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The COVID-19 caused by the SARS-CoV-2 has rapidly spread throughout more than 200 countries, with more than 30 million confirmed cases to date. The disease is mainly represented by a respiratory tract illness with a wide severity spectrum. Nevertheless, other organs such as the liver are commonly affected. Since the very beginning of the pandemic, abnormalities in the liver blood tests (LBT) have been described in patients with COVID-19. These alterations have largely been reported as mild to moderate elevations in the serum transaminases.1–3 In a minority of cases, hypertransaminasaemia may be severe or combined with increased levels of cholestatic parameters such as alkaline phosphatase or total bilirubin. The incidence of these LBT abnormalities is variable among studies but it can be present in up to half the hospitalised patients with SARS-CoV-2. The exact mechanisms whereby the virus causes damage in the liver parenchyma are still unknown. A direct cytotoxic injury against hepatocytes has been proposed, while an immune-mediated damage has also been suggested. These hypotheses have been raised since SARS-CoV-2 particles were found in the cytoplasm of hepatocytes of affected individuals.1 In addition, lobular and portal inflammation have been described as the most frequent histhopathological findings, apart from macrovesicular steatosis.4 Another factor that should be considered is the potential role of drug induced liver …
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Contributors PR: interpreted the results, drafted and revised the manuscript. AC: interpreted the results, drafted, revised the manuscript and gave final approval.
Funding Andrés Cárdenas is funded by the Instituto de Salud Carlos III and Plan Estatal de Investigación Ciéntifica y Técnica y de Innovación-grant no PI19/00752 and has received funding for this work by 'Fundación Marta Balust'.
Competing interests AC is a consultant for Mallinckrodt Pharmaceuticals, Boston Scientific, Shionogi, has participated on Advisory Boards for Mallinckrodt Pharmaceuticals and has received grant support by Mallinckrodt and Boston Scientific.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.