Subsquamous Extension of Intestinal Metaplasia Is Detected in 98% of Cases of Neoplastic Barrett's Esophagus

Anders, Mario; Lucks, Yasmin; El‐Masry, Muhammad Abbas; Quaas, Alexander; Rösch, Thomas; Schachschal, Guido; Bähr, Christina; Gauger, Ulrich; Sauter, Guido; Izbicki, Jakob R.; Marx, Andreas

doi:10.1016/j.cgh.2013.07.013

Cited by 36 publications

(21 citation statements)

References 24 publications

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“…These data underscore the need for more advanced imaging techniques to assess Barrett's neoplasia before and during endoscopic treatment [37]. Furthermore, a recent study reported a subsquamous extension of intestinal metaplasia in 98 % of patients with this condition [38]. The authors consequently advised that any resection of neoplastic Barrett's esophagus should extend for at least 1 cm into the squamous epithelium [38].…”

Section: Discussionmentioning

confidence: 94%

“…Furthermore, a recent study reported a subsquamous extension of intestinal metaplasia in 98 % of patients with this condition [38]. The authors consequently advised that any resection of neoplastic Barrett's esophagus should extend for at least 1 cm into the squamous epithelium [38]. In our study, markings were usually placed 3 mm outside the lesions, and the resection aimed to excise the lesion and all the markings.…”

Section: Discussionmentioning

confidence: 96%

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Clinical outcome in patients treated with endoscopic submucosal dissection for superficial Barrett’s neoplasia

et al. 2014

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 96%

Clinical outcome in patients treated with endoscopic submucosal dissection for superficial Barrett’s neoplasia

et al. 2014

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“…The R0 resection rate can be explained by the difficult delineation of Barrett's neoplasia, which might extend laterally further than a non-magnifying endoscope can show, and even under the squamous epithelium as was demonstrated using optical coherence tomography. 26,27 Therefore, many authors suggest extending the delineation margins 5 to 10 mm away from the visible lesion. 20,24,27 Our choice of only 2-3 mm lateral safety margins was made by analogy with ESD procedures in other organs.…”

Section: Discussionmentioning

confidence: 99%

Endoscopic submucosal dissection for early Barrett’s neoplasia

et al. 2016

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Introduction: The possible benefit of endoscopic submucosal dissection (ESD) for early neoplasia arising in Barrett's esophagus remains controversial. We aimed to assess the efficacy and safety of ESD for the treatment of early Barrett's neoplasia. Methods: All consecutive patients undergoing ESD for the resection of a visible lesion in a Barrett's esophagus, either suspicious of submucosal infiltration or exceeding 10 mm in size, between February 2012 and January 2015 were prospectively included. The primary endpoint was the rate of curative resection of carcinoma, defined as histologically complete resection of adenocarcinomas without poor histoprognostic factors. Results: Thirty-five patients (36 lesions) with a mean age of 66.2 AE 12 years, a mean ASA score of 2.1 AE 0.7, and a mean C4M6 Barrett's segment were included. The mean procedure time was 191 AE 79 mn, and the mean size of the resected specimen was 51.3 AE 23 mm. En bloc resection rate was 89%. Lesions were 12 AE 15 mm in size, and 81% (29/36) were invasive adenocarcinomas, six of which with submucosal invasion. Although R0 resection of carcinoma was 72.4%, the curative resection rate was 66% (19/29). After a mean follow-up of 12.9 AE 9 months, 16 (45.7%) patients had required additional treatment, among whom nine underwent surgical resection, and seven further endoscopic treatments. Metachronous lesions or recurrence of cancer developed during the follow-up period in 17.2% of the patients. The overall complication rate was 16.7%, including 8.3% perforations, all conservatively managed, and no bleeding. The 30-day mortality was 0%. Conclusion: In this early experience, ESD yielded a moderate curative resection rate in Barrett's neoplasia. At present, improvements are needed if ESD is to replace piecemeal endoscopic mucosal resection in the management of Barrett's neoplasia.

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“…3). 73 The overlying squamous epithelium hides this subsquamous intestinal metaplasia from the endoscopist and may protect it from radiofrequency ablation. The rate at which subsquamous intestinal metaplasia progresses to a malignant state is not known, but cancers have been found in these subsquamous metaplastic glands.…”

Section: Radiofrequency Ablation Of Nondysplastic Barrett's Metaplasiamentioning

confidence: 99%

Barrett's Esophagus

Spechler¹,

Souza²

2014

N Engl J Med

452

334

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I t has been estimated that 5.6% of adults in the United States have Barrett's esophagus, 1 the condition in which a metaplastic columnar mucosa that confers a predisposition to cancer replaces an esophageal squamous mucosa damaged by gastroesophageal reflux disease (GERD). 2 GERD and Barrett's esophagus are major risk factors for esophageal adenocarcinoma, a deadly tumor whose frequency in the United States has increased by a factor of more than 7 during the past four decades. 3,4 The metaplastic columnar mucosa of Barrett's esophagus causes no symptoms, and the condition has clinical importance only because it confers a predisposition to cancer. PathogenesisMetaplasia, the process wherein one adult cell type replaces another, is a consequence of chronic tissue injury. 5 In patients with chronic esophageal injury from GERD, Barrett's metaplasia develops when mucus-secreting columnar cells replace reflux-damaged esophageal squamous cells. The cells that give rise to this metaplasia are not known. It has been proposed that GERD might induce alterations in the expression of key developmental transcription factors, causing mature esophageal squamous cells to change into columnar cells (transdifferentiation) or causing immature esophageal progenitor cells to undergo columnar rather than squamous differentiation (transcommitment). 5,6 In a rat model of reflux esophagitis, metaplasia develops from bone marrow stem cells that enter the blood and settle in the reflux-damaged esophagus. 7 Studies in mouse models have suggested that metaplasia might result from upward migration of stem cells from the proximal stomach (the gastric cardia) 8 or from proximal expansion of embryonic-type cells at the gastroesophageal junction. 9 It is not clear which of these processes contribute to the pathogenesis of Barrett's esophagus in humans. Di agnosisThe diagnosis of Barrett's esophagus requires findings on endoscopy that columnar mucosa extends above the gastroesophageal junction, lining the distal esophagus, plus esophageal-biopsy results that confirm the presence of columnar metaplasia. 2 Endoscopically, the gastroesophageal junction is identified as the most proximal extent of gastric folds, and the columnar mucosa is salmon-colored and coarse, in contrast to the pale, glossy esophageal squamous mucosa (Fig. 1). The extent of esophageal columnar metaplasia determines whether long-segment or short-segment Barrett's esophagus (≥3 cm or <3 cm of columnar metaplasia, respectively) is diagnosed. 10 However, authorities disagree on the histologic type of columnar mucosa that establishes a diagnosis of Barrett's esophagus.U.S. gastroenterology societies require esophageal biopsies showing intestinal metaplasia with goblet cells (also called specialized intestinal metaplasia or specialized columnar epithelium) for a definitive diagnosis of Barrett's esophagus The New England Journal of Medicine Downloaded from nejm.org at UNIVERSITY OF NEWCASTLE on August 27, 2014. For personal use only. No other uses without permission.

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Subsquamous Extension of Intestinal Metaplasia Is Detected in 98% of Cases of Neoplastic Barrett's Esophagus

Cited by 36 publications

References 24 publications

Clinical outcome in patients treated with endoscopic submucosal dissection for superficial Barrett’s neoplasia

Clinical outcome in patients treated with endoscopic submucosal dissection for superficial Barrett’s neoplasia

Endoscopic submucosal dissection for early Barrett’s neoplasia

Barrett's Esophagus

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