S2689 Liver Injury in a Patient With Acute Hepatitis B and SARS-CoV-2 Co-Infection: A Case Report

Abstract

INTRODUCTION: Liver injury in patients with COVID 19 have been described with an incidence of 14.8%–78% and characterized by elevated AST and ALT levels. Here we present a case of a man that presented with acute liver injury found to acute HBV and SARS-CoV-2 co-infection. CASE DESCRIPTION/METHODS: A 33 year-old-man presented with jaundice, subjective fever and malaise for 5 days. Physical exam showed jaundice, not hypoxic, hemodynamically stable and afebrile. Investigations on admission AST 2607 U/L, ALT 1187 U/L, TB 27.2 mg/dL (58.2 mg/dL on day 5), GGT 332 U/L, INR 1.49. IgManti-HBc reactive, HBeAg non-reactive, Anti-HBs Non-reactive, HBV viral load 920000 IU/mL. Nasopharyngeal swab for SARS-COV-2 RNA PCR was positive. LDH 1026 U/L, CRP 8.0 mg/L, Ferritin 27,775 ng/ml, D-Dimer: 286 ng/dL. Absolute lymphocyte count 1.90 103/cumm. CT abdomen minimal periportal edema with periportal lymphadenopathy. Tenofovir 300 mg/day for 2 days was given, then switched to Entecavir 0.5 mg/day. He received Acetylcysteine infusion 100 mg/kg for 5 days. On discharge AST 390 U/L, ALT 958 U/L, TB 43.8 mg/dL, INR 1.09. He didn’t develop respiratory symptoms. DISCUSSION: This case rose the question of the interaction between the two viruses and the appropriate treatment in HBV and SARS-CoV-2 co-infection. In a study patients with severe COVID-19 were more likely to have HBV than non-severe cases (2.4% vs 0.6%), it has been proposed that there could be an enhancement of viral replication of HBV due to SARS-CoV-2, and that SARS-CoV-2 may directly bind to ACE2 positive cholangiocytes causing hepatic injury. A CRP >20mg/ L and lymphopenia < 1.1 103/cumm have been independently associated with liver injury in COVID-19, in most studies liver dysfunction appears to be mild and transient. Highly elevated AST and ALT are more commonly seen with HBV, in COVID-19 the median levels of AST and ALT haven been 47 U/L. The above suggested liver injury was mediated by HBV, we did not administer any treatment targeting COVID-19. Whether or not SARS-CoV-2 promotes/enhances HBV replication needs to be further studied. In the setting of emergent COVID-19 its challenging to treat patients presenting like ours given the increasing number of non-respiratory manifestation of the disease, the decision to give treatment for SARS-CoV-2 can be puzzling. Here we have presented a patient with acute HBV and co-infection with SARS-CoV-2 that improved without administering any COVID-19 specific therapy.