Barrett esophagus (BE) is a known risk factor for the development of esophageal adenocarcinoma. Pathologists play a critical role in confirming the diagnosis of BE and BE-associated dysplasia. As these diagnoses are not always straightforward on routine hematoxylin and eosin–stained slides, numerous ancillary stains have been used in an attempt to help pathologists confirm the diagnosis. On the basis of an in-depth review of the literature, the Rodger C. Haggitt Gastrointestinal Pathology Society provides recommendations regarding the use of ancillary stains in the diagnosis of BE and BE-associated dysplasia. Because goblet cells are almost always identifiable on routine hematoxylin and eosin–stained sections, there is insufficient evidence to justify reflexive use of Alcian blue (at pH 2.5) and/or periodic-acid Schiff stains on all esophageal biopsies to diagnose BE. In addition, the use of mucin glycoprotein immunostains and markers of intestinal phenotype (CDX2, Das-1, villin, Hep Par 1, and SOX9) are not indicated to aid in the diagnosis of BE at this time. A diagnosis of dysplasia in BE remains a morphologic diagnosis, and hence, ancillary stains are not recommended for diagnosing dysplasia. Although p53 is a promising marker for identifying high-risk BE patients, it is not recommended for routine use at present; additional studies are needed to address questions regarding case selection, interpretation, integration with morphologic diagnosis, and impact on clinical outcome. We hope that this review and our recommendations will provide helpful information to pathologists, gastroenterologists, and others involved in the evaluation of patients with BE and BE-associated dysplasia.
*Department of Pathology, Brigham and Women’s Hospital
‡Children’s Hospital Boston, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA
†Department of Pathology, University of Michigan, Ann Arbor, MI
§Depatment of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA
∥Department of Pathology, University of Chicago Medical Center, Chicago, IL
¶Department of Pathology and Laboratory Medicine, Emory University Hospital, Atlanta, GA
Conflicts of Interest and Source of Funding: The authors have disclosed that they have no significant relationships with, or financial interest in, any commercial companies pertaining to this article.
Correspondence: Alyssa M. Krasinskas, MD, Department of Pathology and Laboratory Medicine, Emory University Hospital, 1364 Clifton Road NE, Suite H180D, Atlanta, GA 30322 (e-mail: firstname.lastname@example.org).