2020
DOI: 10.14218/jcth.2020.00018
|View full text |Cite
|
Sign up to set email alerts
|

COVID-19 and Liver Dysfunction: Current Insights and Emergent Therapeutic Strategies

Abstract: The outbreak of coronavirus disease 2019 , caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has attracted increasing worldwide attention. Cases of liver damage or dysfunction (mainly characterized by moderately elevated serum aspartate aminotransferase levels) have been reported among patients with COVID-19. However, it is currently uncertain whether the COVID-19related liver damage/dysfunction is due mainly to the viral infection per se or other coexisting conditions, such as the us… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

4
380
0
26

Year Published

2020
2020
2022
2022

Publication Types

Select...
10

Relationship

2
8

Authors

Journals

citations
Cited by 369 publications
(417 citation statements)
references
References 42 publications
4
380
0
26
Order By: Relevance
“…This suggests IL-6 is a key proinflammatory factor that triggers the inflammatory "storm" in patients. [13] In MAFLD patients, particularly those with obesity, increased inflammatory activity in the liver and visceral fat is independently correlated with increased levels of IL-6, [14] which might have an additive/synergistic role in promoting greater severity of COVID-19. It is conceivable that the secretion of hepatokines for example, reduced adiponectin or the altered secretion of inflammatory lipid mediators in obese patients with MAFLD, [15] may also contribute to the current observations.…”
Section: Discussionmentioning
confidence: 99%
“…This suggests IL-6 is a key proinflammatory factor that triggers the inflammatory "storm" in patients. [13] In MAFLD patients, particularly those with obesity, increased inflammatory activity in the liver and visceral fat is independently correlated with increased levels of IL-6, [14] which might have an additive/synergistic role in promoting greater severity of COVID-19. It is conceivable that the secretion of hepatokines for example, reduced adiponectin or the altered secretion of inflammatory lipid mediators in obese patients with MAFLD, [15] may also contribute to the current observations.…”
Section: Discussionmentioning
confidence: 99%
“…It binds to a variety number of eukaryotic and prokaryotic pathogens, facilitating complement activation through classical pathway [8], indicating immune activation, lymphocyte infiltration, immune molecules consumption and inflammation outbreak. Clinically, increased CRP levels might be early indicators of nosocomial infections in COVID-19 patients who were slow to recover, and might aid physicians to administer empirical antibiotics treatment early to prevent worsened outcome [9,10].…”
Section: Table 1 Baseline Characteristics Of Included Patients Stratmentioning
confidence: 99%
“…It remains unclear whether liver injury is caused by the virus itself or reflects a severe inflammatory response with liver damage. 28 SARS-CoV-2 may directly infect liver cells as the receptor of the virus, angiotensin-converting enzyme 2 (ACE2), is expressed by liver and bile duct cells. 29 Data from two independent cohorts revealed ACE2 expression in 2.6% of hepatocytes and 59.7% of cholangiocytes, suggesting that SARS-CoV-2 might directly bind to ACE2-positive cholangiocytes to dysregulate liver function.…”
Section: Covid -19 and Hepati C Inj Urymentioning
confidence: 99%