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Both hypo- and hyper-glycaemia may occur in salicylate poisoning.

Gaseous methyl salicylate (MeSA) is a major volatile in TMV-inoculated tobacco plants, and is produced in parallel with SA.

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Raskin I 1992a Salicylate, a new plant hormone.

A review of 51 fatal cases of acute salicylate poisoning in Ontario during 1983 and 1984, discovered that salicylate was the most common cause of death, due to the ingestion of single drugs.

Toxic doses of salicylate stimulate the respiratory centre leading to respiratory alkalosis.

Lennon AM, Neuenschwander UH, Ribas-Carbo M, Giles L, Ryals JA, Siedow JN 1997 The effects of salicylic acid and tobacco mosaic virus infection on the alternative oxidase of tobacco.

Raskin I 1992b Role of salicylic acid in plants.

Local gastrointestinal (GI) irritation of SA is more marked than ASA (acetylsalicylic acid).

Although the clinical value of screening for salicylates in acute poisoning was emphasized (Chan et al., 1995), determination of plasma salicylate concentration is required to confirm the diagnosis and to estimate the severity of salicylate intoxication.

Chronic salicylate poisoning particularly those with metabolic acidosis, hypoglycaemia, lethargy, coma and fits in malaria endemic areas may mimic severe malaria as was investigated in Kenya (English et al., 1996).

A violet colour indicates the presence of salicylates.

Severe salicylate poisoning is associated with marked respiratory and nervous system toxicity.

Haemodialysis should also be considered in severely poisoned patients with features of central nervous system toxicity, pulmonary oedema, cerebral oedema and in cases of plasma salicylate concentrations of more than 800 mg/L (Proudfoot, 1983).

Fluid retention may occur during forced diuresis and increase the risk of pulmonary oedema in severe salicylate intoxication (Heffner & Sahn, 1981; Balali-Mood, 1981).

In severe salicylate intoxication, haemodialysis and or charcoal haemoperfusion is indicated.
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  • Acetylsalicylic acid may also cause gastric irritation.

    Methyl salicylate poisoning has the odour of the drug which can be detected on the breath and in the urine and vomit.

  • High unbound fraction of salicylate in plasma during intoxication.

    A rapid screening test for the presence of salicylate in the urine may indicate the use of the drug.

  • Unrecognised adult salicylate intoxication.

    The synthetic form is white but if prepared from natural methyl salicylate, it may have a slightly yellow or pink tint.

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Asterixis as a manifestation of salicylate toxicity.

Salicylic acid concentrations above 800 mg/L after 6 hours post exposure is severely toxic and may be lethal (Balali-Mood, 1981). Children 7.2.2 Relevant animal data 7.2.3 Relevant in vitro data

Acute acetylsalicylic acid poisoning.

These effects occur when salicylates are administered during the third trimester, and thus its use during this period of pregnancy should be avoided (Insel, 1996).

Salicylate associated asystole: report of two cases.

The uricosuric activity of phenylbutazone, probenecide and sulphinpyrazone is strongly antagonized by salicylate and maybe completely diminished by small doses due to decreased tubular reabsorption of uric acid (Insel, 1996).

Protein binding of salicylate in uremic and normal plasma.

Fodor J, Gullner G, Adam AL, Barna B, Komives T, Kiraly Z 1997 Local and systemic responses of antioxidants to tobacco mosaic virus infection and to salicylic acid in tobacco.

Salicylate inhibition of antiplatelet effect of aspirin.

Leon J, Shulaev V, Yalpani N, Lawton MA, Raskin I 1995 Benzoic acid 2-hydroxylase, a soluble oxygenase from tobacco, catalyzes salicylic acid biosynthesis.

The clinical value of screening for salicylates in acute poisoning.

Salicylate inhibits the conversion of arachidonic acid to the unstable endoperoxide intermediate PG G2, which is catalyzed by the enzyme cyclo oxygenase.

Hypoglycaemia with salicylate poisoning.

In a report of two cases of severe salicylate poisoning, asystole occurred shortly after the intravenous administration of diazepam (Berk & Anderson, 1989).

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