Author: McConnell, Matthew J; Kondo, Reiichiro; Kawaguchi, Nao; Iwakiri, Yasuko
Title: COVID-19 and liver injury: role of inflammatory endotheliopathy, platelet dysfunction and thrombosis. Cord-id: q370gz3q Document date: 2021_10_18
ID: q370gz3q
Snippet: Liver injury, characterized predominantly by elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT), is a common feature of coronavirus disease-2019 (COVID-19) symptom caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV2). Additionally, SARS-CoV2 infection is associated with acute-on-chronic liver failure in patients with cirrhosis, and has a notably elevated mortality in patients with alcohol-related liver disease compared to other etiologies. Direct viral
Document: Liver injury, characterized predominantly by elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT), is a common feature of coronavirus disease-2019 (COVID-19) symptom caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV2). Additionally, SARS-CoV2 infection is associated with acute-on-chronic liver failure in patients with cirrhosis, and has a notably elevated mortality in patients with alcohol-related liver disease compared to other etiologies. Direct viral infection of the liver with SARS-CoV2 remains controversial, and alternative pathophysiologic explanations for its hepatic effects are an area of active investigation. In this review, we discuss the effects of SARS-CoV2 and the inflammatory environment it creates on endothelial cells and platelets more generally and then with a hepatic focus, presenting vascular inflammation and thrombosis as a potential mechanism of liver injury and liver-related complications in COVID-19.
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