Lamotrigine is not associated with differential clinical outcomes in a real-world sample of patients with unipolar depression receiving ketamine or esketamine.

IF 3.3 3区 医学 Q2 NEUROSCIENCES
Mia C Santucci, Rachel B Katz, Brian Pittman, Sina Nikayin, Samuel T Wilkinson
{"title":"Lamotrigine is not associated with differential clinical outcomes in a real-world sample of patients with unipolar depression receiving ketamine or esketamine.","authors":"Mia C Santucci, Rachel B Katz, Brian Pittman, Sina Nikayin, Samuel T Wilkinson","doi":"10.1007/s00213-025-06896-7","DOIUrl":null,"url":null,"abstract":"<p><strong>Rationale: </strong>Ketamine has emerged as a rapid-acting antidepressant. Lamotrigine is used as an off-label treatment for major depressive disorder. Some theorize, based on mechanism, that lamotrigine might interfere with ketamine's antidepressant effects.</p><p><strong>Objectives: </strong>To report on clinical outcomes for patients with depression treated concomitantly with/without lamotrigine and ketamine/esketamine.</p><p><strong>Methods: </strong>Clinical outcomes based on the Montgomery-Åsberg Depression Rating Scale (MADRS) and the Quick Inventory of Depressive Symptomatology-Self Report (QIDS) were organized from patients with major depressive disorder treated with ketamine/esketamine at Yale Psychiatric Hospital from 2014 through November 2023. Patients were treated with intravenous ketamine (0.5 mg/kg over 40 min) or intranasal esketamine (56 or 84 mg) twice per week for two to four weeks.</p><p><strong>Results: </strong>Overall, 347 patients with depression were treated with ketamine/esketamine, 57 of which were concurrently taking lamotrigine during the treatment period. Most (207/347, 59.7%) patients were women, with an average age of 45.6 (standard deviation [SD] = 16.6). The average dose of lamotrigine was 210.1 (SD = 153.9). In the initial, unadjusted model, there was no group (lamotrigine v. no lamotrigine) by time interaction using the MADRS (F<sub>2,345</sub>=1.19, p = 0.30) or QIDS (F<sub>2,338</sub>=0.51, p = 0.60) as outcomes. Adjusting for concomitant medications (antidepressants, benzodiazepines), prior exposure to electroconvulsive therapy, sex, age, race, history of psychiatric hospitalization, additional psychiatric comorbidities, and whether patients started treatment as an outpatient or inpatient did not affect results.</p><p><strong>Conclusions: </strong>We found no clinical evidence for an interaction between lamotrigine and treatment with ketamine/esketamine in a real-world sample of treatment-seeking patients with major depressive disorder.</p>","PeriodicalId":20783,"journal":{"name":"Psychopharmacology","volume":" ","pages":""},"PeriodicalIF":3.3000,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Psychopharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00213-025-06896-7","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

Rationale: Ketamine has emerged as a rapid-acting antidepressant. Lamotrigine is used as an off-label treatment for major depressive disorder. Some theorize, based on mechanism, that lamotrigine might interfere with ketamine's antidepressant effects.

Objectives: To report on clinical outcomes for patients with depression treated concomitantly with/without lamotrigine and ketamine/esketamine.

Methods: Clinical outcomes based on the Montgomery-Åsberg Depression Rating Scale (MADRS) and the Quick Inventory of Depressive Symptomatology-Self Report (QIDS) were organized from patients with major depressive disorder treated with ketamine/esketamine at Yale Psychiatric Hospital from 2014 through November 2023. Patients were treated with intravenous ketamine (0.5 mg/kg over 40 min) or intranasal esketamine (56 or 84 mg) twice per week for two to four weeks.

Results: Overall, 347 patients with depression were treated with ketamine/esketamine, 57 of which were concurrently taking lamotrigine during the treatment period. Most (207/347, 59.7%) patients were women, with an average age of 45.6 (standard deviation [SD] = 16.6). The average dose of lamotrigine was 210.1 (SD = 153.9). In the initial, unadjusted model, there was no group (lamotrigine v. no lamotrigine) by time interaction using the MADRS (F2,345=1.19, p = 0.30) or QIDS (F2,338=0.51, p = 0.60) as outcomes. Adjusting for concomitant medications (antidepressants, benzodiazepines), prior exposure to electroconvulsive therapy, sex, age, race, history of psychiatric hospitalization, additional psychiatric comorbidities, and whether patients started treatment as an outpatient or inpatient did not affect results.

