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Abstract
More potent gastric acid-inhibiting drugs with a longer duration of action are being produced. The latest H2 receptor antagonists are examples of this tendency, and the first H+-K+ ATPase antagonist omeprazole is the most potent gastric acid-reducing agent currently known. The benefits of profound gastric acid inhibition in the treatment of acid peptic diseases have been demonstrated in clinical studies. Omeprazole achieves faster healing and symptom relief of duodenal ulcer than H2 receptor blockers. Particularly in the treatment of refractory ulcers and reflux oesophagitis, treatment with omeprazole is very effective. However, gastric acid has an important physiologic role. The potential consequences of profound inhibition of gastric acid include intragastric bacterial colonization and hypergastrinaemia. Bacterial overgrowth of the stomach renders the gut more susceptible to enteric infections and may facilitate nosocomial infections in compromised patients. Another possible repercussion of intragastric bacteria is the formation of N-nitroso compounds with carcinogenic potency. Serum gastrin levels increase with decreasing gastric acidity. Hypergastrinaemia has a trophic effect on the gastric mucosa and gastric endocrine cells. In animal experiments ECL-cell hyperplasia and carcinoid formation have been observed as a result of high serum gastrin levels. In man similar abnormalities have been recorded in diseases accompanied by hypergastrinaemia, such as pernicious anaemia or the Zollinger-Ellison syndrome. To date there are no reports in man describing these effects after profound drug-induced hypochlorhydria, but no controlled studies have yet been done. From the available data we may conclude that profound inhibition of gastric acid secretion has clinical advantages. The risks involved will most probably be very small during short periods of treatment. At present it is not possible to establish to what extent and for what time profound acid inhibition is safe.