BARRETTS DISEASE - PATHOPHYSIOLOGY OF METAPLASIA AND ADENOCARCINOMA

Peptic ulceration arising in the lower esophagus lined by columnar epi thelium was described in detail by Tileston in 1906. Although this con cept was challenged in 1950 by Barrett, experimental and clinical evid ence has now conclusively demonstrated that Barrett's metaplasia is an acquired condition and is a consequence of chronic reflux of gastric or duodenal contents or both. Current concepts suggest that unknown tr ophic factors present in these secretions stimulate proliferation Of m ultipotential reserve cells located in the esophageal submucosal gland s resulting in columnar metaplasia of the normal squamous epithelium w ith subsequent potential for malignant degeneration. Today, numerous p atients are affected by reflux esophagitis, a lesser number by Barrett 's metaplasia, and a smaller but ever-enlarging group by adenocarcinom a. Although high-grade dysplasia is considered a precursor to invasive adenocarcinoma, detection of this abnormal mucosa remains controversi al and currently requires esophagoscopy with biopsy. Epithelial marker s, such as increased activity of mucosal ornithine decarboxylase, sulf omucin production, nuclear DNA aneuploidy, and recently molecular anal ysis, have also been proposed to identify those patients at increased risk for malignant degeneration. As more is learned about the pathogen esis of Barrett's disease, perhaps these cancers can ultimately be pre vented.