• Gianni Testino, Antonio DI Biagio, Sharmila Fagoonee, and Rinaldo Pellicano.
• Unit of Addiction and Hepatology, Alcohological Regional Center, IRCCS Ospedale Policlinico San Martino, ASL3 Liguria, Genoa, Italy - gianni.testino@asl3.liguria.it.
• Minerva Med. 2022 Apr 1; 113 (2): 333-342.

AbstractAngiotensin converting enzyme 2 (ACE2) receptor sites for severe acute respiratory syndrome Coronavirus-2 (SARS-CoV-2), responsible for the disease called COVID-19 are present in the liver, especially in correspondence with cholangiocytes. Liver damage during SARS-CoV-2 infection can be due to several mechanism including direct cytopathic effect, synergy of intestinal damage/liver damage (lipopolysaccharides/Kupfer and other cells interaction), uncontrolled immune reaction (lymphopenia and significant increase in C reactive protein, ferritin, lactate dehydrogenase, D-dimer, interleukin (IL)-6, IL- 10, IL-2, interferon-gamma, etc.), sepsis, drug-induced liver injury, hypoxia and thromboembolic events. An increase in aspartate aminotransferase (AST) from 14 to 58% and alanine transaminase (ALT) from 21 to 76% has been reported. The mean level of AST and ALT has been reported to be higher in patients admitted to the intensive care unit than in those hospitalized in the ordinary hospital unit. The correlation of liver damage with worse prognosis is now a known fact, confirmed by numerous studies, in all pandemic phases. The consumption of alcohol reduces both innate and acquired immune activity and it has been hypothesized that this habit is correlated with liver increase of ACE2 receptors. Furthermore, nonalcoholic and alcoholic steatosis/steatohepatitis is a breeding ground for the development of oxidative stress. In this context, any encounter with SARS-CoV-2 infection can support and aggravate the systemic cytokine tsunami.

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