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Fatal 251-NBOMe Intoxication: A New Recreational Risk

Yoshie Umemura, Thomas A. Andrew, Valerie L. Jacobs, Andrew J. Giustini, Lionel D. Lewis, James J. Filiano

Academic Forensic Pathology March 1, 2015 DOI: 10.23907/2015.009 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Case study Case report Peer reviewed
Sample size 1
Population 17-year-old girl with mood disorders who ingested 25I-NBOMe
Measures liquid chromatography/time-of-flight mass spectrometry
Key findings The authors report that a 17-year-old girl died after ingesting 25I-NBOMe on blotter paper, presenting in status epilepticus and progressing to hyperthermia, metabolic acidosis, rhabdomyolysis, acute kidney injury, and irreversible cerebral edema, with brain death declared on hospital day seven. They suggest the cause was fulminant serotonin syndrome, possibly compounded by chronic lithium therapy.

Abstract

Abuse of synthetic drugs is an emerging trend in substance abuse. Identification of exposure to such chemicals is often difficult due to the paucity of specific laboratory assays. One such group of compounds is the 2C class of phenethylamines that include 2-(4-lodo-2, 5-dimethoxyphenyl)-N-I[(2-methyoxyphenyl)methyl]ethanamine, known as 251-NBOMe or the street names “Smiles” and “N-Bomb.” This family of compounds consists of relatively new synthetic drugs, a two-carbon substitute of phenethylamine, which is a highly potent serotonin receptor 2A(5-HT2A) agonist. There are limited data on 251-NBOMe poisoning. We report a 17-year-old girl with mood disorders who died following 251-NBOMe ingestion, revealing its lethality. She presented in status epilepticus shortly after ingesting a substance on a blotter paper at a concert. She then acutely developed hyperthermia, metabolic acidosis, rhabdomyolysis, elevated transaminases, acute kidney injury, hypokalemia, hypocalcemia, and irreversible cerebral edema, and was declared brain dead on hospital day seven. Specific toxicological testing revealed exposure to 251-NBOMe from antemortem whole blood liquid chromatography/time-of-flight mass spectrometry at concentrations above 0.25 ng/mL. We suggest that the patient died from fulminant serotonin syndrome following acute 251-NBOMe intoxication with a possible contribution from chronic lithium therapy.

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