Cyproheptadine for Serotonin Toxicity: an Updated Systematic Review and Grading of Evidence
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ACUTE CARE PHARMACOLOGY AND TOXICOLOGY (A KING, SECTION EDITOR)
Cyproheptadine for Serotonin Toxicity: an Updated Systematic Review and Grading of Evidence Elizabeth T Jacobs 1,2 & Katherine G Akers 3 & Varun Vohra 2,3,4 & Andrew M King 1,2,3,4 Accepted: 23 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review Serotonin toxicity (ST) is a serious clinical entity caused by drug-induced serotonin excess in the central nervous system. Animal studies and some human data indicate that activation of specific serotonin receptor subtypes, namely 5HT1A and 5-HT2A, are involved in ST pathophysiology, suggesting that serotonin antagonists could be used to treat ST. However, to date, high-quality evidence for the clinical utility of the most commonly employed serotonin antagonist, cyproheptadine, is lacking. This systematic review provides a clinical update on the evidence regarding use cyproheptadine for treating ST and compiles cyproheptadine treatment recommendations from recent review articles. Recent Findings Published articles concerning the use of cyproheptadine for treating ST are exclusively case reports and case series (n = 151); most provide very low-quality evidence (i.e., grade D, n = 148) and the remaining few provide low-quality evidence (i.e., grade C, n = 3). Most recent review articles (n = 18) acknowledge this low level of evidence and propose cyproheptadine as an optional treatment, whereas others recommend its use in the clinical setting. Summary Although ST has been recognized as a clinical entity for decades, rigorous trials demonstrating the therapeutic efficacy of cyproheptadine are lacking, warranting large-scale prospective human trials of antiserotonergic agents using a coordinated multicenter approach. Keywords Serotonin syndrome . Serotonin toxicity . Cyproheptadine . Serotonin antagonist . Toxicology . Antidote
Introduction Serotonin toxicity (ST), alternatively known as serotonin syndrome (SS), is the result of excess serotonin receptor stimulation in the central nervous system. The resulting clinical effects are often described as a triad of autonomic hyperactivity, neuromuscular effects, and altered mentation. Pharmacologic mechanisms leading to excessive serotonin receptor stimulation
This article is part of the Topical collection on Acute Care Pharmacology and Toxicology * Andrew M King [email protected] 1
Detroit Medical Center, Detroit, MI, USA
2
Michigan Poison Center, Detroit, MI, USA
3
Wayne State University, Detroit, MI, USA
4
Department of Emergency Medicine, Wayne State University School of Medicine, 4201 St. Antoine, Suite 6G, Detroit, MI, USA 48201
include inhibition of serotonin reuptake, monoamine oxidase inhibition, increased serotonin release, and/or synthesis of precursors. A recent review of hospitalized patients in the United States (US) identified antidepressants, dextromethorphan, lamotrigine, and tramadol as the most frequently implicated medications [1••]. A commonly considered anti-serotonergic agent for t
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