Stress‐Related Mucosal Damage: Critical Evaluation of Potential New Therapeutic Agents

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Abstract
Cell injury produced by hydrochloric acid is the final common denominator for stress-related mucosal damage. Actions of therapeutic agents designed to prevent such damage are directed toward either inhibiting acid secretion or stimulating protective mechanisms. Newer agents that fall into the former category include omeprazole, an inhibitor of the H+-K+–ATPase pump, prostaglandins, and somatostatin. In addition to inhibiting acid, prostaglandins stimulate mucus and bicarbonate secretion and therefore provide a two-pronged protective action. Tranexamic acid is an antifibrinolytic agent that is postulated to promote clotting at bleeding sites in upper gastrointestinal lesions. Analyses of composite data suggest that (1) prostaglandin E preparations appear to be as effective as currently recognized forms of therapy, such as antacid and H2-receptor antagonist administration; (2) little enthusiasm can currently be generated for use of somatostatin or tranexamic acid; and (3) omeprazole is a theoretically attractive agent that remains to be tested in the prophylactic treatment of gastrointestinal ulceration due to severe stress.