Acute Liver Failure in a Child With Adenovirus Detected by PCR in the Explanted Liver

Abstract

As of June 15, 2022, the Centers for Disease Control and Prevention has reported 296 pediatric patients under investigation for hepatitis of unknown etiology in the United States; the World Health Organization has reported 650 probable cases worldwide. One of the leading hypotheses for this cluster of cases is adenovirus, a virus that commonly causes respiratory or gastrointestinal symptoms in healthy children but rarely causes severe hepatitis or acute liver failure in immunocompetent children. The other leading hypothesis is that prior infection with SARS-CoV-2 may predispose children to developing liver injury from a normally innocuous agent. We describe a case of a previously healthy child presenting with acute liver failure who had detectable adenovirus DNA in his stool, whole blood, and in liver explant tissue, suggesting adenovirus as the likely etiology for the liver failure. He had no evidence of prior or current SARS-CoV-2 infection, nor had he received COVID vaccination, suggesting that SARS-CoV-2 did not play a role. Additionally, we report on the ability to provide rapid evaluation of a living donor within 72 hours and successfully perform a lifesaving, left-lobe, living donor liver transplant.

FIGURE 1

(A) Percutaneous liver biopsy at 200× demonstrating severe, diffuse mixed portal, and lobular inflammation with associated hepatocellular ballooning, cholestasis, and piecemeal necrosis. (B) Negative immunohistochemical stain for adenovirus. (C) Reactive nuclear changes suggestive of viral cytopathic effect (arrow). (D) Explant histology at 100× demonstrating fulminant hepatitis with disrupted lobular architecture resulting from extensive portal expansion and diminished residual lobular hepatocytes; marked, primarily lobular, lymphoplasmacytic infiltrate; severe reactive hepatocellular changes with giant cell formation, ballooning degeneration, and cholestasis.