The coronavirus disease 2019 (COVID-19) pandemic imposed arestructuring of global health systems by rethinking spaces used for the care of these patients and the additions of intensive care, infectious diseases and pneumology departments. This paper provides evidence on the presence of severe acute respiratory syndrome coronavirus 2 in hepatocytes and its direct cytopathic activity, as well as the degree of liver damage due to drug toxicity, inflammation and hypoxia in COVID-19. A review of clinical trials has quantified liver damage through both pathology and biochemistry studies. Additionally, we briefly present the results of a study conducted in our clinic on 849 patients admitted for COVID-19 treatment, of which 31 patients had pre-existing chronic liver disease and 388 patients had values above the normal limit for alanine aminotransferase, aspartate aminotransferase, and total bilirubin. It was observed that patients with abnormal liver tests were significantly statistically older, had more comorbidities and had a higher percentage of unfavourable evolution (death or transfer to intensive care). The conclusion of this paper is that the main causes of liver damage are direct viral aggression, coagulation dysfunction and endothelial damage, and patients with impaired liver function develop more severe forms of COVID-19 which requires special care by a multidisciplinary team that includes a hepatologist.
Keywords: Biochemical changes; COVID-19; Cytopathic effect; Drug toxicity; Hyper-inflammatory reaction; Liver injury.
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