Acute Epstein-Barr Virus-Induced Acute Pancreatitis and Cholestatic Hepatitis

Abstract

Epstein-Barr virus (EBV) is a herpesvirus that is spread through saliva between susceptible individuals and asymptomatic EBV shedders. A majority of EBV infections are subclinical and approximately 90% of adults are eventually EBV-seropositive. Infectious mononucleosis is a common clinical manifestation of EBV. Besides fever, adenopathy, fatigue, pharyngitis, and atypical lymphocytosis, other manifestations include splenomegaly, splenic rupture, generalized maculopapular rash, and a variety of neurologic syndromes. EBV can effect any organ system and has reportedly been associated with myocarditis, pneumonia, hepatitis, pancreatitis, acute renal failure, and glomerulonephritis. A 17-year-old female with no significant history presented with non-radiating, dull, epigastric pain with associated decreased appetite, nausea and vomiting. On physical examination, her abdomen was non-distended with mild epigastric tenderness on palpation, without guarding or rebound tenderness, Murphy sign was not present. Initial laboratory data revealed a normal white blood cell count with elevated lymphocytes, alkaline phosphatase 205 IU/L, AST 270 IU/L, ALT 281 IU/L, total bilirubin 2.7 mg/dL, direct bilirubin 1.8, and a lipase of 937 u/L which elevated to 2839 u/L the following day. Right upper quadrant ultrasound was unremarkable. MRCP was negative for choledocholithiasis, but did reveal hepatosplenomegaly. Patient did not endorse a history of alcohol consumption, medications known to cause pancreatitis, trauma, surgery, or family history of pancreatitis. Workup for hypertriglyceridemia, autoimmune pancreatitis, and viral hepatitis was negative. A heterophile antibody test was positive and virology revealed acute infection of Epstein-Barr virus. Acute pancreatitis is not a common complication of acute EBV infection. A recent review of literature revealed acute pancreatitis in 14 patients with acute EBV infection, with five cases being acute pancreatitis with cholestatic hepatitis. In contrast to the review, this patient presented with abdominal pain and vomiting, and did not present with classic infectious mononucleosis symptoms. Mechanism of acute pancreatitis and hepatitis due to infectious mononucleosis are likely due to an inflammatory reaction to the virus, but the underlying mechanism needs further investigation. Although it is rare, EBV infection should be considered in the differential diagnosis if the patient has acute cholestatic hepatitis with acute pancreatitis.