GHB-O-β-glucuronide in blood and urine is not a suitable tool for the extension of the detection window after GHB intake

Because of its small detection window, uncovering drug-facilitated crime after gamma-hydroxybutyric acid (GHB) intake remains a problem. The aim of this experiment was to determine endogenous concentrations of GHB and GHB-O-β-glucuronide (GHB-Gluc) in plasma and urine samples and to compare them with concentrations after GHB intake in humans. Plasma and urine samples of volunteers (n = 50) who had never taken GHB during their lifetime (control group) were collected, and endogenous concentrations of GHB and GHB-Gluc were determined. In addition, plasma and urine samples of patients (n = 3) therapeutically taking sodium oxybate (GHB-sodium salt) were collected prior to and at different time points after the intake. GHB was determined via a liquid chromatography (LC)–tandem mass spectrometry system operated in multiple reaction monitoring mode. GHB-Gluc was detected by LC–quadrupole time-of-flight mass spectrometry. In plasma and urine samples of the control group (n = 50), endogenous concentrations of GHB-Gluc ranged from 0.011 to 0.067 mg/L and from 0.16 to 7.1 mg/L, respectively, while unconjugated GHB concentrations were less than 2 mg/L in both matrices. In contrast, after sodium oxybate administration, GHB concentrations increased markedly, and fell to below the commonly used cutoff value (plasma 4 mg/L and urine 10 mg/L) after 6–8 h in all patients. GHB-Gluc concentrations showed no significant time-dependent increase in plasma samples. In urine, GHB-Gluc concentrations increased after GHB intake, but were generally not higher than the endogenous concentrations of the control group. Therefore, it can be concluded that GHB-Gluc concentrations are not a suitable marker for extending the detection window after GHB intake.