Rabee Tawel

We report a case of fulminant liver failure in a patient with acute active hepatitis B infection who was found to have COVID-19 without lung involvement. A 24-year-old male was brought by ambulance service to Hamad General Hospital, Emergency Department (ED), in Doha on April 8, 2020, with chief complaints of fever and cough for 3 days. Upon initial evaluation, the patient was febrile (39.4°C), jaundiced, and disoriented regarding time, place, and person, with an unremarkable past medical history. Initial blood tests showed severely elevated urea, creatinine, transaminases, and ammonium in addition to an impaired coagulation profile consistent with fulminant liver failure. A swab was taken for COVID-19 PCR testing and found to be positive. Serological tests revealed hepatitis B surface antigen positivity and other serology indicating acute hepatitis B. Initial X-ray and repeat chest X-rays did not show lung infiltrates. On the 6^th day after admission, the patient developed fixed dilated pupils, with brain edema on CT; cardiac arrest occurred on the 10^th day after admission, and the patient died. Although it is still largely unclear, HBV0-activated sudden-onset strong cytotoxic T lymphocyte response and enhanced viral replication and/or retention of the viral capsid in infected hepatocytes may cause the pathogenesis of FH. These pathophysiological events cause extensive hepatocyte apoptosis and necrosis, which results in deadly severe liver failure. Our findings support that the liver damage occurring in COVID-19 is caused by an impaired innate immune system rather than by direct cell damage caused by SARS-CoV-2. We think that more consideration should be given to the presence of acute hepatitis B, especially in COVID-19 patients.