• J. Clin. Gastroenterol. · Apr 2007

    CDX2 expression in columnar metaplasia of the remnant esophagus in patients who underwent esophagectomy.

    • Dorine Bax, Peter D Siersema, Leon M G Moons, Herman van Dekken, Hugo W Tilanus, Johannes G Kusters, and Ernst J Kuipers.
    • Gastroenterology and Hepatology, Erasmus MC--University Medical Center Rotterdam, Rotterdam, The Netherlands.
    • J. Clin. Gastroenterol. 2007 Apr 1;41(4):375-9.

    BackgroundPatients who have undergone esophagectomy with gastric tube reconstruction often have complaints of gastro-esophageal reflux. A subset of these patients will develop columnar epithelium in the remnant esophagus, which can be of the gastric or intestinal type (Barrett esophagus).GoalsTo determine whether gastric-type mucosa (GM) in the esophagus is a precursor stage of intestinal metaplasia (IM).StudyThe medical records of 613 patients having undergone esophagectomy were reviewed for the endoscopic presence of segments with columnar mucosa in the remnant esophagus. Of them, 45 patients underwent endoscopic follow-up at least 6 months after resection. The presence of IM in the remnant esophagus was determined histologically in archival biopsy samples. Intestinal characteristics were identified by immunohistochemistry for CDX2, MUC2, and cytokeratins 7 and 20. CDX2 transcription was assessed by reverse transcription polymerase chain reaction.ResultsIn 18 of 45 patients (40%) GM was identified, and 7 of these patients also had foci of IM. CDX2 and MUC2 expression was observed in IM, and in 2 patients, CDX2 expression was also observed in gastric-type glands at a distance from intestinal glands. CDX2 transcription was identified in 2 patients without IM.ConclusionsIn the majority of patients after esophageal resection, expression of CDX2 and MUC2 in the remnant esophagus was only detectable in IM, but CDX2 was also observed in 4 cases with only GM. This could indicate that induction of formation of GM and IM may share a common pathway, eventually leading to the development of specialized intestinal epithelium.

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