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D. A. Trauner, MD
Dept of Pediatrics Univ of Chicago Chicago, IL 60637

J. J. Stockard, MD
Dept of Neurology Mayo Clinic Rochester, MN 55901

L. Sweetman, PhD
Dept of Pediatrics Univ of California at San Diego La Jolla, CA 92093

Arch Neurol. 1977;34(5):321.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In Reply.—

Dr Holmes' letter points out the continuing dilemma in attempts to define etiological agents in Reye's syndrome; many abnormalities occur simultaneously, and causal relationships are difficult to establish. It is possible that correction of increased intracranial pressure and changes in short-chain fatty acids are interrelated as well. In fact, preliminary data from our laboratory suggest that short-chain fatty acids may produce pericapillary brain edema in experimental animals (D. A. Trauner and J. de la Torre, unpublished observations).

The role of exchange transfusion in Reye's syndrome is also somewhat tenuous. The fact that short-chain fatty acid concentrations may actually be increased by this procedure suggests to us, as to Dr Holmes, that the role of transfusion in this disorder should be reevaluated. . . . [Full Text PDF of this Article]

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