Overview of Amphetamine-Type Stimulant Mortality Data – UK, 1997–2007

Abstract

Background/Aims: Despite being amphetamine derivatives, MDMA and its analogues show a number of clinical pharmacological differences with respect to both amphetamine (AMP) and methylamphetamine (METH). We aimed here at reporting and analysing information relating to the socio-demographics and clinical circumstances of the AMP-type stimulant-related deaths for the whole of the UK. Methods: Data (1997–2007) were taken from the National Programme on Substance Abuse Deaths (np-SAD) database, collecting information from UK coroners/procurators fiscal. To calculate rates of fatalities per 100,000 users, appropriate AMP/METH and ecstasy users’ numbers were taken from the 2001–2007 British Crime Survey. Results: Overall, 832 AMP/METH- and 605 ecstasy (mostly MDMA and methylenedioxyamphetamine/MDA)-related deaths were respectively identified. In comparison with AMP/METH victims, the ecstasy ones were more likely to be younger (28.3 vs. 32.7 years; p < 0.0001) and less likely to be known as drug users (PR = 1.9; CI 1.5–2.6). Ecstasy was more likely to be identified on its own than AMP/METH (p = 0.0192). Contributory factors were more frequently mentioned by coroners in the ‘AMP/METH-only’ (106 cases) group than in the ‘ecstasy-only’ (104 cases) one (p = 0.0043). Both poly- and monodrug AMP/METH fatalities per 100,000 16- to 59-year-old users were significantly more represented than ecstasy fatalities (respectively 17.87 ± 4.77 deaths vs. 10.89 ± 1.27; p = 0.000; 2.09 ± 0.88 vs. 1.75 ± 0.56; p = 0.0096). However, mono-intoxication ecstasy fatalities per 100,000 16- to 24-year-old users were significantly more represented than AMP/METH fatalities (1.67 ± 0.52 vs. 0.8 ± 0.65; p = 0.0007). Conclusion: With respect to AMP/METH, ecstasy was here more typically identified in victims who were young, healthy, and less likely to be known as drug users. AMP/METH high mortality rates may be explained by users’ high levels of physical co-morbidity; excess ecstasy-related fatality rates in young users may be a reason for concern. Although the coroners’ response rate was of 90–95%, study limitations include both reporting inconsistency over time and lack of routine information on drug intake levels prior to death.

Mortality, Causes of Death and Risk Factors for Death Among Primary Amphetamine Users in the Swedish Criminal Justice System

“…Some studies describe causes of death among amphetamine users undergoing medicolegal autopsies (DeLetter, Piette, Lambert, & Cordonnier, 2006;Eksborg & Rajs, 2008;Pilgrim, Gerostamoulos, Drummer, & Bollmann, 2009;Schifano, Corkery, Naidoo, Oyefeso, & Ghodse, 2010), but there is a lack of cohort studies performing analyses of risk factors for death in amphetamine users. A recent review (Singleton, Degenhardt, Hall, & Zabransky, 2009) urged for follow-up studies in this area.…”

Clinical Pharmacology of 3,4-Methylenedioxymethamphetamine (MDMA, “Ecstasy”): The Influence of Gender and Genetics (CYP2D6, COMT, 5-HTT)

“…This increase in abuse has become a growing public health concern since MDMA can produce acute toxicity and fatal episodes [2]. In addition, its chronic consumption is associated with neurocognitive deficits and increased psychopathology prevalence [3]–[6].…”

Δ9-Tetrahydrocannabinol attenuates MDMA-induced hyperthermia in rhesus monkeys

“…These effects are present across a range of ambient temperatures (Von Huben et al, 2007) across which rat (Malberg and Seiden, 1998), but not human (Freedman et al, 2005), temperature responses change from hypo thermia to hyper thermia. Given species differences in thermoregulation, it continues to be critical to determine the degree to which primate responses to MDMA differ from those of rats under conditions likely to contribute to, or protect against, medical emergency and even death in the human user (Patel et al, 2004, Schifano et al, 2010). One such condition that may be important for the human user is the concurrent use of cannabis and the resulting exposure to one of the more active constituents, Δ 9 -tetrahydrocannabinol (THC) (Mohamed et al, 2011).…”