Helicobacter pylori (HP) is known to be one of the most common sources of infection worldwide, with approximately 50% of the world’s population infected with H. pylori, and infections in developing countries are significantly higher than in developed countries. Many diseases of the digestive system such as chronic gastritis, peptic ulcer, MALT lymphoma, and gastric cancer are closely related to H. pylori infection. The pattern of HP infection differs between developing and developed countries, with low infection rates in developed countries, few infections in children and adolescents, and 6-11% infection rates in children under 12 years of age (1). In contrast, acquisition of HP infection in developing countries occurs mainly in childhood, with infection rates of more than 50% in children under 5 years of age in many developing countries and even 80%-90% in some African countries (2). Data from epidemiological surveys in Beijing, Shanghai and Guangzhou, China, showed that the HP infection rate in children was 15.7%-45.2%, and it is noteworthy that the HP infection rate in 119 children aged 4-12 years in Yangzhong, Jiangsu Province, a region with a high incidence of gastric cancer, was 73.11% by urea breath test (3). Therefore, it is an important task for pediatricians to understand HP infection and its related diseases in children and to diagnose, treat and prevent them. （The exact route of HP infection and susceptibility factors is not fully understood, but there is increasing evidence to support the transmission of HP infection from person to person, mainly through “oral-oral” or “fecal-oral” and “gastro-oral” routes. “and “gastric-oral” routes (4). Humans are the only known natural hosts of HP, and HP infection shows a clear family clustering phenomenon. Some specific eating behaviors such as mothers chewing over food to feed their children or sharing utensils during meals significantly increase pediatric HP infection. In rural Bangladesh, it is customary for Hindu mothers to apply their saliva to the nipples before breastfeeding, and a comparison of HP infection rates among Hindu and Muslim children in the same area showed that the former were significantly higher than the latter. A study reported that HP-DNA was detected in the oral tonsils and adenoids of 30% of HP-infected patients, and the cagA gene was detected in five cases, suggesting that the oral tonsils and adenoids may also be the habitat of HP (5), providing evidence of transmission by the “oral-oral” route. Recent studies have provided direct evidence of HP transmission by “fecal-oral” or through contaminated water and food (6). Some scholars have suggested that flies may be intermediate hosts for transmission (7), but their ability to transmit and how to transmit needs further study. Genetic factors may be related to the susceptibility of the organism to HP, but socioeconomic environmental factors are the main influence on the prevalence of HP infection. Socioeconomic environmental factors that are strongly associated with HP infection include overcrowding, poor sanitation, unclean drinking water, lack of bed-sharing during childhood, and lack of education and counseling for mothers about feeding; other factors that can increase the risk of HP infection include the presence of HP-infected individuals in the family, mothers feeding their children with chewed food, non-breastfeeding, and low parental education, among others. Regarding breastfeeding, a study in the United States showed that breast milk has the ability to increase the body’s resistance to HP and that breast milk plays a protective role (8). However, other studies do not seem to support this conclusion, and one study even concluded that the rate of HP infection in breastfed children was high instead, however, further analysis of the reasons revealed that mothers did not wash their hands and nipples before breastfeeding, and the contamination caused by its direct transmission was greater than the protective effect of breast milk. （Like adults, most children with HP infection are asymptomatic, and the detection rate of HP in normal children is 30%. Once HP-infected children become symptomatic, the symptoms are those of chronic gastritis and peptic ulcer, such as abdominal pain, anorexia, bloating, nausea, vomiting, acid reflux, belching, and in severe cases, gastrointestinal bleeding such as fecal occult blood, vomiting blood, and black stools. Systematic etiological studies have demonstrated that there is a clear causal relationship between HP and the development of pediatric chronic gastritis, and the rate of HP positivity in histologically confirmed cases of chronic gastritis in children is more than 60%, while HP is not detected in children with histologic abnormalities, secondary gastritis (drug, bile reflux, eosinophilic gastritis), and gastric crohn’s disease. symptoms are significantly reduced. It is important to note that, like adults, most children with HP-associated chronic gastritis do not exhibit symptoms, and HP is strongly associated with the development and recurrence of peptic ulcers, especially duodenal ulcers, in children, and eradication of HP can promote ulcer healing and reduce ulcer recurrence. Recurrent Abdominal Pain (RAP) is a common problem in pediatrics, occurring in about 10-15% of preschool and school-age children. 54% of children with RAP are reported to be HP positive in the literature, which is clearly associated with HP infection, and anti-HP treatment can lead to relief of RAP symptoms (9), but some scholars disagree, and the correlation between RAP and HP infection is currently uncertain. infection correlation is not certain. HP infection in children can reduce iron stores and lead to iron deficiency anemia, and iron stores increase steadily after HP infection is eradicated. the mechanism of the decrease in iron stores and thus anemia caused by HP infection may be related to the increase of lactoferrin in the stomach, which affects iron absorption by binding to dietary iron. The exact mechanism is currently under investigation (10). Another hematologic disorder, thrombocytopenic purpura (ITP), has been more frequently reported to be associated with HP infection in adults, while no correlation has been seen in children. (iii) Diagnosis and treatment Current methods for diagnosing HP infection include invasive and non-invasive methods. Invasive methods refer to methods by gastroscopy, including gastric mucosal bacterial culture, histological examination, and rapid urease test; non-invasive methods currently applied include urea breath test, fecal HP antigen test, and serum antibody test. Bacteriological examination of the gastric mucosa by gastroscopic biopsy is the “gold standard” for the