Acute liver injury after protracted seizures in children

Xilla T. Ussery, Eric L. Henar, Dennis D. Black, Stuart Berger, Peter F. Whitington*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


Three children were observed to have extensive liver injury following protracted seizures. Two recovered with supportive care and one died from central nervous system complications. When first measured, the levels of aminotransferases were minimally elevated, but they increased to 250 to 8,000 times normal within 12 to 24 h after the seizure episode. They fell to near normal over the next 8 to 11 days in the survivors, and to one sixth of the peak level by 4 days in the patient who died. A percutaneous liver biopsy from one child demonstrated centrolobular necrosis consistent with severe ischemic injury. Common causes for liver dysfunction, including viral hepatitis, drug hepatitis, and Reye syndrome, were excluded on clinical, serologic, and histologic grounds. We reason that hepatic injury resulted from ischemia. We speculate that prior treatment with anticonvulsants, which are capable of inducing mixed-function oxidases in the liver, aggravated the ischemia-reperfusion injury by increasing the production of reactive oxygen intermediates and reducing cytoprotective mechanisms. Prevention of such injury should be directed toward control of seizures and early respiratory support when seizures occur, not restructuring medication regimens.

Original languageEnglish (US)
Pages (from-to)421-425
Number of pages5
JournalJournal of pediatric gastroenterology and nutrition
Issue number4
StatePublished - Jan 1 1989


  • Ischemia in liver
  • Liver injury
  • Seizures in children

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Gastroenterology


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