Consensus on the diagnosis and treatment of Barrett’s esophagus In order to standardize the diagnosis and treatment of Barrett’s esophagus (BE) in China, the Second National Symposium on Barrett’s esophagus was held by the Chinese Society of Gastroenterology in Chongqing on June 4, 2011, and the following consensus was reached. I. Definition BE is a pathological phenomenon in which the compound squamous epithelium of the lower esophagus is replaced by chemosis of a single columnar epithelium, which may or may not be accompanied by intestinalization. Those with intestinal epithelial metaplasia are precancerous lesions of esophageal adenocarcinoma. As for those without intestinal metaplasia, it is still controversial whether they are precancerous lesions. Clinical manifestations of BE are mainly symptoms of gastroesophageal reflux disease (GERD), such as heartburn, acid reflux, retrosternal pain and dysphagia. However, epidemiological data in recent years have found that close to 40070 patients do not have GRED symptoms. It is currently believed that the main clinical significance of BE is its relationship with esophageal adenocarcinoma. For the general population and patients with GERD alone, routine screening for BE is not recommended, but for those patients with multiple other risk factors (age 50 years or older, long-term reflux esophageal disease, diaphragmatic hernia, obesity especially abdominal obesity), BE should be screened. III. Diagnosis The diagnosis of this disease is mainly based on endoscopy and esophageal mucosal biopsy. The diagnosis of BE can be made when the presence of columnar epithelial hyperplasia in the lower esophagus is detected by endoscopy, and the presence of columnar cells is confirmed by pathological examination. (1) Endoscopic diagnosis: (1) Squamous-columnar epithelial junction (SCJ): the gray-red squamous epithelium of the distal esophagus is shifted to orange-red columnar epithelium at the junction of the gastroesophagus, which forms a dentate Z-line at the squamous-columnar epithelial junction, that is, SCJ. (2) Gastroesophageal junction (GEJ): the junction of the tubular esophagus and the sacculated stomach, the endoscopic localization of which is marked by the longitudinal row of the lower esophagus The end of the fenestra-like vessels or the proximal edge of the gastric mucosal folds in the minimally inflated state. A clear distinction between the SCJ and the GEJ is important for the identification of BE. Under normal circumstances, 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, pathological biopsy is needed to confirm the diagnosis of BE. 2. Endoscopic manifestation: When BE occurs, the Z line is shifted upward, which is manifested by the appearance of orange (or) columnar epithelium with fenestrated vascular manifestation at the proximal end of the GEJ, i.e., separation of the SCJ from the GEJ. In recent years, pigmented endoscopy with magnification endoscopy, narrow-band spectral imaging endoscopy (NBI), and laser confocal endoscopy have been applied to the diagnosis of BE. These techniques can clearly show the microstructure of the mucosa, help localize it, and guide biopsy. 3. Endoscopic typing: (1) Classification according to the length of the chemosis columnar epithelium: a. Long-segment BE: the chemosis columnar epithelium involves the whole circumference of the esophagus and is ≥3 cm in length. b. Short-segment BE: the chemosis columnar epithelium does not involve the whole circumference of the esophagus or involves the whole circumference but is <3 cm in length.(2) Classification according to the endoscopic morphology: divided into whole circumference, lingual and insular. (3) Bragg's C&M classification: C represents the length of the chemosis mucosa of the total circumference type, and M represents the maximum length of the chemosis mucosa. For example, C3-M5 indicates that the columnar epithelium of the circumferential segment of the esophagus is 3 cm, and the non-peripheral segment or lingual extension is 5 cm above the GEJ; CO-M3 indicates that there is no full circumferential segment of epithelial metaplasia, and the lingual extension is 3 cm above the GEJ. Such classification has a high sensitivity to ≥1 cm of metaplasia mucosa, while it is less sensitive to those <1 cm. (B) Pathological diagnosis 1. Biopsy sampling: The four-quadrant biopsy method is recommended, that is, biopsies are routinely taken in four quadrants at 2-cm intervals starting from the GEJ, and more than 8 pieces of mucosal tissue are taken at each interval to effectively improve the detection rate of intestinal epithelial metaplasia. For those suspected of BE carcinoma, four quadrant biopsies should be taken at 1cm intervals, and the application of new endoscopic techniques for targeted biopsy is advocated. 