Pyloric duct ulcers often lack the periodic and rhythmic pain of typical ulcers, postprandial epigastric pain is common, poor response to antacids, easy vomiting or pyloric obstruction, and more complications such as perforation or bleeding. Pathogenesis: 1. Helicobacter pylori (Hp) infection is the main cause of peptic ulcer. (1) High rate of Hp infection in patients with peptic ulcer If we can exclude factors such as patients who have taken antibiotics, bismuth or non-steroidal anti-inflammatory drugs (NSAID) before testing, the rate of Hp infection is 90%-100% in DU patients and 80%-90% in GU. the risk of peptic ulcer in Hp-infected patients is also significantly increased. Prospective studies have shown that approximately 15-20% of Hp-infected individuals can develop peptic ulcers. (2) According to Hp can promote ulcer healing and significantly reduce the rate of ulcer recurrence eradication of Hp without suppression of gastric acid secretion can be effective in healing ulcers; the so-called refractory ulcers, which were not treated with conventional drugs that inhibit for secretion, were healed after effective Hp eradication therapy; the application of a highly effective Hp regimen for 1 week, followed by no further anti-ulcer therapy and a review 4 weeks after the end of the course of treatment. The healing rate of ulcers was higher or equal to the healing rate after 4-6 weeks of continuous treatment with the application of conventional acid secretion inhibitors. These results demonstrate, from different perspectives, that Hp eradication promotes ulcer healing. Frequent recurrence of ulcers used to be one of the main features of the natural history of peptic ulcers. The annual recurrence rate of ulcers that healed after treatment with conventional drugs that inhibit gastric acid secretion was 50%-70% after discontinuation of the drugs. Hp eradication can reduce the annual recurrence rate of DU and GU to less than 5%, thus allowing the majority of ulcer patients to be completely cured. In addition, Hp eradication can also significantly reduce the incidence of complications such as bleeding of peptic ulcer. (3) Hp infection alters the balance between mucosal invasive and defensive factors Hp, by virtue of its virulence factor, colonizes the gastric-type mucosa (stomach and duodenum with gastric chemosis), induces local inflammation and immune response, and impairs local mucosal defense repair mechanisms; on the other hand, Hp infection increases the secretion of pro-gastrin and gastric acid, which enhances the invasive factors. The synergistic effect of these two factors causes damage to the gastroduodenal mucosa and ulcer formation. The final formation of peptic ulcer is due to gastric acid-pepsin self-digestion. This concept has remained unchanged in the “Hp era”. Pepsin is a pepsinogen secreted by the main cell and activated by hydrochloric acid, it can degrade protein molecules, so it has an invasive effect on the mucosa.