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Covid-19 and Liver Injury: Role of Inflammatory Endotheliopathy, Platelet Dysfunction, and Thrombosis.

TLDR
In this article, vascular inflammation and thrombosis were presented as a potential mechanism of liver injury and liver-related complications in coronavirus disease 2019 (COVID-19) symptoms caused by SARS-CoV-2.
Abstract
Liver injury, characterized predominantly by elevated aspartate aminotransferase and alanine aminotransferase, is a common feature of coronavirus disease 2019 (COVID-19) symptoms caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2). Additionally, SARS-CoV-2 infection is associated with acute-on-chronic liver failure in patients with cirrhosis and has a notably elevated mortality in patients with alcohol-related liver disease compared to other etiologies. Direct viral infection of the liver with SARS-CoV-2 remains controversial, and alternative pathophysiologic explanations for its hepatic effects are an area of active investigation. In this review, we discuss the effects of SARS-CoV-2 and the inflammatory environment it creates on endothelial cells and platelets more generally and then with a hepatic focus. In doing this, we present vascular inflammation and thrombosis as a potential mechanism of liver injury and liver-related complications in COVID-19.

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COVID-19 and liver disease: where are we now?

TL;DR: In this article , the authors have shown that patients with end-stage liver disease and COVID-19 are at a higher risk of hospitalization, ventilation and death than those without chronic liver disease.
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Histopathological Features of SARS-CoV-2 in Extrapulmonary Organ Infection: A Systematic Review of Literature

TL;DR: An up-to-date view of histopathological observations of the structural and ultrastructural alterations associated with COVID-19 is provided and may contribute to a better knowledge of the physiopathological bases of this disease.
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Disease Severity in Moderate-to-Severe COVID-19 Is Associated With Platelet Hyperreactivity and Innate Immune Activation

TL;DR: In moderate-to-severe COVID-19, but not in other respiratory diseases, disease severity was associated with platelet hyperreactivity and a typical inflammatory signature, pointing to the importance of antithrombotic therapy for reducing disease severity.
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Scavenging ROS to Alleviate Acute Liver Injury by ZnO‐NiO@COOH

TL;DR: ZnO-NiO@COOH particles are synthetically applied to treat acute liver injury (ALI) as discussed by the authors , which significantly reduce the expression levels of inflammatory factors (i.e., IL 1, IL 6, and TNF-α), macrophage infiltration, and granulocyte activation.
Journal ArticleDOI

Pathogenesis and Mechanisms of SARS-CoV-2 Infection in the Intestine, Liver, and Pancreas

TL;DR: In this paper , the authors reviewed various potential mechanisms of gastrointestinal, liver, and pancreatic injury in the SARS-CoV-2 pandemic and found that angiotensin-converting enzyme 2 (ACE2) receptors serve as the cellular entry mechanism for the virus and these receptors are particularly abundant throughout the GI tract, making the intestine, liver and pancreas potential extrapulmonary sites for infection and reservoirs sites for developing mutations and new variants that contribute to the uncontrolled spread of the disease and resistance to treatments.
References
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Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study.

TL;DR: Wang et al. as discussed by the authors used univariable and multivariable logistic regression methods to explore the risk factors associated with in-hospital death, including older age, high SOFA score and d-dimer greater than 1 μg/mL.
Journal ArticleDOI

COVID-19: consider cytokine storm syndromes and immunosuppression

TL;DR: Re-analysis of data from a phase 3 randomised controlled trial of IL-1 blockade (anakinra) in sepsis, showed significant survival benefit in patients with hyperinflammation, without increased adverse events.
Journal ArticleDOI

Structure, Function, and Antigenicity of the SARS-CoV-2 Spike Glycoprotein.

TL;DR: It is demonstrating that cross-neutralizing antibodies targeting conserved S epitopes can be elicited upon vaccination, and it is shown that SARS-CoV-2 S uses ACE2 to enter cells and that the receptor-binding domains of Sars- coV- 2 S and SARS S bind with similar affinities to human ACE2, correlating with the efficient spread of SATS among humans.
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