Author: Portincasa, Piero; Krawczyk, Marcin; Smyk, Wiktor; Lammert, Frank; Di Ciaula, Agostino
Title: COVIDâ€19 and nonalcoholic fatty liver disease: two intersecting pandemics Cord-id: ynflssd7 Document date: 2020_6_26
ID: ynflssd7
Snippet: BACKGROUND: Initial evidence from China suggests that most vulnerable subjects to COVIDâ€19 infection suffer from preâ€existing illness, including metabolic abnormalities. The pandemic characteristics and highâ€lethality rate of COVIDâ€19 infection have raised concerns about interactions between virus pathobiology and components of the metabolic syndrome. METHODS: We harmonized the information from the recent existing literature on COVIDâ€19 acute pandemic and mechanisms of damage in nonâ€
Document: BACKGROUND: Initial evidence from China suggests that most vulnerable subjects to COVIDâ€19 infection suffer from preâ€existing illness, including metabolic abnormalities. The pandemic characteristics and highâ€lethality rate of COVIDâ€19 infection have raised concerns about interactions between virus pathobiology and components of the metabolic syndrome. METHODS: We harmonized the information from the recent existing literature on COVIDâ€19 acute pandemic and mechanisms of damage in nonâ€alcoholic fatty liver disease (NAFLD), as an example of chronic (nonâ€communicable) metabolic pandemic. RESULTS: COVIDâ€19 patients are more fragile with underlying metabolic illness, including hypertension, cardiovascular disease, type 2 diabetes, chronic lung diseases (e.g., asthma, chronic obstructive pulmonary disease, and emphysema), and metabolic syndrome. During metabolic abnormalities, expansion of metabolically active fat (“overfat conditionâ€) parallels chronic inflammatory changes, development of insulin resistance, and accumulation of fat in configuring NAFLD. The deleterious interplay of inflammatory pathways chronically active in NAFLD and acutely in COVIDâ€19 patients, can explain liver damage in a subgroup of patients, and might condition a worse outcome in metabolicallyâ€compromised NAFLD patients. In a subgroup of NAFLD patients, the underlying liver fibrosis might represent an additional and independent risk factor for severe COVIDâ€19 illness, irrespective of metabolic comorbidities. CONCLUSIONS: NAFLD can play a role in the outcome of COVIDâ€19 illness due to frequent association with comorbidities. Initial evidences suggest that increased liver fibrosis in NAFLD might affect COVIDâ€19 outcome. In addition, longâ€term monitoring of postâ€COVIDâ€19 NAFLD patients is advisable, to document further deterioration of liver damage. Further studies are required in this field.
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