Conclusions: We found no clinical evidence for an interaction between lamotrigine and treatment with ketamine/esketamine in a real-world sample of treatment-seeking patients with major depressive disorder.

在接受氯胺酮或艾氯胺酮治疗的单极抑郁症患者的真实样本中,拉莫三嗪与差异临床结果无关。
理由:氯胺酮已成为一种速效抗抑郁药。拉莫三嗪被用作重度抑郁症的标签外治疗。一些理论,基于机制,拉莫三嗪可能会干扰氯胺酮的抗抑郁作用。目的:报道联合/不联合拉莫三嗪和氯胺酮/艾氯胺酮治疗抑郁症患者的临床结果。方法:采用Montgomery-Åsberg抑郁评定量表(MADRS)和抑郁症状快速量表-自我报告(QIDS)对2014年至2023年11月在耶鲁精神病院接受氯胺酮/艾氯胺酮治疗的重度抑郁症患者的临床结果进行整理。患者接受静脉注射氯胺酮(0.5 mg/kg超过40分钟)或鼻内注射艾氯胺酮(56或84 mg)治疗,每周两次,持续2至4周。结果:347例抑郁症患者接受氯胺酮/艾氯胺酮治疗,其中57例患者在治疗期间同时服用拉莫三嗪。大多数(207/347,59.7%)患者为女性,平均年龄为45.6岁(标准差[SD] = 16.6)。拉莫三嗪的平均剂量为210.1 (SD = 153.9)。在初始的、未调整的模型中,使用MADRS (f2345 =1.19, p = 0.30)或QIDS (f2338 =0.51, p = 0.60)作为结果,没有时间相互作用组(拉莫三嗪vs .无拉莫三嗪)。调整伴随药物(抗抑郁药、苯二氮卓类药物)、既往电休克治疗、性别、年龄、种族、精神住院史、其他精神合并症以及患者是作为门诊患者还是住院患者开始治疗都不影响结果。结论:在现实世界中寻求治疗的重度抑郁症患者样本中,我们没有发现拉莫三嗪与氯胺酮/艾氯胺酮治疗之间相互作用的临床证据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Psychopharmacology
Psychopharmacology 医学-精神病学
CiteScore
7.10
自引率
5.90%
发文量
257
审稿时长
2-4 weeks
期刊介绍: Official Journal of the European Behavioural Pharmacology Society (EBPS) Psychopharmacology is an international journal that covers the broad topic of elucidating mechanisms by which drugs affect behavior. The scope of the journal encompasses the following fields: Human Psychopharmacology: Experimental This section includes manuscripts describing the effects of drugs on mood, behavior, cognition and physiology in humans. The journal encourages submissions that involve brain imaging, genetics, neuroendocrinology, and developmental topics. Usually manuscripts in this section describe studies conducted under controlled conditions, but occasionally descriptive or observational studies are also considered. Human Psychopharmacology: Clinical and Translational This section comprises studies addressing the broad intersection of drugs and psychiatric illness. This includes not only clinical trials and studies of drug usage and metabolism, drug surveillance, and pharmacoepidemiology, but also work utilizing the entire range of clinically relevant methodologies, including neuroimaging, pharmacogenetics, cognitive science, biomarkers, and others. Work directed toward the translation of preclinical to clinical knowledge is especially encouraged. The key feature of submissions to this section is that they involve a focus on clinical aspects. Preclinical psychopharmacology: Behavioral and Neural This section considers reports on the effects of compounds with defined chemical structures on any aspect of behavior, in particular when correlated with neurochemical effects, in species other than humans. Manuscripts containing neuroscientific techniques in combination with behavior are welcome. We encourage reports of studies that provide insight into the mechanisms of drug action, at the behavioral and molecular levels. Preclinical Psychopharmacology: Translational This section considers manuscripts that enhance the confidence in a central mechanism that could be of therapeutic value for psychiatric or neurological patients, using disease-relevant preclinical models and tests, or that report on preclinical manipulations and challenges that have the potential to be translated to the clinic. Studies aiming at the refinement of preclinical models based upon clinical findings (back-translation) will also be considered. The journal particularly encourages submissions that integrate measures of target tissue exposure, activity on the molecular target and/or modulation of the targeted biochemical pathways. Preclinical Psychopharmacology: Molecular, Genetic and Epigenetic This section focuses on the molecular and cellular actions of neuropharmacological agents / drugs, and the identification / validation of drug targets affecting the CNS in health and disease. We particularly encourage studies that provide insight into the mechanisms of drug action at the molecular level. Manuscripts containing evidence for genetic or epigenetic effects on neurochemistry or behavior are welcome.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信