Gastric Metaplasia of Oesophageal Mucosa in a Patient With Gerd: Cdx2 Expression as a Possible Prognostic Criterion for Barrett’s Oesophagus

Background Gastroesophageal reflux disease (GERD) is one of the most common acid-dependent diseases with possible formation of intestinal metaplasia of the esophageal mucosa—Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC). Patients with BE require long-term proton pump inhibitors therapy to prevent progression of changes in the esophageal mucosa and dynamic monitoring for screening and early diagnosis of EAC. However, no significant increase in the risk of EAC has been described for patients with gastric metaplasia, and informative histopathological features of BE formation have not been defined. Therefore, testing markers of possible progression of gastric metaplasia to intestinal metaplasia seems relevant. Methods In a pilot study, endoscopic sampling of biopsy material from the esophageal mucosa above the Z-line was performed in 26 GERD patients with morphological findings of gastric metaplasia with cardiac and/or fundal glands. Immunohistochemical evaluation of the expression of intestinal differentiation marker CDX2 with a monoclonal antibody (clone CDX2–88) was performed in all samples studied. Results On endoscopic evaluation the area of glandular epithelium was present within 1–3 cm above the Z-line. Of 26 specimens examined, cardiac mucosa was detected within the biopsy material volume in 14 cases, in 5 cases oxyntic mucosa and in the remaining cases (7) it was mixed phenotypes with the presence of both. In 9 cases CDX-2 expression was detected in gastric epithelium (Fig). Nuclear expression of different degrees of color intensity was presented in individual cells of mucus-producing epithelium and was detected in mucosa samples of cardiac type in 7 cases and in 2 studied samples with mixed phenotype (oxynto-cardiac). Conclusion The revealed expression of CDX2 in the zones of gastric metaplasia of the esophageal mucosa of GERD patients probably characterizes the readiness of stem cells to transform into intestinal epithelium and form BE. The probable trigger of the expression process is components of refluxate. Intestinal metaplasia in this context may be considered as a side effect of gene function, at least in the first stages of intestinal metaplasia development in Barrett’s esophagus. Establishing its role requires further studies with the inclusion of a sufficient number of patients to obtain reliable data on the prognostic value of such trait.