γ-Hydroxybutyric acid (GHB) is a substance frequently abused as a knockout agent.Because of possible amnesia experienced by victims of GHB exposure and the short detection time of GHB in biological samples, the proof of GHB uptake is often challenging for forensic toxicologists. For this reason, various approaches have been evaluated to prolong the detection of GHB intake. In the present study, a fatty acid ester of GHB (4-palmitoyloxy butyrate [GHB-Pal; 3-carboxypropyl hexadecanoate]) was synthesized with the intent of examining whether such esters could be detected as metabolites of GHB in blood samples. Using the structurally elucidated synthesis product (structural elucidation by means of high performance liquid chromatography quadrupole time of flight mass spectrometry [LC-QToF-MS]), an LC triple quadrupole mass spectrometric (LC-MS/MS) method was established for the detection of GHB-Pal. Blood (plasma) samples from four cases in which GHB was previously detected at relevant concentrations (56.1-96.5 μg/ml) were analyzed with respect to GHB-Pal. Signals for GHB-Pal, as well as possible signals for other fatty acid esters of GHB, were detectable in these specimens. (Negative) control samples (20 plasma samples and 20 red blood cell/blood clot samples; from cases in which an intake of GHB or its precursors was not assumed) were all negative for GHB-Pal. To evaluate a possible forensic benefit of GHB fatty acid esters (prolongation of the detection window of a GHB uptake), the analysis of additional plasma samples collected after GHB uptake

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In crimes facilitated by γ‐hydroxybutyric acid (GHB) administration, the frequent occurrence of anterograde amnesia of the victims as well as the short detection window and variations of endogenous GHB concentrations complicate obtaining analytical proof of GHB administration. Because elevated endogenous organic acid concentrations have been found in the urine of patients with succinic semialdehyde deficiency (leading to accumulation of GHB in human specimens) and after GHB ingestion, we searched for an alternative way to prove GHB administration via detection of elevated organic acid concentrations in blood plasma and urine. We collected blood and urine samples from narcolepsy patients (n = 5) treated with pharmaceuticals containing GHB sodium salt (1.86–3.72 g GHB as free acid per dose). Although GHB was detectable only up to 4 h in concentrations greater than the commonly used cutoff levels in blood plasma, 3,4‐dihydroxybutyric acid (3,4‐DHB) could be detected up to 12 h in blood plasma in concentrations exceeding initial concentrations of the same patient before GHB ingestion. Furthermore, four of the five patients showed an increase above endogenous levels described in the scientific literature. In urine, GHB concentrations above commonly used cutoff levels could be observed 4.5–9.5 h after GHB intake. Creatinine standardized initial concentrations were reached again for glycolic acid (GA), 3,4‐DHB, and 2,4‐dihydroxybutyric (2,4‐DHB) acid at 6.5–22, 11.5–22, and 8.5–70 h after GHB intake, respectively. Therefore, 2,4‐DHB, 3,4‐DHB, and GA are promising and should be further investigated as potential biomarkers to prolong the detection window of GHB intake.

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