Barrett MJ, Hurwitz ES, Schonberger LB, Rogers MF. Changing epidemiology of Reye syndrome in the United States . Pediatrics 1986;;77:598-602.
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.
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.
Arrowsmith JB, Kennedy DL, Kuritsky JN, Faich GA. National patterns of aspirin use and Reye syndrome reporting, United States, 1980 to 1985 . Pediatrics 1987;;79:858-63.
Corey L, Rubin RJ, Hattwick MAW, Noble GR, Cassidy E. A nationwide outbreak of Reye's syndrome: its epidemiologic relationship to influenza B . Am J Med 1976;;61:615-25.
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.
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.
According to CDC's case definition, the following conditions must be met for consideration as a RS case: 1) acute, noninflammatory encephalopathy documented a) by alteration in the level of consciousness and, if available, a record of cerebrospinal fluid containing ≤8 leukocytes per mm3 or b) by histologic specimen demonstrating cerebral edema without perivascular or meningeal inflammation; 2) hepatopathy documented either by a liver 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 and hepatic abnormalities.