Omeprazole in the management of refractory duodenal ulcer

Abstract

In about 5-10% of duodenal ulcer patients, ulcer healing is difficult or impossible to achieve with H2-receptor antagonists. Such patients are considered to have a refractory ulcer. The cause of refractoriness remains unknown. Some patients have high acid secretion or inadequate acid suppression on treatment, but this has not been confirmed by all investigators or in all patients. Abnormalities in mucosal defence presumably exist, but none have as yet been identified. The principal medical therapeutic approach has been to continue suppressing acid or to use mucosal protective agents. Increasing the duration of H2-receptor antagonist treatment at the same dose had little effect, but doubling or trebling the dose improved healing rates in open studies. Markedly higher healing rates occurred when treatment was changed from cimetidine to ranitidine (which is more potent) in open studies, but this was not always confirmed in controlled studies. Adding the anti-muscarinic, pirenzepine, to cimetidine to achieve better acid inhibition, improved healing rates in some controlled studies but not in others. The mucosal protectant, colloidal bismuth subcitrate, proved significantly more effective than H2-receptor antagonist treatment, but the drug is suitable only for short-term therapy. Controlled studies with omeprazole confirmed the results of open studies and proved the product to be superior to continued H2-receptor antagonist treatment in healing refractory duodenal ulcer. Open studies using maintenance treatment with low-dose omeprazole suggest that such therapy is effective in keeping refractory duodenal ulcer healed.