title: Intestinal and pancreatic metaplasia at the esophagogastric junction in patients without Barrett's esophagus.
abstract: OBJECTIVE
  A distinctive type of columnar epithelium with intestinal metaplasia is considered diagnostic for Barrett's esophagus. The neoplastic potential of pancreatic metaplasia at the esophagogastric junction is unknown. The aims of the present study were: 1) to characterize both forms of metaplasia at the esophagogastric junction, and to estimate their prevalence; 2) to investigate c-erbB-2 expression and K-ras mutations in pancreatic metaplasia; and 3) to study the relationship between metaplasia, inflammatory changes in the cardiac mucosa, and presence of H. pylori.
  
  
  METHODS
  A total of 76 esophagogastrectomy specimens of patients with a normally located squamocolumnar junction, were investigated immunohistochemically. K-ras mutations were evaluated using PCR.
  
  
  RESULTS
  Intestinal metaplasia in the cardia was found in 12% of patients: six complete-type, and three incomplete-type. Pancreatic metaplasia was demonstrated in 14% of patients, and neither c-erbB-2 expression nor K-ras mutations were found. Intestinal and pancreatic metaplasia were associated with mucosal inflammation. In contrast to generalized gastritis, isolated "carditis" was not associated with H. pylori infection.
  
  
  CONCLUSIONS
  When intestinal metaplasia occurs in a biopsy from the esophagogastric junction, it is not necessarily a marker for Barrett's esophagus. No indication was found that pancreatic metaplasia has neoplastic potential. Both forms of metaplasia reflect mucosal inflammation. Carditis may be a distinct inflammatory condition of the gastric mucosa that is not related to H. pylori infection.
authors.affiliation: Department of Pathology, Academic Medical Center, University of Amsterdam, The Netherlands.
authors.forename: W
authors.initials: W
authors.lastname: Polkowski
authors.forename: J J
authors.initials: JJ
authors.lastname: van Lanschot
authors.forename: F J
authors.initials: FJ
authors.lastname: ten Kate
authors.forename: T M
authors.initials: TM
authors.lastname: Rolf
authors.forename: M
authors.initials: M
authors.lastname: Polak
authors.forename: G N
authors.initials: GN
authors.lastname: Tytgat
authors.forename: H
authors.initials: H
authors.lastname: Obertop
authors.forename: G J
authors.initials: GJ
authors.lastname: Offerhaus
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics / Q000473:pathology*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001471:Barrett Esophagus / Q000235:genetics / Q000473:pathology*; D004848:Epithelium / Q000473:pathology; D004938:Esophageal Neoplasms / Q000235:genetics / Q000473:pathology*; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology; D005756:Gastritis / Q000235:genetics / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology; D016481:Helicobacter Infections / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D011230:Precancerous Conditions / Q000235:genetics / Q000473:pathology*; D016283:Proto-Oncogene Proteins p21(ras) / Q000235:genetics; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000235:genetics
chemical_list: D016283:Proto-Oncogene Proteins p21(ras); D018719:Erb-b2 Receptor Tyrosine Kinases; C501009:HRAS protein, human