Hyperammonemia and Reye's Syndrome

Abstract

To the Editor: The rapidity with which metabolic changes occur in Reye's syndrome interferes with the biochemical definition of the underlying lesion. For instance, one abnormality occurring early and transiently but with many potential consequences and lingering effects is hyperammonemia.¹ The clinical symptoms and neurologic manifestations of affected patients resemble those seen in persons with genetic defects of ammonia disposal.^{2 , 3} The transiency of hyperammonemia suggests that the defect in the conversion of ammonia to urea is functional. Assays of urea cycle enzymes during hyperammonemia are unavailable but necessary for correct interpretation of the mechanism. On the basis of our preliminary . . .