Detection of 25C-NBOMe in Three Related Cases.
John J Kristofic, Jeffrey D Chmiel, George F Jackson, Shawn P Vorce, Justin M Holler, Stephen L Robinson, Thomas Z Bosy
Journal of analytical toxicology July 1, 2016 DOI: 10.1093/jat/bkw035 via PubMed
Summary
AI-generated from the abstractA 23-year-old Caucasian male died after being subdued by military law enforcement, having experienced severe respiratory distress. Autopsy revealed mild to moderate coronary atherosclerosis, biventricular dilation, mild right ventricular hypertrophy, and bilateral pulmonary edema and congestion. Blood contained no drugs or ethanol, but urine had pseudoephedrine, nicotine, and cotinine. A designer drug screen detected 25C-NBOMe, 25C-NBOH, and 2C-C in blood and urine. 25C-NBOMe concentrations were measured in blood (2.07 ng/mL), urine (27.43 ng/mL), and various organs. The medical examiner ruled the cause of death as 25C-NBOMe toxicity temporally associated with excited delirium and forcible restraint, manner accidental.
Study at a glance
| Characteristics | Case study Case report Peer reviewed |
|---|---|
| Sample size | 1 |
| Population | 23-year-old Caucasian male |
| Intervention | 25C-NBOMe |
| Citations | 34 |
| Key finding | Death was caused by 25C-NBOMe toxicity in the context of excited delirium and forcible restraint. |
Abstract
An accidental death associated with the use of the designer drug, 2-(4-chloro-2,5-dimethoxyphenyl)-N-(2-methoxybenzyl)ethanamine (25C-NBOMe), is reported. A 23-year-old Caucasian male experienced severe respiratory distress and died after being subdued by military law enforcement. At autopsy, remarkable findings upon internal examination included mild to moderate coronary atherosclerosis, biventricular dilation, mild right ventricular hypertrophy and bilateral pulmonary edema and congestion. The decedent's blood contained no drugs, ethanol or other volatile compounds. Pseudoephedrine, nicotine and cotinine were detected in his urine. A LC-QTOF designer drug screen, employing a basic solid-phase extraction, was used to isolate 25C-NBOMe, 25C-NBOH and 2C-C from both blood and urine specimens. Quantitative analysis was performed by LC-MS-MS operating in multiple reaction monitoring mode. 25C-NBOMe and 2C-C were present in the blood (2.07 and 0.12 ng/mL) and in the urine (27.43 ng/mL and 0.38 ng/mL), respectively. 25C-NBOMe concentrations were determined by standard addition in the brain (19.10 ng/g), spleen (27.13 ng/g), lung (25.21 ng/g), liver (15.20 ng/g), kidney (25.06 ng/g) and gastric contents (30.24 µg total in 100 mL submitted). On the basis of decedent case history, autopsy and toxicological findings, the medical examiner ruled the cause of death as 25C-NBOMe toxicity temporally associated with excited delirium and forcible restraint. The manner of death was ruled accidental.