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Fulminant hepatitis after grand mal seizures: Mechanisms and role of liver transplantation
Author(s) -
Ichai Philippe,
Huguet Emmanuel,
Guettier Catherine,
Azoulay Daniel,
Gonzalez Maria Eugenia,
Fromenty Bernard,
Masnou Pascal,
Saliba Faouzi,
Roche Bruno,
Zeitoun Fahed,
Castaing Denis,
Samuel Didier
Publication year - 2003
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1053/jhep.2003.50327
Subject(s) - medicine , liver transplantation , fulminant hepatic failure , steatosis , fulminant , transplantation , context (archaeology) , liver biopsy , liver function tests , liver function , epilepsy , gastroenterology , surgery , biopsy , paleontology , psychiatry , biology
Abstract Fulminant liver failure is a rare complication of grand mal seizures with a high mortality, the prognosis being largely determined by the combination of the hepatic and neurologic insults. The mechanisms of acute liver failure secondary to grand mal epilepsy and the place of liver transplantation in this context are poorly defined and are the subject of this report. A series of 6 such patients is presented. All had a history of chronic primary or post‐traumatic epilepsy and presented with acute liver failure shortly after a grand mal fit. Detailed accounts of background, presentation, and management are given and integrated with blood, radiologic, and histologic investigations. Two of the 6 patients survived, 1 making a full recovery and the other with neurologic sequelae. Two patients underwent liver transplantation but died with severe neurologic sequelae despite improving liver function. The remaining 2 patients were considered too unwell to undergo liver transplantation and died in multiple organ failure. Liver histology from needle biopsy and/or native liver explants identified lesions compatible with a combination of steatosis and necrosis. Factor V and transaminase levels may allow early identification of patients in whom liver function is likely to improve spontaneously. In conclusion, the mechanisms of liver failure occurring after grand mal seizures appear multifactorial, including hypoxia, steatosis, and drug‐induced components. The neurological prognosis and overall survival of these patients remains poor.