Drugs, gastritis, and peptic ulcer

Drug damage to the stomach provides a model for study of the development of peptic ulcer, gastritis, and duodenitis in man. Aspirin damage is the best understood. Pathophysiologically, aspirin alters the gastric mucosal barrier to hydrogen ions and lowers gastric potential difference. Ultrastructurally, aspirin damage to surface epithelial cells leads to microerosions. Macroscopically, acute hemorrhage and erosions are seen in both the stomach and duodenum by endoscopy after ingestion of a large dose of aspirin. Patients with chronic rheumatic diseases taking aspirin have a 50% incidence of gastric erosions and 20% incidence of gastric ulcer, suggesting an association between erosions and chronic ulcer formation. Acute gastric damage is lessened by neutralizing acid with bicarbonate, reducing acid secretion with cimetidine, or administering aspirin in enteric-coated form. Rheumatic patients on enteric-coated aspirin have a significantly lower incidence of gastric ulcer (5%) than those taking regular aspirin. Damage may also be prevented by increasing mucosal resistance; acute damage can be prevented by exogenous prostaglandins, regardless of their effect on acid secretion (cytoprotection). Other commonly used drugs, such as alcohol, acetaminophen, and indomethacin, reported to have paradoxical effects with respect to erosions and peptic ulcer, provide additional information on the development of gastric erosions and ulcers.