OBJECTIVE: To summarize the published data on lansoprazole, a proton pump inhibitor approved by the Food and Drug Administration for use in the treatment of duodenal ulcer, erosive esophagitis, and pathologic hypersecretory conditions (e.g., Zollinger-Ellison syndrome). DATA SOURCES: Published data on lansoprazole identified by MEDLINE searches (1985–1996), as well as other pertinent literature. STUDY SELECTION: Clinical efficacy trials discussed were limited to multicenter, double-blind, parallel group, prospective studies, where possible. DATA SYNTHESIS: Lansoprazole inhibits gastric acid secretion via inhibition of gastric hydrogen/potassium adenosine triphosphatase (H+,K+-ATPase), an enzyme of the gastric parietal cell membrane that forms part of the proton pump that performs the final step in the acid secretory process. Lansoprazole binds covalently to parietal cell H+,K+-ATPase, rendering it nonfunctional and inhibiting the secretion of gastric acid. In clinical trials, lansoprazole has been shown to be more effective than placebo and standard doses of histamine (H)2-receptor antagonists and as effective as standard doses of omeprazole for the treatment of peptic ulcer disease, gastroesophageal reflux, Zollinger-Ellison syndrome, and nonsteroidal antiinflammatory drug—induced lesions. CONCLUSIONS: Lansoprazole is safe and effective for the treatment of acid-related disorders. It is more effective than the H2-receptor antagonists and comparable to omeprazole for these indications. The choice between lansoprazole and omeprazole is likely to be institution-specific and pharmacoeconomic.
Modulations in extracellular calcium lead to H+-ATPase-dependent acid secretion: a clarification of PPI failure
