Journal
JOURNAL OF CLINICAL MEDICINE
Volume 12, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/jcm12052067
Keywords
NAFLD; HCV; HBV; COVID-19; cytokine storm; drug-induced liver injury
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Liver injury is common in SARS-CoV-2 infection, caused by both direct viral infection and cytokine release syndrome. COVID-19 can lead to acute-on-chronic liver failure in patients with cirrhosis. Pro-inflammatory cytokines, hypoxia, and coagulopathy contribute to liver damage in COVID-19.
Liver injury occurs frequently as a consequence of SARS-CoV-2 infection. Direct infection of the liver leads to hepatic impairment with elevated transaminases. In addition, severe COVID-19 is characterized by cytokine release syndrome, which may initiate or exacerbate liver injury. In patients with cirrhosis, SARS-CoV-2 infection is associated with acute-on-chronic liver failure. The Middle East and North Africa (MENA) region is one of the world's regions characterized by a high prevalence of chronic liver diseases. Both parenchymal and vascular types of injury contribute to liver failure in COVID-19, with a myriad of pro-inflammatory cytokines playing a major role in perpetuating liver injury. Additionally, hypoxia and coagulopathy complicate such a condition. This review discusses the risk factors, and the underlying causes of impaired liver functions in COVID-19, with a focus on key players in the pathogenesis of liver injury. It also highlights the histopathological changes encountered in postmortem liver tissues as well as potential predictors and prognostic factors of such injury, in addition to the management strategies to ameliorate liver damage.
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