The chapter is a review of current knowledge on the impact of H. pylori infection on the clinical course of patients with various forms of liver damage. H. pylori infection is found in 50–90% of the world population. The bacteria not only mainly contribute to occurrence of gastric mucosa inflammation but also to gastric ulcer and cancer. H. pylori contains an active antioxidative system, which not only neutralizes free radicals but also synthesizes specific VacA toxin, which leads to destruction and apoptosis of the cells. A specific system of bacterial CagA genes has a special role in carcinogenesis. There is an increasing number of reports describing lesions in the circulatory system, pancreas, or the skin, connected with H. pylori infection. Liver colonization by H. pylori happens after transmission of the bacteria from the stomach, with blood, through the portal vein or directly through the bile ducts. The bacteria promote liver function deterioration in the course of toxic injury, autoimmune inflammation, chronic HBV, and HCV infection. Infections among people with liver cirrhosis are especially dangerous. In this group of patients, H. pylori infection may significantly worsen liver function, leading to hyperammonemia, increased portal pressure, and development of esophageal varices. Thus, testing for and treating this infection among patients with liver cirrhosis is especially important.
Part of the book: Helicobacter Pylori