Bech Anne Berit, Clausen Thomas, Waal Helge, Vindenes Vigdis, Edvardsen Hilde Erøy, Frost Joachim, Skeie Ivar
National Advisory Unit on Concurrent Substance Abuse and Mental Health Disorders, Innlandet Hospital Trust, Department of Mental Health, P.O. Box 104, 2381, Brumunddal, Norway.
Norwegian Centre for Addiction Research (SERAF), Institute of Clinical Medicine, University of Oslo, P.O. Box 1171 Blindern, 0318, Oslo, Norway.
Addiction. 2020 Aug 1. doi: 10.1111/add.15211.
To present the substances and their concentrations detected post-mortem in patients receiving opioid agonist treatment (OAT) stratified by cause of death, estimate the pooled opioid and benzodiazepine concentrations using established conversion factors for blood concentrations from the Norwegian Road Traffic Act, and explore the association between drug-induced cause of death and the pooled opioid and benzodiazepine concentrations.
Cross-sectional nationwide study.
Norway.
One hundred and seven patients who died during OAT (i.e. within 5 days after the last intake of OAT medication) between 1 January 2014 and 31 December 2015, with post-mortem femoral blood available for toxicology. Data were collected from hospital records, the Norwegian Cause of Death Registry and autopsy reports.
Presence of alcohol and non-alcohol substances in the bloodstream at time of death, determined through records of toxicology of post-mortem femoral blood.
A median of four substances was detected across the causes of death. At least one benzodiazepine was detected in 81 (76%) patients. The median pooled opioid concentration was significantly higher in drug-induced deaths compared with other causes of death (362 ng/mL versus 182 ng/mL, P < 0.001), in contrast to the pooled benzodiazepine concentration (5466 versus 5701 ng/mL, P = 0.353). The multivariate regression analysis showed that only increasing pooled opioid concentration (ng/ML) was associated with increased odds of a drug-induced cause of death (odds ratio, 1.003; 95% confidence interval: 1.001-1.006).
In Norway, overall opioid concentration seems to play an important role in drug-induced deaths during opioid agonist treatment in patients prescribed methadone or buprenorphine. Patients prescribed buprenorphine tend to replace their agonist with full agonists, while patients prescribed methadone tend to have high opioid concentrations from methadone as the only opioid.
呈现接受阿片类激动剂治疗（OAT）患者死后按死因分层检测到的物质及其浓度，使用挪威道路交通法中既定的血液浓度转换因子估算阿片类药物和苯二氮䓬类药物的合并浓度，并探讨药物诱发的死因与阿片类药物和苯二氮䓬类药物合并浓度之间的关联。
全国性横断面研究。
挪威。
2014年1月1日至2015年12月31日期间在OAT期间（即最后一次服用OAT药物后5天内）死亡且有死后股血可用于毒理学检测的107例患者。数据从医院记录、挪威死亡原因登记处和尸检报告中收集。
通过死后股血毒理学记录确定死亡时血液中酒精和非酒精物质的存在情况。
各死因中检测到的物质中位数为四种。81例（76%）患者检测到至少一种苯二氮䓬类药物。与其他死因相比，药物诱发死亡患者的阿片类药物合并浓度中位数显著更高（362纳克/毫升对182纳克/毫升，P<0.001），而苯二氮䓬类药物合并浓度则相反（5466对5701纳克/毫升，P = 0.353）。多变量回归分析显示，仅阿片类药物合并浓度（纳克/毫升）升高与药物诱发死因的几率增加相关（比值比，1.003；95%置信区间：1.001 - 1.006）。
在挪威，总体阿片类药物浓度似乎在接受美沙酮或丁丙诺啡治疗的患者阿片类激动剂治疗期间药物诱发的死亡中起重要作用。接受丁丙诺啡治疗的患者倾向于用完全激动剂替代其激动剂，而接受美沙酮治疗的患者倾向于仅将美沙酮作为唯一阿片类药物而具有高阿片类药物浓度。
