Published online Dec 28, 2022. doi: 10.3748/wjg.v28.i48.6875
Peer-review started: September 5, 2022
First decision: November 5, 2022
Revised: November 7, 2022
Accepted: November 27, 2022
Article in press: November 27, 2022
Published online: December 28, 2022
Processing time: 112 Days and 16.1 Hours
The coronavirus disease 2019 (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Hepatic involvement is common in SARS-CoV-2-infected individuals. It is currently accepted that the direct and indirect hepatic effects of SARS-CoV-2 infection play a significant role in COVID-19. In individuals with pre-existing infectious and non-infectious liver disease, who are at a remarkably higher risk of developing severe COVID-19 and death, this pathology is most medically relevant. This review emphasizes the current pathways regarded as contributing to the gastrointestinal and hepatic ailments linked to COVID-19-infected patients due to an imbalanced interaction among the liver, systemic inflammation, disrupted coagulation, and the lung.
Core Tip: Clinical manifestations of coronavirus disease 2019 (COVID-19) may be triggered by the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in the liver. SARS-CoV-2 genomic RNA and its replicative intermediates were found in liver tissues. SARS-CoV-2 causes direct cholangiocyte damage. Systemic inflammation due to COVID-19 correlated with the degree of acute liver injury as revealed by the rise in aspartate aminotransferase levels. SARS-CoV-2 infection increased the risk of morbidity and mortality in patients with a history of advanced liver disease.