Methanol ingestion results in the formation of formic acid, a toxic metabolite that can cause metabolic acidosis. Methanol toxicity is therefore dependent on the amount of methanol ingested, the nature of treatment received, elapsed time since ingestion, and the accumulation of formic acid. Both methanol and formic acid concentrations are determined at this laboratory using headspace gas chromatography. An examination of 12 fatalities attributed to methanol poisoning is presented. Six individuals were found deceased, and their postmortem methanol and formic acid concentrations ranged from 84 to 543 mg/dL and 64 to 110 mg/dL, respectively. In the other six individuals, hospital treatment such as bicarbonate, ethanol infusion, and hemodialysis was administered. Antemortem methanol and formic acid concentrations ranged from 68 to 427 mg/dL and 37 to 91 mg/dL, respectively, whereas corresponding postmortem methanol and formic acid levels ranged from undetectable to 49 mg/dL and undetectable to 48 mg/dL, respectively. Hospital treatment of formic acid toxicity resulted in significantly reduced postmortem methanol and formic acid concentrations. Furthermore, the toxicological relevance of nine methanol-positive cases where postmortem methanol concentrations ranged from 3 to 142 mg/dL, with corresponding formic acid levels of less than 10 mg/dL, is discussed.
Despite the reported increased use of ketamine as a recreational drug, relatively few fatalities attributed to ketamine poisoning have been documented. Two recent fatalities in which ketamine was detected are described and compared with cases previously reported in the scientific literature. Concentrations of ketamine were measured in the heart and femoral blood samples using gas chromatography with nitrogen phosphorus detection. Ketamine concentrations in a 26-year-old man whose death was attributed to ketamine intoxication were 6.9 and 1.8 mg/L in heart and femoral blood, respectively. In this case, the ketamine concentration detected in the heart blood is in agreement with the lowest concentration reported in the literature, in which ketamine intoxication was ruled as the cause of death and no other drugs were present. Ketamine concentrations in a 20-year-old man, whose death was attributed to asthma and ketamine was considered an incidental finding, were 1.6 and 0.6 mg/L in heart and femoral blood, respectively. Marked differences between heart and femoral blood ketamine concentrations were observed in both of the reported cases. This may be indicative of incomplete distribution prior to death and/or postmortem redistribution of ketamine.
The interpretation of drug intoxication in death investigations is based on the available published literature. In the case of hydromorphone, the literature is limited. This report serves to facilitate the evaluation of cases where hydromorphone may be implicated in a fatality through the examination of 251 hydromorphone-positive cases in the province of Ontario from 1985 to 2003. Thirty-three of these cases were selected for review in greater detail. In four cases in which hydromorphone was the sole drug detected and death was attributed to hydromorphone toxicity, concentrations ranged from 77 to 2684 ng/mL. Hydromorphone concentrations ranged from 21 to 441 ng/mL in 28 cases in which at least one other drug was detected. In five deaths attributed to natural causes, blood hydromorphone concentrations ranged from 75 to 423 ng/mL. The results of this study emphasize the importance of case specific information. Fatalities due to hydromorphone occurred at 51 ng/mL and greater; however, tolerant users of this drug, as seen in the deaths attributed to natural causes, may achieve incidental concentrations that would otherwise be considered fatal. Hydromorphone was detected and quantitated using gas chromatography-mass spectrometry.
This case report details an individual arrested for drug-impaired driving after leaving the scene of multiple motor vehicle collisions and evading police. The driver was examined by a drug recognition expert and failed the drug recognition evaluation. The driver admitted to using cocaine, marijuana, an antidepressant medication and "N-bomb," a novel psychoactive substance that possesses hallucinogenic properties. Toxicological analyses at the Centre of Forensic Sciences' Toronto laboratory revealed only the substance 2-[4-chloro-2,5-dimethoxyphenyl]-N-[(2-methoxyphenyl)methyl]ethanamine (25C-NBOMe) in the accused's urine. This is the first report in which 25C-NBOMe was identified through DRE and toxicological analyses in a drug-impaired driver.
Infection of fourth-instar Aedes aegypti (L.) with the entomopathogenic digenean Plagiorchis elegans (Rudolphi) alters the carbohydrate metabolism of the insect. Within 24 h of cercarial penetration, total body extracts of infected fourth instars exhibited decreased trehalase activity, increased trehalose-6-phosphatase activity, and a concomitant accumulation of trehalose when compared with uninfected larvae. The amounts of glucose, glycogen and lipids, and the activity of glycogen phosphorylase a were similar in extracts of infected and control larvae. The predominant fatty acids, in both control and infected larvae, were C 18:0, C 18:1, and C 18:3. There were no significant differences in the types or proportions of fatty acids found in control and infected larvae. Parasitic infection is discussed in terms of impaired trehalose metabolism.
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