BACKGROUND: Barrett's esophagus is caused by gastroesophageal reflux and may progress towards esophageal adenocarcinoma. Currently diagnosis is established upon a mixture of endoscopic and histopathologic criteria. Recently a novel histopathology classification questions current policies regarding diagnosis of Barrett's esophagus. METHODS: Review on published frequency of Barrett's esophagus and critical analysis of the novel histopathology classification of columnar lined esophagus. RESULTS: Our review, including 40 studies and 95,386 persons (mean age 53 years) undergoing endoscopy and biopsy sampling from the esophagogastric junction revealed Barrett's esophagus (BE) in 1.6–2.0% of controls and 0.8–36% of individuals with dyspepsia and GERD symptoms and was similar for those with and without endoscopic visible columnar lined esophagus. BE seems to be predominant in males and BE-frequency increases with length of visible columnar lined esophagus and age. The novel histopathology classification (Paull-Chandrasoma classification) of columnar lined esophagus indicates that currently used endoscopic "model anatomy" is based on invalid criteria and should be given up. The endoscopic proximal stomach (cardia) is identified as "dilated end stage esophagus", which may give rise for intestinal metaplasia, dysplasia and adenocarcinoma. Critical analysis of a population-based study indicates that the frequency of BE is largely underestimated owing to misclassification of endoscopic and histopathologic findings. CONCLUSIONS: The frequency of Barrett's esophagus seems to be higher than estimated, shows a large variation and may be also present in asymptomatic controls. Uniform endoscopy, biopsy sampling and histopathology should be included for future Barrett management.

were not significantly associated factors.Esophagitis was associated with GERD based on the symptom criteria specified (OR: 3.0; 95% CI: 1.1-8.1),although most subjects with esophagitis (90.9%) did not meet symptom criteria for GERD.Subjects with esophagitis experienced more severe and more frequent epigastric burning than subjects without esophagitis (p = 0.050), but no difference was seen for epigastric pain or typical GERD symptoms.Hiatus hernia was associated with the presence of GERD based on symptoms (OR: 25.1; 95% CI: 1.5-426.2) and with esophagitis (OR: 17.8; 95% CI 2.8-113.02).The prevalence of H. pylori infection was 70.8%.No significant associations with H. pylori infection for either esophagitis or symptom-based GERD were found.Conclusions.The spectrum of symptoms and esophageal complications associated with GERD in Shanghai differs from that in Western countries.This has implications for future studies of the epidemiology of GERD in Asia.

SqM = squamous;CM = cardiac mucosa; OCM = oxyntocardiac mucosa; IM = intestinal metaplasia within CM; OM = gastric oxyntic mucosa. Unlabeled areas = no biopsy

BACKGROUND: Gastroesophageal reflux disease (GERD) is associated with columnar lined esophagus (CLE) and Barrett's esophagus (BE), which may progress towards esophageal adenocarcinoma. Currently a mixture of symptoms, endoscopic and histopathologic criteria and results obtained from esophageal function tests define GERD. We searched for a histopathology-based definition of GERD. METHODS: Review on GERD-histopathology. RESULTS: Multilevel biopsies and the novel Paull-Chandrasoma histopathology-classification of CLE define those with reflux and risk for development of esophageal adenocarcinoma (those with Barrett's esophagus and dysplasia) and list three abnormal nondysplastic epithelia between squamous and gastric oxyntic mucosa: cardiac mucosa (CM), oxyntocardiac mucosa (OCM), and CM with intestinal metaplasia (=Barrett's esophagus, with 0.5% annual cancer risk). Frequency of intestinal metaplasia (IM) is 15–24% at an endoscopically normal junction and increases towards 100% if CLE is ≥5 cm. IM develops at the squamocolumnar junction. Dilated end stage esophagus (DESE) is a novel concept and defines the early stage of reflux disease. The pathophysiology of DESE involves gastric distention-induced shortenings of the lower esophageal sphincter (LES) with reflux favoring damage and columnar metaplasia of the most distal esophagus. Over time permanent LES shortening and proximal dislocation of the squamocolumnar junction result in gastric-type appearance of DESE, which is mistaken for proximal stomach. The majority of adenocarcinomas of the "esophagogastric" junction arise within DESE. CONCLUSIONS: CLE is abnormal, results from reflux and is a disease if associated with life quality-impairing symptoms and/or intestinal metaplasia and dysplasia (cancer risk). Presence of CLE, IM, and dysplasia cannot be excluded from endoscopy, but requires histopathology of biopsies from the squamocolumnar junction.

