In 1980, studies in Ohio, Michigan and Arizona by Starko, et al. []pointed to the use of aspirin during an upper respiratory tract infection and chicken pox as a potential indicator for the syndrome.
Aspirin use in children and adolescents decreased sharply in the mid-1980’s in North America, the UK, Europe and Australia. A decline in the incidence of Reye’s syndrome was almost immediately observed. The decrease in the number of cases of Reye’s syndrome was once thought to directly correspond to a decrease in aspirin use [] but that surmise has since come under some scrutiny. The decrease in the number of cases may also reflect a concurrent increased accuracy in diagnosis and the redesignation of misdiagnosed cases since the mid-1980’s — i.e., initially there were thought to be some 47 cases of Reye’s Syndrome in the UK in 1980/1981 but after a reassessment of susbsequent rediagnoses, that figure was revised downward to just 7 cases.
How many reported cases prior to 1980 might also be removed from the tallies, resulting in a decrease, if reassesments were conducted where possible? It is worth noting that a decrease in the number of cases has also been observed in countries where children’s aspirin is still in use. A dramatic worldwide decrease since 1996, regardless of salicylate use, has not been satisfactorily accounted for. Further case studies, primarily in the UK and Australia, have revealed 19 viruses singly and in conjunction with salicylates, pesticides and aflatoxin as potential factors contributing to the disease.
Reye’s syndrome tends to occur in previously healthy children about a week after common viral infections such as influenza or chickenpox. It can also develop after an ordinary upper respiratory infection such as a cold. The precise reason is unknown, but using aspirin to treat a viral illness or infection may trigger the condition in children.
Reye’s syndrome may be a metabolic condition — one without symptoms (asymptomatic) — that’s unmasked by viral illnesses. Reye’s syndrome occurs most commonly in children between the ages of 4 and 12.
While most children who survive Reye’s syndrome don’t suffer any long-term damage, this disorder can occasionally result in permanent liver damage, irreversible nervous system damage, coma and death.
Reye’s syndrome may include a combination of the following problems:
§ High levels of ammonia and acidity and a low level of sugar in the blood (hypoglycemia)
§ Fatty deposits in the liver and abnormal liver function tests
§ Poor blood clotting and bleeding caused by liver failure
§ Swelling of the brain, sometimes with coma and brain death
Earlier diagnosis and treatment can greatly reduce the chance of death.