In order to standardize the diagnosis and treatment of Barrett’s esophagus (BE) in China, the Second National Symposium on Barrett’s Esophagus of the Chinese Medical Association (CMA) Division of Digestive Diseases was held in Chongqing, China on June 4, 2011, where the issues related to BE were extensively discussed and the following consensus was reached. I. Definition BE is a pathological phenomenon in which the complex squamous epithelium of the lower esophagus is replaced by a chemotaxic single-layer columnar epithelium, either with or without intestinalization. Those with intestinal metaplasia are precancerous lesions of esophageal adenocarcinoma. As to whether those without intestinal metaplasia are precancerous lesions, it is still controversial. Yan Mingxian, Department of Gastroenterology, Thousand Buddha Mountain Hospital, Shandong Province, China Clinical manifestations BE is mainly characterized by symptoms of gastroesophageal reflux disease (GERD), such as heartburn, acid reflux, retrosternal pain and dysphagia. However, in recent years, epidemiologic data found that close to 40070 patients did not have GRED symptoms. At present, it is believed that the main clinical significance of BE is its relationship with esophageal adenocarcinoma, and routine screening for BE is not recommended for the general population and patients with simple GERD, but for those patients with multiple other risk factors (age 50 years or older, long-term reflux esophageal disease, diaphragmatic hernia, and obesity, especially abdominal obesity), screening for BE should be performed. Diagnosis The diagnosis of this disease is mainly based on endoscopic examination and esophageal mucosal The diagnosis of this disease is mainly based on endoscopy and esophageal mucosal biopsy. When endoscopic examination reveals columnar epithelial hyperplasia in the lower esophagus, it is called “endoscopic suspected BE”, and BE can be diagnosed when the presence of columnar cells is confirmed by pathological examination, and the presence of intestinal epithelial hyperplasia is found to be more supportive of the diagnosis of BE. (I) Endoscopic diagnosis 1. Endoscopic signs: (1) squamous-columnar epithelial junction (SCJ): grayish-red squamous epithelium of the distal esophagus migrates into orange-red columnar epithelium at the gastroesophageal junction, and constitutes a toothed Z line at the squamous-columnar epithelial junction, i.e., SCJ. (2) Gastroesophageal Junction (GEJ): it is the junction of the tubular esophagus and the cystic stomach, and the signs of endoscopic localization are longitudinal rows of blood vessels or fenestrated vessel ends or fenestrated blood vessels of the lower esophagus, which can be seen as the markers for BE in the lower esophagus. The markers for endoscopic localization are the endings of the longitudinal fenestrated vessels in the lower esophagus or the proximal margin of the gastric mucosal folds in the minimally inflated state. A clear distinction between SCJ and GEJ is important for recognizing BE. Normally, the SCJ (Z line) and GEJ should be located at the same site, with the mucosa of the gastric cardia below the Z line and the squamous epithelium above the Z line. Because the mucosa of reflux esophagitis can be confused with BE in appearance, pathologic biopsy is needed to confirm the diagnosis of BE. 2. Endoscopic manifestations: When BE occurs, the Z line is shifted upward, which is manifested by the appearance of orange-red (or) columnar epithelium with fenestrated blood vessels proximal to the GEJ, i.e., separation of the SCJ from the GEJ. In recent years, pigment endoscopy and magnifying endoscopy, narrow band spectral imaging endoscopy ( NBI), laser confocal endoscopy have been applied to the diagnosis of BE, these techniques can clearly show the microstructure of the mucosa, help to localize and guide biopsy. (3)Endoscopic classification:(1)According to the length of pyogenic columnar epithelium: a. Long-segment BE: the pyogenic columnar epithelium involves the whole periphery of the esophagus and the length is ≥3 cm. b. Short-segment BE: the pyogenic columnar epithelium does not involve the whole periphery of the esophagus or it involves the whole periphery but the length is <3 cm. (2)According to the classification of the morphology under endoscopy: it is classified into peripheral, lingual, and insular. c. Endoscopic classification: it is classified into peripheral, lingual, and insular. d. Endoscopic classification: the endoscopic classification of BE: it is classified into peripheral and insular. (3) Bragg's C&M classification: C represents the length of the peripheral type of septated mucosa, and M represents the maximum length of septated mucosa. For example, C3-M5 indicates that the columnar epithelium of the esophageal circumferential segment is 3 cm, and the non-circumferential segment or lingual extension is 5 cm above the GEJ; CO-M3 indicates that there is no epithelialized peripheral segment, and the lingual extension is 3 cm above the GEJ. This classification is highly sensitive to ≥1 cm of chemotaxis mucosa, and poorly sensitive to those <1 cm. (II) Pathological diagnosis 1. Biopsy sampling: Four-quadrant biopsy is recommended, i.e., biopsies are routinely taken at 2 cm intervals from GEJ upward in 4 quadrants, and more than 8 pieces of mucosal tissues are taken at each interval, which can effectively improve the detection rate of intestinal epithelial hyperplasia. For those who are suspected to have BE carcinoma, four-quadrant biopsies should be taken at 1 cm intervals, and the application of new endoscopic techniques for targeted biopsy is advocated. (2) Histologic typing of columnar epithelium of lower esophageal metaplasia: (1) Gastric fundus type: it is similar to gastric fundus epithelium, with visible principal cells and wall cells, but BE epithelial atrophy is more obvious, and the glands are fewer and shorter. This type is mostly distributed in the distal end of the BE near the cardia. (2) Cardia type: similar to cardia epithelium, with small gastric recesses and mucous glands, but without principal cells and mural cells. (3) Intestinal chemotaxis type: microvilli and crypts on the surface, and cup cells are the characteristic cells. histochemical staining with AB (pH 2.5) or sulfate mucus, and immunohistochemical staining for Cdx2 and mucin help to identify cup cells. 3. BE with anisocytosis: (1) Mild anisocytosis: normal structure, enlarged and densely stained nuclei, but the nuclei do not exceed 1/2 of the cell size, and a mitotic image is seen. The mucin of cup and columnar cells is reduced, and atrophic cup cells can be seen. (2) Severe heterogeneous hyperplasia: the structure is altered, and there may be branching out buds, which are villous and extend to the mucosal surface. The nuclei of the cells are densely stained and exceed 1/2 of the cell size. they may be irregularly layered, mitosis is common, cup cells and columnar cells are usually absent, mucus production is absent or reduced, and this abnormality may extend to the mucosal surface. IV. Treatment The principle is to control gastroesophageal reflux, eliminate symptoms, prevent and treat complications, including heterogeneous hyperplasia and carcinoma. 1. Drug therapy: acid suppressants are the main drugs for the treatment of reflux symptoms. Among the acid-suppressing drugs, proton pump inhibitors are better than H2 receptor antagonists, but there is no conclusive evidence that proton pump inhibitors can reverse columnar epithelial chemotaxis or prevent adenocarcinoma, and the use of proton pump inhibitors should be in accordance with the regular dose and full course of gastroesophageal reflux disease. Most of the poor results of proton pump inhibitors are due to inappropriate dosage or method of administration. In some patients, proton pump inhibitors and H2 receptor antagonists can be combined. Promotive drugs, mucosal protective agents, analgesics, smooth muscle transient relaxation inhibitors are also effective in controlling symptoms and treating reflux esophagitis. 2. Endoscopic treatment: It is suitable for BE patients with severe heterogeneous hyperplasia and cancer confined to the mucosal layer. At present, endoscopic treatments often used include argon plasma coagulation, high-frequency electrotherapy, laser therapy, radiofrequency ablation, photodynamic therapy, endoscopic mucosal resection and cryoablation, etc. For patients without heterogeneous hyperplasia, endoscopic treatment is also effective. Endoscopic treatment is not advocated for BE not accompanied by heterogeneous hyperplasia because of its low probability of becoming cancerous. The probability of cancer in BE with mild heterotrophic hyperplasia is also low, so endoscopic follow-up can be carried out first, and endoscopic treatment should be carried out if severe heterotrophic hyperplasia develops. 3. Surgical treatment: In principle, BE patients with proven carcinoma should be treated surgically. Evidence-based medicine shows that endoscopic and surgical treatments can achieve the same effect for patients with BE accompanied by severe alloplastic hyperplasia and early stage cancer limited to the mucosal layer, and the choice of treatment should be based on the patient's own opinion and the doctor's experience. 4. Anti-reflux surgery: including surgery and endoscopic anti-reflux surgery. Although it can improve the reflux symptoms of BE patients to a certain extent, it does not affect the natural course of the disease, and the long-term efficacy needs to be confirmed. Given the risk of BE developing into esophageal adenocarcinoma, patients with BE should be followed up regularly for early detection of heterogeneous hyperplasia and carcinoma. The interval of endoscopy should be based on the degree of heteroplasia. For those who do not have heteroplasia, the examination should be repeated every 2 years, and if heteroplasia and early cancer are not detected after 2 examinations, the interval can be relaxed to 3 years. For those with mild heterozygous hyperplasia, endoscopic review should be performed every 6 months in the first year, and if the heterozygous hyperplasia has not progressed, the review can be performed once a year. For BE with severe heterogeneous hyperplasia, there are two choices: endoscopic or surgical treatment is recommended, or close monitoring and follow-up with repeat gastroscopy every 3 months until detection of intramucosal cancer. (This article is summarized from: Chinese Journal of Gastrointestinal Endoscopy, Volume 28, Issue 8, August 2011)