Barrett’s esophagus is not a disease, but a pathological change in which the compound squamous epithelium of the lower esophagus is replaced by a single layer of columnar epithelium with or without intestinalization. It is a precancerous lesion of esophageal adenocarcinoma with intestinal epithelial metaplasia. Barrett’s esophagus mainly presents with symptoms of GERD, such as heartburn, acid reflux, retrosternal pain and dysphagia, and is often secondary to GERD. The main clinical significance of Barrett’s esophagus is currently considered to be its association with esophageal adenocarcinoma, and routine screening is not recommended for the general population and patients with GERD alone? but should be screened in those patients with multiple other risk factors, such as age 50 years or older, chronic reflux esophageal disease, diaphragmatic hernia, and obesity, especially abdominal obesity. The diagnosis of this disease is based mainly on endoscopy and esophageal mucosal biopsy. The diagnosis is made when the presence of columnar cells is confirmed by pathological examination, and is further supported by the presence of intestinal epithelial metaplasia. The principles of treatment for this disease are to control GERD, eliminate symptoms, and prevent and treat complications, including heterogeneous hyperplasia and carcinoma. Specifically, these include: 1. Drug therapy: Acid suppressants are the main drugs used to treat reflux symptoms. Among acid-suppressing drugs, proton pump inhibitors are superior to H2 receptor antagonists, but there is no conclusive evidence that proton pump inhibitors can reverse columnar epithelial hyperplasia or prevent the occurrence of adenocarcinoma. The use of proton pump inhibitors should be carried out in accordance with the conventional dose and full course of 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. Given the risk of developing adenocarcinoma of the esophagus in Barrett’s esophagus, patients should be followed up regularly for early detection of heterogeneous hyperplasia and cancer. The interval of endoscopy should depend on the degree of heterogeneous growths. 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.