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?