Liver injury in COVID-19: two clinical cases

Abstract

COVID-19 (coronavirus disease 2019, a disease caused by a new coronavirus 2019) continues to threaten world public healthcare. Epidemiological data indicate that patients with metabolic disorders and chronic illnesses are most susceptible to SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). Potential factors for organ involvement include systemic hyperimmune-mediated inflammation due to the “cytokine storm”, cytopathic effects, hypoxia, drug toxicities, etc. In addition, SARS-CoV-2, by interaction with ACE2 (angiotensin-converting enzyme 2) receptors in the vasculature endothelium results in endothelial dysfunction, increased permeability, microcirculatory abnormalities, vascular thrombophilia and thrombus formation. The diagnosis of COVID-19 is confirmed by detection of SARS-CoV-2 RNA in biological samples and serum antibodies. The infection is associated with leukopenia and thrombocytopenia, increased С-reactive protein, ferritin, lactate dehydrogenase, and D-dimer. Abnormalities in functional liver tests seen in COVID-19 are associated with progression and severity of the infection. The mechanism of direct cytotoxicity due to active SARS-CoV-2 replication in hepatocytes are not fully understood and is likely to be related to potential proliferation of hepatocytes, liver injury in response to systemic inflammation, and development of drug hepatic toxicity. We present a clinical case of drug-induced hepatitis in a patient with COVID-19 treated with tocilizumab, an inhibitor of interleukin 6 receptors. Prolonged increase in blood enzymes after treatment cessation is likely related to a longer half-elimination time of tocilizumab, which affects the oxidation-reduction system of liver cytochromes. Patients with chronic liver disorders are more vulnerable to clinical sequelae of СOVID-19, while the infection is frequently associated with hypoxia and hypoxemia due to severe pneumonia or the “cytokine storm”. In addition, patients who have been diagnosed with liver cirrhosis are at high risk of morbidity and mortality due to their higher proneness to infections, first of all, due to systemic immune deficiency that was demonstrated in the second clinical case. Decompensated liver cirrhosis is related not only to a higher risk of more severe COVID-19, but also to progression of chronic liver disease as such. To achieve effective results of causal and nosotropic therapy for COVID-19, it is highly significant to provide thorough clinical monitoring, tailored approach to the treatment of each patient with consideration of their comorbidities, immune status, and drug interactions.