Chronic atrophic gastritis is a chronic gastritis characterized by atrophy of the epithelium and glands of the gastric mucosa, reduction in the number of intrinsic glands, thinning of the gastric mucosa, thickening of the mucosal base, or with pyloric glandular hyperplasia and intestinal glandular hyperplasia, or with atypical hyperplasia. It often presents with vague pain in the upper abdomen, fullness, belching, loss of appetite, or wasting, anemia, etc. The symptoms are non-specific. Its causative factor is mainly H. pylori. When H. pylori enters the stomach through the mouth, part of it will be killed by gastric acid, and part of it will adhere to the mucus layer of the gastric sinus, settling in the mucus layer on the surface of the mucosal epithelial cells of the gastric sinus, and generally not invading into the gastric glands and the lamina propria. The urease produced by H. pylori can decompose urea, and the ammonia produced can neutralize the gastric acid that re-infiltrates into the mucus, forming a local microenvironment favorable to the settlement and reproduction of H. pylori, making the infection chronic. In addition, dietary habits, immune factors, physical factors, and genetics can also contribute to the appearance of the disease. When the lesion extends deep into the gland, the gland is destroyed, the number is reduced, the lamina propria is fibrotic, and the mucosa is thinned. The disease is classified into non-chemotropic atrophy and chemo-chemotropic atrophy depending on whether it is accompanied by chemosis, etc. Multifocal atrophy centered on the gastric horn and spreading to the gastric sinus and body has an increased risk of developing into gastric cancer. In conclusion, when similar symptoms appear or the diagnosis of atrophic gastritis is made, early medical consultation and treatment should be carried out under the guidance of doctors.