Current Trends
Reye Syndrome Surveillance -- United States, 1987 and 1988
For the 1987 and 1988 surveillance years, 36 and 20 cases,*
respectively, of Reye syndrome (RS)** were reported to the National
Reye Syndrome Surveillance System. These years have the lowest
number
of cases reported since continuous national surveillance was
established in December 1976 (Table 1). For both years,
approximately
80% of reported patients had an antecedent illness within 3 weeks
before onset of vomiting or neurologic symptoms. Eighteen RS
patients
in 1987 and nine in 1988 had respiratory illnesses; seven and four
had
varicella; three and two had diarrhea without respiratory symptoms.
In
both years, approximately 50% of cases occurred in January,
February,
and March--the peak months for respiratory viral infections,
including
varicella and influenza (type A(H1N1) in 1987 and type A(H3N2) in
1988).
In 1987, 17 (47%) of the 36 reported RS patients and, in 1988, 16
(80%) of the 20 patients were female; 33 (92%) and 19 (95%),
respectively, were white, two (6%) and one (5%) were black, and one
patient (3%) in 1987 was Asian. Seventeen patients each year were
greater than or equal to 5 years old, representing a 75% decline in
the
number of cases in this age group from 1986. Nineteen reported
patients
in 1987 and three in 1988 were less than 5 years old, representing
a
42% and a 91% decline, respectively, in this age group from 1986.
Approximately 75% of patients in both 1987 and 1988 were admitted
to
hospitals in precomatose stages of RS--stages 0, 1, or 2.*** In
each
year, stage 2 was the classification for the largest number of
patients
upon admission (47% and 55%, respectively), followed by stage 1 for
1987 (31%) and stages 0, 1, and 3 (10% each) for 1988. In 1987, the
most severe phases of illness after hospitalization were stage 1
(25%),
stage 2 (8%), stage 3 (8%), stage 4 (11%), and stage 5 (30%).
Eleven
percent of patients received treatment that precluded
classification
(i.e., they had received anesthetic or paralyzing agents in their
treatment); the most severe stage was not reported for 7%. In 1988,
25%
reached stage 1 only; 5% reached stage 2, 20% reached stage 3, 20%
reached stage 5, and 30% received treatment that precluded
classification.
The case-fatality rates for these 2 years were 29% and 30%,
respectively, based on patients for whom short-term outcome was
reported (35 (97%) of the 36 patients in 1987 and 17 (85%) of the
20
patients in 1988).
Reported by: Epidemiology Office, Div of Viral and Rickettsial
Diseases, Center for Infectious Diseases, CDC.
Editorial Note
Editorial Note: The annual number of RS cases reported to CDC has
decreased steadily since 1980. Major studies on RS and medications
(1-3) have confirmed prior reports (4-6) of an association between
ingestion of aspirin during antecedent viral illness and subsequent
development of RS. The decline in the number of RS cases since late
1980 coincides with the increased publicity about this association
and
with the decrease in the frequency and/or dose of
aspirin-containing
medication used in treating children with influenza-like illness or
varicella (7,8). In addition, since 1986, labels of all
aspirin-containing medications have been required to provide a
warning
about the risk of RS in association with aspirin use in children
with
influenza-like illness and varicella.
Before diagnosing RS, physicians should rule out any of the
approximately 20 metabolic disorders that may mimic RS,
particularly in
infants and small children (2,9-11). Because 40%-65% of reported RS
patients since 1985 have been greater than or equal to 10 years of
age,
health-care providers and public health agencies also should advise
older children and their parents about warnings concerning aspirin
use.
Interest in reporting RS may wane as the number of cases decreases
in
the United States. Health-care providers and public health agencies
are
urged to continue reporting to the National Reye Syndrome
Surveillance
System to assure adequate epidemiologic monitoring of this illness.
References
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.
2.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.
3.Pinsky PF, Hurwitz ES, Schonberger LB, Gunn WJ. Reye's syndrome
and
aspirin: evidence for a dose-response effect. JAMA 1988;260:657-61.
4.Starko KM, Ray CG, Dominguez LB, Stromberg WL, Woodall DF. Reye's
syndrome and salicylate use. Pediatrics 1980;66:859-64.
5.Waldman RJ, Hall WN, McGee H, Van Amburg G. Aspirin as a risk
factor
in Reye's syndrome. JAMA 1982;247:3089-94.
6.Halpin TJ, Holtzhauer FJ, Campbell RJ, et al. Reye's syndrome and
medication use. JAMA 1982;248:687-91.
7.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.
8.Barret MJ, Hurwitz ES, Schonberger LB, Rogers MF. Changing
epidemiology of Reye syndrome in the United States. Pediatrics
1986;77:598-602.
9.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.
10.Greene CL, Blitzer MG, Shapira E. Inborn errors of metabolism
and
Reye syndrome: differential diagnosis. J Pediatr 1988;113:156-9.
11.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).
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