title: Amiodarone-induced liver cirrhosis and parkinsonism: a case report.
abstract: BACKGROUND
  Amiodarone-induced hepatotoxicity consists of mild liver test abnormalities and rare cases of acute hepatitis and chronic hepatic lesions, and histologically resembles the whole spectrum of alcoholic liver disease, i.e., non-alcoholic steatohepatitis. Amiodarone-induced neurotoxicity, including tremor, ataxia and peripheral neuropathy, is known, and some cases of parkinsonism following amiodarone use have also been reported.
  
  
  OBJECTIVE
  To study the pathology of amiodarone-associated parkinsonism.
  
  
  METHODS
  Light and electromicroscopic examinations of a patient with liver cirrhosis and amiodarone-induced parkinsonism.
  
  
  RESULTS
  On postmortem examination, the liver showed micronodular cirrhosis. Striking steatosis and frequent Mallory bodies were present on light microscopy. There were lysosomal inclusion bodies on electron microscopy. From these findings, amiodarone-induced liver cirrhosis was diagnosed. Brain atrophy and infarcts were not observed, and pigmentation in the substantia nigra was preserved. Histologically, there was a slightly lesser degree of neuronal loss with astrocytosis in the substantia nigra, locus ceruleus, and dorsal vagal nucleus. Lewy bodies were not found. In the cerebral white matter and basal ganglia, Alzheimer Type II astrocytes, which are abundant in hepatic encephalopathy, had deposition of electron-dense materials within the lysosomes and mitochondrial matrices. The materials were compatible with the accelerated amiodarone.
  
  
  CONCLUSIONS
  This is the first case in which the accumulation of amiodarone in the brain was morphologically observed. Amiodarone accumulation in the brain may play a role in neurotoxicity inducing parkinsonism.
authors.affiliation: First Department of Internal Medicine, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki City, Osaka, Japan. in1212@poh.osaka-med.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Ishida
authors.forename: M
authors.initials: M
authors.lastname: Sugino
authors.forename: T
authors.initials: T
authors.lastname: Hosokawa
authors.forename: T
authors.initials: T
authors.lastname: Sato
authors.forename: D
authors.initials: D
authors.lastname: Furutama
authors.forename: A
authors.initials: A
authors.lastname: Fukuda
authors.forename: F
authors.initials: F
authors.lastname: Kimura
authors.forename: H
authors.initials: H
authors.lastname: Kuwabara
authors.forename: Y
authors.initials: Y
authors.lastname: Shibayama
authors.forename: T
authors.initials: T
authors.lastname: Hanafusa
mesh_terms: D000368:Aged; D000638:Amiodarone / Q000009:adverse effects*; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects*; D001921:Brain / Q000473:pathology*; D006801:Humans; D002479:Inclusion Bodies / Q000648:ultrastructure*; D008099:Liver / Q000473:pathology; D008103:Liver Cirrhosis / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D046529:Microscopy, Electron, Transmission; D020734:Parkinsonian Disorders / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D017180:Tachycardia, Ventricular / Q000188:drug therapy
chemical_list: D000889:Anti-Arrhythmia Agents; D000638:Amiodarone