The relationship between H. pylori and chronic gastritis and peptic ulcers has become familiar. As research has progressed, some new findings have initially revealed that HP is also inextricably linked to other diseases. The occurrence of hepatic encephalopathy (hepatic coma) in patients with cirrhosis is often associated with elevated blood ammonia, and HP may be one of the “culprits” of ammonia production. It has been proved that the eradication of HP can improve the efficacy of hepatic encephalopathy and facilitate the recovery of encephalopathy. Experts also found that there is a kind of bacteria in liver cancer tissue that is very similar to HP. The pathogenic mechanism of HP 1. Flagellar power of HP: HP relies on flagellar power to cross the mucus layer and reach the surface of gastrointestinal mucosa. 2.Urease: HP can produce a large amount of urease, which has high enzymatic activity and damages the epithelium of gastric mucosa through the immune pathway. 3, HP virulence: the infection rate of HP in the population is high, but not exactly proportional to the onset of chronic gastritis and peptic ulcer. There are some carriers without disease, which may have two reasons, namely the strength of HP virulence and the body’s ability to defend. Intragastric infection due to H. pylori has been shown to be the main cause of gastritis. HP detection rate in active, severe gastritis is 90-100%. The HP detection rate in pediatric duodenal ulcers is about 52.6-62.9%. The recurrence rate of ulcers is low (less than 4%) in those who turn negative for HP. H. pylori detection 1, gastric mucosa tissue section staining and culture: HP culture needs to be carried out in a micro-oxygen environment with special media for 3-5 days to produce results, is the most accurate diagnostic method. 2, urease test: urease reagent contains urea and phenol red, the enzyme produced by HP can decompose the urea in it to produce ammonia, the latter makes the PH value in the reagent rise, thus making the phenol red change from brownish yellow to red. The biopsy stomach mucosa into the above reagent (filter paper sheet), if the gastric mucosa contains HP then the reagent turns red. This method is rapid, simple, specificity and sensitivity of up to 90% or more. 3, serological detection of anti-HP antibodies: but even IgM antibodies can remain positive for several months after the clearance of HP, limiting its diagnostic significance. The DNA of HP in the blood can also be detected by PCR. 4. Nuclide labeled urea respiratory test: Let the child take a certain amount of isotope 13C labeled urea orally. If the child’s digestive tract contains HP, the urease produced by HP can break down the urea to produce CO2, which is exhaled by the lungs. The degree of HP infection in the stomach can be determined by measuring the 13C content in the exhaled gas, with a specificity and sensitivity of more than 90%.