Helicobacter pylori (Hp), a Gram-negative bacillus that infects the gastric mucosa, is one of the most frequently infected pathogens in humans worldwide, with a population prevalence of approximately 40%. Because Hp infection is closely associated with a range of diseases such as chronic active gastric sinusitis, peptic ulcer, gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue lymphoma, it has been a hot topic of research in the field of digestive diseases since its discovery in 1982. Hp infection is associated with many diseases, for example, Hp infection causes chronic inflammation of the gastric mucosa. The mechanisms that cause this process are not fully understood and may be related to enzymes released by Hp (e.g. urease), bacterial adhesion to the gastric epithelium, and cytotoxins released by bacteria (e.g. vacuolar toxin A). Unlike other chronic inflammatory conditions (dominated by lymphocytic infiltration), inflammation due to Hp infection is accompanied by a large neutrophil infiltration (active inflammation). Peptic ulcer is a condition in which Hp infection is located mainly in the non-acid-secreting gastric sinus, causing increased secretion of gastrin, which stimulates increased gastric acid secretion. The high acid load causes damage to the duodenal mucosa, forming ulcers and duodenal mucosal gastric epithelial metaplasia, and Hp can colonize the metaplastic epithelium, further causing mucosal damage. In contrast, the mechanism of Hp-induced gastric ulcers is mainly through direct mucosal injury. For gastric cancer, a large amount of epidemiological data also shows a strong correlation between Hp infection and gastric carcinogenesis, and WHO has designated Hp as a class I carcinogen for gastric cancer. The risk of gastric carcinogenesis is higher in patients with infection involving both the gastric body and the gastric sinus. This type of infection causes decreased gastric acid secretion, which leads to atrophic gastritis, intestinal chemosis, heterogeneous hyperplasia, and eventually the development of gastric cancer. Urea breath test Specific sensitivity is good The diagnosis of Hp infection can be divided into non-invasive and invasive tests depending on whether endoscopy is required. Non-invasive tests have good sensitivity but poor specificity. Since Hp infection is often a long-term process, detection of IgM antibodies is not clinically relevant. Currently, IgG antibodies are mainly tested clinically. Because IgG antibodies persist for months or longer after the infection has been eradicated, serologic testing cannot distinguish between current and previous infection and cannot be used to determine whether eradication has been successful. The urea breath test works by having the patient drink C13 or C14-labeled urea, which is broken down in the stomach by Hp’s urease enzyme into carbon dioxide and ammonia. The presence of Hp infection in the patient is diagnosed by analyzing the percentage of labeled carbon dioxide in the exhaled breath. This method has high sensitivity and specificity and is the most commonly used non-invasive diagnostic method today. There is also an invasive test that includes a rapid urease test, histology, and bacterial culture. Among them, bacterial culture can also be used for the diagnosis of Hp infection, but its technique is more complex and requires specialized laboratory and technical personnel, and is generally not used as a routine diagnostic method. For patients who fail initial treatment, Hp culture can be accompanied by drug sensitivity testing, which is valuable for individualized treatment. Quadruple therapy can improve Hp eradication rates First-line treatment options for Hp infection include: triple therapy, quadruple therapy, and sequential therapy. Triple therapy refers to a standard dose of PPI plus two antibiotics. Due to the high primary resistance rate of metronidazole in China, PPI (Bid) + amoxicillin (1.0g Bid) + clarithromycin (0.5g Bid) is generally recommended as the initial treatment regimen for 7 to 14 days. For patients with penicillin allergy, a quadruple therapy based on bismuth can be used. Quadruple therapy is PPI, bismuth plus two antibiotics (usually metronidazole 250mg Qid and tetracycline 500mg Qid) for 10 to 14 days. This therapy has a high eradication rate in patients with clarithromycin resistance or penicillin allergy. The course of sequential therapy is 10 days, with PPI(Bid) + amoxicillin (1.0g Bid) for the first 5 days and PPI(Bid) + clarithromycin (0.5g Bid) and tinidazole (0.5g Bid) for the second 5 days. The rationale is that amoxicillin weakens the structure of the bacterial cell wall, thereby preventing clarithromycin resistance due to efflux channels through the drug and increasing its susceptibility. However, the efficacy of this therapy in Asian populations remains to be confirmed by further studies.