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©The Author(s) 2023.
World J Hepatol. Jan 27, 2023; 15(1): 41-51
Published online Jan 27, 2023. doi: 10.4254/wjh.v15.i1.41
Published online Jan 27, 2023. doi: 10.4254/wjh.v15.i1.41
Pathophysiologic mechanism of virus | Clinical impact | Considerations for clinical management |
Direct influence of the virus on the liver cells | Significant ACE2 expression in parenchymal liver cells contributing to virulence and further damaging effect of the virus on the cells | Several antiviral agents are approved for treatment of SARS-CoV-2 infection e.g. remdesivir and ritonavir-boosted nirmatrelvir, which can inhibit viral replication. Also, monoclonal antibodies reduce the binding ability of SARS-CoV-2 to the ACE2 receptor |
Drug-induced liver injury | Drug metabolized by cytochrome P-450 could contribute to secondary toxicity of several drugs (paracetamol, antibiotics) | Following the strict rules for avoidance of hepatotoxic drugs if possible. Standard use of hepatoprotective medications |
Results of systemic inflammation response and general hypoxia | The hypoxic damage of hepatocytes, platelet activation, endotheliopathy, immune-mediated response related to liver damage | Administration of corticosteroids and other immunomodulators can reduce or modulate the adverse impact of immune over-response |
Role of immunity | Impaired synthesis of PRRs are toll-like receptors, activation of the pro-inflammatory cytokines such as IL-1, IL-6, TNF-alpha | Use of IL-1 and IL-6 inhibitors, such as anakinra or tocilizumab, as well as Janus kinase inhibitors, such as baricitinib, can decrease the excessive effect of pro-inflammatory cytokines |
- Citation: Liptak P, Nosakova L, Rosolanka R, Skladany L, Banovcin P. Acute-on-chronic liver failure in patients with severe acute respiratory syndrome coronavirus 2 infection. World J Hepatol 2023; 15(1): 41-51
- URL: https://www.wjgnet.com/1948-5182/full/v15/i1/41.htm
- DOI: https://dx.doi.org/10.4254/wjh.v15.i1.41