Published online Apr 14, 2023. doi: 10.3748/wjg.v29.i14.2064
Peer-review started: September 28, 2022
First decision: October 17, 2022
Revised: October 23, 2022
Accepted: March 21, 2023
Article in press: March 21, 2023
Published online: April 14, 2023
Processing time: 196 Days and 20.2 Hours
As of June 2022, more than 530 million people worldwide have become ill with coronavirus disease 2019 (COVID-19). Although COVID-19 is most commonly associated with respiratory distress (severe acute respiratory syndrome), meta-analysis have indicated that liver dysfunction also occurs in patients with severe symptoms. Current studies revealed distinctive patterning in the receptors on the hepatic cells that helps in viral invasion through the expression of angiotensin-converting enzyme receptors. It has also been reported that in some patients with COVID-19, therapeutic strategies, including repurposed drugs (mitifovir, lopinavir/ritonavir, tocilizumab, etc.) triggered liver injury and cholestatic toxicity. Several proven indicators support cytokine storm-induced hepatic damage. Because there are 1.5 billion patients with chronic liver disease world
Core Tip: Several review articles have contributed to the pathophysiology, therapeutic strategies, vaccine development, and clinical trials of coronavirus disease 2019 (COVID-19). Since the liver is the primary site of immune protein synthesis, any liver defect may compromise the immune system. Patients with chronic liver disease are at a higher risk of severe COVID-19. This review article demonstrated the pathophysiology and molecular mechanisms responsible for more severe outcomes in patients with hepatic defects. Further, we critically evaluated the molecular mechanisms concerning hepatotropism in patients with COVID-19, which could lead to the development of new therapeutics.