Abstract

Concurrent acute hepatitis and acute pancreatitis is a rare disease entity. Most commonly it can be attributed to infectious etiologies such as hepatitis A, Hepatitis B and Hepatitis E. Although not as common, Epstein Barr Virus (EBV) should be considered in the differential diagnosis in patients with combined hepatitis and pancreatitis. We report a case of a 25 year-old male admitted with 2-day history of abdominal pain, nausea and dark stools. Laboratory findings were significant for mixed hepatocellular and cholestatic liver injury. Abdominal imaging showed evidence of acute pancreatitis, without biliary obstruction. Serologic tests and radiologic imaging excluded common infectious, autoimmune and/or structural etiologies. The diagnosis of EBV infection was made by a positive IgM antibody to the viral capsid antigen and Epstein-Barr nuclear antigen. The patient had a prolonged hospitalization for persistent abdominal pain and lag in improvement in his cholestatic liver injury. This disease process has been described in 6 children and no cases in adults have been reported to our knowledge.

Highlights

  • A 25-year-old healthy male was admitted with a 2day history of severe right upper quadrant and epigastric abdominal pain with radiation to the back

  • The patient was medically managed for acute hepatitis and acute pancreatitis of unknown etiology

  • Epstein-Barr Virus is a double helix DNA virus from the Herpesviridae family, which infects B cells and epithelial cells. It is most commonly implicated in Infectious Mononucleosis and Burkitt’s lymphoma, other rare presentations have been reported

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Summary

Introduction

A 25-year-old healthy male was admitted with a 2day history of severe right upper quadrant and epigastric abdominal pain with radiation to the back. Abdominal ultrasound was obtained on admission, which showed a normal Common Bile Duct (CBD), no gallstones and no evidence of acute cholecystitis. Magnetic resonance cholangiopancreatography was obtained, which showed severe acute pancreatitis with marked progression in edema and fluid retention and mildly distended gallbladder without evidence of acute cholecystitis (see Fig. 2).

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