Histopathology of<unk> , showing intestinalized epithelium with goblet cells, as opposed to normal stratified squamous epithelium of the esophagus, and pseudostratified columnar epithelium of the fundus of the stomach. The submucosa displays an infiltrate including lymphocytes and plasma cells, constituting an underlying chronic inflammation. The area between the stratified and the intestinalized epithelium displays reactive changes, but there is no secondary dysplasia in this case. H&E stain.<unk>  occurs due to chronic inflammation. The principal cause of chronic inflammation is gastroesophageal reflux disease, GERD (UK: GORD). In this disease, acidic stomach, bile, and small intestine and pancreatic contents cause damage to the cells of the lower esophagus. In turn, this provokes an advantage for cells more resistant to these noxious stimuli in particular HOXA13-expressing stem cells that are characterised by distal (intestinal) characteristics and outcompete the normal squamous cells. This mechanism also explains the selection of HER2/neu (also called ERBB2) and the overexpressing (lineage-addicted) cancer cells during the process of carcinogenesis, and the efficacy of targeted therapy against the Her-2 receptor with trastuzumab (Herceptin) in the treatment of adenocarcinomas at the gastroesophageal junction. Researchers are unable to predict who with heartburn will develop<unk> . While no relationship exists between the severity of heartburn and the development of<unk> , a relationship does exist between chronic heartburn and the development of<unk> . Sometimes, people with<unk>  have no heartburn symptoms at all. Some anecdotal evidence indicates those with the eating disorder bulimia are more likely to develop<unk>  because bulimia can cause severe acid reflux, and because purging also floods the esophagus with acid. However, a link between bulimia and<unk>  remains unproven. During episodes of reflux, bile acids enter the esophagus, and this may be an important factor in carcinogenesis. Individuals with GERD and BE are exposed to high concentrations of deoxycholic acid that has cytotoxic effects and can cause DNA damage.
Barrett's esophagus
Nutcracker esophagus
Herpes esophagitis
Zenker's diverticulum
Esophageal candidiasis
Lymphocytic esophagitis
Esophageal achalasia
Eosinophilic esophagitis