introduction / background

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].


COVID-19 is a dominant pulmonary disease, with multisystem involvement, depending upon comorbidities. Its profile in patients with pre-existing chronic liver disease (CLD) is largely unknown. We studied the liver injury patterns of SARS-Cov-2 in CLD patients, with or without cirrhosis.

Materials & Methods

The retrospectively collected data was analysed as groups i.e. patients having CLD without cirrhosis, those having cirrhosis with or without decompensation, those with or without acute liver injury during COVID-19 infection. Descriptive statistics were expressed as mean ± SD or median (IQR). The Student’s t-test for continuous data, Fisher’s exact test or Pearson’s Chi-square test for categorical data and Kaplan–Meier curve with long-rank test was considered for survival outcomes. AUROC was used to derive the applicability and cut-off for CTP score to predict mortality. The proportional risk between the groups was calculated as odds ratio. All statistical tests were two-tailed, and a significance level (p) of 0.05 was used. All statistical tests were performed using SPSS.


Altogether, 228 patients [185 CLD without cirrhosis and 43 with cirrhosis] were enrolled, with comorbidities in nearly 80%. Metabolism associated fatty liver disease (113, 61%) and viral etiology (26, 60%) were common. In CLD without cirrhosis, diabetes [57.7% vs 39.7%, OR = 2.1 (1.1–3.7), p = 0.01] and in cirrhotics, obesity, [64.3% vs. 17.2%, OR = 8.1 (1.9–38.8), p = 0.002] predisposed more to liver injury than those without these. Forty three percent of CLD without cirrhosis presented as acute liver injury and 20% cirrhotics presented with either acute-on-chronic liver failure [5 (11.6%)] or acute decompensation [4 (9%)]. Liver related complications increased (p < 0.05) with stage of liver disease; a Child-Turcotte Pugh score of 9 or more at presentation predicted high mortality [AUROC 0.94, HR = 19.2 (95 CI 2.3–163.3), p < 0.001, sensitivity 85.7% and specificity 94.4%). In decompensated cirrhotics, the liver injury was progressive in 57% patients, with 43% mortality. Rising bilirubin and AST/ALT ratio predicted mortality among cirrhosis patients.


SARS-Cov-2 infection causes significant liver injury in CLD patients, decompensating one fifth of cirrhosis, and worsening the clinical status of the already decompensated. The CLD patients with diabetes and obesity are more vulnerable and should be closely monitored.


Coronavirus disease (COVID-19) Situation Report – 113. Data as received by WHO from national authorities. 2020. 2. Lu R, Zhao X, Li J, Niu P, Yang B, Wu H, et al. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet. 2020;395(10224):565–574. doi: 10.1016/S0140-6736(20)30251-8. 3. Guan WJ, Ni ZY, Hu Y, Liang WH, Ou CQ, He JX, et al. Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med. 2020

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