Published online Apr 28, 2023. doi: 10.3748/wjg.v29.i16.2397
Peer-review started: October 31, 2022
First decision: February 2, 2023
Revised: February 17, 2023
Accepted: April 7, 2023
Article in press: April 7, 2023
Published online: April 28, 2023
Core Tip: Following respiratory system, liver is the second most involved organ in coronavirus disease 2019 (COVID-19). Besides the well-observed cholangiocyte tropism, typical severe acute respiratory distress syndrome corona virus-2 (SARS-CoV-2) Lesions indicated by ultrastructural and histological evidence, identification of replicating SARS-CoV-2, S and nucleocapsid proteins RNAs within hepatocytes, as well as intrahepatic virus observation by electron microscopy and in-situ hybridization, converge to the conclusion that SARS-CoV-2 may also be hepatotropic. Most prevalent mechanisms of COVID-19-related liver injury are hypercytokinemia with “bystander hepatitis”, cytokine storm syndrome with subsequent oxidative stress, endotheliopathy and immuno-thromboinflammation. Depending on the grade of their abnormalities, increased serum aspartate aminotransferase, (mostly peak) alanine aminotransferase, alkaline phosphatase, total bilirubin, inflammatory markers (C-reactive protein, ferritin, interleukin-6, -10) and decreased albumin levels are independent discriminators of COVID-19 severity and mortality. Age, male gender, chronic liver disease, liver cirrhosis, obesity, diabetes, and non-alcoholic fatty liver disease are independent prognostic factors of unfavorable COVID-19 outcomes.