COVID-19 and Liver Dysfunction: Current Insights and Emergent Therapeutic Strategies

Original Article: Gong Feng, Kenneth I. Zheng, Qin-Qin Yan, Rafael S. Rios, Giovanni Targher, Christopher D. Byrne, Sven Van Poucke, Wen-Yue Liu and Ming-Hua Zheng, COVID-19 and Liver Dysfunction: Current Insights and Emergent Therapeutic Strategies, J Clin Transl Hepatol.

Author of summary: Gabriella Assante; Reviewer: Giulia Peserico

This is an overview of liver damage characteristics during COVID19 pandemic in 14 Chinese studies, by reporting demographic and clinical analysis, potential mechanism and treatments for liver dysfunction related to Sars-CoV-2 infection.

Between December 11th2019 and February 20th2020, along with severe pneumonia and related symptoms, Covid19+ patients have also described liver damage as consequence of increase AST and/or ALT values. In the specific, studies performed in Wuhan and Zhejiang Province, have reported that men were more infected than women. Besides, in Wuhan from 24.1% to 36.6% of infected patients had increased levels of AST compared to 16.1 % in Zhejiang Province. As the proportion of people infected with AST increment, is greater in Wuhan rather than in the province, this leads to think that the viral load of COVID19 in exposed patients where the infection began was higher.

Although lungs are the main target of SARS-CoV2, ACE2 have been found high expressed also in the bile duct 20 times more than in the hepatocytes. As consequence, the liver dysfunction reported several times in COVI19+ patients, is may due to a secondary liver damage. For instance, during the treatment of SARS-CoV-2 infection, many drugs such as Lopinavir, Abidol, Oseltamivir are used along with antipyretic agents containing acetaminophen which is known to induce liver damage when ingested between 7.5 to 10g. On the other hands, the virus leads to multiple proinflammatory signals as TLRs and T Lymphocytes. The activated T lymphocytes attack the infected body cells, leading to their apoptosis and necrosis, until T lymphocytes are depleted. Damage-related pattern molecules released by dead infected cells, can further amplify some inflammatory signals, such as TLRs. T-lymphocyte depletion cannot control viral and bacterial infections, thereby activating multiple inflammatory signaling pathways, which lead to macrophage activation and secondary inflammatory reactions. As result, the organ failure could be due to the inflammatory storm where a huge number of Cytokines are released causing cell damage.  Moreover, also the oxygen reduction and the lipid accumulation in the hepatocytes, as consequence of hypoxia and shock induced by COVID19 complication, can lead to a liver damage though the activation of proinflammatory factors.

As ACE2 is widely expressed not only in lung tissue but also in GI tract, vascular and arterial cells, oral mucosa basal cells as well as liver, it could be potential target treatment in COVID19+ patents by activating ACE2/Ang1-7/ Mas or inhibiting ACE/Ang II/AT1R pathways.


The cause of liver damage in CVOID19+ patient needs to be further investigated as wells as new drugs for patients with pre-existing liver disease in order to attenuate the worse impact of SarS-CoV-2 infection related liver injury/dysfunction.

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