Typical acute phase laboratory findings in admitted COVID-19 patients are elevated C - reactive protein and ferritin. Lactate dehydrogenase, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are also often elevated in COVID-19 patients, indicating liver damage. 

SARS-CoV-2 penetrates the cell by attaching to angiotensin-converting enzyme 2 (ACE2). A recent, non-peer-reviewed, article has reported its expression in cholangiocytes.

SARS-CoV infection is accompanied by an abnormal liver function which could be due to viral replication in the liver. 

It has been reported that patients suffering from certain viral infections, like infections caused by hepatitis C and human immunodeficiency viruses, are more predisposed for developing drug-induced liver injury (DILI), particularly when associated with highly active antiretroviral therapy. Recently it was hypothesised that liver impairment in COVID-19 patients could also be drug-related. 

Hydroxychloroquine is applied as an antiviral drug, whose effect on hepatic tissue seems unclear since it is used to treat liver infection with protozoa (i.e. malaria) but cases of fulminant hepatic failure have been reported. Azithromycin may have additional effects to hydroxychloroquine. azithromycin-induced hepatotoxicity only emerges 1–3 weeks after its initiation.

Patients with diabetes type 1 or 2, or developing hypertension, often receive blood pressure reducing ACE inhibitors and angiotensin II type I receptor blockers, which may cause ACE2 overexpression, which may act as at the origin of a higher susceptibility for developing COVID-19. Likewise, these patients frequently suffer from metabolic syndrome, which is a major risk factor for non-alcoholic fatty liver disease (NAFLD). NAFLD can sensitize the liver for hepatotoxicants such as acetaminophen, which is a widely used antipyretic symptomatic drug treatment. 

A recent post-mortem histopathological analysis of a liver biopsy of a COVID-19 patient showed microvesicular liver steatosis. It has also been demonstrated that patients suffering from COVID-19 have increased serum levels of monocyte chemoattractant protein-1 (MCP-1), which is a chemokine known to heighten steatohepatitis. Consequently, predisposing factors for developing steatohepatitis, like intake of steatosis-inducing drugs (e.g. sodium valproate, amiodarone, tamoxifen and methotrexate), could play a role in combined COVID-19 and DILI. 

Thus it is wise to carefully monitor COVID-19 patients for drug treatment that could lead to DILI.

SOURCE-  Arch Toxicol,2020; 94, 1367–1369. https://doi.org/10.1007/s00204-020-02734-1