The pandemic of respiratory infection with Severe Acute Respiratory Syndrome Corona Virus -2 (SARS-CoV-2) has already infected 7 million people globally, leaving 4 lacs dead [1]. SARS-Cov-2 is an enveloped, non-segmented, positive-sense RNA virus belonging to β-coronavirus family [2] and causes fever, dry cough and breathing difficulty, which can progress to respiratory distress due to interstitial pneumonia and multi-organ involvement [3, 4]. The latter is due to systemic inflammation leading to a cytokine storm and immune dysfunction often with features of macrophage activation syndrome, as evidenced by hyperferritinaemia, hepatic dysfunction and diffuse intravascular coagulation [5]. Viral entry is through the ACE-2 receptor; high expression of which is noted in type II alveolar cells, enterocytes, cholangiocytes, myocardial cells and proximal tubule cells of kidney, predisposing the concerned organs to the risk of developing complications [6, 7].
Deranged liver functions, mainly raised alanine aminotransferase (ALT) and aspartate aminotransferase (AST), have been reported in 14–53% patients without known liver disease [8, 9]. Patients with severe disease showed higher frequency and degree of liver dysfunction while in milder cases, the liver injury was transient [10]. The mechanisms of hepatic injury include immune-mediated inflammation, hypoxic injury due to severe pneumonia and drug related [11]. It is also postulated that expression of ACE2 receptor on cholangiocytes may predispose to cholestatic injury [12]. Data on post-mortem liver biopsies is limited and demonstrates moderate microvascular steatosis and mild lobular and portal activity [13].