Published online Dec 7, 2021. doi: 10.3748/wjg.v27.i45.7855
Peer-review started: May 4, 2021
First decision: June 12, 2021
Revised: June 13, 2021
Accepted: September 8, 2021
Article in press: September 8, 2021
Published online: December 7, 2021
Processing time: 212 Days and 22.6 Hours
Patients with severe liver disease who have been infected with severe acute respiratory syndrome coronavirus-2 (coronavirus disease 2019) frequently develop acute respiratory distress syndrome and multiple organ failure, with a high mortality rate, as a result of the hyper-proinflammatory state known as the cytokine storm. Clinicians must recognize cytokine storms earlier to avoid intensive care admission and multi-organ damage, a critical life-threatening condition with prognostic and therapeutic implications
Core Tip: Understanding the hepatic consequences of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and its molecular mechanism has greatly evolved. Evidence suggests that coronavirus disease 2019 fatalities are primarily due to cytokine storm and abnormal immune function. Throughout the infection, interleukin-6, nuclear factor kappa B, and tumor necrosis factor-alpha are inflammatory cytokines released by SARS-CoV-2-infected macrophages and monocytes that cause acute liver injury. Anti-viral treatment with anti-inflammatory receptors, such as monoclonal antibodies, can be used to reduce the morbidity and mortality associated with SARS-CoV-2 infection.