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Advanced precancerous lesions in the lower oesophageal mucosa: High-grade dysplasia and intramucosal carcinoma in Barrett's oesophagus

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Abstract

Adenocarcinoma developed in Barrett's oesophagus is a tumour with an increasing incidence and still a poor prognosis. The only marker that can be used for surveillance remains dysplasia (intraepithelial neoplasia), especially when it is high-grade, that precedes intramucosal carcinoma. New forms of dysplasia have been described in complement to the classical intestinal type (foveolar dysplasia, basal crypt dysplasia). High-grade dysplasia and intramucosal carcinoma are diagnosed on biopsies taken during endoscopy. Standard endoscopy is now challenged by various techniques that represent recent major technical improvements (chromoendoscopy, virtual chromoendoscopy, optical frequency domain imaging, confocal laser endomicroscopy). In numerous cases, high-grade dysplasia and intramucosal carcinoma can be treated by endoscopic procedures, allowing a precise histopathological diagnosis on the resected specimen (endoscopic mucosal resection, submucosal endoscopic dissection) or destroying the neoplastic tissue. Radiofrequency ablation is currently considered as the best available technique for treatment of flat high grade dysplasia and for eradication of residual Barrett's mucosa after focal endoscopic mucosal resection.

Introduction

During recent decades, the incidence of oesophageal adenocarcinoma has risen dramatically in most Western countries. This tumour is now the most common type of oesophageal cancer in the United States and in parts of Western Europe [1], [2]. The prognosis of oesophageal adenocarcinoma remains poor, with a five-year survival less than 15 percent [3]. Barrett's oesophagus (BO) is recognized as the precursor of almost all cases of oesophageal adenocarcinoma [4]. Two systematic reviews and meta-analyses of 47 and 51 studies found an average cancer incidence of 0.6% per year in patients with BO [5], [6]; however, this risk may be lower than it was estimated previously: in a recent population-based study in Denmark, the absolute annual risk of cancer was only 0.12% [7]. Nevertheless, BO surveillance has been recommended to detect dysplasia and early carcinoma. The diagnosis of these early neoplastic lesions has been very much improved with recent innovations in endoscopic techniques, and their treatment now relies on non-surgical procedures in most cases.

Section snippets

Barrett's oesophagus, Barrett's dysplasia and Barrett's carcinoma: definition and main molecular changes

BO is defined by the American Gastroenterological Association (AGA) as ‘the condition in which any extent of metaplastic columnar epithelium that predisposes to cancer development replaces the stratified epithelium that normally lines the distal oesophagus’ [8]. Whether or not this definition implies the presence of intestinal-type columnar epithelium with goblet cells is still a matter of debate, which will not be discussed in detail in this article (for review, ref. [9], [10]). The

Pathological features of high-grade dysplasia and intramucosal carcinoma

HGD is characterized by marked cellular atypia and complex architectural changes. Adenomatous (also called intestinal) dysplasia is the most frequent histological subtype, but two other types can be observed: non-adenomatous or foveolar type dysplasia and basal crypt dysplasia [16], [17]. IMC invades the lamina propria, and is defined primarily by its architectural properties.

Cancer risk in patients with dysplasia in BO

Although it is well established that patients with dysplasia in BO have an increased risk of cancer, the exact risk of progression to carcinoma is difficult to establish with certainty. One of the reasons of the variable results published in the literature is the high number of prevalent carcinomas missed on the initial endoscopy, resulting in some studies in a risk of progression from HGD to carcinoma as high as 90%. In a meta-analysis that excluded prevalent carcinomas, the incidence of

Diagnostic criteria of BO

The diagnosis of BO is suspected at endoscopy and confirmed with histology [39]. Indeed, endoscopic suspicion of BO appears like an abnormal salmon-coloured mucosa in the lower oesophagus, above the top of gastric folds, replacing the normal pale pink-coloured oesophageal mucosa. At this stage, the term ‘endoscopic suspicion of oesophageal metaplasia’ (ESEM) should be used by the endoscopist in the endoscopy report, and biopsies should be taken in order to confirm the presence of intestinal

Management of high-grade dysplasia and early carcinoma in Barrett's oesophagus

Until recently, surgical resection was the treatment of choice for early stage lesions in BO, but this paradigm is currently challenged by interventional endoscopy [55]. Oesophagectomy is associated with significant mortality and morbidity even when surgery is performed in high volume expert centres. Operative mortality rate for oesophagectomy for HGD and early adenocarcinoma ranges from 0% to 4%, with an overall operative 30-day mortality rate of approximately 2% [56]. The management of early

Conflict of interest

None.

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