Thomsen Ragnar, Rasmussen Brian Schou, Johansen Sys Stybe, Linnet Kristian
Section of Forensic Chemistry, Department of Forensic Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Frederik V's vej 11, DK-2100 Copenhagen, Denmark.
Section of Forensic Chemistry, Department of Forensic Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Frederik V's vej 11, DK-2100 Copenhagen, Denmark.
Forensic Sci Int. 2017 Mar;272:154-158. doi: 10.1016/j.forsciint.2016.12.038. Epub 2017 Jan 5.
Gamma-hydroxybutyrate (GHB) is a recreational drug, a drug of abuse, as well as an endogenous molecule in mammals. The drug has become infamous as a tool for drug-facilitated sexual assault. GHB is found in low concentrations in living humans, while at postmortem the concentration of GHB rises due to fermentation processes. The endogenous nature of GHB leads to difficulty in interpretation of concentrations, as the source of GHB is not obvious. Postmortem brain and blood samples were collected from 221 individuals at autopsy. Of these, 218 were not suspected of having ingested GHB, while GHB intake was reported for the last three (cases A-C). Decomposition level was estimated and cases classified into no/minor and advanced decomposition. Brain samples were extracted from the frontal lobe; only gray matter from the cerebral cortex was used. Blood was drawn from the femoral vein. Brain samples were homogenized and diluted with water. Brain homogenates or femoral blood were then prepared using protein precipitation and GHB was quantified with UHPLC-MS/MS. For 189 cases where ingestion of GHB was not suspected and where no/minor decomposition had occurred the concentrations were in the range 4.8-45.4mg/kg (median 15.3mg/kg) in blood and not-detected to 9.8mg/kg (median 4.8mg/kg) in brain tissue. For case A, where intoxication with GHB was deemed to be the sole cause of death, the concentrations were 199 and 166mg/kg in blood and brain, respectively. For case B, where intoxication with GHB was a contributing factor of death, the respective concentrations were 142 and 78.4mg/kg. For case C, where GHB was ingested but the cause of death was opioid poisoning, the concentrations were 40.3 and 12.7mg/kg. The results demonstrate that postmortem-formed levels of GHB are much lower in brain than peripheral blood. Analysis of GHB in brain tissue thus provides for an improved capability to identify an exogenous source of GHB. By measuring GHB in brain tissue and employing a cut-off concentration of 10mg/kg, a tentative distinction can be made between an endo- and exogenous source of GHB. An exception to this strategy is for extensively decomposed corpses, where endogenous GHB concentrations can be high even in brain.
γ-羟基丁酸（GHB）是一种消遣性药物、滥用药物，也是哺乳动物体内的一种内源性分子。这种药物因作为协助实施性侵犯的工具而声名狼藉。在活着的人体内，GHB的浓度较低，而在死后，由于发酵过程，GHB的浓度会升高。GHB的内源性导致难以解释其浓度，因为GHB的来源并不明显。在尸检时从221名个体身上采集了死后的脑和血样本。其中，218人未被怀疑摄入过GHB，而据报告最后三人（病例A - C）摄入过GHB。估计了尸体的腐败程度，并将病例分为无/轻度腐败和重度腐败。从额叶提取脑样本；仅使用大脑皮质的灰质。从股静脉采集血液。将脑样本匀浆并用水稀释。然后通过蛋白质沉淀法制备脑匀浆或股静脉血，并采用超高效液相色谱 - 串联质谱法对GHB进行定量。对于189例未怀疑摄入GHB且未发生/轻度腐败的病例，血液中GHB浓度范围为4.8 - 45.4mg/kg（中位数15.3mg/kg），脑组织中未检测到至9.8mg/kg（中位数4.8mg/kg）。对于病例A，GHB中毒被认为是唯一死因，血液和脑组织中的浓度分别为199和166mg/kg。对于病例B，GHB中毒是死亡的一个促成因素，相应浓度分别为142和78.4mg/kg。对于病例C，摄入了GHB但死因是阿片类药物中毒，浓度分别为40.3和12.7mg/kg。结果表明，死后脑组织中GHB的生成水平远低于外周血。因此，分析脑组织中的GHB能够更好地识别GHB的外源性来源。通过测量脑组织中的GHB并采用10mg/kg的临界浓度，可以初步区分GHB的内源性和外源性来源。这种策略的一个例外是对于腐败严重的尸体，即使在脑组织中内源性GHB浓度也可能很高。
