Helicobacter pylori, people have always thought that they are only bacteria that infect the stomach disease, there is only so little territory, otherwise how to call such a name? Actually, they are not. Although H. pylori is small, the locomotor organ is very advantageous: each bacterial body end has 2-6 flagella, the flagellum is 1.5 times longer than the body, and the flagellum end has a spherical expansion, like a high-efficiency battery, to ensure the supply of energy for flagellar movement. When moving forward, the long flagellum is a high-powered propeller; when retreating, the flagellum immediately becomes an effective brake, even in the slimy gastric juice, they can still move freely, while the E. coli can not move. As we know from the history of microbiology, it has always been the open secret of various pathogenic bacteria to start from the point of invasion and keep expanding their territory. Syphilis spirochetes, for example, invade from the genitals and then move throughout the body, reaching organs such as the eyes, mouth, bones, and even the brain; Mycobacterium tuberculosis often uses the lungs as a base, conquering the intestines, genitals, and large and small joints; and the hepatitis B virus damages the kidneys in no small number. H. pylori can enter the portal system from the gastric mucosa to reach the liver, where it produces urease with various toxins, causing proliferation of blastocytes and then liver fibrosis, among other things. It can also release cytotoxins, urease, phospholipase, hemolysin, and even toxic ammonia in the gastric mucosa, striking remote targets like mines with the help of flowing blood and lymphatic fluid. What does H. pylori do in the hepatobiliary area? It promotes the development of NAFLD. When a person is infected with H. pylori, the blood levels of triglycerides and LDL increase significantly, and the ratio of HDL to total cholesterol decreases significantly. These changes in lipid metabolism are the basic factors that promote the development of NAFLD. The risk of NAFLD in those with H. pylori infection is 4.68 times higher than in those without infection. Associated with autoimmune liver disease, H. pylori leaves a large amount of genetic material in the liver that can alter the normal immune response process of the liver, thus contributing to the development of autoimmune liver disease. Affecting chronic hepatitis B, C and cirrhosis in the gastric mucosa and liver tissues of patients with these liver diseases, there is not only H. pylori antigen with genetic material, but also a positive rate of H. pylori antibodies in the serum up to 70%, far exceeding the level of healthy people. After anti-H. pylori treatment, patients’ liver cells were repaired and hepatitis symptoms and liver function improved significantly. Aggravated hepatic encephalopathy is a variety of acute and chronic liver disease, patients can develop a variety of neuropsychiatric symptoms, ranging from mild to severe, called hepatic encephalopathy. H. pylori contains high concentrations of urease on the surface and inside the bacterium, which can break down urea to produce ammonia. Ammonia can interfere with the brain’s energy metabolism and is highly toxic to the brain, and ammonia has been thought to be the cause of the development of hepatic encephalopathy. Experimental cirrhotic animals infected with Helicobacter pylori had significantly elevated levels of ammonia in the peripheral and portal blood flowing to the liver. Indirectly, it causes alcoholic liver disease: trying to detoxify the alcohol toxins entering the body depends on the liver’s ethanol dehydrogenase (liver enzymes) to work, and gastric enzymes in the gastric mucosa can share 10% of the detoxification function and are a good helper to reduce the burden of liver enzymes. Helicobacter pylori can disable gastric enzymes, and without the helper liver enzymes are naturally overwhelmed, detoxification capacity is weakened, alcohol toxicity increases, and alcoholic liver disease naturally occurs. Becoming the core of gallstone disease: H. pylori can enter the liver from the duodenum through the sphincter of Addison and also directly from the hepatic portal vein with the lymphatic vessels, reaching the bile through the secretory action. Scientists have characterized the genetic material left behind by gallstone bacteria and found that about 50% of them belong to H. pylori.