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Reyes Syndrome--PhARMA's attack upon aspirin

Another example of Big PhARMA going after the use of aspirin.  They chose an extremely rare condition (2 cases per year since 1994) when it was not so rare because of inadequate diagnostic technique.  PhARMA has ran with Reyes Syndrome as part of their smear aspirin—aspirin cuts in to their profits from Warfin and other blockbusters.  Every pharmacist and doctor knows of Reye’s Syndrome, but probably less than 5% know that it is exceedingly rare and limited to those with a metabolic disorder resulting in excessive ammonia. {See the bracketed commentary in green}



Reye's syndrome is a potentially fatal disease that causes numerous detrimental effects to many organs, especially the brain and liver, as well as causing hypoglycemia.[1] The exact cause is unknown, and while it has been associated with aspirin consumption by children with viral illness, it also occurs in the absence of aspirin use.  The disease causes fatty liver with minimal inflammation and severe encephalopathy (with swelling of the brain). The liver may become slightly enlarged and firm, and there is a change in the appearance of the kidneys. Jaundice is not usually present.[2] {Note the symptomatic diagnosis.}

Early diagnosis is vital; while most children recover with supportive therapy, severe brain injury or death are potential complications.


The precise mechanism by which Reye's syndrome occurs remains unknown. This serious condition is described as a "syndrome" rather than a disease as the clinical features that physicians use to diagnose it are quite broad.  The serious symptoms of Reye's syndrome appear to result from damage to cellular mitochondria,[7] at least in the liver, and there are a number of ways that aspirin could cause or exacerbate mitochondrial damage. A potential increased risk of developing Reye's syndrome is one of the main reasons that aspirin has not been recommended for use in children and teenagers, the age group for which the risk of lasting serious effects is highest. No research has found a definitive cause of Reye's syndrome, and association with aspirin has only been shown through epidemological studies. The diagnosis of "Reye's Syndrome" greatly decreased in the 1980s, when genetic testing for inborn errors of metabolism was becoming available in first world countries.[8] A retrospective study of 49 survivors of cases diagnosed as "Reye's Syndrome" showed that the majority of the surviving patients had various metabolic disorders.[9]


Some studies have demonstrated an association between aspirin taken for viral illnesses and the development of Reye’s syndrome.[4] One small study presented findings that acetaminophen (paracetamol) is a greater risk,[5


Documented cases of Reye’s syndrome in adults are rare. The recovery of adults with the syndrome is generally complete, with liver and brain function returning to normal within two weeks of the illness. In children, however, mild to severe permanent brain damage is possible, especially in infants. Over thirty percent of the cases reported in the United States from 1981 through 1997 resulted in fatality.


In 1980, after CDC began cautioning physicians and parents about the association between Reye’s syndrome and the use of salicylates in children with chickenpox or virus-like illnesses, the incidence of Reye's syndrome in the United States began to decline. In the United States between 1980 and 1997, the number of reported cases of Reye’s syndrome decreased from 555 cases in 1980 to about 2 cases per year since 1994.  {Given this dramatic drop and diagnosis is based upon symptoms, it seems that recent developments in diagnosis have removed many children from the pool of those who would have been labeled as having Reyes Syndrome}.   During this time period 93% of reported cases for which racial data were available occurred in whites and the median age was six years. A viral illness occurred in 93% of cases in the preceding three week period. For the period 1991-1994, the annual rate of hospitalizations due to Reye’s syndrome in the US was estimated to be between 0.2 and 1.1 per million population less than 18 years of age. {This rate is inconsistent with “Reye’s syndrome decreased from 555 cases in 1980 to about 2 cases per year since 1994” same article.  Almost every drug has more total sum of negative consequences than aspirin, and given the many long-term benefits, the current warrants against aspirin usage for children are not properly founded.   See for example acetaminophen--jk}

This ties together the specific, extremely rare metabolic disorder that involves mitochondria and affects the liver, a condition that is exacerbated in children (but not adults) by taking aspirin.  Reyes Syndrome is almost unknown among adults, and that this level of occurrence among children as dropped to nearly that level because of the development of laboratory tests.  Reyes syndrome has dropped to under 1/75,000,000 children per year.*  It is a medical historical note.  Thus for example, Googling in aspirin + Reye's Syndrome, the first 3 pages had no article published later than 2000.  Yet the drug industry and health associations continue to issue the warring as though it occurs at the pre 1985 rate.--jk   


*  Reye’s syndrome decreased from 555 cases in 1980 to about 2 cases per year since 1994. (



Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Volume 1454, Issue 1, 31 May 1999, Pages 115-125

John F. T. Glasgowa, Bruce Middletonb, , , Raymond Moorea, Alison Graya and Joanne Hilla

a Nuffield Department of Child Health, The Queen’s University of Belfast, Royal Belfast Hospital for Sick Children, Belfast BT12 6BA, UK

b School of Biomedical Sciences, University of Nottingham Medical School, Queen’s Medical Centre, Nottingham NG7 2UH, UK

Received 22 February 1999;

accepted 10 March 1999.

Available online 14 October 1999.



The effects of aspirin metabolites on β-oxidation were studied in skin fibroblasts from eight typical Reye’s syndrome (RS) patients and controls. RS patients’ cells did not differ from controls in rates of palmitate oxidation or in the three component activities of the mitochondrial trifunctional enzyme (MTE), indicating no inherited β-oxidation defect. Aspirin metabolites salicylate, hydroxyhippurate and gentisate, but not aspirin, directly inhibited palmitate oxidation in control and RS cells. RS cells were significantly more sensitive to inhibition than controls at 0.5 to 5 mM salicylate. Inhibition was concentration-dependent and reversible. Inhibition did not occur in fibroblasts lacking activity of the long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) activity of MTE. Salicylate was therefore inhibiting β-oxidation at this step. Hydroxyhippurate and salicylate reversibly inhibited HAD activities in extracts of control and RS cells. Studies with pure short-chain HAD and LCHAD (MTE) showed hydroxyhippurate and salicylate were competitive inhibitors of the former but mixed (not competitive) inhibitors of the latter. Both compounds inhibited the combined, three-step, MTE reaction measured in the physiological direction. We conclude that (1) salicylate and hydroxyhippurate decrease β-oxidation in intact cells by reversible inhibition of LCHAD activity of the MTE, and (2) β-oxidation in RS cells is inherently more sensitive to inhibition by low concentrations of salicylate than controls.

Author Keywords: Reye’s syndrome; Salicylate; Hydroxyhippurate; Gentisate; Fatty acid β-oxidation; 3-Hydroxyacyl-CoA dehydrogenase; Mitochondrial trifunctional enzyme

Abbreviations: ASA, acetylsalicylic acid (aspirin); ECH, 2-enoyl-CoA hydratase; FBS, foetal bovine serum; KAT, 3-ketoacyl-CoA thiolase; LCHAD or SCHAD, long-chain or short-chain 3-hydroxyacyl-CoA dehydrogenase; MTE, mitochondrial trifunctional enzyme; PBS, phosphate-buffered saline; RS, Reye’s syndrome

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Disclaimer:  The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for any medical advice, diagnosis, and treatment.