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阿片类药物使用障碍患者的潜在药物动力学因素导致中毒,随后使用丁丙诺啡/纳洛酮治疗。

A Case of Potential Pharmacokinetic Kratom-drug Interactions Resulting in Toxicity and Subsequent Treatment of Kratom Use Disorder With Buprenorphine/Naloxone.

机构信息

From the Psychiatry Residency Spokane, Providence Sacred Heart Medical Center, Spokane, WA (HDB, AGB); College of Osteopathic Medicine, Pacific Northwest University of Health Sciences, Yakima, WA (MMM); Department of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University Spokane, WA (MFP); Providence Medical Research Center, Providence Health Care, Spokane, WA (EJC).

出版信息

J Addict Med. 2022;16(5):606-609. doi: 10.1097/ADM.0000000000000968. Epub 2022 Feb 14.

Abstract

The botanical product kratom produces opioid-like effects at high doses and is sometimes used for opioid replacement by individuals with opioid use disorder. Mitragynine, a major alkaloid contained in kratom leaves, has been shown to inhibit multiple cytochromes P450 (CYPs) in vitro, including CYP2D6 and CYP3A. As such, kratom may precipitate pharmacokinetic drug interactions when co-consumed with certain medications. We present a case of a patient taking 150 mg venlafaxine (CYP2D6/3A substrate), 300 mg quetiapine (CYP3A substrate), and a high amount of kratom (~90 g) daily. The patient presented to the emergency department with serotonin syndrome and corrected electrocardiogram abnormalities that may have been secondary to supratherapeutic exposure to venlafaxine and/or quetiapine. The patient's symptoms resolved after discontinuation of venlafaxine and quetiapine. He was amenable to medication therapy for kratom discontinuation and successfully completed an at-home induction with buprenorphine/naloxone. This case report adds to the literature about potential pharmacokinetic kratom-drug interactions and suggests that buprenorphine/naloxone can facilitate recovery from kratom use disorder.

摘要

植物产品卡痛在高剂量下会产生类阿片样效应,有时被阿片类药物使用者用于替代阿片类药物。卡痛叶中的主要生物碱之一——美沙酮,已被证明可在体外抑制多种细胞色素 P450(CYP),包括 CYP2D6 和 CYP3A。因此,卡痛可能会与某些药物同时使用时引发药物的药代动力学相互作用。我们报告了一例患者每天服用 150 毫克文拉法辛(CYP2D6/3A 底物)、300 毫克喹硫平(CYP3A 底物)和大量卡痛(~90 克)。该患者因出现血清素综合征和纠正的心电图异常而到急诊就诊,这些异常可能是文拉法辛和/或喹硫平超治疗浓度暴露引起的。停止使用文拉法辛和喹硫平后,患者的症状得到缓解。他愿意接受药物治疗以戒除卡痛,并成功在家中使用丁丙诺啡/纳洛酮进行诱导。本病例报告增加了关于潜在药代动力学卡痛-药物相互作用的文献,并表明丁丙诺啡/纳洛酮可以促进戒除卡痛成瘾的康复。

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