Barrett’s esophagus (BE) is a pathology in which the compound squamous epithelium of the lower esophageal mucosa is replaced by a single layer of columnar epithelium. The broad concept includes gastroepithelial metaplasia or ectasia of the esophagus and columnar epithelial metaplasia. To distinguish it from the columnar epithelium of the cardia mucosa in the lower esophagus, it was once specified that the lesion was more than 3 cm from the gastroesophageal junction (GEJ) (the so-called 3-cm rule). In recent years, the concept tends to refer to any length of pre-existing squamous epithelium replaced by columnar epithelium found endoscopically and confirmed by pathological histology above the junction of the esophageal and gastric mucosa (GEJ). A stricter definition refers to the replacement of the original squamous epithelium above the GEJ line by a specific columnar epithelium containing cupped cells. These new definitions are inclusive of short-segment BE, which specifically defines intestinal epithelial metaplasia as BE only when it is closely related to carcinoma, and proposes the concept that BE is a precancerous lesion, while excluding gastric mucosal ectasia and gastric epithelial metaplasia from BE. The etiology of this disease is unknown, and it is mostly secondary to gastroesophageal reflux (GERD) and hiatal hernia in clinical practice. The various components of reflux, including gastric juice, alkaline bile and pancreatic juice, can cause damage to the squamous epithelium of the lower esophagus, which is repaired by the columnar epithelium with acid resistance and strong regenerative ability, thus forming BE. Barrett’s esophagus is a precancerous lesion that can develop into esophageal culpable adenocarcinoma, which accounts for about 30% to 50% of esophageal cancer in the UK and US. This disease is not uncommon in clinical practice, but some physicians often only define orange-red islands of mucosa as BE because of conceptual confusion, so the detection rate reported in the literature is low. The diagnosis of BE must be based on endoscopy and histopathology, and endoscopic findings of squamous-columnar epithelial lines displaced away from the EGJ (marked by the presence of fenestrated vessels in the orange mucosa at the mouth of the longitudinal folds of the stomach or in the distal esophagus) may lead to a suspicious diagnosis of BE, pending tissue biopsy. Further confirmation is needed. The diagnosis of BE can be made if the endoscopic sampling site is between the distal end of the Z line and the EGJ, which is upward shifted, and an enteric epithelium with cupped cells, or if there is no cupped cells but only cardia epithelium or fundic gland epithelium, the diagnosis of “esophagitis with cardia or fundic gland hyperplasia”. However, it can also be diagnosed clinically as “Barrett’s esophagus, cardia type or fundic gland type”. The criteria for biopsy biopsy are generally 4 biopsies taken every 2 cm circumferentially along the entire long axis of the lesion (4-quadrant biopsy). Since the discovery of entericized columnar epithelium containing cupped cells is the true meaning of BE, the sampling site, tissue block size and sampling depth have a greater impact on the diagnostic rate of BE. Larger biopsy forceps retrieval can not only obtain larger tissue blocks, but also reach deeper tissues, which is more helpful in determining the cancer potential of BE. Endoscopic pigment staining is important in guiding BE biopsy. BE is usually divided into three types according to the type of columnar epithelium, namely junctional (cardia type), fundic (acid-secreting-cardia type) and special type (intestinal epithelial metaplasia type). Since the narrow concept of only intestinal epithelial metaplasia is considered as a histological basis for the diagnosis of BE, only the specific type is a true BE according to this definition. cupula cells can be easily identified in routine HE staining, and whether they can be used as a characteristic structure of intestinal epithelial metaplasia remains controversial. Adenocarcinoma of the esophagus accounts for about 5-10% of all esophageal cancers, and since esophageal adenocarcinoma only occurs in the specific type of BE epithelium, “enteric” BE is a precancerous lesion. It is important to note that the presence of cupped cells does not imply cancerous potential, but the mucus secretion is different and the cancerous potential is completely different. The rate of cancer is generally lower in cupular cells containing salivary acid mucus, while the rate of cancer is higher in cupular cells containing sulfate mucus. This difference in the nature of mucus can only be distinguished by special histochemical staining (e.g. AB-PAS/HID) or immunohistochemical staining, which is not routinely performed in clinical diagnosis, but rather by the evaluation of heterotypy to determine the carcinogenic potential. The term dysplasia has different terms in China, including atypical hyperplasia or interstitial lesions, which can be judged by pathological examination and thus has the operability of clinical application.BE heterogeneity mainly refers to abnormal epithelial structure (disorder of glandular epithelial arrangement, loss of polarity, sieve-like structure or epithelial back-to-back, etc.) and abnormal cell nuclei (large deep stained nuclei, increased nuclear plasma ratio, pathological nuclear division, etc.), and is classified as mild or severe. It was classified into 2 grades: mild and severe. Mild anisotropy is dominated by the heterogeneity of the nucleus, which is pencil-shaped, crowded, and arranged in complex layers, but the height does not exceed 1/2 of the cell. severe anisotropy is characterized by significant heterogeneity of both cellular and tissue structures, with the nucleus in complex layers, occupying the entire cytoplasm of the epithelial cells, and loss of epithelial cell polarity. Glandular ducts are prolonged, twisted, and of different sizes, etc. Glandular ducts with common walls and back-to-back are common, and some appear sieve-like structures. The main difference between them and carcinoma is the absence of infiltrative growth, and carcinoma shows obvious heterogeneity of the nucleus and incomplete glandular structure. Due to the lack of uniform criteria, the grading of heterogeneous hyperplasia varies widely even among experienced gastrointestinal pathologists. The nuclear staining of regenerating epithelial cells appearing in response to inflammation is deepened, and the boundary between nucleus and nucleus can still be distinguished, but sometimes it is not easily distinguished from mild heterogeneity, and there is no consensus on whether severe heterogeneity is cancerous epithelium, which is currently advocated as high-grade intraepithelial neoplasia. Regarding treatment strategies The aim of treatment is to reduce gastroesophageal reflux and to manage complications. Pharmacological treatment is the same as that for GERD. For histologically confirmed esophageal columnar epithelial metaplasia or gastric mucosal ectoplasia without cupped cells and heterotypy, the patient can be treated as “reflux esophagitis” if there are clinical symptoms. Since the acid exposure of the esophagus is more severe in patients with BE than in other GERD patients, it is important to consider the presence of intermittent acidic gastric contents. At the same time, intermittent reflux of acidic gastric contents may increase cell proliferation and decrease esophageal cell apoptosis, therefore, complete elimination of acid reflux is required to obtain ideal symptom control, requiring better and higher doses of PPI. If the BE esophagus is confirmed to be enteric then the degree of atypical hyperplasia and cancer potential should be pathologically assessed (combined with mucus histochemical or immunohistochemical staining to determine the type of mucus secretion when available) and such cases should be included in the clinical endoscopic follow-up and surveillance. If atypical hyperplasia is present on biopsy, endoscopic treatment should be performed, and endoscopic dilatation should be performed for complicated esophageal strictures, and active surgical treatment should be performed for suspected cancerous lesions.