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Review
.2014 May;46(5):632-42.
doi: 10.1016/j.jemermed.2013.11.104. Epub 2014 Feb 22.

Synthetic cathinones ("bath salts")

Affiliations
Review

Synthetic cathinones ("bath salts")

Matthew L Banks et al. J Emerg Med.2014 May.

Abstract

Background: Synthetic cathinones are popularly referred to in the media as "bath salts." Through the direct and indirect activation of the sympathetic nervous system, smoking, snorting, or injecting synthetic cathinones can result in tachycardia, hypertension, hyperthermia, myocardial infarction, and death.

Objective: The chemical structures and names of bath salts identified by the Ohio Attorney General's Bureau of Criminal Investigation are presented. Based on their common pharmacophores, we review the history, pharmacology, toxicology, detection methods, and clinical implications of synthetic cathinones. Through the integration of this information, the pharmacological basis for the management of patients using synthetic cathinones is presented.

Discussion: Synthetic cathinones activate central serotonergic and dopaminergic systems contributing to acute psychosis and the peripheral activation of the sympathetic nervous system. The overstimulation of the sympathetic nervous system contributes to the many toxicities reported with bath salt use. The pharmacological basis for managing these patients is targeted at attenuating the activation of these systems.

Conclusions: Treatment of patients presenting after using bath salts should be focused on reducing agitation and psychosis and supporting renal perfusion. The majority of successfully treated synthetic cathinones cases have used benzodiazepines and antipsychotics along with general supportive care.

Keywords: amphetamine; bath salts; phenethylamine; sympathomimetic; synthetic cathinones.

Copyright © 2014 Elsevier Inc. All rights reserved.

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Figures

Figure 1
Figure 1
General chemistry of phenethylamine, amphetamine and 3,4-methylenedioxy-methamphetamine (MDMA). The phenethylamine pharmacophore is bolded in each of the structures. The α and β-carbons are the sites of many substitutions to the “bath salts.”
Figure 2
Figure 2
Comparison of the substituted cathinones (methcathinone) to substituted amphetamines (methamphetamine) and the phenethylamine pharmacophore. The phenethylamine pharmacophore is bolded in each of the structures. Methamphetamine has a methyl (single carbon) off the α-carbon and nitrogen (N) terminus of phenethylamine. Methcathinone has carbonyl group (=O) off the β-carbon of methamphetamine.
Figure 3
Figure 3
Simplified schematic of synaptic neurotransmission for the endogenous monoamine dopamine (DA). Panel A shows that under normal (non-drug) conditions, DA is released from the presynaptic neuron into the synaptic cleft where DA can bind to post-synaptic dopamine receptors on the postsynaptic neuron to promulgate neurotransmission. DA can also bind to the dopamine transporter located on the presynaptic neuron and be translocated back into the presynaptic neuron for repackaging and subsequent release. Dopamine uptake by the dopamine transporter is the primary mechanism of terminating the DA-mediated neurotransmission. Panel B shows that under conditions of methcathinone use, there is an increased concentration of DA in the synaptic cleft that results in increased activation of post-synaptic dopamine receptors. Furthermore, methcathinone is a substrate for the dopamine transporter, blocking the ability of DA to bind to the transporter, and thus reducing one of the main mechanisms of dopaminergic neurotransmission termination.
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Comment in

  • Beta-blocker use for toxicity from "bath salts".
    Richards JR, Laurin EG, Albertson TE.Richards JR, et al.J Emerg Med. 2015 Feb;48(2):e45-6. doi: 10.1016/j.jemermed.2014.09.046. Epub 2014 Nov 18.J Emerg Med. 2015.PMID:25453853No abstract available.

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