The Biochemistry of Reye's Syndrome

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Abstract
And I Daniel fainted, and was sick certain days; afterward I rose up, and did the king's business; and I was astonished at the vision, but none understood it. The Bible Daniel 8:27 On the basis of the findings presented in this biochemical overview, it can be said that Reye's syndrome affects every major category of human metabolism. Such an effect at the molecular level parallels, in scope, the known impact of this disease on the function and/or structure of parenchymal cells from multiple organ systems. In this regard, the student of RS is presented with a unique opportunity to examine, integrate, and correlate a spectrum of morphopathologic and pathophysiologic findings with biochemical derangements as we have attempted to do. An appreciation of the complex interplay of these structural, functional, and biochemical abnormalities and how they might perpetuate or accelerate the disease process would be educationally rewarding in itself. Moreover, because we are handicapped from a therapeutic standpoint in not having identified a single etiologic agent responsible for triggering RS, it is hoped that such an appreciation will lead to the recognition of common denominators in its pathogenesis. In this context, a primary objective of “specific” therapies would be to interrupt the pathogenetic sequence of RS at such common sites thereby obviating further deterioration or death of the patient and permitting the reestablishment of morphologic, physiologic, and biochemical homeostasis. Of the current therapies employed in RS, insulin either administered with or as a consequence of hypertonic glucose appears to be a logical choice by virtue of its ability to retard amino acid efflux from skeletal muscle and block lipolysis.

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