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Introduction - Uppsala Monitoring Centre

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ullous eruption < 1 % and purpura.<br />

B) Opthalmological events (Type B events): ptosis, strabismus and amaurosis may<br />

only be relevant to salicylic acid as I have found no confirmation of a causal<br />

association with Aspirin. There have been two reports of myopia and raised<br />

intraocular pressure, but these are only likely to have been tested if there were<br />

ocular symptoms, which had been referred to an ophthalmologist. Similarly<br />

papilloedema. They might be more frequent than this figure suggests.<br />

C) Aspirin idiosyncrasy (Type B events): These are substantiated by many papers,<br />

but the mechanism is not certain. It is likely that hypotension is secondary to<br />

anaphylactoid shock (or poisoning) and that hypersensitivity is part of the same<br />

syndrome, which is not an allergy since no antigen–antibody reactions have<br />

been identified (Freie, 2000).<br />

D) Haematological events (Type B events): There is some evidence supporting<br />

thrombocytopenia, agranulocytosis and aplastic anaemia. The relative risks were<br />

1.9 and 2.9 respectively and, according to Dr Shapiro, the results were equivocal<br />

(IAAAS, 1986) slightly elevated, but the relative risks were of borderline statistical<br />

significance (Scrip, 1986).<br />

E) Renal events: oliguria, renal failure, acute and/or chronic interstitial nephritis,<br />

acute tubular necrosis, papillary necrosis, analgesic nephropathy: haematuria,<br />

nocturia, symptoms of urinary tract infection, renal colic, renal calculi, renal<br />

failure, dehydration, acidosis, anaemia, hypertension, dyspepsia, peptic ulcers<br />

with haemorrhage are common. ‘Reported in a considerable number of patients<br />

who have consumed a large amount of Aspirin’, (Wigley, 1973).<br />

F) Salicylism - mild chronic intoxication (Type A events): tinnitus, dizziness,<br />

diminished vision, hearing loss, headache, feeling of intoxication, nausea,<br />

vomiting. The onset of these symptoms indicates that the plasma concentration<br />

was approaching 35 mgm per 100cc. (Graham & Parker, 1948). To keep below<br />

the threshold for salicylism a dose of 12 to 20 gr every 4 hours to start with and<br />

then every six hours maintained a plasma salicylate value of 20 – 25 mgm per<br />

100cc. The threshold for salicylism was 30 mgm per 100cc. (Hoffman et al.,<br />

1949).<br />

G) Reproductive events (Type A events): prolonged labour, teratogenicity (animals<br />

only), increased bleeding.<br />

H) Reye’s Syndrome is a rare paediatric disorder characterized by an initial<br />

febrile illness, commonly influenza or varicella, followed in several days by<br />

vomiting, disorientation, seizures and loss of consciousness. Signs – liver<br />

histology, hyperammonemia, lactic acidemia, elevated free fatty acids and<br />

amino acids (Raye et al., 1963). Most of the children died within a few days<br />

and at autopsy there was diffuse fatty infiltrate of the liver and severe cerebral<br />

oedema. The clinical and pathological features of the syndrome were first<br />

clearly defined by Dr. Reye and his associates in 1963 in Australia. Numerous

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