Endoscopy 2002; 34(12): 1007-1009
DOI: 10.1055/s-2002-35845
Editorial
© Georg Thieme Verlag Stuttgart · New York

Is Barrett's Esophagus Dangerous?

W.  M.  Weinstein1
  • 1Dept. of Medicine, Division of Digestive Diseases, Center for Health Sciences, University of California, Los Angeles, California, USA
Further Information

Publication History

Publication Date:
02 December 2002 (online)

A campaign of ablation against Barrett's esophagus has been initiated at a number of centers. This campaign is not confined just to “rogue Barrett's” - where tissue has gone awry, with the development of dysplasia or very early cancer. It has also been directed at ordinary, everyday Barrett's esophagus [1] [2].

In this issue of Endoscopy, Kahaleh and colleagues [3] report long-term results (median 36 months) with ablation of Barrett's esophagus using argon plasma coagulation (APC) in 39 patients. Thirty-two of the 39 had no dysplasia, and the remaining seven had low-grade dysplasia. The results presented by the authors, and their analytical discussion of them, show that ablation treatment for Barrett's esophagus is at a relatively early stage of technical assessment with regard to both feasibility and durability.

Barrett's esophagus is a remarkable biological phenomenon. When the gut becomes stressed, it wants to be something else (Henry Appelman, personal communication). This something else is metaplasia - a response to injury throughout the gastrointestinal tract in which one type of adult tissue replaces another. What is amazing is that when Barrett's metaplasia is, in turn, injured by a variety of treatment modalities, then it too wants to be something else. In this case, the something else is to disappear and be replaced by the original squamous lining epithelium.

The metaplasia of Barrett's esophagus would be simply a curiosity if it were not for the fact that it carries a slight increase in cancer risk, as does intestinal metaplasia in the stomach. Other types of metaplasia - e. g., gastric metaplasia of the duodenal bulb surrounding duodenal ulcers, and pseudopyloric (mucous gland) metaplasia in Crohn’s disease - do not carry an increased risk of cancer.

References

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  • 2 Walker S J, Selvasekar C R, Birbeck N. Mucosal ablation in Barrett's esophagus.  Dis Esophagus. 2002;  15 22-29
  • 3 Kahaleh M, Van Laethem J L, Nagy N. et al . Long-term follow-up and factors predictive of recurrence in Barrett's esophagus treated by argon plasma coagulation and acid suppression.  Endoscopy. 2002;  34 950-955
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  • 8 Cameron A J. Epidemiology of Barrett's esophagus and adenocarcinoma.  Dis Esophagus. 2002;  15 106-108
  • 9 Gerson L B, Shetler K, Triadafilopoulos G. Prevalence of Barrett's esophagus in asymptomatic individuals.  Gastroenterology. 2002;  123 461-467
  • 10 Incarbone R, Bonavina L, Szachnowicz S. et al . Rising incidence of esophageal adenocarcinoma in Western countries: is it possible to identify a population at risk?.  Dis Esophagus. 2000;  13 275-278
  • 11 Dulai G S, Guha S, Kahn K L. et al . Preoperative prevalence of Barrett's esophagus in esophageal adenocarcinoma: a systematic review.  Gastroenterology. 2002;  122 26-33

W. M. Weinstein, M.D.

Dept. of Medicine, Division of Digestive Diseases

UCLA Center for Health Sciences 44-138 · Box 951684 · Los Angeles · CA 90095-1684 · USA

Fax: + 1-310-825-1700

Email: wweinste@ucla.edu

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