diagnosis of HP presenting infection. In children with upper gastrointestinal symptoms suggestive of organic disease, after excluding other causes (e.g., lactose indigestion, celiac disease, constipation, hepatobiliary disease), gastroscopy with multiple biopsies is the best test. Urea breath test includes 13C urea breath test and 14C urea breath test. 13C urea breath test is preferred in children, and it has been widely used in children because of its non-radioactive characteristics, with high sensitivity and specificity, and is a reliable non-invasive diagnostic method for diagnosing HP presenting infection and evaluating drug efficacy. However, the urea breath test is not suitable for young children, especially those under 2 years of age, because the accuracy is affected by the lack of cooperation of young children. The fecal antigen test (HPSA) is a new non-invasive diagnostic method with similar sensitivity and specificity as the urea breath test, and is used as a diagnostic tool in adults, but its application in children has also shown high sensitivity and specificity. Since fecal HPSA is susceptible to the influence of various factors, especially drugs, its value in evaluating drug efficacy needs to be further observed. Monoclonal antibodies for the detection of fecal HP antigens are already available (12). In addition, PCR technology for the detection of fecal HP-DNA will provide new non-invasive diagnostic methods, and it is believed that more non-invasive methods will be used for clinical diagnosis in the future. In children, serological methods to detect H. pylori infection are unreliable. Which children need to be tested for HP? HP should be routinely tested in those with chronic gastritis and peptic ulcer; MALT lymphoma, despite its low incidence, is routinely tested for HP once diagnosed; routine testing for HP is not recommended in children with dyspeptic symptoms, but only when symptoms are severe enough not to exclude organic disease and influence therapeutic judgment; and review after eradication of HP infection. The review is done by reliable non-invasive methods, with the 13C urea breath test currently being preferred. Routine screening for HP infection is not currently advocated for those children with a family history of peptic ulcer and a family history of gastric cancer. Treatment of HP infection begins with determining the indications for eradication therapy (13, 14). HP eradication should be performed in children with HP-positive chronic gastritis, peptic ulcer, MALT, and in HP-positive children with severe and recurrent dyspeptic symptoms to improve symptoms. It is important to emphasize that the primary goal of H. pylori eradication therapy in children is to heal peptic ulcers and relieve symptoms. In children who are asymptomatic or have only non-specific mild symptoms, eradication therapy for the purpose of preventing later life complications (peptic ulcer or malignancy) can be delayed until safer treatment options are available later. Because of the association between HP infection and iron deficiency anemia in children, it has been suggested that children with iron deficiency anemia who are HP positive should be treated with concomitant anti-HP infection. Drugs used to treat HP infection in children include clarithromycin, metronidazole, amoxicillin, bismuth complexes (mainly bismuth potassium subcitrate), proton pump inhibitors (PPI) or H2 receptor inhibitors (H2RI). Many second-line agents (e.g., tetracycline, rifabutin, ciprofloxacin) are contraindicated or have not been approved for use in children. Combinations are required, and some of the reported treatment regimens and eradication rates are shown in Table 2. Treatment should be selected for high eradication rates to avoid causing widespread antibiotic resistance to HP and other bacteria nationwide. The triple therapy of “PPI plus two antibiotics for 7-14 days” is the best treatment method at present. (iv) Antibiotic resistance The eradication rate of HP has decreased in recent years, and the emergence of drug-resistant strains and the increase of drug resistance rate year by year are the main reasons. The rate of drug resistance varies in different countries and regions, the rate of HP resistance to metronidazole in adults ranges from 20%-80%, the rate of resistance to clarithromycin was 0 when it was first applied, in recent years Europe reported 10%-15% resistance, domestic Shanghai, Beijing and other places reported 5.1%-10%, most scholars believe that HP is less resistant to amoxicillin. The resistance of HP infected in children to antibiotics has been reported one after another, Poland and Japan reported the eradication rate of HP and the resistance rate and variation of HPi to several commonly used antibiotics, HP strains infected in children have the same 8% – 16% resistance to metronidazole and a slightly higher resistance to clarithromycin (18%), no resistant strains to amoxicillin have been reported. We have tested the susceptibility and resistance of strains isolated from the gastric mucosa of children undergoing gastroscopy, and the results showed that HP in children is 18.2% resistant to clarithromycin, 31.8% resistant to metronidazole, and 9.1% resistant to amoxicillin, and there are multi-drug resistant strains, therefore, HP resistance in children and the resulting therapeutic difficulties should be given sufficient attention by clinicians. Although routine antibiotic sensitivity testing is not currently advocated, the proposed establishment of regional surveillance of drug resistance rates will help to understand the variability of HP resistance rates in the population and guide the selection of antibiotics for HP eradication. In conclusion, H. pylori infection is a health hazard in children in developing countries, and in China, where the prevalence of HP infection is high, the majority of infections are acquired in childhood. HP infection is the cause of chronic inflammation and peptic ulcers in children, and eradication of HP infection in children may reduce the incidence of peptic ulcers in adulthood and may reduce the incidence of gastric cancer. . The current regimen for treating children has mostly evolved from the adult regimen, and the triple therapy of “acid suppressant + two antibiotics” is the most commonly used treatment method, which makes treatment difficult due to the increasing resistance to antibiotics. Therefore, it is important to further clarify the transmission route of HP infection and the main risk factors for HP transmission to prevent HP infection and reduce the infection rate in the population. Looking to the future, a vaccine would be the best way to prevent and treat the infection, but there is currently no practical option.