Introduction - Uppsala Monitoring Centre

(ADEC, 1971). It is unlikely that clioquinol was the only causative factor in
the production of SMON as has been pointed out by Meade:
The possibility of protopathic bias since the early symptoms of SMON can be
diarrhoea and abdominal pain.
The absence of SMON prior to about 1955 despite being on the market since
1934.
The decline in incidence before the drug was suspended.
A large proportion of patients with SMON had not taken clioquinol.
The virtual absence outside Japan.
Some cases of SMON had not taken clioquinol (Meade, 1975).
On the other hand, there are observations inexplicable by the infection
hypothesis:
SMON is a new disease seldom reported in other counties.
Rare in children and high morbidity in middle or old aged women.
The disease was sporadic: it was hard to trace contact between cases.
No fever, rash and other symptoms suggesting infection; blood or spinal fluid
showed no abnormality.
Pathohistology: no inflammatory change. Changes reminiscent of outcomes of
metabolic disorder, vitamin deficiency or intoxication (Kono, 1971). Further
reading: KK Jain’s Drug-induced Neurological Disorders, Hogrefe & Huber
2001, 435-441.Venning said that there was no satisfactory evidence
concerning the incidence of the adverse reaction, but this was almost certainly
too low for a cohort approach to post-marketing surveillance to be effective for
either alerting or verification (Venning, 1983).
1899 Aspirin
Use: anti-inflammatory agent and analgesic
ADR: Reye’s syndrome (acute encephalopathy associated with selective hepatic
abnormality and metabolic decompensation).
SED 1952: acetylsalicylic acid should not be given in the first years of life,
because young children are particularly sensitive.
Reye’s syndrome was named after Dr R Douglas Reye, who along with Dr
Graeme Morgan and Dr Jim Baral, reported on a series of children admitted to
the Royal Alexandra Hospital for Children in Sydney. The original report by
Reye et al (1963) did not mention Aspirin use and the author did not believe
that it was due to Aspirin. However, in a letter to the editor of ‘Pediatrics’ in
1988, Dr Baral claimed that 11 of the 21 patients in the original study were
given Aspirin before the onset of their syndrome and that exposure to other
sources of salicylates (such as topical creams, gels or shampoos) was
possible (Baral 1988). This is in contrast to a statement by Dr Morgan in 1985
that ‘We enquired into the use of medications, including Aspirin, but the