Abstract

We read with great interest the letter by Mitchell and Arcinue concerning our finding of hypertyraminemia in Reye's syndrome patients. Since the acceptance of our manuscript we have confirmed this finding in an additional 16 patients with biopsy-proven Reye's syndrome. The discovery of depressed hepatic monoamine oxidase activity described by the authors confirms our preliminary findings in four patients whose hepatic monoamine oxidase levels were measured in our laboratories. We feel that the work of Mitchell and Arcinue supports our hypothesis that derangement in biogenic amine metabolism may contribute to the encephalopathy of Reye's syndrome.

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