Update: histopathology-based definition of gastroesophageal reflux disease and Barrett's esophagus

BACKGROUND: Gastroesophageal reflux disease (GERD) is associated with columnar lined esophagus (CLE) and Barrett's esophagus (BE), which may progress towards esophageal adenocarcinoma. Currently a mixture of symptoms, endoscopic and histopathologic criteria and results obtained from esophageal function tests define GERD. We searched for a histopathology-based definition of GERD. METHODS: Review on GERD-histopathology. RESULTS: Multilevel biopsies and the novel Paull-Chandrasoma histopathology-classification of CLE define those with reflux and risk for development of esophageal adenocarcinoma (those with Barrett's esophagus and dysplasia) and list three abnormal nondysplastic epithelia between squamous and gastric oxyntic mucosa: cardiac mucosa (CM), oxyntocardiac mucosa (OCM), and CM with intestinal metaplasia (=Barrett's esophagus, with 0.5% annual cancer risk). Frequency of intestinal metaplasia (IM) is 15-24% at an endoscopically normal junction and increases towards 100% if CLE is >= 5 cm. IM develops at the squamocolumnar junction. Dilated end stage esophagus (DESE) is a novel concept and defines the early stage of reflux disease. The pathophysiology of DESE involves gastric distention-induced shortenings of the lower esophageal sphincter (LES) with reflux favoring damage and columnar metaplasia of the most distal esophagus. Over time permanent LES shortening and proximal dislocation of the squamocolumnar junction result in gastric-type appearance of DESE, which is mistaken for proximal stomach. The majority of adenocarcinomas of the "esophagogastric" junction arise within DESE. CONCLUSIONS: CLE is abnormal, results from reflux and is a disease if associated with life quality-impairing symptoms and/or intestinal metaplasia and dysplasia (cancer risk). Presence of CLE, IM, and dysplasia cannot be excluded from endoscopy, but requires histopathology of biopsies from the squamocolumnar junction.