During the clinical course of coronavirus disease 2019 (COVID‐19), it has been observed that hepatic injury occurs in a significant proportion of patients, particularly in those with severe or critical illness. Mild increase in sinusoidal lymphocytic infiltration, sinusoidal dilatation, steatosis and multifocal hepatic necrosis are the pathologic changes reported. Direct viral‐induced cellular injuries and potential hepatotoxicity from therapeutic drugs are two likely underlying mechanisms. In addition, the pre‐existing chronic liver disease exacerbated during COVID‐19, and COVID‐19‐related hyperinflammatory reactions may contribute to liver injury as well. Further studies of additional autopsy cases will help clarifying these possibilities.

The largest study on COVID-19 to date1 showed that the prevalence of elevated aminotransferases and bilirubin in people faring worst was at least double that of others. Although clinically significant liver dysfunction was not quantified, this and other studies have led some to suggest that this finding might present clinical challenges.2Close inspection of the available data supports a higher prevalence of abnormal aminotransferase levels in severe COVID-19 disease, but these studies actually suggest that clinically significant liver injury is uncommon, even when data for the most severely ill patients are selected (table).

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