[Optimal use of acid-inhibitors in acid-related diseases. Physiological and physiopathological considerations with implications on therapeutic choice].

Most animal species produce gastric acid. This acid denaturates the proteins in the food and thus makes them accessible to the proteolytic enzymes. The main function of the gastric acid is probably to kill swallowed microorganisms. However, the gastric acid plays an essential role in the pathogenesis of common and important diseases like peptic ulcer and reflux oesophagitis. Drugs that inhibit the secretion of gastric acid suppress both symptoms as well as lesions in patients with peptic ulcer or reflux oesophagitis. However, both reflux oesophagitis and peptic ulcer tend to recur when the acid-inhibitory treatment is stopped. In this overview the author warns against long-term profound inhibition of acid, since, in the long term, both the reduced killing of microorganisms as well as the secondary hypergastrinemia may induce increased risk of gastric cancer. In this context the role of the enterochromaffin-like (ECL) cell in gastric carcinogenesis is thoroughly discussed. There is probably a spectrum of neuroendocrine tumours in the stomach as like in the lungs, which also are foregut derived. Gastrin regulates the function (release of histamine) as well as the growth of the ECL cell, and a maximal trophic effect seems to be reached at a lower gastrin concentration than previously realized.