What is the pathophysiology of Reye syndrome?

Updated: Apr 02, 2018
  • Author: Debra L Weiner, MD, PhD; Chief Editor: Kirsten A Bechtel, MD  more...
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Answer

The pathogenesis of Reye syndrome, while not precisely elucidated, appears to involve mitochondrial injury resulting in dysfunction that disrupts oxidative phosphorylation and fatty-acid beta-oxidation in a virus-infected, sensitized host potentially with an underlying occult inborn error of fatty acid oxidation, urea cycle or mitochondrial disorder. [2, 16] The host has usually been exposed to mitochondrial toxins, most commonly salicylates (>80% of cases).

Histologic changes include cytoplasmic fatty vacuolization in hepatocytes, astrocyte edema and loss of neurons in the brain, and edema and fatty degeneration of the proximal lobules in the kidneys. All cells have pleomorphic, swollen mitochondria that are reduced in number, along with glycogen depletion and minimal tissue inflammation. Hepatic mitochondrial dysfunction results in hyperammonemia, which is thought to induce astrocyte edema, resulting in cerebral edema and increased intracranial pressure (ICP).


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