SUPPRESSION OF ACID-SECRETION IN PEPTIC-ULCER DISEASE

Until recently, suppression of gastric acid secretion in patients with peptic ulcer was empirical and of unproven value. Anticholinergic dru gs had only modest inhibitory effects on acid secretion, many side eff ects, and uncertain efficacy. Controlled trials using antacids demonst rated the value of reducing gastric acidity for healing duodenal ulcer . The discovery of histamine-2 (H-2) receptor antagonists in the 1970s and the introduction of H+,K+-ATPase inhibitors in the 1980s made red uction of acid secretion the first-choice modality for healing and pre venting recurrences of duodenal and gastric ulcers. The demonstration in the late 1980s and early 1990s that Helicobacter pylori (Hp) was a major risk factor for duodenal and gastric ulcer recurrences suggested that peptic ulcer could be cured by eradicating this organism from th e stomach. However, antibiotic eradication of Hp can be difficult, oft en requiring simultaneous administration of a drug that suppresses aci d secretion. Therefore, H-2 and proton pump inhibitors continue to pla y a role in the management of duodenal and gastric ulcers associated w ith Hp and also play a primary role in the therapy of other acid-relat ed disorders, such as gastroesophageal reflux diseases, stress ulcers, ulcers associated with nonsteroidal anti-inflammatory drugs, and gast rinoma (Zollinger-Ellison syndrome) and other acid hypersecretory stat es.