Although Australian scholars Barry J. Marshall and J. Robin Warren were not awarded the Nobel Prize in Physiology or Medicine until 2005 for the discovery of Helicobacter pylori (Hp), H. pylori, or Hp, is no stranger to people. There have been statistics that the global Hp infection rate is more than 50%, developing countries than developed countries, by the Chinese Medical Association Digestive Diseases Branch of the H. pylori group made a natural population involving 20 provinces and cities, 40 centers of the epidemiological survey of Hp infection: China’s infection rate of 40-90%, an average of 59%; the current infection rate of 42-64%, an average of 55%. Digestive system diseases are common and prevalent in the population, and the medical profession has gradually recognized that Hp is the main cause of chronic gastritis, an important causative factor of peptic ulcer (including gastric ulcer and duodenal ulcer), and plays an important role in the occurrence of gastric cancer, and has been recognized by the World Health Organization as the number one carcinogenic factor of gastric cancer, even with a kind of gastric lymphoma – It is also closely related to the occurrence of a type of gastric lymphoma, mucosa-associated lymphoid tissue (MALT) lymphoma. In fact, besides digestive system diseases, Hp is also correlated with diseases of other systems. For example, Hp infection is closely associated with a number of hematologic diseases, including iron deficiency anemia, megaloblastic anemia, idiopathic thrombocytopenic purpura, and allergic purpura, and the aforementioned gastric mucosa-associated lymphoma is also a hematologic disease. Hp and iron deficiency anemia: In addition to causing peptic ulcers and long-term chronic bleeding in the digestive tract, Hp infection also causes diffuse atrophic gastritis, which reduces gastric acid secretion and affects iron absorption; the growth and reproduction of Hp requires iron consumption, making the body iron deficiency “worse”. In addition, Hp itself can interfere with iron metabolism. Therefore, the relationship between Hp and iron deficiency anemia is relatively close. Usually, iron deficiency anemia can be treated satisfactorily with bleeding control and iron supplementation, but in case of refractory iron deficiency anemia, the presence of Hp infection should be noted. Some refractory iron deficiency anemias can be improved with Hp eradication therapy, even if iron supplementation is not continued, so that the anemia can be corrected. Hp and megaloblastic anemia: megaloblastic anemia is mainly due to a deficiency of vitamin B12 or folic acid in the body. endotoxin produced by the Hp strain causes the infected organism to produce antibodies that damage gastric mucosal cells through autoimmune mechanisms, leading to atrophic gastritis and a decrease in gastric acid, pepsin and endocannabinoid secretion. Vitamin B12 in food must be released by the action of gastric acid and pepsin to be utilized via binding to endokines. Therefore, Hp infection can affect the absorption of vitamin B12 and lead to megaloblastic anemia due to vitamin B12 deficiency. In addition, vitamin B12 deficiency affects the nervous system, manifesting as numbness in the distal extremities, profound sensory disturbances, ataxia, vertebral fasciculation signs, depression, memory impairment, and in severe cases, abnormal psychiatric symptoms. Hp and idiopathic thrombocytopenic purpura: Idiopathic thrombocytopenic purpura is an autoimmune bleeding disorder in which the abnormality of autoimmunity causes insufficient production and excessive destruction of platelets, and patients have different degrees of bleeding symptoms due to thrombocytopenia. As early as 1998, some foreign scholars found that Hp infection was associated with the disease and that platelet counts could be rebounded to varying degrees after successful eradication of Hp. Therefore, if idiopathic thrombocytopenic purpura is not effective, you may consider checking for Hp infection, and perhaps the platelet count will be effectively rebounded with the eradication of Hp. Hp and allergic purpura: Allergic purpura, also known as allergic cutaneous vasculitis, is characterized by non-thrombocytopenic skin purpura, abdominal pain, arthritis, and nephritis, and is a common condition in childhood and can also develop in adults. Some scholars found that there is a correlation between allergic purpura and Hp infection, and the clinical symptoms of purpura completely disappeared when Hp was cleared. chronic persistent stimulation of Hp itself and its metabolites will stimulate the body to produce a series of immune reactions and clinical symptoms of allergic purpura, meanwhile, Hp infection will also weaken the barrier function of gastric mucosa and increase the exposure of the body to food, drugs, pathogens, etc. in the digestive tract. Hp infection also weakens the gastric mucosal barrier function, increases the exposure of the body to food, drugs, pathogens and other allergens in the digestive tract and amplifies the degree of allergic reaction. Hp and gastric mucosa-associated lymphoid tissue lymphoma: Gastric mucosa-associated lymphoma is a low-grade malignant lymphoma with limited lesion development. Currently, the idea that Hp infection can cause gastric mucosa-associated lymphoma has been generally accepted by domestic and international academics, and anti-Hp therapy has become the first-line treatment option for gastric mucosa-associated lymphoma. Hp is mainly transmitted by the “human-to-human” and “fecal-to-mouth” routes, but it can also be transmitted by endoscopy, and there are obvious clusters in families. Hp usually resides in the pylorus, but the oral cavity is also a parasitic area, especially in dental plaque, which is an important cause of recurrent Hp infections, so use a mouthwash with antiseptic properties. There are many diagnostic methods for Hp infection, commonly used include invasive tests such as gastric mucosal biopsy by gastroscopy and non-invasive tests such as serum Hp antibodies, 13C- or 14C-urea breath test, and fecal Hp antigen. For hematologic patients with iron deficiency anemia, megaloblastic anemia, idiopathic thrombocytopenic purpura, and allergic purpura, if conventional treatment is not effective, it is worthwhile to check for Hp infection by non-invasive 13C- or 14C-urea breath test and treat accordingly. With the rising rate of resistance to certain antibiotics in the population, the treatment regimen for Hp eradication has been updated from triple therapy to quadruple therapy containing a proton pump inhibitor (PPI), bismuth plus two antibiotics for 10 or 14 days, and if the patient’s GI symptoms are not relieved at the end of the course, antacid therapy with a PPI can be continued for 2 to 4 weeks. Pay attention to the Hp review after treatment.