title: Distribution of body fat and its influence on esophageal inflammation and dysplasia in patients with Barrett's esophagus.
abstract: OBJECTIVE
  Increased waist circumference and visceral fat are associated with increased risk of Barrett's esophagus (BE) and esophageal adenocarcinoma. This association might be mediated by mechanical and endocrine mechanisms. We investigated the distribution of fat in subjects with BE and its association with esophageal inflammation and dysplasia.
  
  
  METHODS
  We collected data from 50 BE cases and 50 controls (matched for age and sex, identified from a radiology trauma database) seen at the Mayo Clinic in 2009. Abdominal (subcutaneous and visceral) and gastroesophageal junction (GEJ) fat area was measured using computed tomography with standard techniques. Esophageal inflammation (based on a histologic score) and dysplasia grade were assessed from esophageal biopsies of BE cases by a gastrointestinal pathologist. Conditional logistic regression was used to assess the association of body fat depot area with BE status, esophageal inflammation, and dysplasia.
  
  
  RESULTS
  All BE subjects had controlled reflux symptoms without esophagitis, based on endoscopy. The GEJ fat area (odds ratio [OR], 6.0; 95% confidence interval [CI], 1.3-27.7; P = .02), visceral fat area (OR, 4.9; 95% CI, 1.0-22.8; P = .04), and abdominal circumference (OR, 9.1; 95% CI, 1.4-57.2; P = 0.02) were associated with BE, independent of body mass index (BMI). The subcutaneous fat area was not associated with BE. Visceral and GEJ fat were significantly greater in BE subjects with esophageal inflammation (compared with those without, P = .02) and high-grade dysplasia (compared with those without, P = .01), independent of BMI.
  
  
  CONCLUSIONS
  GEJ and visceral fat are associated with BE, and with increased esophageal inflammation and high-grade dysplasia in BE subjects, independent of BMI. Visceral fat therefore might promote esophageal metaplasia and dysplasia.
authors.affiliation: Division of Internal Medicine, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, USA.
authors.forename: Eric M
authors.initials: EM
authors.lastname: Nelsen
authors.forename: Yujiro
authors.initials: Y
authors.lastname: Kirihara
authors.forename: Naoki
authors.initials: N
authors.lastname: Takahashi
authors.forename: Qian
authors.initials: Q
authors.lastname: Shi
authors.forename: Jason T
authors.initials: JT
authors.lastname: Lewis
authors.forename: Vikneswaran
authors.initials: V
authors.lastname: Namasivayam
authors.forename: Navtej S
authors.initials: NS
authors.lastname: Buttar
authors.forename: Kelly T
authors.initials: KT
authors.lastname: Dunagan
authors.forename: Ganapathy A
authors.initials: GA
authors.lastname: Prasad
mesh_terms: D000273:Adipose Tissue / Q000473:pathology*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001471:Barrett Esophagus / Q000150:complications*; D001706:Biopsy; D050218:Body Fat Distribution / Q000706:statistics & numerical data*; D016022:Case-Control Studies; D004941:Esophagitis / Q000453:epidemiology* / Q000473:pathology*; D007887:Fabaceae; D005260:Female; D006651:Histocytochemistry; D006801:Humans; D008297:Male; D008679:Metaplasia / Q000453:epidemiology* / Q000473:pathology*; D008875:Middle Aged