S2959 COVID-19-Induced Liver Injury: A Rare Cause of Acute Cholestasis in a High Risk Population

Introduction: Within the COVID-19 pandemic, hepatic dysfunction is common in the elderly population and ICU patients. Hepatic injury may be multifactorial including direct cytopathic effects after entry via host angiotensin-converting enzyme 2 (ACE2) receptors which are highly expressed in cholangiocytes. We describe an 82 year old female presenting with sudden jaundice and pruritus with marked elevation in bilirubin and transaminitis secondary to COVID-19 infection. Case Description/Methods: Patient presented with sudden jaundice and pruritus without respiratory distress, pain, fevers, or bowel movement changes. She tested positive for COVID-19 however didn't require supplemental oxygen, steroids or antiviral therapy. Notable labs included AST 260 IU/L, ALT 260 IU/L, ALP 1015 IU/L, total bilirubin 28 umol/L, direct bilirubin over 15 umol/L and INR 1.03. All toxicology was negative. ANA was positive at 1:320, anti-smooth muscle antibody level 22 and normal total IgG. Viral hepatitis panel, EBV, CMV, TTG, AMA were not detected. MRI/MRCP demonstrated mild fatty liver, with normal gallbladder and pancreas without biliary dilatation or obstruction. Liver biopsy demonstrated cholestatic changes including bile plugging, portal fibrosis, and scattered inflammatory cells. She was prescribed cholestyramine and Ursodeoxycholic acid and her condition was self limiting with continued monitoring as an outpatient. Discussion: Liver injury ranges from 2.5-76.3% of all COVID-19 cases. In vitro studies identify that coronavirus enters host cells via the ACE2 host receptor. Immunohistochemistry shows high ACE2 expression in vascular endothelium, type 2 alveolar cells, gastrointestinal tract and cholangiocytes. COVID-19 liver injury is likely multifactorial, including direct viral cytopathic injury, hypercoagulation and thrombosis in the porta-hepatic system, and hypoxia-induced reactive oxygen species. Innate immune response dysregulation contributes to pulmonary and extrapulmonary injuries and hepatotoxic agents such as antivirals are known to also cause drug-induced liver injury (DILI). COVID-19 liver histology shows moderate microvesicular steatosis, mild inflammatory infiltrates in the hepatic lobule and portal tract with instances of portal fibrosis and acute liver necrosis, as seen in our patients pathology report. Covid-19 liver injury is mainly self limiting however risk of severe injury have been seen in elderly and the critically ill.