title: The role of a defective lower esophageal sphincter in the clinical outcome of treatment for gastroesophageal reflux disease.
abstract: OBJECTIVE
  To evaluate the clinical role of a defective lower esophageal sphincter in the long-term outcome of medical and surgical treatment for gastroesophageal reflux disease.
  
  
  METHODS
  Nonrandomized control study (median follow-up, 33 months).
  
  
  METHODS
  Referred care.
  
  
  METHODS
  Fifty-five patients with gastroesophageal reflux disease were prospectively evaluated using a symptom questionnaire, upper endoscopy, esophageal manometry, and 24-hour pH monitoring. Patients were classified into three groups: (1) those with a manometrically defective lower esophageal sphincter, treated surgically; (2) those with a manometrically defective lower esophageal sphincter, treated medically; and (3) those with a manometrically normal lower esophageal sphincter, treated medically.
  
  
  METHODS
  Nissen antireflux procedure and medical therapy with H2-blockers and/or omeprazole.
  
  
  METHODS
  Symptomatic improvement after treatment and need for continuous medication.
  
  
  RESULTS
  After therapy, symptoms improved significantly in all three groups (P < .05), but least in the patients who declined surgery. Among patients with a defective lower esophageal sphincter, medical therapy could be discontinued in 13 of 14 patients who had surgery compared with one of 14 who declined surgery. Of the 27 patients with a normal lower esophageal sphincter who were treated medically, medical therapy could be discontinued in 12.
  
  
  CONCLUSIONS
  In patients with gastroesophageal reflux disease who have a defective lower esophageal sphincter, surgery can ensure durable symptom control. Patients with a defective sphincter who decline surgery are destined for lifelong therapy, whereas in approximately half of those with a normal sphincter, medical therapy can eventually be discontinued.
authors.affiliation: Department of Surgery, University of Padua Medical School, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Costantini
authors.forename: G
authors.initials: G
authors.lastname: Zaninotto
authors.forename: M
authors.initials: M
authors.lastname: Anselmino
authors.forename: C
authors.initials: C
authors.lastname: Boccù
authors.forename: L
authors.initials: L
authors.lastname: Nicoletti
authors.forename: E
authors.initials: E
authors.lastname: Ancona
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D003627:Data Interpretation, Statistical; D004943:Esophagogastric Junction / Q000502:physiology*; D005260:Female; D005500:Follow-Up Studies; D018662:Fundoplication; D005764:Gastroesophageal Reflux / Q000188:drug therapy / Q000503:physiopathology / Q000601:surgery*; D006635:Histamine H2 Antagonists / Q000627:therapeutic use; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008365:Manometry; D008875:Middle Aged; D008991:Monitoring, Physiologic; D009853:Omeprazole / Q000627:therapeutic use; D011446:Prospective Studies; D012984:Software; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D000897:Anti-Ulcer Agents; D006635:Histamine H2 Antagonists; D009853:Omeprazole