Background: Initial evidence from China suggests that most vulnerable subjects to COVID-19 infection suffer from pre-existing illness, including metabolic abnormalities. The pandemic characteristics and high-lethality rate of COVID-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 COVID-19 acute pandemic and mechanisms of damage in non-alcoholic fatty liver disease (NAFLD), as an example of chronic (non-communicable) metabolic pandemic.
Results: COVID-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 condition") 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 COVID-19 patients, can explain liver damage in a subgroup of patients, and might condition a worse outcome in metabolically-compromised NAFLD patients. In a subgroup of NAFLD patients, the underlying liver fibrosis might represent an additional and independent risk factor for severe COVID-19 illness, irrespective of metabolic comorbidities.
Conclusions: NAFLD can play a role in the outcome of COVID-19 illness due to frequent association with comorbidities. Initial evidences suggest that increased liver fibrosis in NAFLD might affect COVID-19 outcome. In addition, long-term monitoring of post-COVID-19 NAFLD patients is advisable, to document further deterioration of liver damage. Further studies are required in this field.
Keywords: SARS-CoV-2; fatty liver; mitochondria; nitrosative stress; oxidative stress.
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