (production and release of histamine) and growth of the enterochromaffin‐like (ECL) cell. Hitherto, the role that this cell plays in gastric carcinogenesis appears to have been underestimated.