Erythrocyte Lipid Abnormalities in Reye's Syndrome

Abstract

ABSTRACT. Previous studies have demonstrated alterations in plasma free fatty acid content in Reye's syndrome (RS). We have therefore studied erythrocyte membrane lipids to determine if there are concomitant structural and functional modifications attributable to RS. Erythrocyte lipids were measured in children with RS and in critically ill children also requiring intensive care (ICU). In comatose RS patients erythrocyte phospholipid arachidonate was increased 2-fold relative to control ICU patients: 20.46 f 2.14 versus 10.41 f 2.32% of total erythrocyte phospholipid, p < 0.05. RS coma patients also demonstrated an increased ratio of erythrocyte phospholipid polyunsaturatedlsaturated fatty acids (0.76 f 0.10) compared to ICU controls (0.48 f 0.08, p < 0.05). Erythrocyte cholesterol was higher in RS patients (79.00 f 6.61 pg/mg protein) than in ICU controls (59.74 f 6.09, p < 0.05). Erythrocyte malondialdehyde generation was decreased in comatose RS patients (404 rl: 28 nmol malondialdehyde/g hemoglobin) versus ICU (517 f 29, p < 0.05). Although plasma vitamin E was depressed in RS patients, the erythrocyte vitamin E concentrations were no different in RS patients than in ICU patients. All RS patients had a typical viral prodrome and either a history of aspirin intake and/or measurable serum salicylate on admission. All of the biochemical abnormalities in RS patients listed above returned to values comparable to those of healthy RS siblings on recovery. The transient nature of these phenomena suggests that they were related to viral infection and/or aspirin rather than to intrinsic differences in lipid metabolism between RS patients and controls. (Pediatr Res 21: 352-356,1987)

Induction of omega-oxidation of monocarboxylic acids in rats by acetylsalicylic acid.

“…The mechanism of this increase is unclear. The increase in free fatty acids could be due to the activation of endogenous phospholipase activity which has been postulated previously in Reye's syndrome (54).…”

Animal Models for Reye’s Syndrome

“…Tonsgard (1989) recently reported that serum levels of both monocarboxylic and dicarboxylic fatty acids are elevated at certain stages of the disease. There is also evidence that the relative proportions of unesterified polyunsaturated fatty acids are increased in serum (Ogburn et al, 1982) and in erythrocytes (Schwarz et al, 1987) of RS patients. Contiguous withserum lipid abnormalities, the cells of the visceral organs, particularly the liver, are loaded with fat that is stored as microvesicular droplets (Brown and Forman, 1982).…”