Distinguishing Barrett gastric foveolar dysplasia from reactive cardiac mucosa in gastroesophageal reflux disease.
ABSTRACT Morphologic dysplasia remains the criterion standard of cancer risk in Barrett esophagus but poses many challenges including distinction from reactive inflammatory change. Gastric foveolar dysplasia, a newly described subtype comprising 15% to 20% of Barrett dysplasia, overlaps with reactive cardiac mucosa in gastroesophageal reflux disease (GERD). Despite the clinical importance of accurate distinction, the issue has not been studied. Review of 3698 biopsies from 461 Barrett patients yielded 160 biopsies with Barrett gastric foveolar dysplasia (74 low grade and 86 high grade). These were compared with inflamed cardia from 80 patients with GERD. Immunohistochemistry was performed for Lgl2, MUC2, MUC5AC, and MUC6. Comparing GERD with Barrett gastric foveolar dysplasia, surface nuclear stratification (85% versus 0%, P < .00001), upper mucosa-limited atypia (80% versus 0%, P < .0001), villiform architecture (52% versus 4%; P < .0001), full-thickness mucosal atypia (0% versus 100%, P < .00001), and crowded glandular architecture (0% versus 75%, P < .00001) all proved useful. Cytologic features were less helpful. Comparing low-grade gastric dysplasia alone, because its distinction from reactive cardia may be even more challenging, the listed features all remained significant. Loss or aberrant Lgl2 expression was much more typical of dysplasia (12% versus 99%; P = .0001). MUC proteins did not distinguish the groups. Surface nuclear stratification, "top-heavy" atypia, and noncrowded, villiform architecture were highly characteristic of reactive cardiac atypia in GERD, in comparison with the monolayered nuclei in crowded glands occupying the full mucosal thickness in Barrett gastric foveolar dysplasia. Loss or aberrant Lgl2 staining was useful in identifying Barrett gastric foveolar dysplasia.
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ABSTRACT: Foveolar dysplasia is an uncommon form of dysplasia that is encountered in the stomach and oesophagus in the context of Barrett's oesophagus. Glands displaying foveolar dysplasia also show architectural abnormalities that are similar to those encountered in adenomatous dysplasia. However, from a cytological point of view, foveolar dysplasia glands are lined by low-cuboidal to columnar epithelium, the cytoplasm is often clear with round-to-oval nuclei. Nuclear stratification as seen in adenomatous dysplasia is not common, although there is loss of nuclear polarity, pleomorphism and mitotic activity. It is important to distinguish low-grade foveolar dysplasia from regenerative change.Journal of Clinical Pathology 09/2014; · 2.55 Impact Factor
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ABSTRACT: The following, from the 12th OESO World Conference: Cancers of the Esophagus, includes commentaries on the clinical differences between carcinomas arising slightly above, slightly below, and within the gastroesophageal junction (GEJ); information provided by biopsies; information provided by resection specimens following neoadjuvant therapy; histologic differences existing between carcinomas arising slightly above, slightly below, and within the GEJ; differences provided by immunohistochemistry in these tumors; information given by endoscopic mucosal resection specimens; the role of esophageal pyloric gland adenomas as precursors of adenocarcinomas in the region of the cardia; the role of pancreatic metaplasia; Her2 immunoreactivity to make distinctions in the site of origin; and intestinal metaplasia limited to the cardia as a precursor of adenocarcinoma.Annals of the New York Academy of Sciences 09/2014; 1325(1). · 4.38 Impact Factor
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ABSTRACT: This review summarizes the endoscopic and histologic features of Barrett’s esophagus (BE) as well as some of the recent advancements and controversies. BE represents metaplastic conversion of normal squamous epithelium of tubular esophagus to columnar epithelium. The diagnosis of BE requires a combination of endoscopic and histopathologic findings. There is worldwide controversy regarding the exact definition of BE, particularly with regard to the requirement to histologically identify goblet cells in biopsies. The presence and detectability of goblet cells might vary depending on a variety of factors and is subject to sampling error. Therefore, a systematic biopsy sampling with sufficient number of biopsies is currently recommended to limit the likelihood of a false negative result for detection of goblet cells. There are both endoscopic and pathologic challenges in evaluating gastroesophageal junction biopsies in patients with irregular Z lines to determine the exact location of the sample (i.e., esophagus versus stomach). Recently, several, novel endoscopic techniques have been developed to improve BE detection. However, none have been validated yet in clinical practice. The surveillance of patients with BE relies on histologic evaluation of dysplasia; however there are significant pathologic limitations and diagnostic variability in evaluating the presence and grading of BE dysplasia, particularly with regard to the more recently recognized non-intestinal types of dysplasia. All BE dysplasia samples should be reviewed by an expert gastrointestinal pathologist to confirm the diagnosis. Finally, it is important to emphasize that close interaction between gastroenterologists and pathologists is essential to ensure proper evaluation of endoscopic biopsies in order to optimize the surveillance and clinical management of patients with BE.Baillière' s Best Practice and Research in Clinical Gastroenterology 11/2014; · 3.28 Impact Factor