title: Gastroesophageal reflux disease: an update on management.
abstract: Gastroesophageal reflux is commonplace; all humans experience it. For many patients, gastroesophageal reflux disease (GERD) is a manageable condition. For others, GERD can progress to severe symptoms, inflammation, and disruption of the mucosal lining. Effective therapy calls for a clear understanding of the pathogenesis of GERD. The final common denominator to GERD is a lower esophageal sphincter 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: is therapy directed toward eliminating the symptoms or is therapy designed to eliminate gastroesophageal reflux? Unfortunately, effective therapy for GERD usually does not affect 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 modalities 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.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, Medical College of Wisconsin, Milwaukee.
authors.forename: W J
authors.initials: WJ
authors.lastname: Hogan
mesh_terms: D004941:Esophagitis / Q000209:etiology / Q000517:prevention & control; D004943:Esophagogastric Junction / Q000503:physiopathology; D005764:Gastroesophageal Reflux / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology / Q000601:surgery; D006635:Histamine H2 Antagonists / Q000627:therapeutic use; D006801:Humans
chemical_list: D006635:Histamine H2 Antagonists