Cardiac mucosa indicates risk for Barrett esophagus

Abstract

Key Words: Columnar lined esophagus; Barrett esophagus; Gastroesophageal reflux disease

TO THE EDITOR

With interest we read the article by Bani-Hani et al[1] entitled “Pathogenesis of columnar-lined esophagus", which has been published in the recent issue of World Journal of Gastroenterology. The review profoundly adds to our understanding of columnar-lined esophagus (CLE) and clearly indicates that CLE represents an acquired condition and develops as a consequence of gastroesophageal reflux disease (GERD)[1]. However, it should be pointed out that inclusion of CLE-histopathology helps to define those at risk for dysplastic and malignant transformation. Histopathology characterizes nondysplastic and dysplastic (low-, high grade dysplasia) CLE[2-4]. Going in line with the Paull-Chandrasoma classification[2], nondysplastic CLE includes oxyntocardiac mucosa, cardiac mucosa, multilayered epithelium (a mixture of basal layer of squamous epithelium and cardiac mucosa) and cardiac mucosa with goblet cells (i.e. intestinal metaplasia; Barrett esophagus, BE). In contrast to cardiac mucosa, goblet cells have never been detected within oxyntocardiac mucosa[2,3]. Consequently, following a 4-quadrant biopsy protocol of the esophagogastric junction (including squamous and gastric type mucosa, irrespective of the presence or absence of endoscopic CLE) presence of oxyntocardiac mucosa in all biopsies indicates absence of risk to progress towards intestinal metaplasia and dysplasia[2,3]. In contrast to that, presence of cardiac mucosa indicates risk to undergo intestinal metaplasia and progress towards dysplasia and adenocarcinoma of the esophagus (annual incidence for BE 0.2%-2.0%). Controversy still exists if CLE is esophageal or gastric. Normally the esophagus is lined by squamous epithelium and the stomach is covered by oxyntic mucosa. Recently Chandrasoma et al[4] showed that CLE, but not oxyntic mucosa, is present above submucosal glands and adjacent to submucosal gland ducts. Since submucosal glands are absent in the stomach, CLE is considered to be esophageal, irrespective of endoscopic appearance[2-4]. Taken together, CLE represents the morphologic consequence of GERD. GERD should be included into histopathologic routine. Hopefully, future studies will evaluate the incidence and prevalence of CLE subtypes in the normal population for identification of those at risk for intestinal metaplasia and adenocarcinoma of the esophagus.