Discussion
Liver function affected by SARS-COV-2 (9,10). However, there are currently few investigations on the pathogenesis of liver damage in patients with COVID-19. The liver biochemistry abnormalities in COVID-19 patients are moderate (1-2 times the upper limit of normal) increases of serum ALT and AST values, observed in an estimated 29-39% and 38-63% of patients, respectively (12–14). There is no consensus on the association between liver enzyme level elevations and mortality in COVID-19 patients. In this regard, some studies have reported that there is no apparent association (15,16).
On the contrary, several studies have revealed that elevations in the AST and ALT levels that are more than five times the upper limit of normal are linked with an increased risk of mortality (11,17–19). Here, our patient on day 11 had a higher level of AST (105 times the upper limit of normal) and ALT (more than 62 times the upper limit of normal). A tentative explanation is that patients might have a robust immune response. Another reason is that aggressive therapies and anti-viral medication may lead to liver damage (20). It is noteworthy that the possibility of drug-induced liver damage due to hepatotoxicity is associated with drugs used in the treatment of COVID-19 such as lopinavir, ritonavir, and hydroxychloroquine should be taken into consideration by clinicians (6).
It is crucial to develop effective treatment regimens for COVID-19 patients with the fewest side effect on the liver. Further observations will be required to understand the hepatic SARS-CoV-2 infection comprehensively. There is a salient question in this regard. Is the drastic increase in serum AST and ALT caused by hepatic SARS-CoV-2 infection?