Endoscopy 2009; 41(1): 46-50
DOI: 10.1055/s-2008-1077782
Endoscopy essentials

© Georg Thieme Verlag KG Stuttgart · New York

Upper gastrointestinal tumors

R.  Lambert1
  • 1Screening group, International Agency for Research on Cancer (IARC), Lyon, France
Further Information

Publication History

Publication Date:
04 December 2008 (eFirst)

Intestinal metaplasia and risk of cancer in Barrett’s esophagus

Barrett’s esophagus, which is more frequent in Caucasians and in males, is associated with an increased risk for adenocarcinoma in the esophagus. The endoscopic diagnosis of Barrett’s esophagus is easy and reliable when the distal esophagus is lined with a long segment of metaplastic columnar epithelium. The detection of short (< 3 cm) or ultra-short (< 1 cm) segments of columnar metaplasia in the esophagus requires more attention and a precise analysis of the landmarks at the esophagogastric junction. The extremely precise anatomical study of the esophagogastric junction conducted in Japan by Takubo et al. [1] applies to the landmarks that are accessible to the endoscopist. The squamocolumnar epithelial junction is a major landmark between the squamous lining of the distal esophagus and the columnar lining of the short segment of gastric cardiac epithelium. The islands of esophageal cardiac epithelium, unstained by Lugol and located in the squamous epithelium above the squamocolumnar epithelial junction, should not be mistaken for an ultra-short Barrett’s segment. When small islands of squamous epithelium are detected by Lugol at this level they point to an ultra-short segment of Barrett’s because they correspond to the opening of ducts of submucosal glands that are located in the esophagus.

Three epithelial types can be sampled by biopsy in a segment of columnar metaplasia lining the esophagus: gastric oxyntic type, gastric cardiac type, and intestinal type. Western specialists, particularly in the USA, consider that intestinal metaplasia in the esophagus is the precursor of adenocarcinoma, and require the presence of this epithelial type for the diagnosis of Barrett’s esophagus [2]. This restriction is not required in Japan because pathologists consider that in the esophagus adenocarcinoma often arises from areas with an esophageal cardiac epithelium. Areas of intestinal metaplasia can also be sampled in biopsies from the gastric cardiac mucosa, and distinct criteria have been described by Western specialists for intestinal metaplasia occurring in the esophagus or at the gastric cardia in carditis [3].

The presence of intestinal metaplasia in the tissue samples collected in a segment of columnar-lined esophagus is not always confirmed. This was evaluated by Wang et al. [2], who found intestinal metaplasia in only 48 % of 2511 endoscopic procedures carried out in 13 distinct centers in the USA. The question is whether the risk of cancer and the surveillance of individuals with a columnar-lined esophagus without dysplasia should concern only those showing intestinal metaplasia in the histological control evaluation. An answer has recently been given in a study by Gatenby et al. [4] of seven centers in the UK: a 5- and 10-year follow-up was conducted with histological control evaluation in 322 patients who were negative for intestinal metaplasia and in 612 patients who were positive. After 5 years, 54.8 % of the negative patients had developed intestinal metaplasia, and the proportion was 90.8 % after 10 years. There was no difference in the development of dysplasia between patients with or without intestinal metaplasia. Out of the 322 patients who did not have intestinal metaplasia at the index endoscopy, 3.7 % developed high-grade dysplasia or cancer. The respective proportion for the 612 patients who had been positive for intestinal metaplasia was 4.7 %. Therefore, the presence or absence of intestinal metaplasia at the index endoscopy does not appear to play a significant role in the risk of cancer.

In conclusion, individuals with a columnar-lined esophagus are exposed to an increased risk of adenocarcinoma. After the initial detection, an extremely careful endoscopic exploration is required. The aim of the exploration is the detection of flat areas with dysplasia, and the clinical relevance of the detection of intestinal metaplasia is very low!