In order to standardize the diagnosis and treatment of Barrett’s esophagus (BE) in China, the Chinese Society of Gastroenterology of the Chinese Medical Association held the 2nd National Symposium on Barrett’s Esophagus in Chongqing 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. 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 do 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 patients with multiple other risk factors (age over 50 years, long-term reflux esophageal disease, diaphragmatic hernia, and obesity, especially abdominal obesity) should be screened for BE. 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 endoscopy finds 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 examination mark: (1) squamous-columnar epithelial junction (SCJ): the distal esophagus gray-red squamous epithelium in the gastroesophageal junction to move into the orange-red columnar epithelium, in the squamous-columnar epithelial junction constitutes a toothed Z line, that is, the SCJ. (2) Gastroesophageal conjunction: for the tubular esophagus and the cystic stomach of the junction, and the mark of endoscopic localization for the esophagus lower end of the longitudinal fenestration-like blood vessel endings 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 in the same place, 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, the diagnosis of BE needs to be confirmed by pathologic biopsy. 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), and laser confocal endoscopy have been applied to the diagnosis of BE, and these techniques can clearly display the microstructure of the mucosa, which helps to localize and guide biopsy. 3.Endoscopic typing: (1)Classification according to the length of the pyogenic columnar epithelium: a. Long-segment BE: the pyogenic columnar epithelium involves the whole circumference of the esophagus and the length is ≥3cm. b. Short-segment BE: the pyogenic columnar epithelium does not involve the whole circumference of the esophagus or it involves the whole circumference but the length is <3cm.(2)Classification according to the endoscopic morphology: it is classified into the whole circumference type, the lingual type, and the insular type. (3) Bragg's C&M classification: C represents the length of septated mucosa in the peripheral type, and M represents the maximum length of septated mucosa. For example, C3-M5 indicated that the columnar epithelium of the esophageal circumferential segment was 3 cm, and the non-circumferential segment or lingual extension was 5 cm above the GEJ; CO-M3 indicated that there was no peripheral epithelialization, and the lingual extension was 3 cm above the GEJ. This classification had a higher sensitivity for ≥1 cm of chemotaxis, while the sensitivity for those with <1 cm was poorer. (II) Pathological diagnosis 1. Biopsy sampling: It is recommended to use four-quadrant biopsy method, i.e., biopsies are routinely taken from GEJ upward at 2 cm intervals in four 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 1cm intervals, and the application of new endoscopic technology for targeted biopsy is advocated. The histologic typing of columnar epithelium of lower esophageal metaplasia: (1) Gastric fundus type: similar to the gastric fundus epithelium, the main cells and wall cells are visible, 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-shaped cells are its characteristic cells. histochemical staining of AB (pH 2.5) or sulfate mucus, immunohistochemical staining of Cdx2 and mucin help to identify cup-shaped cells. 3.BE with anisocytosis: (1)Mild anisocytosis: normal structure, enlarged and densely stained nuclei, but the nucleus is not more than 1/2 of the cell size, 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 extend to the mucosal surface in the form of villi. 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. Treatment The principle is to control gastroesophageal reflux, eliminate symptoms, prevent and treat complications, including heterotrophic 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 treatment for GERD. 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. Promotional 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 treatment methods often used include argon plasma coagulation, high-frequency electrotherapy, laser therapy, radiofrequency ablation, photodynamic therapy, endoscopic mucosal resection and cryoablation, etc. For patients with BE 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 cancerous transformation of 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. Surgery: In principle, BE patients with proven cancer should be treated with surgery. Evidence-based medicine shows that endoscopic and surgical treatments can achieve the same effect for patients with BE accompanied by severe heterotrophic hyperplasia and early cancer limited to the mucosal layer, and the choice of treatment should be based on the patients' own opinion and doctors' 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 options: endoscopic or surgical treatment is recommended, or close monitoring and follow-up with repeat gastroscopy every 3 months until detection of intramucosal cancer.