[Intoxation with paramethoxymethamphetamine]. / Forgiftning med parametoksymetamfetamin.

BACKGROUND: Since the summer of 2010, there has been an epidemic of deaths related to paramethoxymethamphetamine (PMMA) in Norway. We present a review of the pharmacology and toxicology of the substance. MATERIAL AND METHOD: The review is based on a literature search in the databases PubMed, Ovid and MEDLINE. A discretionary selection was made of relevant articles. RESULTS: Paramethoxymethamphetamine and paramethoxyamphetamine (PMA) are two so-called designer amphetamines which appear from time to time on the illegal narcotics market in many countries. They are frequently sold as ecstasy or amphetamine, often mixed with amphetamine or methamphetamine. The substances, known on the street as «Death¼, have potent serotonergic effects and are associated with significant toxicity. Many deaths have been reported worldwide, even after intake of an «ordinary user dose¼. The narcotic effect is not very pronounced and the onset is slow, which may lead to unintentional overdosing. INTERPRETATION: In cases of severe intoxation that are apparently related to intake of amphetamine or ecstasy, PMMA/PMA intoxation should be suspected.

Blood GHB concentrations and results of medical examinations in 25 car drivers in Norway.

PURPOSE: information on the clinical effects associated with whole blood gamma-hydroxybutyrate (GHB) concentrations is sparse. We have investigated possible relationships between GHB blood concentrations and clinical effects in car drivers. METHODS: in Norway, the police stop car drivers suspected of drug-driving. Medical doctors perform a clinical test of impairment (CTI) and blood samples are screened for drugs/medicines by immunological, enzymatic and chromatographic methods at the Division of Forensic Toxicology and Drug Abuse. GHB is a part of our extended drug-testing programme. GHB is standardly measured as GBL by gas chromatographic method. All the results were stored in a database. This database was searched between 2000 and 2007 for car drivers positive only for GHB, called GHB-drivers. A control group with a completely negative blood analysis, including GHB, called control-drivers, was included in the study. RESULTS: twenty-five car drivers had only GHB in their blood. The police reported that 78% showed unsafe driving behaviour and seven were involved in car accidents, without serious injury. A total of 61% of the drivers were found to be sleepy or in an even more reduced state of consciousness. The median GHB blood concentration was 1,262 (range 592-2,191) µmol/L, measured a median of 69 min after the police had stopped the driver from driving. The GHB blood concentration tended to increase with increasing impairment and reduced consciousness. Clinical findings were normal- to large-sized pupils (86%), impairment as the final conclusion (84%), impaired balance/nystagmus (62 and 54%, respectively), congested/shiny conjunctiva (67%), apathetic, aggressive or abnormal behaviour (65%), reduced short-term memory (67%), reduced/absent pupillar reaction to light (65%), heart rate ≤ 70 beats/min (56%), and some level of reduced consciousness (56%). In the control-drivers, 15.6% were found by the medical doctors to have reduced consciousness or impaired. CONCLUSIONS: the median GHB blood concentration of the 25 car drivers was high. Most drivers had clinical impairment that was not explainable by injuries, with depressive effects on the central nervous system and sympathomimetic effects on eyes. Effects on impairment and consciousness tended to be concentration-dependent. The number of drivers who were impaired or had reduced consciousness was highly increased in GHB-drivers compared to controls. Based on these results, we conclude that the GHB-drivers most probably drove in an unsafe manner due to impairment by GHB.

Lethal poisoning with ethiofencarb and ethanol.

Ethiofencarb is one of the carbamate compounds, which are, in general, less toxic than organophosphorus insecticides. This is due to their reversible acetylcholinesterase inhibition and relative inability to cross the blood-brain barrier. Generally, ethiofencarb is regarded to be of low toxicity (LD(50) > 200 mg/kg); however, severe poisoning and death are not uncommon. To our knowledge, no measurements of ethiofencarb and its metabolites in human postmortem whole blood have been published. We present here a case report of fatal ethiofencarb intoxication with quantitative analysis of ethiofencarb and its metabolites in ante- and postmortem blood. In addition, postmortem urine was collected and analyzed. A 56-year-old man, who worked as a gardener, was found in poor condition, sitting in his car seat. He had been vomiting. The man was admitted to the local hospital about 1 h later. At admission, he was conscious, but unable to speak clearly. His condition deteriorated, and he developed severe pulmonary edema. Resuscitation with atropine and adrenaline were attempted, but he died approximately 3 h after admission. The analysis of postmortem peripheral blood revealed 0.12 g/100 mL ethanol, 26.4 mg/L ethiofencarb, 37.9 mg/L ethiofencarbsulfoxide, and 0.9 mg/L ethiofencarbsulfone. Ethanol (0.26 g/100 mL), ethiofencarb, ethiofencarbsulfoxide, and ethiofencarbsulfone were also detected in urine.