Clinical Features of COVID-19-Related Liver Damage

Fan, Zhichao; Chen, Liping; Li, Jun; Tian, Cheng; Zhang, Yajun; Huang, Shaoping; Liu, Zhanju; Cheng, Jun

doi:10.2139/ssrn.3546077

Cited by 83 publications

(132 citation statements)

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“…ACE2 is localized in various human tissues including the liver [8]. Several clinical studies have shown biochemical evidence of liver injuries [14,15]. However, only limited histologic hepatic abnormalities are noted in our patients.…”

Section: Discussionmentioning

confidence: 69%

Pathological study of the 2019 novel coronavirus disease (COVID-19) through postmortem core biopsies

et al. 2020

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Data on pathologic changes of the 2019 novel coronavirus disease are scarce. To gain knowledge about the pathology that may contribute to disease progression and fatality, we performed postmortem needle core biopsies of lung, liver, and heart in four patients who died of COVID-19 pneumonia. The patients' ages ranged from 59 to 81, including three males and one female. Each patient had at least one underlying disease, including immunocompromised status (chronic lymphocytic leukemia and renal transplantation) or other conditions (cirrhosis, hypertension, and diabetes). Time from disease onset to death ranged from 15 to 52 days. All patients had elevated white blood cell counts, with significant rise toward the end, and all had lymphocytopenia except for the patient with leukemia. Histologically, the main findings are in the lungs, including injury to the alveolar epithelial cells, hyaline membrane formation, and hyperplasia of type II pneumocytes, all components of diffuse alveolar damage. Consolidation by fibroblastic proliferation with extracellular matrix and fibrin forming clusters in airspaces is evident. In one patient, the consolidation consists of abundant intra-alveolar neutrophilic infiltration, consistent with superimposed bacterial bronchopneumonia. The liver exhibits mild lobular infiltration by small lymphocytes, and centrilobular sinusoidal dilation. Patchy necrosis is also seen. The heart shows only focal mild fibrosis and mild myocardial hypertrophy, changes likely related to the underlying conditions. In conclusion, the postmortem examinations show advanced diffuse alveolar damage, as well as superimposed bacterial pneumonia in some patients. Changes in the liver and heart are likely secondary or related to the underlying diseases.

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Section: Discussionmentioning

confidence: 69%

Pathological study of the 2019 novel coronavirus disease (COVID-19) through postmortem core biopsies

et al. 2020

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“…[4][5][6] In a study of 148 infected patients in Shanghai, 50.7% (75/148) had abnormal liver function tests (LFTs). 4 However, 29.7% (44/148) had abnormal LFTs before admission including eight patients with known chronic hepatitis B and C. Pre-existing liver disease in the remaining 36 patients before admission was indeterminate. 14.9% (22/148) of patients with normal tests on admission developed abnormal LFTs, although antiviral therapy may have contributed to this.…”

Section: Covid-19 In Gastroenterology: a Clinical Perspectivementioning

confidence: 99%

COVID-19 in gastroenterology: a clinical perspective

Ong

Young

Ong

2020

Gut

116

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“…The clinical presentation and transmission of COVID-19 is complex. Common symptoms include fever, cough, shortness of breath, chest pain, malaise, fatigue, headache, myalgias, anosmia, and diarrhea, while laboratory and radiographic findings include lymphopenia and ground-glass opacities on chest imaging, respectively [1][2][3][4][5][6][7][8] . Of an initial cohort of 1,099 hospitalized patients diagnosed with COVID-19, many developed diffuse alveolar damage (DAD) 1 , pneumonia (79.1%), not infrequently complicated by acute respiratory distress syndrome (ARDS, 3.4%), and shock (1.0%), with 5.0% of patients requiring ICU admission and 2.2% requiring ventilation 4 .…”

