Anatomic Pathology / ESOPHAGEAL AND JUNCTIONAL INTESTINAL METAPLASIA Intestinal Metaplasia of the Esophagus or Esophagogastric Junction Evidence of Distinct Clinical, Pathologic, and Histochemical Staining Features

نویسندگان

  • Johanna W. van Sandick
  • Jan B. van Lanschot
  • Lonneke van Felius
  • Jelle Haringsma
  • Wim Dekker
  • Johan A. Offerhaus
چکیده

Our purpose was to evaluate the clinical, histologic, and histochemical staining characteristics of intestinal metaplasia (IM) at an endoscopically normalappearing esophagogastric junction (IM-EGJ) compared with IM in a columnar-lined esophagus (IMCLE). A prospective study included 253 patients referred for elective upper gastrointestinal endoscopy. Biopsy specimens were obtained from 2 cm above and immediately distal to the squamocolumnar junction, the gastric corpus, and the antrum. Any red mucosa above the EGJ was sampled. IM-CLE (prevalence, 5.5%) typically occurred in white male smokers with a long history of reflux symptoms. IM-EGJ (prevalence, 9.1%) was associated with corpus and antrum gastritis and with IM at these sites. IM-CLE usually (13/14 [93%]) was the incomplete type IM, whereas only 12 (52%) of 23 patients in the IM-EGJ group had incomplete IM. IM-EGJ and IM-CLE should be considered as separate entities. Further research is needed to evaluate whether neoplastic progression of IM-EGJ is related to its mucin profile. The predisposition of patients with a columnar-lined esophagus, traditionally called Barrett esophagus, to develop esophageal adenocarcinoma is well documented.1 The recognition that cancer complicating Barrett esophagus originates from intestinal-type columnar epithelium has led to redefinition of Barrett esophagus by the presence of intestinal metaplasia (IM) in the esophagus.2,3 Initially, histologic evidence of IM on biopsy specimens obtained from the lower esophagus was considered sufficiently distinctive to use its detection as the “gold standard” for a diagnosis of Barrett esophagus. Later on, it was shown that biopsy specimens immediately distal to the squamocolumnar junction also could reveal IM when Barrett esophagus was unsuspected endoscopically.4 The pathogenesis of IM at an endoscopically normalappearing esophagogastric junction (EGJ) is subject to ongoing discussion. Some studies have indicated a relationship with gastroesophageal reflux disease,5-7 while others have implicated a role for Helicobacter pylori infection.8-10 Importantly, dysplasia and adenocarcinoma have been noted in association with IM just distal to a normally located squamocolumnar junction.10,11 The increasing frequency of adenocarcinoma of the EGJ, in parallel with the rising incidence of adenocarcinoma of the esophagus,12 further enhances the importance of identifying preceding pathologic conditions. Histochemically, IM in a columnar-lined esophagus (IMCLE) resembles incomplete IM of gastric mucosa.13-16 It differs from complete IM by the presence of mucus-secreting columnar cells that contain both neutral and acid mucins. As part of this study, we investigated the relative frequencies of incomplete vs complete IM at an endoscopically normalappearing esophagogastric junction (IM-EGJ). Am J Clin Pathol 2002;117:117-125 117 © American Society for Clinical Pathology van Sandick et al / ESOPHAGEAL AND JUNCTIONAL INTESTINAL METAPLASIA The objectives of this prospective biopsy study were to (1) assess the overall prevalence of IM-EGJ compared with IM-CLE in patients undergoing elective upper endoscopy; (2) evaluate the clinical, endoscopic, and histologic associations with special reference to features of gastroesophageal reflux disease (GERD) and gastric pathology; and (3) study the histochemical staining characteristics of IM-EGJ compared with IM-CLE. Materials and Methods

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تاریخ انتشار 2002