Abstract
Omeprazole, at present the only substituted benzimidazole in clinical evaluation for the treatment of acid related diseases, shows a novel mechanism of action. It interferes with the proton pump in the secretory membrane of the parietal cell, the H+K+ATPase, an enzyme unique to the gastric mucosa (1). Due to its potent and long lasting antisecretory activity, omeprazole may be used in a once daily regimen for ulcer therapy. Omeprazole is the only anti-secretory drug known to reduce gastric acidity during both the day and the night, by almost 100% and 85% respectively (2, 3). While very high 14-day healing rates can be achieved in duodenal ulcer disease (4–6), nothing is known of the efficacy of omeprazole in the treatment of gastric ulcer.