A 44–year–old woman with a past medical history of reflux presented with jaundice. Ten days prior to presentation, she noticed dark urine but did not seek medical attention. Five days prior, she developed jaundice, fatigue, and a cramping pain in her epigastric region and right upper quadrant. She denied fever, chills, cough, sore throat or rash. She had a small amount of diarrhea and a decrease in her appetite. She did not work in the healthcare field, never had a blood transfusion, had no tattoos, did not drink alcohol, and denied intravenous drug use. She did have sexual relations with someone with hepatitis in college but subsequent testing was negative. Her only medications were pantoprazole and a multivitamin. She denied any over the counter supplements or recent acetaminophen ingestion. Family history was negative for any autoimmune processes or liver conditions. Physical exam was notable for jaundice and tenderness to palpation in the right upper quadrant without hepatosplenomegaly. Laboratories were remarkable for an aspartate aminotransferase of 2690 IU/L, an alanine transaminase of 4920 IU/L, a bilirubin of 22.1 mg/dl and an international normalized ratio of 2.8. Acute hepatitis serologies, anti–nuclear antibody, ceruloplasmin, ferritin, and acetaminophen level were unremarkable. A right upper quadrant ultrasound with dopplers was also negative. She was given N–Acetyl–Cysteine and vitamin K. Her mental status and liver function tests both worsened and she underwent a liver transplant 4 days after presentation. Epstein–Barr virus titers were suggestive of an acute infection with a polymerase chain reaction confirming the diagnosis. She was subsequently treated with ganciclovir following her liver transplant.
Hospitalists frequently encounter acute liver failure, and a timely diagnosis can be lifesaving. Epstein–Barr virus, a herpes virus spread by intimate contact between hosts, can cause a range of diseases from infectious mononucleosis to Burkitt’s lymphoma. Infecting more than 90% of humans and persisting throughout life, it typically is an asymptomatic infection. Although viral hepatitis is a leading cause of fulminant liver failure, Epstein–Barr virus generally causes a benign, self–limited process in immunocompetent patients causing only a mild transaminitis in about 80% of people infected, with jaundice occurring in 1.8–5% of cases. Acute liver failure caused by Epstein–Barr virus has rarely been reported and among those reported there is a 87% mortality rate. In these extreme cases, orthotopic liver transplantation is the only effective therapy.
Although acute Epstein–Barr virus infections often cause only mild transaminitis, it must remain on the differential for fulminant liver failure.