Barrett's Esophagus: Evolutionary Insights From Genomics Janusz A. Jankowski  Gastroenterology  Volume 144, Issue 4, Pages 667-669 (April 2013) DOI: 10.1053/j.gastro.2013.02.014 Copyright © 2013 AGA Institute Terms and Conditions

Figure 1 Model of pathogenesis. New genetic determinants, established environmental triggers, and immune and structural changes. (A) Normal mucosal anatomy at the gastroesophageal junction. (B) Four types of pathology seen in gastroesophageal reflux disease (esophagitis, hiatus hernia, BE, and visceral fat). Diagram bottom to top: Gastroesophageal junction, diaphragm, subhiatal fat ring, cardiac notch, hiatal hernia, BE, and reflux esophagitis. Vertical arrow of gastroesophageal reflux of acid and/or bile into esophagus. On the BE segment, mucosal inflammation is associated with the 6p SNP and this has a greater association in men compared with women (OR, 1.38 vs 1.11). Hiatal hernia may have a defect in the submucosal layer, which in turn is associated with the 16q SNP. Twenty-nine obesity SNPs point to a mechanism that compromises sphincter tone by increasing body mass index directly as well as circulating cytokines indirectly. Gastroenterology 2013 144, 667-669DOI: (10.1053/j.gastro.2013.02.014) Copyright © 2013 AGA Institute Terms and Conditions