Non-steroidal anti-inflammatory drug gastropathy: clinical results with H2 antagonists and proton pump inhibitors.

While the most effective strategy to prevent non-steroidal anti-inflammatory drug-related gastrointestinal toxicity is not to prescribe the medication, this option is often impractical. The use of specific agents to heal mucosal lesions or to prevent non-steroidal anti-inflammatory drug toxicity, has focused upon two approaches: replacement of prostaglandin deficiency and inhibition of acid secretion. Acid suppression with traditional ulcer healing doses of H2-blockers is effective in the cure of gastric and duodenal ulcers upon discontinuation of the offending drug. In the event the non-steroidal anti-inflammatory drug must be continued, the use of H2-RAs is associated with a slight decrease in the healing rate. In long-term prevention studies, H2-blockers significantly reduce duodenal ulcer rates, but are ineffective in reducing gastric ulceration. More potent acid inhibition with double-doses of H2-blockers may also reduce the risk of gastric (famotidine 80 mg) and duodenal ulcers (famotidine 80 mg or ranitidine 600 mg daily). Proton pump inhibitors (omeprazole 20-40 mg, lansoprazole 30 mg daily) appear more effective in healing gastric and duodenal ulcers in patients continuing the offending drug. Comparative studies of omeprazole vs ranitidine, misoprostol and sucralfate show a therapeutic gain in favour of the proton pump inhibition, ranging from 10 to 40%. In long-term prevention studies, omeprazole (20 mg daily) and pantoprazole (40 mg daily) have also been shown to reduce the risk of gastric and duodenal ulcers. Comparative studies of omeprazole (20 mg daily) vs ranitidine (150 mg daily) and misoprostol (200 micrograms daily) showed that after 6 months' follow-up the proton pump inhibition was significantly superior to control drugs in reducing the risk of both gastric and duodenal ulcer.