Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Esophagogastric  Junction

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Volume: Barrett's Esophagus
Chapter: Short Barrett's esophagus

Can histologic demonstration of sulphomucins in columnar cells in and around the gastroesophageal junction help in detecting short segment Barrett's mucosa?

S.J. Spechler (Dallas)

The columnar epithelium characteristic of Barrett's esophagus is a form of intestinal metaplasia (IM). Several systems have been proposed for the classification of IM in the stomach [1-3]. These systems focus on how "complete" is the metaplasia (how strongly does the epithelium resemble that of the normal small intestine) and, if the metaplasia is incomplete, on whether the mucus-secreting cells contain colonic-type sulphomucins that stain with high iron-diamine. The normal small bowel epithelium is comprised largely of: 1) absorptive cells that do not secrete mucus and that have a well-defined brush border containing distinctive enzymes such as alkaline phosphatase, aminopeptidase, and disaccharidases; 2) numerous goblet cells containing sialomucins that stain with alcian blue; and 3) occasional Paneth cells. IM that exhibits these same features is considered the complete, or type I, variety. Incomplete forms of IM have few or no absorptive cells and generally are devoid of Paneth cells. In incomplete IM, the predominant cell type is a columnar "intermediate" cell that secretes mucus. Incomplete forms of IM also contain numerous goblet cells that secrete sialomucins, sulphomucins, or both. The IM is categorized as type II if the intermediate cells secrete neutral mucins (as do normal gastric foveolar cells) and acid sialomucins, and as type III if the intermediate cells secrete predominantly acid sulphomucins. Type I appears to be the predominant form of IM found in the stomach, both in benign conditions and in patients with gastric cancer [3, 4]. Type III IM is the least common form, but the one most strongly associated with gastric cancer [5]. One recent investigation suggested that the risk of gastric cancer for patients with type III metaplasia is more than 4.5-fold higher than that for patients with type I metaplasia [6]. Some investigators even have suggested that type III metaplasia is a form of low-grade dysplasia [7]. One recent report has suggested that the specialized IM of Barrett's esophagus is almost exclusively type III [8]. The demonstration of sulphomucins in biopsy specimens taken at the gastroesophageal junction suggests a substantial cancer risk, but this finding alone does not indicate specifically that the biopsy specimen was taken from the esophagus and not the stomach. Therefore, staining for sulphomucins is of limited value for confirming a diagnosis of short-segment Barrett's esophagus.


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2. Jass JR, Filipe MI. The mucin profiles of normal gastric mucosa, intestinal metaplasia and its variants and gastric carcinoma. Histochem J 1981;13:931-939.

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4. Craanen ME, Blok P, Dekker W, Ferwerda J, Tytgat GNJ. Subtypes of intestinal metaplasia and Helicobacter pylori. Gut 1992;33:597-600.

5. Stemmermann GN. Intestinal metaplasia of the stomach. A status report. Cancer 1994;74:556-564.

6. Filipe MI, Munoz N, Matko I, Kato I, Pompe-Kirn V, Jutersek A, Teuchmann S, Benz M, Prijon T. Intestinal metaplasia types and the risk of gastric cancer:a cohort study in Slovenia. Int J Cancer 1994;57:324-329.

7. Tosi P, Filipe MI, Luzi P, Miracco C, Santopietro R, Lio R, Sforza V, Barbini P. Gastric intestinal metaplasia type III cases are classified as low-grade dysplasia on the basis of morphometry. J Pathol 1993;169:73-78.

8. Glickman JN, Wang HH, Das KM, Goyal RK, Spechler SJ, Antonioli DA, Odze RD. Phenotype of Barrett's esophagus and intestinal metaplasia of the distal esophagus and gastroesophageal junction. Am J Surg Pathol 2001;25:87-94.

Publication date: August 2003 OESO©2015