Barrett's oesophagus and oesophageal adenocarcinoma

Abstract

Oesophageal adenocarcinoma (OAC) has increased dramatically in Western countries, including the UK, over the past 30 years. It usually presents de novo, but is often preceded by Barrett's oesophagus (BO), a premalignant condition whereby the normal squamous epithelium is replaced by columnar lined epithelium with intestinal metaplasia. The main risk factors for BO include male sex, obesity and chronic gastro-oesophageal reflux of acid and bile. The estimated annual risk of BO progression is 0.3%, increasing substantially, up to 30%, when dysplasia is present. Endoscopic surveillance is recommended to detect neoplastic changes at an early stage and considerable evidence supports endoscopic treatment for confirmed low- and high-grade dysplasia, and intramucosal adenocarcinoma. Most OACs are diagnosed at a more advanced stage requiring CT-PET assessment and multi-modal treatment. Surgical treatment is performed in specialist centres, increasingly combined with cytotoxic chemotherapy and radiotherapy, involving close liaison between members of the multidisciplinary team. Molecular targeted therapies, such as HER2 and VEGFR-inhibitors, are beginning to penetrate clinical practice, but high molecular heterogeneity has impeded progress. In view of the overall dismal survival (<20%) for advanced OAC, there is renewed interest in screening techniques for early detection and intervention of dysplastic BO.

Keywords: Ablation; Barrett’s oesophagus; MRCP; adenocarcinoma; biomarkers; dysphagia; endoscopic mucosal resection; endoscopy; oesophagectomy; radiofrequency; screening; staging; surveillance.

Figure 1

Endoscopic appearance of BO. The transition between the pale pink squamous oesophagus and the darker columnar metaplasia that has replaced it in the lower oesophagus can easily be detected endoscopically.

Figure 2

A schematic representation of Prague classification used to measure the length of the Barrett's oesophagus and the Seattle biopsy protocol for diagnosis and surveillance of Barrett's oesophagus

Figure 3

Summary of updated British Society of Gastroenterology guidelines for surveillance of Barrett's oesophagus

Figure 4

Advanced endoscopic imaging techniques to identify dysplasia in BO. (a, b) 2.5% Acetic acid staining in a long segment of BO. Arrows indicate an area of HGD, characterized by earlier loss of acetowhitening compared with the surrounding Barrett’s mucosa. (c, d) NBI. Arrows indicate a slightly raised area of early adenocarcinoma with irregular vessels. (e, f) Autofluorescense imaging. Arrows indicate an area of early adenocarcinoma characterized by abnormal autofluorescense signal (dark red compared with bright green).

Figure 5

RFA treatment for BO with dysplasia. (a, b) RFA 360 balloon to treat a circumferential segment of BO. (c, d) RFA 90 to treat small areas of residual BO.

Figure 6

EMR for early adenocarcinoma in BO. (a) Nodular lesion corresponding to early adenocarcinoma. (b) Marking the lesion before resection. (c) A transparent suction cap is fitted to the tip of the endoscope, the targeted tissue is sucked inside, and a ligation band is then deployed, creating a pseudopolyp. (d) Resection with a metal polypectomy snare.

Figure 7. Siewert classification of gastro-oesophageal cancers

Siewert 1, cancer of the distal oesophagus; Siewert 2, gastric cardia cancer; Siewert 3, subcardial gastric cancer.

Figure 8

The TNM classification (8th edition) of malignant oesophageal tumours