S2703 A Rare Case of EBV Reactivation in an Immunocompetent Patient

Abstract

Introduction: Hepatic involvement during an active primary Epstein-Barr virus (EBV) infection often results in mild, self-resolving elevation of transaminases and is associated with infectious mononucleosis (IM). EBV rarely reactivates, and most cases occur in immunocompromised individuals. We present a rare case of EBV reactivation in an immunocompetent patient only presenting with cholestatic liver injury. Case Description/Methods: A 19-year-old female with a history of resolved EBV IM one year prior presented with dark urine and jaundice. She had no fever, abdominal pain, nausea, vomiting, weight changes or night sweats. She had no history of illicit drug, tobacco or alcohol use, recent travel, or sick contacts. Her medications were loratadine and an OCP;she denied use of acetaminophen or herbal supplements. Family history was unrevealing. On exam she was jaundiced but otherwise normal. Initial laboratory tests showed AST 97 U/L, ALT 75 U/L, ALP 165 U/L, T-BILI 8.1 mg/dL, D-BILI 5.7 mg/dL. CT abdomen revealed splenomegaly. Work up revealed ASMA titer (1:40), but otherwise negative/ normal ANA, IgG, AMA, HCV Ab, HBV serologies, HAV IgM, CMV PCR, iron studies, tick borne serologies, SARS CoV-2 PCR, A1AT and ceruloplasmin. On the second day, the T-BILI peaked to 12.4 mg/dL, AST 151 U/L, ALT 131 U/L, ALP 237 U/L. (Fig.1) EBV serologies were positive (EBV VCA IgG >750.0 U/ml, EBV VCA IgM >160.0 U/ml), EBV viral load of 23,500 copy/ ml and negative monospot test. On day four, the LFTs improved and she was discharged. One month later LFTs had normalized, and she was asymptomatic. Discussion: EBV reactivation causing cholestatic liver injury is extremely rare in immunocompetent individuals. Furthermore, EBV-induced hepatitis is usually associated with IM but our patient's sole complaint was jaundice and dark urine. Interestingly, she had mononucleosis due to EBV one year prior with unremarkable LFTs. The fact that the hepatitis was caused by the reactivation of the virus instead of a primary infection may be the reason for lack of other symptoms. It is unclear whether EBV reactivation increases the risk of hepatitis. The diagnosis can be made without a liver biopsy if thorough work up for hepatitis is negative and the EBV serologies are positive. The disease is often self-limited and the use of antivirals is controversial and thus there is no clear indication. Our case demonstrates that EBV reactivation presenting without the 'classic' IM symptoms may be under-recognized as a cause of cholestatic liver injury. (Figure Presented).