Holmgren P, Jones A W
Department of Forensic Toxicology, University Hospital, 581 85 Linköping, Sweden.
J Forensic Sci. 2003 Nov;48(6):1416-21.
Both ethanol and diazepam are classified as depressants of the central nervous system and exert their effects via the GABAA receptor complex. We report the coexistence and concentrations of ethanol, diazepam, and its primary metabolite nordiazepam in a case series of 234 forensic autopsies collected over a ten-year period. Diazepam, nordiazepam, and ethanol were determined in femoral venous blood by highly selective gas chromatographic methods. The mean (median) femoral blood concentrations were ethanol 0.24 g/100 mL (0.25 g/100 mL), diazepam (D) 0.23 microg/g (0.10 microg/g), nordiazepam (ND) 0.24 micro/g (0.20 microg/g), sum (D + ND) 0.43 microg/g (0.30 microg/g), and the ratio D/ND was 1.19 (1.0). When cause of death was attributed to alcohol and/or drug intoxication (N = 50), the mean and median blood-ethanol concentration was higher, being 0.36 g/100 mL and 0.38 g/100 mL, respectively, whereas the mean (median) and range of blood-diazepam concentrations were about the same, 0.23 microg/g (0.10 microg/g) and 0.05 to 1.2 microg/g. The femoral-blood concentrations of diazepam and nordiazepam were highly correlated (r = 0.73), but there was no correlation between the concentrations of ethanol and diazepam (r = -0.15). In another 114 fatalities (all causes of death) with diazepam and/or nordiazepam as the only drugs present, the mean (median) and range of blood-diazepam concentrations were 0.22 microg/g (0.10 microg/g) and 0.03 to 3.5 microg/g. The pathologists report showed that none of these deaths were classed as drug intoxications. The impression gleaned from this study of ethanol-diazepam deaths is that high blood-ethanol concentration is the major causative factor. We found no evidence that concurrent use of diazepam enhanced the acute toxicity of ethanol, although interpretation is complicated by the high blood-ethanol concentration (median 0.38 g/100 mL), making it difficult to discern an added effect of diazepam.
乙醇和地西泮均被归类为中枢神经系统抑制剂，它们通过GABAA受体复合物发挥作用。我们报告了在十年期间收集的234例法医尸检案例系列中乙醇、地西泮及其主要代谢产物去甲地西泮的共存情况和浓度。采用高选择性气相色谱法测定股静脉血中的地西泮、去甲地西泮和乙醇。股静脉血中乙醇的平均（中位数）浓度为0.24 g/100 mL（0.25 g/100 mL），地西泮（D）为0.23 μg/g（0.10 μg/g），去甲地西泮（ND）为0.24 μg/g（0.20 μg/g），总和（D + ND）为0.43 μg/g（0.з0 μg/g），D/ND比值为1.19（1.0）。当死亡原因归因于酒精和/或药物中毒（N = 50）时，血液乙醇浓度的平均值和中位数较高，分别为0.36 g/100 mL和0.38 g/100 mL，而血液地西泮浓度的平均（中位数）和范围大致相同，为0.23 μg/g（0.10 μg/g）和0.05至1.2 μg/g。地西泮和去甲地西泮的股静脉血浓度高度相关（r = 0.73），但乙醇和地西泮的浓度之间没有相关性（r = -0.15）。在另外114例以地西泮和/或去甲地西泮为唯一存在药物的死亡案例（所有死亡原因）中，血液地西泮浓度的平均（中位数）和范围为0.22 μg/g（0.10 μg/g）和0.03至3.5 μg/g。病理学家的报告显示，这些死亡案例均未被归类为药物中毒。从这项关于乙醇 - 地西泮死亡案例的研究中得出的印象是，高血液乙醇浓度是主要致病因素。我们没有发现证据表明同时使用地西泮会增强乙醇的急性毒性，尽管由于高血液乙醇浓度（中位数0.38 g/100 mL）使得难以辨别地西泮的附加作用，解释变得复杂。
