Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fulminant hepatic failure is a rare complication of status epilepticus. Although many of the anticonvulsants used to treat the seizures are known to have hepatotoxic properties, the exact mechanism leading to massive destruction of the liver following a prolonged seizure remains unclear. Three children are presented who developed fulminant hepatic failure following status epilepticus and subsequently died of multiple organ failure. The literature is reviewed with particular attention to the possible interaction between the anticonvulsants and the metabolic consequences of status epilepticus. We postulate that it is a combination of hypoxia and ischemia that occurs during a prolonged seizure with altered metabolism of free radicals secondary to the anticonvulsant drugs which leads to widespread hepatocyte membrane damage.
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PMID:Fulminant hepatic failure associated with status epilepticus in children: three cases and a review of potential mechanisms. 793 35

Acute hepatic failure develops as a disease entity of rather diverse origin. With disease progression, toxic bilirubin levels may cause severe complications which include AV-nodal blockage, cardiac arrhythmia, impaired consciousness, generalized seizures, and status epilepticus. Treatment choices to prevent clinical deterioration comprise of costly and limited available orthotopic liver transplantation, utilization of extracorporeal bioartificial liver support devices and haemoperfusion/plasmaperfusion treatment with activated charcoal/anion exchange filters. Here, we present a patient with acute drug-induced cholestatic hepatitis. Excessively elevated bilirubin levels were accompanied by cardiac and cerebral complications. Extracorporeal resin perfusion treatment (Plasorba, BR-350) was successfully performed over a 50-day period without activation of the coagulation system or side effects. Bilirubin levels were lowered to a minimum of 225 micromol/l, with concurrent clinical improvement. In conclusion, extracorporeal anion exchange plasmaperfusion may be a viable long-term treatment for hyperbilirubinaemic side effects in overt cholestatic hepatitis.
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PMID:Long-term extracorporeal bilirubin elimination: A case report on cascade resin plasmaperfusion. 1034 81