2020
DOI: 10.1016/j.jhep.2020.06.021
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Hepatocellular type II fibrinogen inclusions in a patient with severe COVID-19 and hepatitis

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Cited by 12 publications
(11 citation statements)
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“…Direct infection of liver cell types including cholangiocytes[ 28 , 29 ] and hepatocytes[ 30 ] has been suggested, but the latter requires confirmatory testing since single cell RNA sequencing has shown relatively sparse hepatocyte expression of the receptors necessary for viral uptake[ 31 ]. However, given the profound multi-systemic involvement of COVID-19, particularly in the severe and critical forms of disease, liver injury is likely to be multifactorial with contributions from systemic inflammation, intrahepatic immune activation, microvascular thrombosis, perturbations of the gut-liver-axis, and drug toxicity[ [32] , [33] , [34] , [35] , [36] ]. In our cohort, patients who suffered acute hepatic decompensation had a 2-fold increased rate of mortality compared to those without and case fatality strongly correlated with degree of organ failure.…”
Section: Discussionmentioning
confidence: 99%
“…Direct infection of liver cell types including cholangiocytes[ 28 , 29 ] and hepatocytes[ 30 ] has been suggested, but the latter requires confirmatory testing since single cell RNA sequencing has shown relatively sparse hepatocyte expression of the receptors necessary for viral uptake[ 31 ]. However, given the profound multi-systemic involvement of COVID-19, particularly in the severe and critical forms of disease, liver injury is likely to be multifactorial with contributions from systemic inflammation, intrahepatic immune activation, microvascular thrombosis, perturbations of the gut-liver-axis, and drug toxicity[ [32] , [33] , [34] , [35] , [36] ]. In our cohort, patients who suffered acute hepatic decompensation had a 2-fold increased rate of mortality compared to those without and case fatality strongly correlated with degree of organ failure.…”
Section: Discussionmentioning
confidence: 99%
“…Given the profound multi-systemic involvement of COVID-19, particularly in the severe and critical forms of disease, liver injury is likely to be multifactorial with contributions from systemic inflammation, intrahepatic immune activation, microvascular thrombosis, hepatic congestion, perturbations of the gut-liver-axis, as well as drug toxicity. [45] , [46] , [47] , [48] The prognostic significance of deranged biochemistry in COVID-19 remains unresolved 49 ; some groups have demonstrated a strong correlation with duration of hospitalisation, organ failure and intensive care unit admission 37 , 41 , 50 whilst others have failed to observe any significant associations with outcome. 39 , 40 …”
Section: Liver Injury Secondary To Covid-19mentioning
confidence: 99%
“…The increased fibrin formation and breakdown correlated with the high level of D-dimers observed in the COVID-19 patients with the worst outcomes . The increasing levels of FGG in severe cases might be due to liver injury, impairing hepatic fibrinogen secretion with acquired fibrinogen storage disease (Fraga, 2020).…”
Section: Ll Open Access Isciencementioning
confidence: 99%