Section: Introductionmentioning

confidence: 99%

“…Of an initial cohort of 1,099 hospitalized patients diagnosed with COVID-19, many developed diffuse alveolar damage (DAD) 1 , pneumonia (79.1%), not infrequently complicated by acute respiratory distress syndrome (ARDS, 3.4%), and shock (1.0%), with 5.0% of patients requiring ICU admission and 2.2% requiring ventilation 4 . As the number of patients has surged, multi-system pathologies have been increasingly described, including kidney injury 9 , liver injury, gastrointestinal symptoms 4 , cardiac injury and dysfunction 2,5,10 , and multiorgan failure [1][2][3][4] . In addition to nasal and throat secretions, SARS-CoV-2 RNA has also been detected in saliva and stool specimens 10,11 , suggesting possible alternative routes of transmission beyond respiratory droplets 12, 13 .…”

Section: Introductionmentioning

confidence: 99%

Integrated analyses of single-cell atlases reveal age, gender, and smoking status associations with cell type-specific expression of mediators of SARS-CoV-2 viral entry and highlights inflammatory programs in putative target cells

Muus

Luecken

Eraslan

et al. 2020

Preprint

250

326

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The COVID-19 pandemic, caused by the novel coronavirus SARS-CoV-2, creates an urgent need for identifying molecular mechanisms that mediate viral entry, propagation, and tissue pathology. Cell membrane bound angiotensin-converting enzyme 2 (ACE2) and associated proteases, transmembrane protease serine 2 (TMPRSS2) and Cathepsin L (CTSL), were previously identified as mediators of SARS-CoV2 cellular entry. Here, we assess the cell type-specific RNA expression of ACE2, TMPRSS2, and CTSL through an integrated analysis of 107 single-cell and single-nucleus RNA-Seq studies, including 22 lung and airways datasets (16 unpublished), and 85 datasets from other diverse organs. Joint expression of ACE2 and the accessory proteases identifies specific subsets of respiratory epithelial cells as putative targets of viral infection in the nasal passages, airways, and alveoli. Cells that co-express ACE2 and proteases are also identified in cells from other organs, some of which have been associated with COVID-19 transmission or pathology, including gut enterocytes, corneal epithelial cells, cardiomyocytes, heart pericytes, olfactory sustentacular cells, and renal epithelial cells. Performing the first meta-analyses of scRNA-seq studies, we analyzed 1,176,683 cells from 282 nasal, airway, and lung parenchyma samples from 164 donors spanning fetal, childhood, adult, and elderly age groups, associate increased levels of ACE2, TMPRSS2, and CTSL in specific cell types with increasing age, male gender, and smoking, all of which are epidemiologically linked to COVID-19 susceptibility and outcomes. Notably, there was a particularly low expression of ACE2 in the few young pediatric samples in the analysis. Further analysis reveals a gene expression program shared by ACE2 + TMPRSS2 + cells in nasal, lung and gut tissues, including genes that may mediate viral entry, subtend key immune functions, and mediate epithelial-macrophage cross-talk. Amongst these are IL6, its receptor and co-receptor, IL1R, TNF response pathways, and complement genes. Cell type specificity in the lung and airways and smoking effects were conserved in mice. Our analyses suggest that differences in the cell type-specific expression of mediators of SARS-CoV-2 viral entry may be responsible for aspects of COVID-19 epidemiology and clinical course, and point to putative molecular pathways involved in disease susceptibility and pathogenesis.

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Clinical Features of COVID-19-Related Liver Damage

Cited by 83 publications

References 0 publications

Pathological study of the 2019 novel coronavirus disease (COVID-19) through postmortem core biopsies

Pathological study of the 2019 novel coronavirus disease (COVID-19) through postmortem core biopsies

COVID-19 in gastroenterology: a clinical perspective

Integrated analyses of single-cell atlases reveal age, gender, and smoking status associations with cell type-specific expression of mediators of SARS-CoV-2 viral entry and highlights inflammatory programs in putative target cells

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