S2614 Cholestatic Hepatitis From Acute Epstein-Barr Virus Infection

Abstract

INTRODUCTION: Primary Epstein-Barr Virus infection (EBV) presents as a triad of fever, posterior lymphadenopathy and pharyngitis. Hepatocellular involvement is limited to transient, mild, asymptomatic elevations of aminotransferases. Clinical manifestations of hepatitis are rarely the presenting feature of the disease and severe cholestasis is exceedingly rare. We present a patient with atypical presenting features found to have cholestatic hepatitis due to acute EBV infection. CASE DESCRIPTION/METHODS: A 38-year-old male with no medical history presented with right upper quadrant (RUQ) abdominal pain for 1 week associated with malaise, dyspnea, nausea, emesis, and fever to 38.8 degrees Celsius. His social history consisted of safe sex practices, no sick contacts, and no drug or alcohol use. On examination, he was afebrile and hemodynamically stable. There was no jaundice, scleral icterus or lymphadenopathy. There was mild tonsillar erythema without edema or exudate. He had RUQ and epigastric tenderness to palpation without notable hepatosplenomegaly. His labs showed no leukocytosis with elevated aspartate aminotransferase (AST) 234 IU/L, alanine aminotransferase (ALT) 383 IU/L, alkaline phosphatase 432 IU/L, and total and direct bilirubin of 3.4 and 1.6 mg/dL, respectively. ALT and AST peaked at 743 and 582 IU/L, respectively. HIV and hepatitis panel were negative. RUQ ultrasound showed normal gallbladder (GB) wall thickness of 2.7 mm with mild distention, trace pericholecystic fluid, and no biliary dilation. Magnetic resonance cholangiopancreatography showed mild hepatosplenomegaly, a normal GB and no biliary obstruction. Further workup revealed a positive Monospot with >160 units/ml of EBV antibodies to viral capsid antigen IgM and indeterminate EBV antibody to viral capsid antigen IgG, indicating acute EBV infection. DISCUSSION: EBV cholestasis is thought to be secondary to inflammation of the bile duct and direct damage to hepatic cells by autoantibody-mediated activation of free radicals. A literature review revealed that EBV has been reported to cause a hepatocellular pattern of elevated aminotransferases however cholestatic patterns are infrequently reported and thus may cause a diagnostic dilemma. The existing literature reports this phenomenon in pediatrics, adolescents, or patients in the second decade of life. Our case highlights the importance of including EBV infection in the differential diagnosis of cholestatic hepatitis at any age, particularly when no demonstrable cholecystitis is present.Table 1.: Liver and biliary marker trend throughout hospitalizationFigure 1.: Abdominal MRI demonstrating hepatomegaly and splenomegaly, measuring 15.1 cm anterior-posteriorly, and 13.9 cm craniocaudally.Figure 2.: Abdominal MRI demonstrating hepatosplenomegaly.