title: Central adiposity is associated with increased risk of esophageal inflammation, metaplasia, and adenocarcinoma: a systematic review and meta-analysis.
abstract: OBJECTIVE
  Central adiposity has been implicated as a risk factor for Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), possibly promoting the progression from inflammation to metaplasia and neoplasia. We performed a systematic review and meta-analysis of studies to evaluate the association between central adiposity and erosive esophagitis (EE), BE, and EAC, specifically exploring body mass index (BMI)-independent and gastroesophageal reflux (GERD)-independent effects of central adiposity on the risk of these outcomes.
  
  
  METHODS
  We performed a systematic search of multiple databases through March 2013. Studies were included if they reported effect of central adiposity (visceral adipose tissue area, waist-hip ratio, and/or waist circumference) on the risk of EE, BE, and EAC. Summary adjusted odds ratio (aOR) estimates with 95% confidence intervals (CIs), comparing highest category of adiposity with the lowest category of adiposity, were calculated by using random-effects model.
  
  
  RESULTS
  Forty relevant articles were identified. Compared with patients with normal body habitus, patients with central adiposity had a higher risk of EE (19 studies; aOR, 1.87; 95% CI, 1.51-2.31) and BE (17 studies; aOR, 1.98; 95% CI, 1.52-2.57). The association between central adiposity and BE persisted after adjusting for BMI (5 studies; aOR, 1.88; 95% CI, 1.20-2.95). Reflux-independent association of central adiposity and BE was observed in studies that used GERD patients as controls or adjusted for GERD symptoms (11 studies; aOR, 2.04; 95% CI, 1.44-2.90). In 6 studies, central adiposity was associated with higher risk of EAC (aOR, 2.51; 95% CI, 1.54-4.06), compared with normal body habitus.
  
  
  CONCLUSIONS
  On the basis of a meta-analysis, central adiposity, independent of BMI, is associated with esophageal inflammation (EE), metaplasia (BE), and neoplasia (EAC). Its effects are mediated by reflux-dependent and reflux-independent mechanisms.
authors.affiliation: Division of Gastroenterology and Hepatology, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota.
authors.forename: Siddharth
authors.initials: S
authors.lastname: Singh
authors.forename: Anamay N
authors.initials: AN
authors.lastname: Sharma
authors.forename: Mohammad Hassan
authors.initials: MH
authors.lastname: Murad
authors.forename: Navtej S
authors.initials: NS
authors.lastname: Buttar
authors.forename: Hashem B
authors.initials: HB
authors.lastname: El-Serag
authors.forename: David A
authors.initials: DA
authors.lastname: Katzka
authors.forename: Prasad G
authors.initials: PG
authors.lastname: Iyer
mesh_terms: D000230:Adenocarcinoma / Q000453:epidemiology*; D015992:Body Mass Index; D004941:Esophagitis / Q000453:epidemiology*; D006801:Humans; D008679:Metaplasia / Q000453:epidemiology*; D056128:Obesity, Abdominal / Q000150:complications*; D018570:Risk Assessment
keywords: BE; BMI; Barrett's Esophagus; Barrett's esophagus; Body Habitus; CI; CT; EAC; EE; Esophageal Cancer; GERD; OR; RR; Visceral Fat; WC; WHR; aOR; adjusted odds ratio; body mass index; computed tomography; confidence interval; erosive esophagitis; esophageal adenocarcinoma; gastroesophageal reflux disease; odds ratio; relative risk; waist circumference; waist-hip ratio