Lenglinger, Johannes M.D.; Eisler, Margit M.D.; Riegler, Franz M. M.D. Author Information

BACKGROUND: Discrepancy exists between the endoscopic (rugal folds) and the histopathologic (oxyntic mucosa) definition of proximal stomach. We compared endoscopy and histopathology of the esophagogastric junction in patients with gastroesophageal reflux disease. METHODS: A total of 102 consecutive patients (60 women) with gastroesophageal reflux disease prospectively underwent endoscopy including multilevel biopsy sampling at the level of the rise of rugal folds (level 0), and also 0.5 cm and 1.0 cm distal and 0.5 cm and ≥ 1 cm proximal to this point. Columnar lined esophagus (CLE) was cataloged according to the histopathologic Paull-Chandrasoma classification and esophagitis according to the endoscopic Los Angeles classification. Hiatal hernia was diagnosed if the endoscopic rugal folds commenced ≥ 2 cm above the diaphragm; competency of the esophagogastric valve was graded according to the Hill classification. RESULTS: All patients had histopathologic CLE with maximal presence at level 0 (97%) and a decrease towards proximal and distal biopsy levels (level −0.5 cm, 81%; level −1.0, 28%; level + 0.5 cm, 40%; level + 1.0 cm, 18%). Histopathologic CLE (distance between CLE-positive biopsy levels) was longer than endoscopic CLE (P < 0.001). All 19 patients with intestinal metaplasia (18.6%) were identified from 4-quadrant biopsies obtained at the squamocolumnar junction and at 0.5 cm distal from it. Persons with intestinal metaplasia were significantly older, had increased frequency of endoscopic hiatal hernia, higher Hill grade and presence of endoscopic CLE (P < 0.05); no significant difference was observed regarding sex, endoscopic esophagitis or length of endoscopic and histopathologic CLE (P > 0.05). None of the patients had dysplasia or carcinoma. CONCLUSIONS: In patients with gastroesophageal reflux disease the esophagogastric junction cannot be identified by endoscopy but requires histopathology of multilevel biopsies. The squamocolumnar junction harbors the highest yield of intestinal metaplasia.

Sirs, We read with interest the article by Ferraris et al.,1 entitled ‘Barrett’s oesophagus: longterm follow up after complete ablation with argon plasma coagulation and the factors that determine its recurrence’. The work profoundly contributes to our understanding of the management of columnar-lined oesophagus containing intestinal metaplasia (=Barrett’s oesophagus).2, 3 Patients with Barrett’s oesophagus underwent ablation with argon plasma coagulation and treatment with a proton pump inhibitor (PPI). If PPI treatment failed to cure reflux symptoms, individuals underwent laparoscopic fundoplication (all had pathological pH monitoring). It is well accepted that persistence of symptoms indicates more severe disease.3 In keeping with this notion it is to be assumed that fundoplication was conducted in the more severe cases of reflux disease. Follow-up showed that frequency of relapse of Barrett’s oesophagus was increased in those under PPI treatment, when compared with individuals who underwent fundoplication. This striking observation is in line with recent studies showing that antireflux surgery favours regression of Barrett’s oesophagus,4, 5 the precursor of oesophageal adenocarcinoma.2, 3 In addition, Lagergren et al.6 recently found an oncopreventive effect of antireflux surgery in a population-based case–control study. It remains to be clarified, however, how an effective fundoplication is adequately defined: by symptoms vs. function tests? We agree with Ferraris et al.1 and Parilla et al.4 that this is best accomplished by pH monitoring (or combined impedance- and pH-monitoring).3 Histopathology shows that Barrett’s oesophagus is preceded by cardiac mucosa, the first step in the columnar-lined oesophagus – intestinal metaplasia – dysplasia – adenocarcinoma sequence.2, 3 It would be interesting to learn if the authors could provide the histopathology of those who were free of intestinal metaplasia (=Barrett’s oesophagus). Did they have cardiac or oxyntocardiac mucosa? Taken together, evidence increases that effective antireflux surgery may in fact be oncopreventive.1, 4-6 Furthermore, ablation with argon plasma coagulation followed by antireflux surgery represents a highly effective alternative in the management of Barrett’s oesophagus.1

Manometry Lab & Department of General Surgery, University Clinic of Surgery, Medical University Vienna, Vienna, Austria, [email protected]

Manometry Lab & Department of General Surgery, University Clinic of Surgery, Medical University Vienna, Vienna, Austria, [email protected]

With interest we read the article by Hansen et al. ( Gut 2007; 56 :918–25). The authors have to be congratulated on their contribution which profoundly adds to our understanding of the pathophysiology leading to oesophageal and gastric cancer. In addition, the paper points out the difficulties we have to correctly assign tumours of the oesophago-gastric junction (oesophageal vs gastric?). Cardiac cancers were subtyped for their associations with serum anti- Helicobacter pylori IgG antibody titer and biochemical markers of loss of gastric secretory function associated with atrophy (pepsinogen I/II ratio and serum gastrin concentration). However, the anatomic criterium to define cardiac carcinoma, that is, tumours centred within 2 cm distal to the oesophago-gastric junction, is inaccurate. Interpretation of the data should be conducted with the inclusion of clear, anatomical and histopathological criteria. It is well accepted that cardiac cancer and adenocarcinoma of the oesophagus share epidemiological and pathogenetic features.1,2 After birth the oesophagus is lined by squamous epithelium, whereas the stomach is lined by gastric oxyntic mucosa (with parietal and chief cells).1,3 Due to gastro-oesophageal reflux, squamous epithelium is …