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Mireia Segura

5 papers in the library · 808 citations · publishing 2001-2007

Papers

Human Pharmacology of MDMA

Therapeutic Drug Monitoring March 19, 2004 Rafael de la Torre, Magı́ Farré, Pere N. Roset et al. 445 citations

MDMA (ecstasy) is a widely misused psychostimulant that increases energy, euphoria, and sociability while also producing distinctive 'entactogen' effects such as feeling close to others and increased empathy. It works by promoting the release and blocking the reuptake of serotonin, dopamine, and norepinephrine. Acute toxic effects include serotonin syndrome, characterized by muscle rigidity, hyperreflexia, and hyperthermia. MDMA metabolism involves two main pathways; one is partially regulated by the polymorphic enzyme CYP2D6, but mechanism-based inhibition after two consecutive doses limits the impact of CYP2D6 genetics on acute toxicity. Metabolism may also contribute to long-term neurotoxic effects through progressive degeneration of the serotonergic system.

γ‐Hydroxybutyrate (GHB) in Humans

Annals of the New York Academy of Sciences August 1, 2006 Sergio Abanades, Magı́ Farré, Mireia Segura et al. 124 citations

Gamma-hydroxybutyrate (GHB) produces dose-related changes in subjective effects, showing a mixed stimulant-sedative pattern: initial feelings of euphoria, high, and liking, followed by mild-to-moderate sedation with impaired performance and balance. Single oral doses of 40, 50, 60, and 72 mg/kg were given to eight volunteers. Mean peak plasma concentrations ranged from 79.1 to 130.1 μg/L. Physiological and subjective effects were dose-dependent and related to plasma concentrations. Urinary excretion was mainly related to dose. The results suggest high abuse liability at the doses typically consumed.

3,4-Dihydroxymethamphetamine (HHMA). A Major in Vivo 3,4-methylenedioxymethamphetamine (MDMA) Metabolite in Humans

Chemical Research in Toxicology August 2, 2001 Mireia Segura, Jordi Ortuño, Magı́ Farré et al. 105 citations

A new method using strong cation-exchange solid-phase extraction and high-performance liquid chromatography with electrochemical detection was validated for measuring the metabolite 3,4-dihydroxymethamphetamine (HHMA) in plasma and urine. Applied to samples from healthy volunteers given MDMA (ecstasy), HHMA appeared as a major metabolite, with peak plasma concentrations (154.5 microg/L) and overall exposure (AUC 1990.9 microg/L h) similar to those of MDMA itself. Urinary recovery of HHMA over 24 hours accounted for 17.7% of the 100 mg MDMA dose, raising total recovery of MDMA and its metabolites to 58%. The method is accurate and precise for pharmacokinetic studies, and measuring HHMA may help clarify its role in MDMA metabolism and potential neurotoxicity.

A comparative study on the acute and long‐term effects of MDMA and 3,4‐dihydroxymethamphetamine (HHMA) on brain monoamine levels after i.p. or striatal administration in mice

British Journal of Pharmacology January 1, 2005 Isabel Escobedo, Esther O’shea, Laura Orío et al. 68 citations

MDMA itself does not cause the immediate release of dopamine or serotonin in the mouse brain; instead, peripheral injection of MDMA reduced striatal dopamine and modestly reduced serotonin one hour after the last dose, but direct injection into the striatum did not produce these acute effects. The metabolite HHMA also did not contribute to acute dopamine depletion, as its effects differed from MDMA after peripheral injection. Long-term dopamine loss seven days later was not due to MDMA itself, since only very high intrastriatal doses caused such loss, and HHMA did not alter striatal dopamine after peripheral injection. HHMA crossed the blood–brain barrier but was not detected in brain after peripheral MDMA, suggesting it is metabolized to other active compounds.

Disposition of Gamma-Hydroxybutyric Acid in Conventional and Nonconventional Biologic Fluids After Single Drug Administration: Issues in Methodology and Drug Monitoring

Therapeutic Drug Monitoring February 1, 2007 Sergio Abanades, Magı́ Farré, Mireia Segura et al. 66 citations

After a single oral dose of 50 mg/kg sodium GHB, mean peak plasma concentrations reached 83.1 μg/mL at 30 minutes, then declined to 0.9 μg/mL at 6 hours. GHB appeared in oral fluid at levels one-third to one-fourth of plasma concentrations, with a half-life of about 1.2 hours compared to 0.7 hour in plasma. Less than 2% of the dose was excreted in urine, and sweat contained only low concentrations. Subjective effects followed a mixed sedative-stimulant pattern, peaking between 1 and 1.5 hours and lasting 2 hours, and were related to plasma concentrations. Oral fluid and sweat were not suitable for monitoring GHB consumption.