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Review
. 2021;11(1):11.
doi: 10.1186/s43066-021-00082-y. Epub 2021 Jan 27.

The risks of liver injury in COVID-19 patients and pharmacological management to reduce or prevent the damage induced

Affiliations
Review

The risks of liver injury in COVID-19 patients and pharmacological management to reduce or prevent the damage induced

Antonio Vitiello et al. Egypt Liver J. 2021.

Abstract

Background: The global pandemic COVID-19 caused by the new coronavirus SARS-CoV-2 has already caused about 1.4 million deaths, and to date, there are no effective or direct antiviral vaccines. Some vaccines are in the last stages of testing. Overall mortality rates vary between countries, for example, from a minimum of 0.05% in Singapore to a maximum of 9.75 in Mexico; however, mortality and severity of COVID-19 are higher in the elderly and in those with comorbidities already present such as diabetes, hypertension, and heart disease.

Main text: Recent evidence has shown that an underlying liver disease can also be a risk factor, and SARS-CoV-2 itself can cause direct or indirect damage to liver tissue through multisystem inflammation generated especially in the more severe stages. In the current pandemic, liver dysfunction has been observed in 14-53% of patients with severe COVID-19. In addition, drugs administered during infection may be an additional factor of liver damage. The mechanism of cellular penetration of the virus that occurs by viral entry is through the receptors of the angiotensin 2 conversion enzyme (ACE-2) host that are abundantly present in type II pneumocytes, heart cells, but also liver cholangiocytes.

Conclusion: In this manuscript, we describe the clinical management aimed at preserving the liver or reducing the damage caused by COVID-19 and anti-COVID-19 drug treatments.

Keywords: COVID-19-SARS-CoV-2; Liver damage; Liver fibrosis; Obeticholic acid.

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Conflict of interest statement

Competing interestsNone of the authors has conflicts of interest to disclose.

Figures

Fig. 1
Fig. 1
COVID-19 can cause direct liver damage, either through ACE-2 entry or indirect through generalized inflammation caused by the cytokine cascade. In addition, the administration of drugs with DILI potential may be an additional cause of liver damage

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