S2587 COVID-19 Virus Causing Fulminant Liver Failure

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Introduction: SARS-CoV-2 has now infected 179 million people worldwide. The virus is known to effect multiple organ systems, most commonly the lungs, but it is also well known that the virus affects the liver. Elevations in AST and ALT have frequently been observed in COVID-19 infection, however these elevations are usually mild to moderate. We present an extremely rare case of COVID-19 causing severe acute liver failure. Case Description/Methods: A 76 year-old male with a past medical history of hypertension and atrial fibrillation presented to the ED with fevers, altered mental status, shortness of breath, fatigue, and nausea. A SARS-CoV-2 nasal swab performed in the ED was positive. The patient had asterixis on physical examination. The patient was found to have severe transaminitis (AST 812, ALT 810, INR 2.51, T-bili 2.4) on admission. The patient had no prior history of liver disease. The patient was admitted to the ICU for acute liver failure in the setting of COVID-19 pneumonia. The patient was intubated for worsening acute hypoxic respiratory failure. The patient expired on hospital day 17. Discussion: Based on the patient’s encephalopathy on presentation, asterixis on physical exam, and severely elevated LFTs, the diagnosis of acute liver failure can be made. The patient was not hypotensive on admission and had SpO2 > 88%, so shock liver was a less likely etiology of the liver failure. Furthermore, LFTs are generally ∼35-50x the upper limit of normal in shock liver. Other causes of liver failure, such as viral hepatitis, drug induced liver injury, and acetaminophen toxicity were ruled out. The pathogenesis of hepatocellular damage seen in COVID-19 infection is still unknown. One proposed mechanism of acute liver failure as a result of COVID-19 infection is through the ACE2 receptor. It is known that SARS-CoV-2 uses the ACE2 receptor to enter and subsequently infect cells of the respiratory tract. However, ACE2 receptors are also expressed on hepatocytes and cholangiocytes. Therefore, our proposed mechanism for how our patient developed such a severe case of acute liver failure was via entry of the SARS-CoV-2 virus into hepatocytes through ACE2 receptors. This is an extremely rare case of SARS-CoV-2 causing acute liver failure. This case emphasizes the importance of monitoring liver function tests closely in COVID-19 patients. More research needs to be performed on the outcomes and possible prognostic indicators for these patients.Table 1.: Progression of Liver Disease During Hospital Course.