Classical Barrett esophagus contrasted with Barrett-type epithelium at normal-appearing esophagogastric junction - Demographic, endoscopic, and histologic features

Background: Incomplete intestinal metaplasia or specialized columnar epithe lium (SCE) is the histologic hallmark of Barrett esophagus (BE), but it may also occur at a normal-appearing gastroesophageal junction without BE; We studied whether differences occur between BE patients and those with SCE at the squamocolumnar junction but without BE (abbreviated JSCE), in terms of endoscopic and histologic signs of gastroesophageal reflux disease (GERD) and Helicobacter pylori gastritis. Methods: A total of 1059 consecutive pat ients referred for endoscopy in one hospital district in Finland were enrol led in the study. Biopsy specimens (at least two from each site) were obtai ned from the gastric antrum and the corpus of the stomach and from the esop hagogastric junction and distal esophagus. Results: Classical BE was detect ed in 25 (2%) and JSCE in 99 (9%) patients. Dysplasia in the metaplastic mu cose was observed in six BE patients but in none of the JSCE patients (P < 0.001). In multivariate analysis the independent risk factors for BE were e ndoscopic erosive esophagitis (odds ratio (OR), 6.08; 95% confidence interv al (CI), 2.50-14.82), male sex (OR, 3.02; 95% CI, 1.20-7.65), and age (OR, 1.02 per year; 95% CI, 1.00-1.06). The independent risk factors for JSCE we re endoscopic erosive esophagitis (OR, 1.88; 95% CI, 1.08-3.29) and age (OR , 1.03; 95% CI, 1.02-1.05) but not H. pylori infection (OR, 1.57; 95% CI, 0 .83-2.97) or chronic gastritis (OR, 0.88; 95% CI, 0.44-1.75). In univariate analysis, however, JSCE was associated with antral-predominant atrophic ga stritis (77% H. pylori-positive). Unlike in JSCE patients, male sex strongl y predominated among BE patients (P = 0.01). The mean ages of BE and JSCE p atients did not differ. Conclusions: Both BE and JSCE without BE increase i n prevalence with age, and both associate with endoscopic erosive esophagit is but not with H. pylori gastritis. However, because of the marked sex dis parity, JSCE cannot be a direct precursor of BE, and some factors other tha n GERD alone also play a role in the pathogenesis of BE. Compared with BE, dysplasia is a rare finding: in JSCE, and endoscopic surveillance with biop sy specimens from JSCE patients without dysplasia is nor recommended.