Helicobacter pylori (Hp) is a Gram-negative, spiral, microaerobic bacterium that is closely associated with the development of chronic gastritis, peptic ulcer, gastric cancer, and gastric mucosa-associated lymphoid tissue lymphoma, and was therefore classified as a class I carcinogen by the WHO in 1994. There is growing evidence that Hp infection is mostly acquired in childhood, and once infected, it is rarely eradicated spontaneously and can cause tissue malignancy in severe cases. Epidemiology: The prevalence of H. pylori infection is closely related to the economic status of the population. In developed countries, children younger than 6 years old are rarely infected and the infection rate is less than 10%. The World Gastroenterology Organization reports that the infection rate of Hp in children is 10% to 80%, and more than 50% of children are infected before the age of 10. Childhood is the period of dramatic increase in H. pylori infection: the rate of increase is 3% to 8% per year, and by age 10 about 40% to 60% of people are infected. Children in developing countries are a high-risk group for H. pylori infection. Transmission route: Human is the only known natural host of Hp, and Hp infection shows a clear family aggregation phenomenon. The specific route of transmission of H. pylori is not well understood. Socioeconomic environmental factors are the main influence on the rate of Hp infection, and known risk factors include population crowding, poor hygiene, unclean drinking water, lack of bed-sharing during childhood, and lack of education and counseling for mothers about feeding. Additional factors that can increase the risk of Hp infection include the presence of an Hp-infected person in the family, the mother feeding the child with chewed food, non-breastfeeding, and low parental education. Detection methods and diagnosis: Detection methods for Hp infection include both invasive and non-invasive methods. Invasive methods rely on gastroscopic biopsy and include rapid urease test (RUT), staining of gastric mucosal tissue sections and bacterial culture of gastric mucosa. Non-invasive testing methods include urea breath test, fecal Hp antigen test (HpSA) and serum Hp antibody test. Except for the serum antibody test, PPI preparations should be discontinued for 2 weeks and antibiotics and bismuth for 4 weeks before all other tests. The results of the rapid urease test are affected by the pH of the reagent, the site of sampling, the size of the tissue, the amount of bacteria, the observation time, and the ambient temperature. The sensitivity of the test can be improved by taking 2 pieces of tissues for testing at the same time (1 piece each from the gastric sinus and body). This method is rapid, convenient and accurate. The detection of Hp can be accompanied by the diagnosis of gastric mucosal lesions (HE staining). There are some differences in the detection results of different staining methods. Immunohistochemical staining has high specificity but is more expensive; fluorescence in situ hybridization (FISH) has high sensitivity for Hp detection and is also used for the detection of Hp resistance to clarithromycin. Bacterial culture is the “gold standard” for the diagnosis of Hp presenting infection. However, it is complex, time-consuming, and requires certain laboratory conditions, and specimens need to be transferred to culture in a special transfer solution and kept cold. The culture can be used for drug sensitivity testing and bacteriological studies. The urea breath test is highly accurate, easy to perform, and can reflect the status of whole stomach Hp infection. The fecal antigen test is safe, easy to perform, and has good sensitivity and specificity. It does not require any oral reagents and is suitable for all ages and types of patients. The international consensus is that the method is comparable in accuracy to the breath test. Serum antibodies detect IgG, reflecting Hp infection over a period of time, and some kits can detect both CagA and VacA antibodies. Serum antibodies can be maintained for a long time after Hp eradication and therefore cannot be used for post-treatment review. Serological methods for Hp detection are mostly used in young children and epidemiological investigations. Current Hp infection can be determined by one of the following three criteria: (1) positive gastric mucosal tissue RUT, tissue section staining or culture; (2) positive UBT; (3) positive HpSA test. Positive serum Hp antibody test indicates previous infection, and those who have never been treated can be considered as presenting infection. Treatment: The efficacy of Hp infection eradication treatment should be determined at least 4 weeks after the end of the course of treatment, with UBT being the first choice. Hp eradication can be judged by meeting one of the following three criteria: (1) negative UBT; (2) negative HpSA; (3) negative RUT based on both sinus and gastric body sampling. Indications for the treatment of Hp infection are unspecified dyspepsia in a population with an Hp infection rate greater than 20%; patients with duodenal and gastric ulcers; MALT lymphoma; unexplained iron deficiency anemia and idiopathic thrombocytopenic purpura; and patients who wish to receive treatment (the appropriate risks and benefits should be described prior to treatment). Commonly used drugs include: (1) antibiotics: amoxicillin 30-50mg/kg/d in 2-3 doses; metronidazole 15-20mg/kg/d in 2-3 doses; tinidazole 15-20mg/kg/d in 2-3 doses; clarithromycin 15-20mg/kg/d in 2-3 doses. (2) Bismuth: colloidal bismuth subcitrate (CBS), 6～8mg/kg/d in 3 times (orally before meals). (3) Antacid secretagogue: H2-receptor antagonist: cimetidine, 20-30mg/kg/d, taken orally every 12 hours or once before bedtime; proton pump inhibitor (PPI): omeprazole, 0.6-0.8mg/kg/d, taken early in the morning daily. Treatment regimen: Preferred regimen (first-line regimen): PPI + clarithromycin + amoxicillin (for people with clarithromycin resistance <15%-20%), or switch to metronidazole if penicillin allergy. The recommended course of treatment in children is 7-14 days. Second-line regimen: for those who fail the first-line regimen (suitable for areas with a high rate of clarithromycin resistance and a low rate of metronidazole resistance) PPI + amoxicillin + metronidazole + colloidal bismuth subcitrate. Modified regimen: sequential treatment: PPI (1mg/kg/d, maximum amount is 20mg bid) + amoxicillin (50mg/kg/d, maximum amount is 1g bid) for 5 days; PPI (1mg/kg/d, maximum amount is 20mg bid) + clarithromycin (15mg/kg/d, maximum amount is 500mg bid) + tinidazole (20mg/kg/ d, maximum 500 mg bid) for 5 days. Whether sequential therapy can be used as a first-line regimen is still controversial, and there is a lack of corresponding multicenter randomized controlled studies in our children. "Individualized treatment" is a way to analyze the reasons for failure and propose treatment for patients who have failed Hp eradication therapy several times. The following methods are recommended for patients who have failed in eradication therapy: ① Understand the patient's compliance with medication in previous treatment and determine the reasons for treatment failure; ② Select effective antibiotics according to the results of drug sensitivity test if available; ③ Avoid repeating the antibiotics used in the initial treatment or adding bismuth agent when treating again if there is no condition to perform drug sensitivity test; ④ Extend the treatment time; ⑤ Consider stopping the medication for those who have failed in multiple treatments (5) For those who have failed in multiple treatments, consider stopping the drug for a period of time (2-3 months or half a year) to allow the bacteria to return to their original active state in order to improve the Hp eradication rate with the next treatment.