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Barrett's esophagus.

Abstract

Barrett's esophagus denotes the presence of columnar epithelium in the esophagus instead of the usual stratified squamous epithelium. Barrett's esophagus had been thought to represent a mediastinal extension of the stomach in patients with a congenital short esophagus. Subsequent clinical and experimental data have established the abnormality as an acquired condition resulting from chronic gastroesophageal reflux. Although roentgenographic studies may show a mild-esophageal stricture or an esophageal ulcer, definitive diagnosis requires endoscopy with directed biopsy of erythematous mucosa in the esophagus, or manometrically guided biopsies for showing the presence of columnar epithelium above the lower esophageal sphincter. Although the origin of the cells causing this epithelium is still unclear, three distinct epithelial types have been found: atrophic gastric-fundic, junctional, and specialized columnar. Esophageal strictures and esophageal ulcers are complications associated with Barrett's esophagus, but its major significance is the association with the development of adenocarcinoma of the esophagus. Treatment of Barrett's esophagus is aimed at preventing gastroesophageal reflux with the additional need for close endoscopic surveillance for the development of dysplasia or early adenocarcinoma. Whether the diagnosis of Barrett's esophagus mandates anti-reflux surgery (fundoplication) remains controversial.

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BibTeXRIS

E M Bozymski, K J Herlihy, R C Orlando. 1982. Barrett's esophagus.. https://doi.org/10.7326/0003-4819-97-1-103

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Expression of the Na+/I- symporter (NIS) is markedly decreased or absent in gastric cancer and intestinal metaplastic mucosa of Barrett esophagus.

BACKGROUND: The sodium/iodide symporter (NIS) is a plasma membrane glycoprotein that mediates iodide (I-) transport in the thyroid, lactating breast, salivary glands, and stomach. Whereas NIS expression and regulation have been extensively investigated in healthy and neoplastic thyroid and breast tissues, little is known about NIS expression and function along the healthy and diseased gastrointestinal tract. METHODS: Thus, we investigated NIS expression by immunohistochemical analysis in 155 gastrointestinal tissue samples and by immunoblot analysis in 17 gastric tumors from 83 patients. RESULTS: Regarding the healthy Gl tract, we observed NIS expression exclusively in the basolateral region of the gastric mucin-producing epithelial cells. In gastritis, positive NIS staining was observed in these cells both in the presence and absence of Helicobacter pylori. Significantly, NIS expression was absent in gastric cancer, independently of its histological type. Only focal faint NIS expression was detected in the direct vicinity of gastric tumors, i.e., in the histologically intact mucosa, the expression becoming gradually stronger and linear farther away from the tumor. Barrett mucosa with junctional and fundic-type columnar metaplasia displayed positive NIS staining, whereas Barrett mucosa with intestinal metaplasia was negative. NIS staining was also absent in intestinalized gastric polyps. CONCLUSION: That NIS expression is markedly decreased or absent in case of intestinalization or malignant transformation of the gastric mucosa suggests that NIS may prove to be a significant tumor marker in the diagnosis and prognosis of gastric malignancies and also precancerous lesions such as Barrett mucosa, thus extending the medical significance of NIS beyond thyroid disease.

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