Karch S B, Stephens B G, Nazareno G V
Assistant Medical Examiners, City and County of San Francisco, CA 94103, USA.
Am J Forensic Med Pathol. 2001 Sep;22(3):266-9. doi: 10.1097/00000433-200109000-00013.
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.
γ-羟基丁酸(GHB)既可以生前产生,也可以死后产生。作者描述了两例检测到GHB的案例,并讨论了确定GHB在每个案例中作用的问题。在这两个案例中,使用气相色谱法分析了用氟化钠保存的血液和尿液。第一名死者是已知的甲基苯丙胺滥用者,其GHB浓度与亚麻醉剂量时观察到的浓度相似(股血中为159微克/毫升;尿液中为1100微克/毫升)。与兴奋剂滥用相关的心肌纤维化也很明显。第二名死者心脏正常,但GHB浓度较高(股血中为1.4毫克/毫升;右心为1.1毫克/毫升;尿液中为6.0毫克/毫升)。血液中可卡因和摇头丸水平分别为420和730纳克/毫升。两名死者都曾饮酒,且处于吸收后状态,血玻璃体比小于0.90。如果不使用氟化钠作为防腐剂,GHB会作为死后产物产生。因此,仅仅证明GHB的存在并不能证明因果关系,甚至不一定能证明摄入了GHB。案例1中的血液和尿液GHB浓度可以由100毫克的治疗剂量产生,心肌纤维化可能与死亡原因的关系比GHB更大。案例2中的病史与大量摄入GHB相符,但也检测到了其他药物,包括乙醇。乙醇会干扰GHB代谢,阻止GHB分解,提高血液浓度,并增加呼吸骤停的可能性。综合调查、尸检和毒理学数据表明,GHB是案例2的死亡原因,但不是案例1的死亡原因。鉴于最近发现即使在储存的生前血液样本中(前提是用柠檬酸盐保存)也会发生死后GHB产生,以及早期观察到尿液中不会发生新生GHB产生,除非满足以下条件,否则推断因果关系是不明智的:(1)同时分析血液和尿液并发现两者升高;(2)血液收集于含氟化钠的试管中;(3)获得详细的病史。