Reye syndrome without initial hepatic involvement.

We report Reye syndrome in an 11-year-old boy whose first symptoms were generalized convulsions and coma without clinical or laboratory evidence of liver disease. Serum glutamic oxaloacetic transaminase and lactate dehydrogenase (LDH) values increased strikingly on the third day after the onset of coma. These enzymatic changes were associated with prolongation of prothrombin time. A rise in blood ammonia concentrations began on the fourth day of coma. The diagnosis of Reye syndrome was confirmed by a liver biopsy and at autopsy. This case demonstrates that encephalopathy in Reye syndrome can develop prior to detectable hepatic involvement, and suggests that factors unrelated to generalized liver damage may occasionally play a role in the pathogenesis of this obscure disorder.