COVIDâ€19 and nonâ€alcoholic fatty liver disease
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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.
The harmonized 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.
COVIDâ€19â€infected 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 COVIDâ€19â€infected 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 patients with NAFLD, the underlying liver fibrosis might represent an additional and independent risk factor for severe COVIDâ€19 illness, irrespective of metabolic comorbidities.
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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Regards,
Jessica Celina
Managing Editor
Pancreatic disorders and Therapy