Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Esophagogastric  Junction

  Browse by Author
  Browse by Movies
Volume: The Esophagogastric Junction
Chapter: Esophageal columnar metaplasia (Barrett s esophagus)

What does the simultaneous expression of Lewis antigen and sulphomucins tell about patients at risk for dysplasia and carcinoma?

J. Torrado, J. Garay (San Sebastián)

The evolution of adenocarcinoma in the distal esophagus follows a sequence of alterations including reflux esophagitis and Barrett's esophagus of gastric and specialized types [1-3]. Histologically, the specialized type of Barrett's esophagus is analogous to the intestinal metaplasia in the gastric mucosae and also indicates a greater risk of malignant transformation [4-7].

Sulphomucins characterize the so-called colonic or incomplete type of intestinal metaplasia in the stomach [8]. However, the significance of such finding in Barrett's esophagus remains controversial [9-11]. Although we have linked the simultaneous expression of sulphomucins and Lewis a antigen in areas of intestinal metaplasia in the stomach to an increased risk of premalignant progression [12-14], the prevalence and significance of aberrant expression of Lewis a antigen and sulphomucins in Barrett's esophagus have not been explored.

We have studied a group of 155 consecutive patients with Barrett's esophagus (unpublished results) referred at our hospital for upper gastrointestinal endoscopy and biopsy. The specific aims were to correlate the different histological stages of Barrett's esophagus, including adenocarcinoma, with the expression of sulphomucins and aberrant Lewis a antigen.

Table I shows the prevalence of sulphomucins by type of Barrett's esophagus. Cancer patients expressed sulphomucins in columnar cells in specialized-type areas of Barrett's esophagus more often than patients with specialized Barrett's esophagus without cancer (93.8% vs 58.6%, age-adjusted OR = 9.84, p < 0.05).
Table I. Expression of sulphomucins by type of B

Table II shows the prevalence of aberrant Lewis a antigen expression in Lewis (a-b+) patients by type of Barrett's esophagus. Cancer patients expressed Lewis a antigen in columnar cells in specialized type areas more often than patients with specialized Barrett's esophagus without cancer (100% vs 35.4%, OR = 63.5, p < 0.001).
Table II. Expression of Lewis a antigen among Le

While none of the 36 Lewis (a-b+) patients with gastric type of Barrett's esophagus expressed sulphomucins or Lewis a antigen, all nine Lewis (a-b+) patients with cancer expressed both markers. Only 4 (6.2%) of the 65 Lewis (a-b+) with specialized type of Barrett's esophagus expressed neither sulphomucins nor aberrant Lewis a antigen, 6 (9.2%) expressed only the aberrant Lewis a antigen, 20 (30.8%) expressed only sulphomucins and 35 (53.8%) expressed both markers.


In summary, we propose the existence of a specialized type of Barrett's esophagus similar to the incomplete or colonic type of gastric intestinal metaplasia which expresses sulphomucins and aberrant Lewis a antigen in goblet and columnar cells, and is associated with a higher risk of malignant transformation.


1. Reid BJ. Barrett's esophagus and esophageal adenocarcinoma. Gastroenterol Clin N Am 1991;20:817-834.

2. Hameeteman W, Tyggat GNJ, Houthoff HJ, Van der Tweel JG. Barrett's esophagus: development of dysplasia and adenocarcinoma. Gastroenterology 1989;96:1249-1256.

3. Reid BJ, Blount PL, Rubin CE, Levine DS, Haggit RC, Rabinovitch PS. Flow-cytometric and histological progression to malignancy in Barrett's esophagus: prospective endoscopic surveillance of a cohort. Gastroenterology 1992;102:1212-1219.

4. Spechler SJ. Barrett's esophagus. Semin Oncol 1994;21:431-437.

5. Haggitt RC. Barrett's esophagus, dysplasia and adenocarcinoma. Hum Pathol 1994;25:982-993.

6. McArdle JE, Lewin KJ, Randall G, Weinstein WM. Distribution of dysplasias and early invasive carcinoma in Barrett's esophagus. Hum Pathol 1992;23:479-482.

7. Reid BJ, Weinstein WM. Barrett's esophagus and adenocarcinoma. Annu Rev Med 1987;38:477-492.

8. Filipe MI, Muñoz N, Matko Y, et al. Intestinal metaplasia types and the risk of gastric cancer: a cohort study in Slovenia. Int J Cancer 1994;57:324-329.

9. Lapertosa G, Baracchini P, Fulcheri E, Gospe. Mucin histochemical analysis in the interpretation of Barrett's esophagus. Am J Clin Pathol 1992;

10. Haggitt RC, Reid BJ, Rabinovitch PS, Rubin CE. Barrett's esophagus. Correlation between mucin histochemistry, flow cytometry, and histologic diagnosis for predicting increased cancer risk. Am J Pathol 1988;131:53-61.

11. Jass JR. Mucin histochemistry of the columnar epithelium of the oesophagus: a retrospective study. J Clin Pathol 1981;34:866-870.

12. Torrado J, Blasco E, Cosme A, Gutierrez-Hoyos A, Arenas JI. Expression of type 1 and type 2 blood group antigens in normal and neoplastic gastric mucosa. Am J Clin Pathol 1989;91:249-254.

13. Torrado J, Correa P, Ruiz B, Bernardi P, Zavala D, Bara J. Lewis antigen alterations in gastric cancer precursors. Gastroenterology 1992;102:424-430.

14. Torrado J, Correa P, Ruiz B, Zavala D, Bara J. Prospective study of Lewis antigens in the gastric precancerous process. Cancer Epidemiol Biomark Prev 1992;1:199-205.

Publication date: May 1998 OESO©2015