Skip to content

Mechanisms underlying the hepatotoxic effects of ecstasy.

Márcia Carvalho, Helena Pontes, Fernando Remião, Maria L Bastos, Félix Carvalho

Current Pharmaceutical Biotechnology August 1, 2010 DOI: 10.2174/138920110791591535 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics MDMA
Keywords Liver Animals Humans N-methyl-3,4-methylenedioxyamphetamine Hallucinogens Models, biological
Key findings MDMA is known to be hepatotoxic in humans, producing jaundice, hepatomegaly, centrilobular necrosis, hepatitis, and fibrosis. The review argues that while metabolism of MDMA into reactive metabolites is a leading proposed mechanism, other factors such as hyperthermia, neurotransmitter efflux, biogenic amine oxidation, polydrug abuse, and environmental features may also increase the risk of liver complications.

Abstract

3,4-Methylenedioxymethamphetamine (MDMA or ecstasy) is a worldwide illegally used amphetamine-derived designer drug known to be hepatotoxic to humans. Jaundice, hepatomegaly, centrilobular necrosis, hepatitis and fibrosis represent some of the adverse effects caused by MDMA in the liver. Although there is irrefutable evidence of MDMA-induced hepatocellular damage, the mechanisms responsible for that toxicity remain to be thoroughly clarified. One well thought-of mechanism imply MDMA metabolism in the liver into reactive metabolites as responsible for the MDMA-elicited hepatotoxicity. However, other factors, including MDMA-induced hyperthermia, the increase in neurotransmitters efflux, the oxidation of biogenic amines, polydrug abuse pattern, and environmental features accompanying illicit MDMA use, may increase the risk for liver complications. Liver damage patterns of MDMA in animals and humans and current research on the mechanisms underlying the hepatotoxic effects of MDMA will be highlighted in this review.

Comparable studies

Other narrative reviews on MDMA, most cited first.

Citations in the library

Explore topics