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Pathology of deaths associated with "ecstasy" and "eve" misuse.

Christopher M. Milroy, Jenny Clark, A.r.w. Forrest

Journal of Clinical Pathology February 1, 1996 DOI: 10.1136/jcp.49.2.149 (opens in new tab) via OpenAlex

Summary

AI-generated from the abstract

In seven young white men aged 20 to 25 who died after using ring-substituted amphetamines (MDMA or MDEA), autopsies revealed liver damage ranging from individual cell death to widespread centrilobular necrosis, with one case of massive hepatic necrosis. Heart changes consistent with catecholamine-induced damage appeared in five cases, and brain perivascular hemorrhagic or hypoxic changes in four. Four cases showed changes similar to those seen in heat stroke, though only two had documented hyperthermia. One man died from fulminant liver failure, one from water intoxication, and one likely from a cardiac arrhythmia linked to myocardial fibrosis. The findings suggest multiple injury mechanisms: hyperthermia in some cases and direct toxic effects on liver and other organs even without hyperthermia.

Study at a glance

Characteristics Case series Case report Peer reviewed
Sample size 7
Population Young white men aged 20 to 25 who died after using ring-substituted amphetamines (MDMA or MDEA)
Topics MDMA
Keywords Hyperthermia Pathology Centrilobular necrosis Steatosis
Citations 275
Key finding Ring-substituted amphetamines cause liver, heart, and brain damage through both hyperthermia-related and direct toxic mechanisms.

Abstract

AIMS: To study the postmortem pathology associated with ring substituted amphetamine (amphetamine derivatives) misuse. METHODS: The postmortem findings in deaths associated with the ring substituted amphetamines 3,4-methylenedioxymethyl-amphetamine (MDMA, ecstasy) and 3,4-methylenedioxyethylamphetamine (MDEA, eve) were studied in seven young white men aged between 20 and 25 years. RESULTS: Striking changes were identified in the liver, which varied from foci of individual cell necrosis to centrilobular necrosis. In one case there was massive hepatic necrosis. Changes consistent with catecholamine induced myocardial damage were seen in five cases. In the brain perivascular haemorrhagic and hypoxic changes were identified in four cases. Overall, the changes in four cases were the same as those reported in heart stroke, although only two cases had a documented history of hyperthermia. Of these four cases, all had changes in their liver, three had changes in their brains, and three in their heart. Of the other three cases, one man died of fulminant liver failure, one of water intoxication and one probably from a cardiac arrhythmia associated with myocardial fibrosis. CONCLUSIONS: These data suggest that there is more than one mechanism of damage in ring substituted amphetamine misuse, injury being caused by hyperthermia in some cases, but with ring substituted amphetamines also possibly having a toxic effect on the liver and other organs in the absence of hyperthermia.

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