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  • Review Article
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Barrett esophagus: histology and pathology for the clinician

Nature Reviews Gastroenterology & Hepatology volume 6, pages 478–490 (2009)Cite this article

Abstract

The incidence of adenocarcinoma of the esophagus and gastroesophageal junction has increased dramatically over the past 30 years. The major precursor to this type of adenocarcinoma is Barrett esophagus, which is defined as the conversion of normal squamous epithelium into metaplastic columnar epithelium. Abundant evidence suggests that adenocarcinoma in the setting of Barrett esophagus develops via a progressive sequence of histological and molecular events. Consequently, patients with Barrett esophagus routinely undergo endoscopic surveillance for early detection of neoplasia. Histological evaluation of mucosal biopsy samples from the esophagus and gastroesophageal junction for identification of goblet cells and evaluation of the presence, grade and extent of dysplasia is the mainstay of risk assessment for these patients. This Review provides physicians with a summary of the pertinent, clinically relevant histological features of Barrett esophagus and its neoplastic complications. The histology of Barrett esophagus and the gastroesophageal junction is summarized, and an overview of information necessary to interpret pathology reports from patients either with or without endoscopic evidence of Barrett esophagus is provided to appropriately guide management of patients. Close interaction between the clinician and the pathologist is essential for proper interpretation of biopsy results and to provide optimal surveillance or treatment strategies.

Key Points

  • The presence of goblet cells depends on a variety of factors, including patients' age, length of Barrett esophagus, presence of neoplasia, and location from which biopsy samples were obtained

  • Mesenchymal changes, such as duplication of the muscularis mucosa in addition to columnar metaplasia, are common and make interpretation of depth-of-invasion of adenocarcinoma difficult in mucosal biopsy specimens

  • Emerging evidence suggests that the background nongoblet columnar epithelium in patients with Barrett esophagus demonstrates intestinal differentiation and molecular abnormalities, which suggests it is at risk of neoplastic change

  • Interobserver variability in diagnosis of dysplasia in Barrett esophagus is high; all biopsy samples identified as indefinite or positive for dysplasia should, therefore, be reviewed by an expert gastrointestinal pathologist

  • The incidence, natural history, and risk of malignancy for patients with extremely short segments of esophageal columnar metaplasia is unknown and requires further study

  • Evaluation and treatment of patients with dysplasia should take into consideration the number of pathologists who have agreed with the diagnosis, as well as the endoscopic appearance and location of the lesion

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Figure 1: Histological appearance of Barrett epithelium.
Figure 2: Histological appearance of multilayered epithelium in the setting of Barrett esophagus.
Figure 3: The location of the Z-line can vary.
Figure 4: Mucosal biopsy of the distal esophagus located proximal to the anatomic gastroesophageal junction and distal to a proximally displaced Z-line.
Figure 5: Histological features of low-grade dysplasia in Barrett esophagus.
Figure 6: Histological features of high-grade dysplasia in Barrett esophagus.
Figure 7: Biopsy sample from the neosquamocolumnar junction of a patient with a slightly irregular Z-line at endoscopy.
Figure 8: Histological appearance of a biopsy sample from a patient with Barrett esophagus, which contains a focus of epithelial atypia considered indefinite for dysplasia.

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Charles P. Vega, University of California, Irvine, CA, is the author of and is solely responsible for the content of the learning objectives, questions and answers of the MedscapeCME-accredited continuing medical education activity associated with this article.

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    Robert D. Odze

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Odze, R. Barrett esophagus: histology and pathology for the clinician. Nat Rev Gastroenterol Hepatol 6, 478–490 (2009). https://doi.org/10.1038/nrgastro.2009.103

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