In December, 2019, an outbreak of a novel coronavirus (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2], previously 2019-nCoV) started in Wuhan, China, and has since become a global threat to human health. The number of confirmed cases of 2019 coronavirus disease (COVID-19) has reached 87 137 worldwide as of March 1, 2020, according to WHO COVID-19 situation report 41; most of these patients are in Wuhan, China. Many cases of COVID-19 are acute and resolve quickly, but the disease can also be fatal, with a mortality rate of around 3%. 1 Onset of severe disease can result in death due to massive alveolar damage and progressive respiratory failure. 2 SARS-CoV-2 shares 82% genome sequence similarity to SARS-CoV and 50% genome sequence homology to Middle East respiratory syndrome coronavirus (MERS-CoV)—all three coronaviruses are known to cause severe respiratory symptoms. Liver impairment has been reported in up to 60% of patients with SARS3 and has also been reported in patients infected with MERS-CoV. 4 At least seven relatively large-scale case studies have reported the clinical features of patients with COVID-19. 1, 5–10 In this Comment, we assess how the liver is affected using the available case studies and data from The Fifth Medical Center of PLS General Hospital, Beijing, China. These data indicate that 2–11% of patients with COVID-19 had liver comorbidities and 14–53% cases reported abnormal levels of alanine aminotransferase and aspartate aminotransferase (AST) during disease progression (table). Patients with severe COVID-19 seem to have higher rates of liver dysfunction. In a study in The Lancet by Huang and colleagues, 5 elevation of AST was observed in eight (62%) of 13 patients in the intensive care unit (ICU) compared with seven (25%) of 28 patients who did not require care in the ICU. Moreover, in a large cohort including 1099 patients from 552 hospitals in 31 provinces or provincial municipalities, more severe patients with disease had abnormal liver aminotransferase levels than did non-severe patients with disease. 1 Furthermore, in another study, 8 patients who had a diagnosis of COVID-19 confirmed by CT scan while in the subclinical phase (ie, before symptom onset) had significantly lower incidence of AST abnormality than did patients diagnosed after the onset of symptoms. Therefore, liver injury is more prevalent in severe cases than in mild cases of COVID-19.

Liver damage in patients with coronavirus infections might be directly caused by the viral infection of liver cells. Approximately 2–10% of patients with COVID-19 present with diarrhoea, and SARS-CoV-2 RNA has been detected in stool and blood samples. 11 This evidence implicates the possibility of viral exposure in the liver. Both SARS-CoV-2 and SARS-CoV bind to the angiotensin-converting enzyme 2 (ACE2) receptor to enter the target cell, 7 where the virus replicates and subsequently infects other cells in the upper respiratory tract and lung tissue; patients then begin to have clinical symptoms and manifestations. Pathological studies in patients with SARS confirmed the presence of the virus in liver tissue, although the viral titre was relatively low because viral inclusions were not observed. 3 In patients with MERS, viral particles were not detectable in liver tissue. 4 Gamma-glutamyl transferase (GGT), a diagnostic biomarker for cholangiocyte injury, has not been reported in the existing COVID-19 case studies; we found that it was elevated in 30 (54%) of 56 patients with COVID-19 during hospitalisation in our centre (unpublished). We also found that elevated alkaline phosphatase levels were …