Buprenorphine, oxycodone, hydrocodone, and methadone mortality in the United States (2010‒2017)

Karilynn M. Rockhill PhD, Gabrielle E. Bau MS, Angela DeVeaugh-Geiss PhD, Howard Chilcoat ScD, Richard Dart MD, PhD, Janetta Iwanicki MD, Joshua C. Black PhD
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Abstract

Objective

Opioid overdose survivors present to emergency departments (EDs) and many EDs have developed programs to initiate buprenorphine. The impact of the increasing use of buprenorphine in ED and by other providers is unknown while opioid mortality continues to rise. Public mortality data do not distinguish buprenorphine from other prescription opioids. Our objective was to determine when changes in overdose mortality trends occurred comparing deaths involving buprenorphine to oxycodone, hydrocodone, and methadone.

Methods

This observational study utilized the drug-involved mortality database including US death certificates (2010‒2017) in which buprenorphine, oxycodone, hydrocodone, or methadone were contributing causes of death (determined through textual analysis). Population- and drug utilization-adjusted mortality rates were examined using disjointed linear regression. Buprenorphine-involved deaths were stratified by polysubstance involvement.

Results

The population-adjusted mortality rates for buprenorphine-involved deaths were lowest compared to other opioids; however, the change in rate for buprenorphine increased faster than oxycodone, hydrocodone, and methadone at 8.9% each quarter-year (95% confidence interval [CI]: 8.0, 9.8) from 2010 to mid-2016 when it stabilized. After adjusting for changes in dispensing over the study period, buprenorphine-involved mortality rates were increasing at 5.3% (95% CI: 4.6, 6.1) each quarter-year. In 2017, 94% buprenorphine-involved deaths had at least one other drug contributing to the cause of death.

Conclusions

Given the low mortality, high proportions of polysubstance mortality, and the mixed agonist/antagonist mechanism of action, use of buprenorphine alone likely presents a lower risk for overdose than comparators. Mortality rose faster than dispensing, signaling need to ensure people understand buprenorphine risks, particularly polysubstance use, balanced against importance for treating opioid use disorders.

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美国的丁丙诺啡、羟考酮、氢可酮和美沙酮死亡率(2010-2017 年)。
目的:阿片类药物过量幸存者来到急诊科(ED),许多急诊科已制定了启动丁丙诺啡的计划。在阿片类药物死亡率持续上升的同时,急诊科和其他医疗机构越来越多地使用丁丙诺啡所产生的影响尚不清楚。公开的死亡率数据并未将丁丙诺啡与其他处方类阿片区分开来。我们的目标是通过比较涉及丁丙诺啡与羟考酮、氢可酮和美沙酮的死亡案例,确定过量死亡趋势何时发生变化:这项观察性研究利用了包括美国死亡证明在内的药物致死数据库(2010-2017 年),其中丁丙诺啡、羟考酮、氢可酮或美沙酮是导致死亡的原因(通过文本分析确定)。使用非连续线性回归法对人口和药物使用调整后的死亡率进行了研究。涉及丁丙诺啡的死亡病例按涉及多种物质进行了分层:与其他阿片类药物相比,丁丙诺啡致死的人口调整死亡率最低;但是,从2010年到2016年中期,丁丙诺啡的死亡率变化比羟考酮、氢可酮和美沙酮的变化快,每季度为8.9%(95%置信区间[CI]:8.0, 9.8),之后趋于稳定。在对研究期间的配药变化进行调整后,涉及丁丙诺啡的死亡率以每季度 5.3% (95% 置信区间 [CI]:4.6, 6.1)的速度上升。2017 年,94% 涉及丁丙诺啡的死亡病例的死因至少与一种其他药物有关:鉴于丁丙诺啡的低死亡率、多物质死亡的高比例以及激动剂/拮抗剂的混合作用机制,单独使用丁丙诺啡的用药过量风险可能低于同类药物。死亡率的上升速度比配药速度快,这表明需要确保人们了解丁丙诺啡的风险,尤其是多种药物的使用,同时还要权衡治疗阿片类药物使用障碍的重要性。
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