Gastroesophageal reflux is commonplace; all humans experience it. For many patients, gastroesophageal reflux disease (GERD) is a manageable condition. For others, GERD an progress to severe symptoms, inflammation, and disruption of the mucosal lining. Effective therapy calls for unclear understanding of the pathogenesis of GERD. The renal common denominator to GERD is a lower esophageal phincter mechanism that relaxes or is incompetent and allows gastroesophageal reflux to occur. Key factors associated with GERD are (a) gastric content, (b) potency of refluxate, (c) esophageal clearance, (d) tissue resistance, and e) disruption of the anatomic hiatus. GERD is generally a chronic condition characterized by recurrent symptoms. treatment goals for the GERD patient need to be defined: a therapy directed toward eliminating the symptoms or is therapy designed to eliminate gastroesophageal reflux? Unfortunately, effective therapy for GERD usually does not effect the mechanism(s) underlying the problem. The broad goals of therapy in GERD are to decrease gastroesophageal reflux and neutralize it, to enhance esophageal clearance, and to protect esophageal mucosa. The therapeutic modalises related to each of these situations are numerous and overlap, but treatment strategies for managing the GERD patient can be used in clinical “stages” or as the clinical situation dictates. H2-receptor antagonist therapy has become the “keystone” in management of GERD. Unfortunately, not all GERD patients respond to conventional H2-receptor antagonist dosage treatment; high-dose H2-receptor antagonist therapy recently has been demonstrated to be more effective in a greater number of GERD patients with severe esophagitis. The introduction of the acid-pump inhibitor omeprazole has been an important step in treating refractory, severe, erosive esophagitis. Unfortunately, GERD recurrence still occurs at a high rate and long-term management remains a problem yet to be solved. © 1990 Raven Press, Ltd., New York.