Peptic ulcers are mainly chronic ulcers that occur in the stomach and duodenum, i.e. gastric and duodenal ulcers, named because ulcer formation is associated with the digestive action of gastric acid/pepsin. Ulcers have a mucosal defect beyond the mucosal muscle layer, unlike erosions. Etiology and pathogenesis 1, H. pylori Confirmation of H. pylori as an important cause of peptic ulcer is based on evidence from two sources: (1) the detection rate of H. pylori in patients with peptic ulcer is significantly higher than that in the general population of controls, with a detection rate of about 90% in DU and 70% to 800% in GU (H. pylori-negative peptic ulcer patients can often find a history of NSAID use, etc. (2) A large number of clinical studies affirm that the recurrence rate of ulcers decreases significantly after successful eradication of H. pylori, and the annual recurrence rate of ulcers healed with conventional acid suppression therapy is 50% to 70%, while eradication of H. pylori can reduce the recurrence rate of ulcers to less than 5%, which indicates that peptic ulcers can be cured after removing the cause. As for why only a small percentage of people (about 15%) in the population infected with H. pylori develop peptic ulcers, it is generally believed that this is the result of the different interactions between H. pylori, the host and environmental factors. 2, non-steroidal anti-inflammatory drugs NSAID is another common cause of peptic ulcers. A large number of studies have shown that the risk of peptic ulcer and its complications is significantly higher in patients taking NSAIDs than in the general population. Clinical studies have reported that gastric or duodenal ulcers can be found in about 10%-25% of patients taking NSAID for a long time, and ulcer complications such as bleeding and perforation occur in about 1%-4% of patients. ulcers caused by NSAID are more common in GU than in DU. The risk of ulcer formation and its complications is related to the type, dose and duration of NSAID, but also to advanced age, simultaneous use of anticoagulants, glucocorticoids and other factors. 3. Gastric acid and pepsin The final formation of peptic ulcer is due to the digestion of mucosa by gastric acid/pepsin itself. Since pepsin activity is pH-dependent, it loses its activity at pH>4. Therefore, gastric acid is the main consideration when discussing the pathogenesis and treatment of peptic ulcer. The rare occurrence of ulcers in the absence of acid and the fact that drugs that inhibit gastric acid secretion promote ulcer healing confirm the decisive role of gastric acid in the formation of ulcers, which is the direct cause of ulcer formation. This damaging effect of gastric acid can generally only occur when the normal mucosal defense and repair function is damaged. 4, other factors (1) smoking: smokers peptic ulcer incidence is higher than non-smokers, smoking affects ulcer healing and promotes ulcer recurrence. The exact mechanism by which smoking affects ulcer formation and healing is not known, but may be related to factors such as increased gastric acid secretion, reduced duodenal and pancreatic bicarbonate secretion, coordinated gastroduodenal motility, and increased mucosal damaging oxygen radicals. (2) Genetics: Genetic factors were once considered important in the development of peptic ulcer, but with the recognition of the important role of Helicobacter pylori in the development of peptic ulcer, the importance of genetic factors has been challenged. For example, the family history of peptic ulcer may be a “family aggregation” phenomenon of H. pylori infection; O-type blood gastric epithelial cells express more adhesion receptors on the surface and favor H. pylori colonization. Therefore, the role of genetic factors remains to be further investigated. (3) Acute stress: It is a consensus that stress ulcers can be caused, but in patients with chronic ulcers, the pathogenic role of emotional stress and psychological disorders is inconclusive. Clinical observations have found that chronic mental stress and overwork do predispose to ulcer attacks or exacerbations, but this occurs mostly when chronic ulcers are already present, so emotional stress may play a primarily causative role and may affect the regulation of gastroduodenal secretion, motility, and mucosal blood flow through neuroendocrine pathways. (4) Gastroduodenal motility abnormalities: Studies have found that some DU patients have increased gastric emptying, which can increase the acid load in the duodenal bulb, and some GU patients have delayed gastric emptying, which can increase the reflux of duodenal fluid into the stomach and aggravate gastric mucosal barrier damage. However, it is now believed that gastrointestinal motility disorders are unlikely to be the primary cause, but can exacerbate mucosal damage from H. pylori or NSAID.