Citation

Schep LJ, Slaughter RJ, Vale JA, Beasley DM, Gee P. Clin. Toxicol. (Phila) 2011; 49(3): 131-141.

Affiliation

Department of Preventive and Social Medicine, National Poisons Centre, University of Otago, Dunedin, New Zealand.

Copyright

(Copyright © 2011, Informa - Taylor and Francis Group)

DOI

10.3109/15563650.2011.572076

PMID

21495881

Abstract

Introduction. Benzylpiperazine (BZP) and trifluoromethylphenylpiperazine (TFMPP) are synthetic phenylpiperazine analogues. BZP was investigated as a potential antidepressant in the early 1970s but was found unsuitable for this purpose. More recently, BZP and TFMPP have been used as substitutes for amfetamine-derived designer drugs. They were legally available in a number of countries, particularly in New Zealand, and were marketed as party pills, but are now more heavily regulated. This article will review the mechanisms of toxicity, toxicokinetics, clinical features, diagnosis, and management of poisoning due to BZP and TFMPP. Methods. OVID MEDLINE and ISI Web of Science were searched systematically for studies on BZP and TFMPP and the bibliographies of identified articles were screened for additional relevant studies including nonindexed reports. Nonpeer-reviewed sources were also accessed. In all, 179 papers excluding duplicates were identified and 74 were considered relevant. Mechanisms of action. BZP and TFMPP have stimulant and amfetamine-like properties. They enhance the release of catecholamines, particularly of dopamine, from sympathetic nerve terminals, increasing intra-synaptic concentrations. The resulting elevated intra-synaptic monoamine concentrations cause increased activation of both central and peripheral α- and