2. Histological typing of chemosis of columnar epithelium in lower esophagus: (1) fundic type: similar to fundic epithelium, main cells and mural cells can be seen, but epithelial atrophy of BE is more obvious, and glands are less and shorter. This type is mostly distributed in the distal part of the BE near the cardia. (2) Cardia type: similar to cardia epithelium, with gastric hollows and mucus glands, but without main cells and mural cells. (3) Intestinal chemosis type: microvilli and crypt on the surface, cup-shaped cells are its characteristic cells. AB (pH 2.5) or mucus histochemical staining of sulfate, Cdx2 and immunohistochemical staining of mucin help to identify cup-shaped cells. 3. BE with heterogeneous hyperplasia: (1) Mild heterogeneous hyperplasia: normal structure, enlarged and densely stained nuclei, but the nuclei do not exceed 1/2 of the cell size, and mitotic signs are visible. The mucin in the cup and columnar cells was reduced, and atrophied cup cells could be seen. (2) Severe heterogeneous hyperplasia: the structure is changed, and there may be branching out buds that extend to the mucosal surface in a villi-like manner. The nucleus is densely stained and exceeds 1/2 of the cell size. irregular stratification may occur, 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 principles are to control GERD, eliminate symptoms, and prevent and treat complications, including heterogeneous hyperplasia and carcinoma. 1.Pharmacological treatment: Acid suppressants are the main drugs used to treat reflux symptoms. Among acid suppressants, proton pump inhibitors are better than H2 receptor antagonists, but there is no conclusive evidence that proton pump inhibitors can reverse columnar epithelial hyperplasia or prevent the occurrence of adenocarcinoma, and the use of proton pump inhibitors should be carried out in accordance with the conventional dose and full course of treatment for GERD. Most of the reasons for the poor effect of proton pump inhibitors are inappropriate doses or inappropriate dosing methods. In some patients, proton pump inhibitors and H2 receptor antagonists can be combined. The prokinetic drugs, mucosal protective agents, analgesics, smooth muscle transient relaxation inhibitors, etc. 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. The commonly used endoscopic treatment methods include argon plasma coagulation, high frequency electric therapy, laser therapy, radiofrequency ablation, photodynamic therapy, endoscopic mucosal resection and cryoablation. For BE without heterogeneous hyperplasia, endoscopic treatment is not advocated because of its low probability of carcinogenesis. BE with mild heterogeneous hyperplasia also has a low probability of cancer, so it can be followed up by endoscopy first, and if it progresses to severe heterogeneous hyperplasia, endoscopic treatment should be performed. 3.Surgical treatment: In principle, BE patients with confirmed carcinoma should be treated surgically. Evidence-based medical evidence shows that for BE with severe heterogeneous hyperplasia and early carcinoma limited to the mucosal layer, endoscopic treatment and surgical treatment can achieve the same effect, and the choice of treatment method should be based on the patient's opinion and the doctor's experience. 4.Anti-reflux surgery: including surgical and endoscopic anti-reflux surgery. Although it can improve the reflux symptoms of BE patients to some extent, it does not affect the natural course of the disease, and the long-term efficacy is yet to be confirmed. V. Monitoring and follow-up In view of 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 depend on the degree of heterogeneous hyperplasia. If no heterogeneous hyperplasia or early carcinoma is detected after 2 examinations, the interval between examinations can be relaxed to 3 years. For those with mild heterogeneous hyperplasia, endoscopic review should be conducted once every 6 months in the first year, and if the heterogeneous hyperplasia does not progress, the review can be conducted 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 gastroscopy every 3 months until intra-mucosal cancer is detected.