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Review
. 2010 Aug 14;16(30):3780-5.
doi: 10.3748/wjg.v16.i30.3780.

Endoscopic treatment of Barrett's esophagus: From metaplasia to intramucosal carcinoma

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Review

Endoscopic treatment of Barrett's esophagus: From metaplasia to intramucosal carcinoma

Jennifer Chennat et al. World J Gastroenterol. .

Abstract

The annual incidence of adenocarcinoma arising from Barrett's esophagus (BE) is approximately 0.5%. Through a process of gradual transformation from low-grade dysplasia to high-grade dysplasia (HGD), adenocarcinoma can develop in the setting of BE. The clinical importance of appropriate identification and treatment of BE in its various stages, from intestinal metaplasia to intramucosal carcinoma (IMC) hinges on the dramatically different prognostic status between early neoplasia and more advanced stages. Once a patient has symptoms of adenocarcinoma, there is usually locally advanced disease with an approximate 5-year survival rate of about 20%. Esophagectomy has been the gold standard treatment for BE with HGD, due to the suspected risk of harboring occult invasive carcinoma, which was traditionally estimated to be as high as 40%. In recent years, the paradigm of BE early neoplasia management has recently evolved, and endoscopic therapies (endoscopic mucosal resection, radiofrequency ablation, and cryotherapy) have entered the clinical forefront as acceptable non-surgical alternatives for HGD and IMC. The goal of endoscopic therapy for HGD or IMC is to ablate all BE epithelium (both dysplastic and non-dysplastic) due to risk of synchronous/metachronous lesion development in the remaining BE segment.

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References

    1. Drewitz DJ, Sampliner RE, Garewal HS. The incidence of adenocarcinoma in Barrett's esophagus: a prospective study of 170 patients followed 4.8 years. Am J Gastroenterol. 1997;92:212–215. - PubMed
    1. Hameeteman W, Tytgat GN, Houthoff HJ, van den Tweel JG. Barrett's esophagus: development of dysplasia and adenocarcinoma. Gastroenterology. 1989;96:1249–1256. - PubMed
    1. Shaheen NJ, Crosby MA, Bozymski EM, Sandler RS. Is there publication bias in the reporting of cancer risk in Barrett's esophagus? Gastroenterology. 2000;119:333–338. - PubMed
    1. Haggitt RC. Pathology of Barrett's esophagus. J Gastrointest Surg. 2000;4:117–118. - PubMed
    1. Gillison EW, Powell J, McConkey CC, Spychal RT. Surgical workload and outcome after resection for carcinoma of the oesophagus and cardia. Br J Surg. 2002;89:344–348. - PubMed

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