Hurwitz ES, Barrett MJ, Bregman D, et al. Public Health Service study on Reye's syndrome and medications: report of the pilot phase . N Engl J Med 1985;;313:849-57.
Hurwitz ES, Barrett MJ, Bregman D, et al. Public Health Service study of Reye's syndrome and medications: report of the main study . JAMA 1987;;257:1905-11, 3366.
Pinsky PF, Hurwitz ES, Schonberger LB, Gunn WJ. Reye's syndrome and aspirin: evidence for a dose-response effect . JAMA 1988;;260:657-61.
Starko KM, Ray CG, Dominguez LB, Stromberg WL, Woodall DF. Reye's syndrome and salicylate use . Pediatrics 1980;;66:859-64.
Waldman RJ, Hall WN, McGee H, Van Amburg G. Aspirin as a risk factor in Reye's syndrome . JAMA 1982;;247:3089-94.
Halpin TJ, Holtzhauer FJ, Campbell RJ, et al. Reye's syndrome and medication use . JAMA 1982;;248:687-91.
Remington PL, Rowley D, McGee H, Hall WN, Monto AS. Decreasing trends in Reye syndrome and aspirin use in Michigan, 1979 to 1984 . Pediatrics 1986;;77:93-8.
Barret MJ, Hurwitz ES, Schonberger LB, Rogers MF. Changing epidemiology of Reye syndrome in the United States . Pediatrics 1986;;77:598-602.
Hurwitz ES. The changing epidemiology of Reye's syndrome in the United States: further evidence for a public health success (Editorial). JAMA 1988;;260:3178-80
Greene CL, Blitzer MG, Shapira E. Inborn errors of metabolism and Reye syndrome: differential diagnosis . J Pediatr 1988;;113:156-9.
Rowe PC, Valle D, Brusilow SW. Inborn errors of metabolism in children referred with Reye's syndrome: a changing pattern . JAMA 1988;;260:3167-70.
Reporting year begins December 1 of previous year. Data for 1988 are provisional.
According to CDC's case definition, the following conditions must be met to be considered an RS case: 1) acute, noninflammatory encephalopathy documented by alteration in the level of consciousness and either a) a record (if available) of cerebrospinal fluid containing less than or equal to 8 leukocytes per mm3 or b) histologic sections of the brain demonstrating cerebral edema without perivascular or meningeal inflammation; 2) hepatopathy documented either by biopsy or autopsy considered to be diagnostic of RS or by a threefold or greater rise in the levels of either serum aspartate aminotransferase, serum alanine aminotransferase, or serum ammonia; and 3) no more reasonable explanation for the cerebral or hepatic abnormalities.
Clinical staging of encephalopathy in RS is based on the level of consciousness and corresponding physical signs. Stages 0-2 are precomatose, with the level of consciousness deteriorating progressively from stage 0 to stage 2. Stages 3-5 are characterized by coma, progressing from early (stage 3) to deep coma (stage 5).