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• W3023107955 abstract "Non-alcoholic fatty liver diseases in patients with COVID-19: A retrospective studyJournal of HepatologyVol. 73Issue 2PreviewLiver injury has been observed in patients with COVID-19, at an incidence ranging from 14–53%.1–3 We examined the liver injury patterns and implication of non-alcoholic fatty liver diseases (NAFLD) on clinical outcomes in Chinese patients with COVID-19. Full-Text PDF No evidence for an increased liver uptake of SARS-CoV-2 in metabolic-associated fatty liver diseaseJournal of HepatologyVol. 73Issue 3PreviewWe read with interest the research article published by Ji and colleagues, in the Journal of Hepatology, showing that patients with metabolic-associated fatty liver disease (MAFLD) have a higher risk of COVID-19 disease progression and higher likelihood of abnormal liver blood tests from admission to discharge than patients without MAFLD.1 Given the absence of data on medical history of these patients, this persistence of liver blood test abnormalities could be either a mere reflection of pre-existing abnormalities related to MAFLD or could alternatively be due to a higher susceptibility of the fatty liver to SARS-CoV-2 infection. Full-Text PDF We read with interest the letter by Biquard et al.[1]Biquard L. Valla D. Rautou P.E. No evidence for an increased liver uptake of SARS-CoV-2 in metabolic associated fatty liver disease.J Hepatol. 2020; 73: 717-718Abstract Full Text Full Text PDF PubMed Scopus (38) Google Scholar In their study, mRNA expression of SARS-CoV-2 infection critical genes, such as angiotensin-converting enzyme 2 (ACE2), transmembrane protease serine 2 (TMPRSS2), phosphatidylinositol 3-phosphate 5-kinase (PIKFYVE) and cathepsin L were found not to be enhanced in patients with metabolic-associated fatty liver disease (MAFLD, previously called non-alcoholic fatty liver disease [NAFLD]) or obesity. This finding is of potential added value to our observation that patients with COVID-19 had worse outcomes if they had underlying MAFLD. Firstly, persistent liver injury observed in our patients was unlikely to be related to the direct cytopathic effects of the virus. Though ideally, one should compare hepatocyte expression of these 4 genes in patients with/without MAFLD that do not have COVID-19. Secondly, this is in keeping with our hypothesis that dysregulated hepatic innate immunity in patients with MAFLD contributes to the pathogenesis of COVID-19. Apart from lung alveolar epithelial cells, the enterocytes of the small intestine also have abundant expression of ACE2 receptors and thus could be another portal of entry for SARS-CoV-2. In keeping with this, gastrointestinal manifestations, such as diarrhoea and abdominal pain occurred in up to one-quarter of patients with COVID-19, without cough. Overall about half of the patients with COVID-19 tested positive for SARS-CoV-2 RNA in faecal and respiratory specimens concomitantly.[2]Cheung K. Hung I.F. Chan P.P. Lung K.C. Tso E. Liu R. et al.Gastrointestinal manifestations of SARS-CoV-2 infection and virus load in fecal samples from the Hong Kong cohort and systematic review and meta-analysis.Gastroenterology. 2020; https://doi.org/10.1053/j.gastro.2020.03.065Abstract Full Text Full Text PDF PubMed Scopus (1047) Google Scholar The liver is enriched with innate immune cells (such as macrophages, natural killer, natural killer T, and γδ T cells)[3]Gao B. Jeong W.I. Tian Z. Liver: an organ with predominant innate immunity.Hepatology. 2008; 47: 729-736Crossref PubMed Scopus (708) Google Scholar and due to its rich blood supply from the small bowel, circulation of the virus via the hepatic reticular system is expected. Hepatic innate immunity populations are potent cytokine producers and there are reports that obesity and NAFLD were associated with increased production of pro-inflammatory cytokines like tumour necrosis factor-α by adipose cells and Kupffer cells.[4]Honce R. Schultz-Cherry S. Impact of obesity on influenza A virus pathogenesis, immune response, and evolution.Front Immunol. 2019; 10: 1071Crossref PubMed Scopus (271) Google Scholar,[5]Lefere S. Tacke F. Macrophages in obesity and non-alcoholic fatty liver disease: crosstalk with metabolism.JHEP Rep. 2019; 1: 30-43Abstract Full Text Full Text PDF PubMed Scopus (144) Google Scholar This may lead to an increased likelihood of symptomatic SARS-CoV-2 infections and the high prevalence of NAFLD in our study populations. Further studies are required to enhance our understanding of the link between the dysregulated hepatic innate immunity and COVID-19. This could be the missing link between the well-recognized risk factors of diabetes mellitus, obesity, chronic liver diseases and age and the outcome of COVID-19 in humans.[6]Ji D. Zhang D. Xu J. Chen Z. Yang T. Zhao P. et al.Prediction for progression risk in patients with COVID-19 pneumonia: the CALL score.Clin Infect Dis. 2020; https://doi.org/10.1093/cid/ciaa414Crossref Scopus (415) Google Scholar This work is funded by the Capital Characteristic Clinic Project of Beijing Municipal Science and Technology Commission (Z181100001718034) and Key Project of Jumei Special Fund for Hepatobiliary Disease Prevention and Treatment (2018JM12603003). DJ, EQ, JX, and DZ treated the patients. DJ, GC, YW and GL processed statistical data and drafted the manuscript. DJ and GL had the idea for and designed the study. We declare no competing interests. Please refer to the accompanying ICMJE disclosure forms for further details. We acknowledge all patients and health-care workers involved in the diagnosis and treatment of patients with COVID-19 in our hospitals. Download .pdf (.2 MB) Help with pdf files disclosures.pdf" @default.
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• W3023107955 title "Reply to: ‘No evidence for an increased liver uptake of SARS-CoV-2 in metabolic-associated fatty liver disease’" @default.
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