GHB
- 1 September 2001
- journal article
- case report
- Published by Wolters Kluwer Health in American Journal of Forensic Medicine & Pathology
- Vol. 22 (3) , 266-269
- https://doi.org/10.1097/00000433-200109000-00013
Abstract
GHB can be produced either as a pre- or postmortem artifact. The authors describe two cases in which GHB was detected and discuss the problem of determining the role of GHB in each case. In both cases, NaF-preserved blood and urine were analyzed using gas chromatography. The first decedent, a known methamphetamine abuser, had GHB concentrations similar to those observed with subanesthetic doses (femoral blood, 159 microg/ml; urine, 1100 microg/ml). Myocardial fibrosis, in the pattern associated with stimulant abuse, was also evident. The second decedent had a normal heart but higher concentrations of GHB (femoral blood, 1.4 mg/ml; right heart, 1.1 mg/ml; urine, 6.0 mg/ml). Blood cocaine and MDMA levels were 420 and 730 ng/ml, respectively. Both decedents had been drinking and were in a postabsorptive state, with blood to vitreous ratios of less than 0.90. If NaF is not used as a preservative, GHB is produced as an artifact. Therefore, the mere demonstration of GHB does not prove causality or even necessarily that GHB was ingested. Blood and urine GHB concentrations in case 1 can be produced by a therapeutic dose of 100 mg, and myocardial fibrosis may have had more to do with the cause of death than GHB. The history in case 2 is consistent with the substantial GHB ingestion, but other drugs, including ethanol, were also detected. Ethanol interferes with GHB metabolism, preventing GHB breakdown, raising blood concentrations, and making respiratory arrest more likely. Combined investigational, autopsy, and toxicology data suggest that GHB was the cause of death in case 2 but not case 1. Given the recent discovery that postmortem GHB production occurs even in stored antemortem blood samples (provided they were preserved with citrate) and the earlier observations that de novo GHB production in urine does not occur, it is unwise to draw any inferences about causality unless (1) blood and urine are both analyzed and found to be elevated; (2) blood is collected in NaF-containing tubes; and (3) a detailed case history is obtained.Keywords
This publication has 22 references indexed in Scilit:
- Determination of γ-Hydroxybutyrate (GHB) in Biological Specimens by Gas Chromatography-Mass SpectrometryJournal of Analytical Toxicology, 2000
- Analysis of Gamma-Hydroxybutyrate (GHB) in Urine by Gas Chromatography-Mass SpectrometryJournal of Analytical Toxicology, 1999
- Gamma-hydroxybutyric acid: an endogenous neuromodulator with abuse potential?Trends in Pharmacological Sciences, 1999
- Sudden Cardiac DeathCirculation, 1998
- A Tale of Novel Intoxication: Seven Cases of γ-Hydroxybutyric Acid OverdoseAnnals of Emergency Medicine, 1998
- Driving Under the Influence of GHB?Journal of Analytical Toxicology, 1994
- Dose-dependent absorption and elimination of gamma-hydroxybutyric acid in healthy volunteersEuropean Journal of Clinical Pharmacology, 1993
- Pharmacokinetics of gamma‐hydroxybutyric acid in alcohol dependent patients after single and repeated oral doses.British Journal of Clinical Pharmacology, 1992
- GABAA and GABAB receptor site distribution in the rat central nervous systemNeuroscience, 1987
- Correlation of Blood Levels of 4-Hydroxybutyrate with State of ConsciousnessAnesthesiology, 1964