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Case Reports
. 2010 Nov;48(9):924-7.
doi: 10.3109/15563650.2010.531021.

Case series of individuals with analytically confirmed acute mephedrone toxicity

Affiliations
Case Reports

Case series of individuals with analytically confirmed acute mephedrone toxicity

David M Wood et al. Clin Toxicol (Phila). 2010 Nov.

Abstract

Context: Previous reports of acute toxicity/harm associated with mephedrone use have been based on self-reported mephedrone use; toxicological screening has not been undertaken in these cases to determine whether mephedrone has been used.

Objective: To report the first case series of analytically confirmed mephedrone-related acute toxicity.

Materials and methods: Serum samples were collected from individuals presenting to an emergency department (ED) with acute toxicity related to self-reported mephedrone use. Toxicological analysis, by gas-chromatography coupled with mass-spectrometry and liquid chromatography with tandem mass-spectrometry was performed to qualitatively confirm mephedrone use. Symptoms/signs of acute mephedrone toxicity and basic physiological parameters were extracted from the routine ED records.

Results: Acute mephedrone-related toxicity was analytically confirmed in seven male patients; the mean ± SD age was 24.6 ± 6.5 years (range 16-36 years). Agitation (four patients) was the most common symptom/sign reported; other common symptoms/signs included: palpitations (two patients); chest pain (two patients); self-limiting pre-hospital seizures (one patient) and headaches (one patient). The mean heart rate was 109.1 ± 21.8 (range 80-140) beats per minute; one patient had a "severe" tachycardia (heart rate of ≥ 140 bpm). The mean systolic blood pressure was 153.0 ± 39.6 (range 110-210) mmHg; three patients had clinically significant hypertension (systolic blood pressure ≥ 160 mmHg).

Discussion: These analytically confirmed acute mephedrone toxicity presentations had clinical features of toxicity consistent with an acute sympathomimetic toxidrome (e.g. hypertension, tachycardia and agitation). These findings are similar to the pattern of toxicity seen with other sympathomimetic recreational drugs such as 3,4-Methylenedioxymethamphetamine (MDMA) and cocaine.

Conclusion: The process for determining whether a novel psychoactive substance should be controlled often relies on demonstrated/proven acute harm associated with its use. It is important that clinical toxicologists undertake appropriate biological sampling and toxicological analyses in suspected cases of "novel psychoactive drug" toxicity. This will ensure that both clinicians and legislative authorities are informed of the confirmed pattern of toxicity associated with these drugs.

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