Epidemiology A large number of domestic and international data show that the detection rate of Hp in patients with duodenal ulcer is 80% to 90%, and eradication of H. pylori infection in patients with DU can reduce the recurrence rate of ulcers. Pathogenic mechanism 1. Increased gastric acid secretion – Acute H. pylori infection causes short-term gastric acid hypoacidity. Conversely, chronic infection often leads to increased secretion of basal and irritated gastric acid, especially in those patients who develop DU; 2. Gastric chemotaxis Hp induces inflammatory cell infiltration, leading to chronic inflammation of the mucosa of the duodenal bulb and gastric epithelial chemotaxis in the duodenum, and colonization of the duodenum. And through local cytotoxic effects, the mucosal resistance decreases and gastric acid and pepsin invade the fragile mucosa, leading to erosive duodenitis and eventually ulcer formation; 3. Immune response Its stimulation induces a strong inflammatory response and immune response, the response includes increased production of inflammatory cytokines, for example, interleukin (IL)-1, IL-6, tumor necrosis factor alpha and, most significantly, IL-8; 4. Downregulation of several important mucosal defense factors and disruption of mucosal defense mechanisms. Principles of management 1. Only 10-15% of patients with H. pylori infection develop ulcer disease, suggesting that other factors are likely to be important in determining the outcome of the infection; 2. Patients with apparent H. pylori negative duodenal ulcers (DU) should be thoroughly examined for the presence of infection, as infection remains the major cause of duodenal ulcers (DU) .