Adenocarcinomas at the gastroesophageal junction appear to arise from loci 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 metaplasia at the gastroesophageal junction develops as a result of chronic inflammation in the epithelia that normally line the junction region. Intestinal metaplasia in the esophagus is known to be a sequela of chronic inflammation in squamous epithelium caused by gastroesophageal reflux disease, whereas intestinal metaplasia in the distal stomach is often a consequence of chronic gastritis caused by Helicobacter pylori infection. For the gastric cardia, the contributions of gastroesophageal reflux disease, H. pylori infection, and other factors to inflammation, metaplasia, and neoplasia are not clear. If physicians are to develop meaningful preventive strategies and specific therapies for tumors of the proximal stomach, a clear understanding of pathogenesis is important. Recent studies on pathogenetic factors for inflammation in cardiac epithelium (gastric carditis) have yielded contradictory results, perhaps because of fundamental differences in the techniques used by different investigators for identifying and sampling the gastric cardia. This report explores the roots of the controversy regarding the role of gastric carditis in the development of metaplasia and neoplasia at the gastroesophageal junction and suggests practical guidelines for biopsy protocols to be used in future studies that will be necessary to resolve these disputes.
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