a National Institute on Drug Abuse, Intramural Research Program , Clinical Pharmacology and Therapeutics Research Branch , Baltimore , MD, USA.
b Department of Psychology , Hartwick College , Oneonta , NY , USA.
Am J Drug Alcohol Abuse. 2018;44(5):502-511. doi: 10.1080/00952990.2018.1454933. Epub 2018 Apr 10.
In a recent clinical trial (NCT00295308), we demonstrated that clonidine decreased the association between opioid craving and moderate levels of stress and affect in patients receiving buprenorphine-based opioid agonist therapy.
To examine the relationship between illicit opioid use and craving and affect during the evaluation of clonidine as an adjunct medication in buprenorphine treatment for opioid use disorder. Secondarily, to examine whether those relationships are driven by within- or between-participant factors.
This was a secondary data analysis from our original trial. Participants (N = 108, female: n = 23, male n = 85) receiving buprenorphine were randomized to receive adjunct clonidine or placebo. Participants used portable electronic devices to rate stress, mood, and craving via ecological momentary assessment (EMA) four times randomly each day. To associate the EMA data with illicit opioid use, each EMA report was linked to participants' next urine drug screen (thrice weekly). We used generalized linear mixed models to examine the interaction between treatment group and illicit opioid use, as well as to decompose the analysis into within- and between-participant effects.
Craving for opioids and cocaine was increased when participants were using illicit opioids; this effect was greater in the clonidine group. For affect, mood was poorer during periods preceding opioid-positive urines than opioid-negative urines for clonidine-treated participants, whereas there was no difference for placebo participants.
This secondary analysis provides evidence that for participants maintained on opioid agonist therapy, clonidine minimized the behavioral impact of moderate levels of negative affect and craving.
在最近的一项临床试验(NCT00295308)中,我们证明了可乐定可降低接受丁丙诺啡类阿片激动剂治疗的患者的阿片类物质渴求与中等程度的压力和情绪之间的关联。
研究氯胺酮作为丁丙诺啡治疗阿片类药物使用障碍的辅助药物的评估过程中,非法阿片类药物使用与渴求及情绪之间的关系。其次,研究这些关系是否由个体内或个体间因素驱动。
这是我们原始试验的二次数据分析。参与者(N=108,女性:n=23,男性 n=85)接受丁丙诺啡治疗,并随机分为接受附加氯胺酮或安慰剂的治疗组。参与者使用便携式电子设备通过生态瞬时评估(EMA)每天随机四次评估压力、情绪和渴求。为了将 EMA 数据与非法阿片类药物使用联系起来,每个 EMA 报告都与参与者的下一次尿液药物筛查(每周三次)相关联。我们使用广义线性混合模型来检验治疗组与非法阿片类药物使用之间的交互作用,并将分析分解为个体内和个体间的影响。
当参与者使用非法阿片类药物时,对阿片类药物和可卡因的渴求增加;氯胺酮组的这种效果更大。对于情绪,与氯胺酮治疗参与者的阿片类药物阴性尿液相比,在阿片类药物阳性尿液之前的时期,情绪较差,而安慰剂参与者则没有差异。
这项二次分析提供了证据,表明对于接受阿片类激动剂治疗的参与者,氯胺酮最大限度地减少了中等程度的负性情绪和渴求对行为的影响。