The 2019 outbreak of coronavirus disease (COVID-19) caused by severe acute coronavirus 2 respiratory syndrome (SARS-CoV-2) has been a  global concern since December 2019. Although most patients with COVID-19  have mild clinical manifestations, in about 5% of these patients the disease eventually progresses to severe lung injury or even multiple organ dysfunction. This situation presents various problems for hepatology. In the context of liver damage in patients with COVID-19, several key problems need to be addressed. For example, it is important to determine whether a SARS-CoV-2 can directly enter the liver, especially when it appears that ACE2 is marginally expressed in hepatocytes. In addition, the mechanisms underlying liver dysfunction in patients with COVID-19 are multifactorial and are associated with hyperinflammation, dysregulated immune responses, abnormal coagulation, and drugs. The  article describes the  potential pathogenesis of  liver damage associated with COVID-19. Histopathological evidence suggests a marked disruption of the intrahepatic network of blood vessels secondary to systemic changes caused by a virus that can trigger a coagulation cascade and damage the endothelial layer of blood vessels. There is also a clinical case of polyethylene damage to the liver in a young man who led to death. Against the background of infection COVID-19 he developed massive thrombosis of the liver vessels, followed by the development of necrosis — fibrosis — cirrhosis — acute liver failure, which caused death.