alexa Effects of Quetiapine on Platelets in Major Depression
ISSN: 2167-1044

Journal of Depression and Anxiety
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Research Article

Effects of Quetiapine on Platelets in Major Depression

John Piletz1,2, Debra Hoppensteadt3, Walter Jeske3, Jawed Fareed3, James Sinacore4, Brittany Garlenski2 and Angelos Halaris2*
1Department of Biology, Mississippi College, Clinton, MS, USA
2Departments of Psychiatry, Loyola University Stritch School of Medicine, Chicago, IL, USA
3Department of Pathology, Loyola University Stritch School of Medicine, Chicago, IL, USA
4Department of Public Health Sciences, Loyola University Stritch School of Medicine, Chicago, IL, USA
Corresponding Author : Angelos Halaris, MD
Professor of Psychiatry
Department of Psychiatry and Behavioral Neuroscience
Loyola University Stritch School of Medicine
2160 South First Avenue, Maywood, IL 60153 USA
Tel: 708-2163275
Fax: 708-216-6840
E-mail: [email protected]
Received: January 07, 2016; Accepted: January 26, 2016; Published: January 28, 2016
Citation: Piletz J, Hoppensteadt D, Jeske W, Fareed J, Sinacore J, et al. (2016) Effects of Quetiapine on Platelets in Major Depression. J Depress Anxiety 5:219. doi:10.4172/2167-1044.1000219
Copyright: © 2016 Piletz J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

1.1 Objectives: Test the prevailing hypothesis that depressive illness is associated with platelet hyperactivity and that treatment with an atypical antipsychotic with established antidepressant efficacy – quetiapine - will normalize platelet activity. 1.2 Methods: Forty-seven outpatients with major depressive disorder (MDD) and 27 healthy controls (HC) without evidence of cardiovascular disease were enrolled. Behavioral rating scales and medical tests preceded baseline assessments of (1) platelet-rich plasma (PRP) aggregometry and (2) whole blood flow cytometry (P-selectin surface labeling). The measures were repeated in those MDD subjects who completed 8 weeks (n=27) or 12 weeks (n=19) of treatment with quetiapine. 1.3 Results: Untreated MDD compared to HC subjects displayed more platelet aggregation when PRP was stirred agonist-free (p=0.021). Other platelet measurements at baseline such as in vitro agonist-stimulated PRP aggregometry or P-selectin expression by flow cytometry did not distinguish MDD from HC subjects. After 8 weeks on quetiapine, a reduced (now normal) agonist-free aggregatory response to stirring (p=0.035) was observed. By 12 weeks the aggregometry response to arachidonic acid (AA) was also lowered (p=0.016 vs. pretreatment; p=0.001 vs. HC). Other agonist additions (ADP, epinephrine, or collagen) failed to distinguish MDD from HC. There were no significant associations between mood rating scores and any form of platelet activity at any time point on quetiapine. 1.4 Limitations: High percentage of dropouts attributable to dose-related side effects limited the post-treatment assessments. 1.5 Conclusions: The hypothesis that untreated depression is associated with more active platelets, was confirmed, but this finding was confined to the “resting”, or agonist-free state. Quetiapine treatment normalized this resting activity and led to a lower-than-normal response to AA-induced aggregation after 12 weeks of treatment. These findings confirm that 8 weeks treatment with quetiapine can normalize at least one form of platelet hyperactivity, but the lower-than-healthy response to AA after 12 weeks on quetiapine warrants further study.

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