Abnormal Liver Biochemistry Tests and Acute Liver Injury in COVID-19 Patients: Current Evidence and Potential Pathogenesis

Abstract

Globally, millions of persons have contracted the coronavirus disease 2019 (COVID-19) over the past several months, resulting in significant mortality. Health care systems are negatively impacted including the care of individuals with cancers and other chronic diseases such as chronic active hepatitis, cirrhosis and hepatocellular carcinoma. There are various probable pathogenic mechanisms that have been presented to account for liver injury in COVID-19 patients such as hepatotoxicity cause by therapeutic drugs, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection of the bile duct cells and hepatocytes, hypoxia and systemic inflammatory response. Liver biochemistry tests such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT) and alkaline phosphatase (ALP) are deranged in COVID-19 patients with liver injury. Hepatocellular damage results in the elevation of serum AST and ALT levels in early onset disease while a cholestatic pattern that develops as the disease progress causes higher levels of ALP, GGT, direct and total bilirubin. These liver biochemistry tests are prognostic markers of disease severity and should be carefully monitored in COVID-19 patients. We conducted a systematic review of abnormal liver biochemistry tests in COVID-19 and the possible pathogenesis involved. Significant findings regarding the severity, hepatocellular pattern, incidence and related clinical outcomes in COVID-19 patients are highlighted.

Prevalence of abnormal liver biochemistry and its impact on COVID-19 patients’ outcomes: a single-center Greek study

“…Interestingly, although the ACE2 receptor is highly expressed in bile duct cells, hepatocellular damage with aminotransferase elevation is more frequent, while a lower prevalence of increased bilirubin and cholestatic enzymes is observed [ 6 ]. On the histological level, it has been shown that COVID-19 patients have mild portal and lobular inflammation and steatosis, as well as hepatocellular necrosis attributable mainly to drug-induced liver injury or systemic inflammatory syndrome caused by the SARS-CoV-2 infection, since no viral inclusions were observed [ 7 , 8 ].…”

Laboratory Profile of COVID-19 Patients with Hepatitis C-Related Liver Cirrhosis

“…The presence of a pre-existing liver condition associated with SARS-CoV-2 infection, such as hepatitis C virus (HCV), may be critical for patient prognosis, since chronic hepatitis C continues to be a health burden in a number of European nations. While the precise effect of COVID-19 on the liver is unclear, abnormalities in liver biochemistry are common in COVID-19 cases, occurring in 15-65% of SARS-CoV-2-infected individuals [11].…”

Multiorgan and Vascular Tropism of SARS-CoV-2

“…The ubiquitous distribution of the ACE2 receptors in several tissues may explain the multi-organ dysfunction linked to COVID-19, as well as the inflammatory and immune components [ 4 ]. Hence, the presence of the SARS-CoV-2 genome has already been reported outside the respiratory tract, most notably in the kidney, gastrointestinal system, nervous system and blood vessels, with some arguments in favor of a local replication [ 5 , 6 , 7 , 8 , 9 , 10 , 11 ].…”

“…Viruses 2022, 14, 515 2 of 10 components [4]. Hence, the presence of the SARS-CoV-2 genome has already been reported outside the respiratory tract, most notably in the kidney, gastrointestinal system, nervous system and blood vessels, with some arguments in favor of a local replication [5][6][7][8][9][10][11].…”