Abstract
The host factors that may be important in the evolution of Reye's syndrome still need clarification. Thaler1,2 has raised the possibility that inborn errors in urea cycle enzymes may be instrumental in the development of the syndrome. He has postulated that such errors may lead to the hyperammonemia that is characteristic early in the illness. This elevated ammonia level may have a significant role in the pathogenesis of Reye's syndrome by virtue of its toxic effects on the brain, liver, and other organs. Cited below are three cases that occurred in one Florida community within one month. These may offer clinical support of the Thaler hypothesis, and they may illustrate an intimate relationship between Reye's syndrome and a less-discussed entity, varicella hepatitis.

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