Abstract
Omeprazole inhibits the final step in the formation of hydrochloric acid by blocking the enzyme H+ —K+ -ATPase on the secretory membrane of the parietal cell [1]. It is a highly effective inhibitor of acid secretion and has been shown to promote the healing of duodenal ulcer, gastric ulcer and reflux oesophagitis [1–3]. The compound is also effective in healing peptic ulcer resistant to high doses of H2-receptor antagonists, in healing ulcers and alleviating symptoms of diarrhoea and malabsorption in patients with Zollinger—Ellison syndrome and enhancing the efficacy of pancreatic enzyme replacement therapy in patients with cystic fibrosis [1–4]. However, little is known of the effect of H+ —K+ -ATPase inhibitors in the prevention of NSAIDs-induced acute gastric lesions and in the healing of peptic ulcer in patients on continuous NSAID therapy.
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© 1992 Springer Science+Business Media Dordrecht
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Lamers, C.B.H.W. (1992). Omeprazole in the prevention and therapy of gastroduodenal lesions on NSAID therapy. In: Rainsford, K.D., Velo, G.P. (eds) Side-Effects of Anti-Inflammatory Drugs 3. Inflammation and Drug Therapy Series, vol 5. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-2982-4_19
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DOI: https://doi.org/10.1007/978-94-011-2982-4_19
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