Helicobacter infection and hepatobiliary cancer: epidemiology and pathogenesis

Abstract

Hepatobiliary cancer is one of the leading causes of cancer death and a major public health problem in both developed and developing countries. Chronic infections are common risk factors for cancer. Animal studies have shown that Helicobacter pylori (H. pylori) infection can cause hepatitis, colitis, and liver cancer in susceptible individuals. Data from clinical and experimental studies point to the involvement of the gastrointestinal microbiota in the pathogenesis of the non-alcoholic fatty liver disease, including H. pylori infection. The researchers included H. pylori infection in the list of etiopathogenetic factors of primary biliary cholangitis due to the detection of its DNA in the liver tissue and antibodies to H. pylori in the bile and serum of patients with primary biliary cholangitis. A growing body of evidence suggests that H. pylori may be a risk factor for the development of liver cirrhosis and hepatocellular carcinoma in patients with viral hepatitis B and C. The contribution of H. pylori infection to the development of hepatic encephalopathy and hyperammonemia has been identified. H. pylori infection is associated with liver inflammation, fibrosis, and necrosis by inducing the synthesis of systemic inflammatory mediators and increasing intestinal permeability. Along with these consequences, bacterial translocation through the biliary tract can also lead to direct liver damage, predisposing or even triggering the carcinogenic process. The study of subspecies of Helicobacter shows that they can lead to the development of not only hepatocellular carcinoma but also other malignant neoplasms of the hepatobiliary system. This review presents current data on the epidemiology and mechanisms of the influence of H. pylori infection on malignant neoplasms of the hepatobiliary tract, with an emphasis on possible prevention strategies.