• Elizabeth D Ballard, Julia S Yarrington, Cristan A Farmer, Erica Richards, Rodrigo Machado-Vieira, Bashkim Kadriu, Mark J Niciu, Peixiong Yuan, Lawrence Park, and Carlos A Zarate.
• Experimental Therapeutics & Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Building 10, CRC Room 7-5341, 10 Center Drive, MSC 1282, Bethesda, MD 20892, United States. Electronic address: Elizabeth.Ballard@nih.gov.
• J Affect Disord. 2018 Dec 1; 241: 86-93.

BackgroundNo pharmacological treatments exist for active suicidal ideation (SI), but the glutamatergic modulator ketamine elicits rapid changes in SI. We developed data-driven subgroups of SI trajectories after ketamine administration, then evaluated clinical, demographic, and neurobiological factors that might predict SI response to ketamine.MethodsData were pooled from five clinical ketamine trials. Treatment-resistant inpatients (n = 128) with DSM-IV-TR-diagnosed major depressive disorder (MDD) or bipolar depression received one subanesthetic (0.5 mg/kg) ketamine infusion over 40 min. Composite SI variable scores were analyzed using growth mixture modeling to generate SI response classes, and class membership predictors were evaluated using multinomial logistic regressions. Putative predictors included demographic variables and various peripheral plasma markers.ResultsThe best-fitting growth mixture model comprised three classes: Non-Responders (29%), Responders (44%), and Remitters (27%). For Responders and Remitters, maximal improvements were achieved by Day 1. Improvements in SI occurred independently of improvements in a composite Depressed Mood variable for Responders, and partially independently for Remitters. Indicators of chronic SI and self-injury were associated with belonging to the Non-Responder group. Higher levels of baseline plasma interleukin-5 (IL-5) were linked to Remitters rather than Responders.LimitationsSubjects were not selected for active suicidal thoughts; findings only extend to Day 3; and plasma, rather than CSF, markers were used.ConclusionThe results underscore the heterogeneity of SI response to ketamine and its potential independence from changes in Depressed Mood. Individuals reporting symptoms suggesting a longstanding history of chronic SI were less likely to respond or remit post-ketamine.Published by Elsevier B.V.

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