COVID-19 and the liver

J Hepatol. 2020 Nov;73(5):1231-1240. doi: 10.1016/j.jhep.2020.06.006. Epub 2020 Jun 15.

Abstract

The current coronavirus disease 2019 (COVID-19) pandemic, caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has become a major public health crisis over the past few months. Overall case fatality rates range between 2-6%; however, the rates are higher in the elderly and those with underlying comorbidities like diabetes, hypertension and heart disease. Recent reports showed that about 2-11% of patients with COVID-19 had underlying chronic liver disease. During the previous SARS epidemic, around 60% of patients were reported to develop various degrees of liver damage. In the current pandemic, hepatic dysfunction has been seen in 14-53% of patients with COVID-19, particularly in those with severe disease. Cases of acute liver injury have been reported and are associated with higher mortality. Hepatic involvement in COVID-19 could be related to the direct cytopathic effect of the virus, an uncontrolled immune reaction, sepsis or drug-induced liver injury. The postulated mechanism of viral entry is through the host angiotensin-converting enzyme 2 (ACE2) receptors that are abundantly present in type 2 alveolar cells. Interestingly, ACE2 receptors are expressed in the gastrointestinal tract, vascular endothelium and cholangiocytes of the liver. The effects of COVID-19 on underlying chronic liver disease require detailed evaluation and, with data currently lacking, further research is warranted in this area.

Keywords: ACE2; COVID-19; Liver; SARS-CoV-2.

Publication types

  • Review

MeSH terms

  • Angiotensin-Converting Enzyme 2
  • Betacoronavirus / physiology*
  • COVID-19
  • Comorbidity
  • Coronavirus Infections* / epidemiology
  • Coronavirus Infections* / physiopathology
  • Humans
  • Liver / metabolism
  • Liver Diseases* / epidemiology
  • Liver Diseases* / metabolism
  • Liver Diseases* / virology
  • Pandemics*
  • Peptidyl-Dipeptidase A / metabolism*
  • Pneumonia, Viral* / epidemiology
  • Pneumonia, Viral* / physiopathology
  • Risk Factors
  • SARS-CoV-2
  • Severity of Illness Index

Substances

  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2