Skip to content

Fatalities Caused by the MDMA-Related Drug Paramethoxyamphetamine (PMA)

James C. Kraner, Damon Mccoy, Mark A. Evans, Larry Evans, Brenda Sweeney

Journal of Analytical Toxicology October 1, 2001 DOI: 10.1093/jat/25.7.645 (opens in new tab)

Relevant Not relevant

Study at a glance

AI-extracted from the abstract
Characteristics Case series Case report Peer reviewed
Sample size 3
Population Three decedents in the midwestern United States who believed they were ingesting MDMA
Topics MDMA
Keywords Drug Pharmacology
Citations 89
Key findings Three fatalities resulted from PMA ingestion mistaken for MDMA, with postmortem blood PMA concentrations of 1.07, 0.60, and 1.90 mg/L and no MDMA detected.

Abstract

The past several years have seen a marked increase in the recreational use of 3,4-methylenedioxymethamphetamine (MDMA) or "Ecstasy". MDMA use is especially common among young people participating in dance parties called "raves". Paramethoxyamphetamine (PMA) exhibits both structural and pharmacological similarity to MDMA. It may, however, be a more potent central stimulant, particularly in its effects on serotonergic transmission. Several fatalities from PMA have been reported in Australia, and here we report three recent fatalities that occurred in the midwestern United States in which each of the decedents believed that they were ingesting MDMA. Symptoms observed included agitation and bruxism, progressing to severe hyperthermia, convulsions, and hemorrhage. Blood was screened for drugs of abuse by enzyme immunoassay with the presence of amphetamines indicated in each case. Confirmation and quantitation for amphetamines was performed by gas chromatography-mass spectrometry. The deceased, two males ages 19 and 24 and a female age 18, had postmortem blood PMA concentrations of 1.07, 0.60, and 1.90 mg/L, respectively. PMA is not a contaminant of MDMA, and no MDMA was found in any of these cases. The primary metabolite of PMA is produced by O-demethylation to 4-hydroxyamphetamine, a reaction catalyzed by cytochrome P450 2D6. This enzyme is noted to be genetically polymorphic. Those with the "slow metabolizer" phenotype may be likely to have higher peak blood concentrations of PMA. Whether any of the decedents described herein were of the slow metabolizer phenotype is not known. Several groups have advocated the onsite use of the Marquis Test for the purpose of pill screening in efforts to distinguish PMA from MDMA. A dark purple is consistent with MDMA, whereas PMA imparts no color change in this test. PMA is often in the form of a white pill with a Mitsubishi symbol on one side. This design has been identified in at least one of these fatalities.

Comparable studies

Other case reports and case series on MDMA, most cited first.

Study Year Design Participants
'Eve' and 'Ecstasy'. A report of five deaths associated with the use of MDEA and MDMA Individuals whose deaths were associated with MDMA or MDEA use 1987 Case series n = 5
Pathology of deaths associated with "ecstasy" and "eve" misuse. Young white men aged 20 to 25 who died after using ring-substituted amphetamines (MDMA... 1996 Case series n = 7
'Eve' and 'Ecstasy' Individuals who died after using MDMA or MDEA 1987 Case series n = 5
A Method of Conducting Therapeutic Sessions with MDMA Clients with clear therapeutic purpose, excluding those with serious functional... 1998 Case study n = 2
Diversity of Psychopathology Associated with use of 3,4-Methylenedioxymethamphetamine (‘Ecstasy’) Psychiatric patients presenting between 1990 and 1992 whose symptoms developed in the... 1994 Case series n = 13

Citations in the library

Cited by 13

and 8 more in the library

Cites 6

and 1 more in the library

Related reading

Explore topics

MDMA Serotonin