The role of gastric carditis in metaplasia and neoplasia at the gastroesophageal junction

Adenocarcinomas at the gastroesophageal junction appear to arise from foci of intestinal metaplasia that develop either in the distal esophagus or the proximal stomach (the gastric cardia). Metaplasia is usually a consequence of chronic inflammation, and it is logical to assume that intestinal metap lasia at the gastroesophageal junction develops as a result of chronic infl ammation in the epithelia that normally line the junction region. Intestina l metaplasia in the esophagus is known to be a sequela of chronic inflammat ion in squamous epithelium caused by gastroesophageal reflux disease, where as intestinal metaplasia in the distal stomach is often a consequence of ch ronic gastritis caused by Helicobacter pylori infection. For the gastric ca rdia, the contributions of gastroesophageal reflux disease, H. pylori infec tion, and other factors to inflammation, metaplasia, and neoplasia are not clear. If physicians are to develop meaningful preventive strategies and sp ecific therapies for tumors of the proximal stomach, a clear understanding of pathogenesis is important. Recent studies on pathogenetic factors for in flammation in cardiac epithelium (gastric carditis) have yielded contradict ory results, perhaps because of fundamental differences in the techniques u sed by different investigators for identifying and sampling the gastric car dia. This report explores the roots of the controversy regarding the role o f gastric carditis in the development of metaplasia and neoplasia at the ga stroesophageal junction and suggests practical guidelines for biopsy protoc ols to be used in future studies that will be necessary to resolve these di sputes.