Publications

The gastric duodenal mucosa normally is protected from the damaging effects of gastric acid and pepsin by ill-defined mechanisms. Ulcers may arise when there is an imbalance between the aggressive and defensive factors that renders the mucosa susceptible to damage. A variety of factors have been identified that may favor the development of peptic ulcers, but no single pathophysiologic defect applies in all ulcer patients. In duodenal ulcers, gastric acid hypersecretion is observed in as many as one third of patients; however, most patients with duodenal ulcers secrete normal amounts of gastric acid. Decreased mucosal bicarbonate secretion may be important in at least some duodenal ulcer patients. Use of NSAIDs may cause either gastric or duodenal ulcers, probably through the inhibition of mucosal prostaglandin synthesis and disruption of mucosal defenses. Finally, a recently identified bacterium, H. pylori, causes a chronic gastritis that is found in the overwhelming majority of patients with duodenal ulcers and non-NSAID-associated gastric ulcers. This bacterium may play a pivotal role in ulcer pathogenesis and, especially, in ulcer recurrences. A number of drugs of proved efficacy are available for the treatment of acute duodenal and gastric ulcers. The H2 receptor antagonists administered once daily remain the mainstay of ulcer therapy because of their efficacy, ease of use, and excellent safety profile. More thorough and long-lasting acid inhibition is afforded by the H+/K(+)-ATPase inhibitor omeprazole. This agent also promotes more rapid ulcer healing, but in most patients, this minor advantage may not justify the higher cost. It is not known whether more rapid healing will translate into lower ulcer complication rates. Until further data are available, this drug may be preferable in patients with large or complicated ulcers. In patients with refractory ulcers, omeprazole is clearly superior to other available agents. Agents that promote mucosal defense mechanisms are becoming increasingly popular in the treatment of duodenal ulcers but have undergone less testing than in gastric ulcers. Sucralfate 1 g four times daily is equivalent to H2 antagonists in the treatment of duodenal ulcers and, probably, gastric ulcers. Its requirement for multiple daily doses makes it somewhat less attractive at present to most patients. Low- to medium-dose Al-containing antacids are inexpensive and efficacious in duodenal ulcer therapy. They should remain as therapeutic options for the compliant patient in whom cost considerations are important. Colloidal bismuth subcitrate 120 mg four times a day is comparable to other agents in the acute treatment of duodenal ulcers and likely gastric ulcers.(ABSTRACT TRUNCATED AT 400 WORDS)