Prostaglandins: viable therapy in gastric ulceration

Gastric ulceration is a complex, multifaceted, pluricausal illness. The pathophysiology of gastric ulcer disease continues to be unclear. The mainstay for pharamacological management of gastric ulceration exists in reduction or neutralization of gastric acid secretion through administration of histamine H2 receptor blockers such as cimetidine and ranitidine. Recent studies show however that the majority of patients experiencing gastric injury exhibit normal or below normal levels of HC1 and pepsin secretion which leaves question to the effectiveness of acid reduction therapy. A viable alternative to H2 receptor blockade is to prevent mucosal injury by maintaining the integrity of the mucosal barrier through administration of prostaglandin analogues. This cytoprotection may reduce gastric damage while maintaining normal acid secretion. Our purpose is to review prostaglandins as a potential therapeutic treatment of gastric and duodenal injury and explore the role of prostaglandins as natural physiological defense mechanisms against gastroduodenal mucosal damage. We also discuss several gastric mucosal damaging agents such as nonsteriodal anti-inflammatory drugs, alcohol, and stress along with comparisons of effectiveness between prostaglandin analogues and H2 receptor blockers in reparation and prevention of injury caused by these agents.