title: Treatment modality and risk of development of dysplasia and adenocarcinoma in columnar-lined esophagus.
abstract: Columnar metaplasia is the precursor lesion for esophageal adenocarcinoma, resulting from prolonged gastroesophageal reflux. The influence of the efficacy of reflux control on the development of neoplastic change in columnar-lined esophagus is not established. This study compares the rate of development of dysplasia and adenocarcinoma in patients with columnar metaplasia of the esophagus between patients treated pharmacologically and those treated with antireflux surgery. This study is a retrospective review of a cohort of patients enrolled in a multicenter national registry involving 738 patients from seven UK centers. Forty-one were treated with antireflux surgery, 42 with H2 receptor antagonist, 532 with proton pump inhibitor, and 114 with a combination of these medications. Nine had none of these medications or surgery. Total follow-up was 3697 years. Mean age and follow-up for patients treated medically were 61.6 and 4.96 years and surgically were 50.5 and 6.19 years, respectively. No patient in the surgical group developed high-grade dysplasia (HGD) or adenocarcinoma. Twenty patients treated medically developed adenocarcinoma and 10 developed HGD. Hazards ratio comparing pharmacological to surgical therapy for development of all grades of dysplasia and adenocarcinoma 1.77 (P = 0.272). Log rank test comparing antireflux surgery to pharmacological therapy for development of HGD or adenocarcinoma P = 0.1287 and for adenocarcinoma P = 0.2125. Although there was a trend towards greater efficacy of antireflux surgery over pharmacological therapy in reducing the development of dysplasia and adenocarcinoma, this did not reach statistical significance.
authors.affiliation: UK National Barrett's Oesophagus Registry, University Department of Surgery, Royal Free and University College Medical School, Royal Free Campus, London, UK. piers.gatenby@btinternet.com
authors.forename: Piers A C
authors.initials: PA
authors.lastname: Gatenby
authors.forename: James R
authors.initials: JR
authors.lastname: Ramus
authors.forename: Christine P J
authors.initials: CP
authors.lastname: Caygill
authors.forename: Andre
authors.initials: A
authors.lastname: Charlett
authors.forename: Marc C
authors.initials: MC
authors.lastname: Winslet
authors.forename: Anthony
authors.initials: A
authors.lastname: Watson
mesh_terms: D000230:Adenocarcinoma / Q000473:pathology*; D001471:Barrett Esophagus / Q000473:pathology*; D018450:Disease Progression; D004938:Esophageal Neoplasms / Q000473:pathology*; D004947:Esophagus / Q000473:pathology*; D005260:Female; D018662:Fundoplication; D005764:Gastroesophageal Reflux / Q000150:complications* / Q000473:pathology / Q000628:therapy*; D006635:Histamine H2 Antagonists / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D011230:Precancerous Conditions / Q000473:pathology*; D054328:Proton Pump Inhibitors / Q000627:therapeutic use; D012189:Retrospective Studies
chemical_list: D006635:Histamine H2 Antagonists; D054328:Proton Pump Inhibitors