title: The effect of medical therapy and antireflux surgery on dysphagia in patients with gastroesophageal reflux disease without esophageal stricture.
abstract: BACKGROUND
  Poor esophageal body motility and trapping of the hernial sac by the hiatal crura are the major pathomechanisms of gastroesophageal reflux disease (GERD)-induced dysphagia. There is only little knowledge of the effect of medical therapy or antireflux surgery in reflux-induced dysphagia.
  
  
  METHODS
  Fifty-nine consecutive GERD patients with dysphagia were studied by means of a symptom questionnaire, endoscopy, barium swallow, esophageal manometry, and 24-hour pH monitoring of the esophagus. Patients had proton pump inhibitor therapy and cisapride for 6 months. After GERD relapsed following withdrawal of medical therapy, 41 patients decided to have antireflux surgery performed. The laparoscopic Nissen fundoplication was chosen in 12 patients with normal esophageal body motility and the laparoscopic Toupet fundoplication in 29 patients with impaired peristalsis. Dysphagia was assessed prior to treatment, at 6 months of medical therapy, and at 6 months after surgery.
  
  
  RESULTS
  Heartburn and esophagitis were effectively treated by medical and surgical therapy. Only surgery improved regurgitation. Dysphagia improved in all patients following surgery but only in 16 patients (27.1%) following medical therapy. Esophageal peristalsis was strengthened following antireflux surgery.
  
  
  CONCLUSIONS
  Medical therapy fails to control gastroesophageal reflux as it does not inhibit regurgitation. Thus, it has little effect on reflux-induced dysphagia. Surgery controls reflux and improves esophageal peristalsis. This may contribute to its superiority over medical therapy in the treatment of GERD-induced dysphagia.
authors.affiliation: Department of Surgery, University of Innsbruck, Austria.
authors.forename: G J
authors.initials: GJ
authors.lastname: Wetscher
authors.forename: K
authors.initials: K
authors.lastname: Glaser
authors.forename: M
authors.initials: M
authors.lastname: Gadenstaetter
authors.forename: C
authors.initials: C
authors.lastname: Profanter
authors.forename: R A
authors.initials: RA
authors.lastname: Hinder
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000328:Adult; D000368:Aged; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D001562:Benzimidazoles / Q000627:therapeutic use; D020117:Cisapride / Q000627:therapeutic use; D003680:Deglutition Disorders / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D004359:Drug Therapy, Combination; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D004940:Esophageal Stenosis; D005260:Female; D005500:Follow-Up Studies; D018662:Fundoplication / Q000379:methods*; D005764:Gastroesophageal Reflux / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D006356:Heartburn / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D006863:Hydrogen-Ion Concentration; D010535:Laparoscopy; D008297:Male; D008365:Manometry; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use; D000077402:Pantoprazole; D011312:Pressure; D011446:Prospective Studies; D054328:Proton Pump Inhibitors; D013454:Sulfoxides / Q000627:therapeutic use; D011795:Surveys and Questionnaires; D016896:Treatment Outcome
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000897:Anti-Ulcer Agents; D001562:Benzimidazoles; D004791:Enzyme Inhibitors; D054328:Proton Pump Inhibitors; D013454:Sulfoxides; D000077402:Pantoprazole; D009853:Omeprazole; D020117:Cisapride