Serotonin syndrome: Preventing, recognizing, and treating it

Wang, Robert Z.; Vashistha, Vishal; Kaur, Sukhdeep; Houchens, Nathan

doi:10.3949/ccjm.83a.15129

Cited by 93 publications

(82 citation statements)

References 32 publications

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“…Our patient exhibited many of the classic symptoms including spontaneous clonus, hyperreflexia, and tremors with ingestion of a known serotonergic agent. The presentation of serotonin syndrome mirrors many of the same signs and symptoms as other life-threatening conditions including malignant hyperthermia, anticholinergic syndrome, and neuroleptic malignant syndrome [15]. Differentiation between these medical issues is essential as treatment differs depending on the diagnosis.…”

Section: Discussionmentioning

confidence: 99%

“…This may progress to life-threatening issues including multiple organ dysfunction, shock, metabolic acidosis, rhabdomyolysis, disseminated intravascular coagulation, renal failure, acute respiratory distress syndrome, and hyperthermia. 5-HT 1A and 5-HT 2A are the receptors thought to be most responsible for serotonin syndrome [15]. Serotonin syndrome may occur in patients of any age and severe systemic manifestations may be seen within minutes of ingestion of a causative agent [13,15].…”

Section: Discussionmentioning

confidence: 99%

“…5-HT 1A and 5-HT 2A are the receptors thought to be most responsible for serotonin syndrome [15]. Serotonin syndrome may occur in patients of any age and severe systemic manifestations may be seen within minutes of ingestion of a causative agent [13,15]. Given its rapid progression, early and accurate diagnosis is essential.…”

Section: Discussionmentioning

confidence: 99%

“…Serotonin syndrome classically has been diagnosed on the basis of a triad of symptoms consisting of autonomic dysfunction, neuromuscular excitation, and altered mental status [13,15]. Recently, two tools have been established to help healthcare professionals ensure an accurate diagnosis of the syndrome, the Hunter and the Sternbach criteria [16][17][18].…”

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

Toxic Leukoencephalopathy in a Teenager Caused by the Recreational Ingestion of 25I-NBOMe: A Case Report and Review of Literature

Humston¹,

Miketic²,

Moon³

et al. 2017

J Med Cases

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Over the past 5 years, the designer drug classification of illicit substances has gained the attention of law enforcement agencies, healthcare providers, and concerned parents around the world. These drugs are often marketed as safe and legal alternatives to their already banned counterparts and are easily acquired online, at "head" shops or behind the counter at local convenient stores. This new drug class includes synthetic cathinones, synthetic cannabinoids, and phenylethylamine derivatives of the 2C class of hallucinogens. Many of these drugs were created for animal research purposes only and were never intended for human consumption. As such, little is known about their pharmacokinetic, pharmacodynamics, and adverse effect profile. Variability in preparation may further alter the already unpredictable safety profile. We report an otherwise healthy 16-year-old adolescent who presented to the emergency department for worsening left-sided weakness, new onset seizure activity, changes in mental status, and an overall decline in health. He self-reported the recreational ingestion of 25I-NBOMe prior to admission. Magnetic resonance imaging and a brain biopsy performed during the course of his admission confirmed the diagnosis of toxic leukoencephalopathy secondary to synthetic hallucinogenic drug use. The basic pharmacology and end-organ effects of 25I-NBOMe are reviewed, their adverse effect profile is presented, and potential anesthetic implications are postulated.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Toxic Leukoencephalopathy in a Teenager Caused by the Recreational Ingestion of 25I-NBOMe: A Case Report and Review of Literature

Humston¹,

Miketic²,

Moon³

et al. 2017

J Med Cases

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“…The use of medication to regulate the melatonin pathway may be crucial [92]. For example, in Poland, the Agency for Health Technology Assessment and Tariff System approved the recommendation of agomelatine in 2014.…”

Section: Melatonin In Treatment For Depressionmentioning

confidence: 99%

Pathophysiology of Depression: Molecular Regulation of Melatonin Homeostasis – Current Status

Dmitrzak‐Węglarz

Reszka

2017

Neuropsychobiology

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Circadian rhythm alterations resulting in disturbed sleep and disturbed melatonin secretion are flagship features of depression. Melatonin, known as a hormone of darkness, is secreted by the pineal gland located near to the center of the brain between the two hemispheres. Melatonin has an antidepressant effect by maintaining the body’s circadian rhythm, by regulating the pattern of expression of the clock genes in the suprachiasmatic nucleus (SCN) and modifying the key genes of serotoninergic neurotransmission that are linked with a depressive mood. Melatonin is produced via the metabolism of serotonin in two steps which are catalyzed by serotonin N-acetyltransferase (SNAT) and acetylserotonin-O-methyltransferase (ASMT). Serotonin, SNAT, and ASMT are key melatonin level regulation factors. Melatonin acts mainly on the MT₁ and MT₂ receptors, which are present in the SCN, to regulate physiological and neuroendocrine functions including circadian entrainment, referred to as a chronobiotic effect. Although melatonin has been known about and refereed to for almost 50 years, the relationship between melatonin and depression is still not clear. In this review, we summarize current knowledge about the genetic and epigenetic regulation of enzymes involved in melatonin synthesis and metabolism as potential features of depression pathophysiology and treatment. Confirmation that melatonin metabolism in peripheral blood partially reflects a disorder in the brain could be a breakthrough in the standardization of measurements of melatonin level for the development of treatment standards, finding new therapeutic targets, and elaborating simple noninvasive clinical tests.

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Adverse reactions caused by high serum concentration of linezolid: Two case reports and literature review

Liu,

Xiao,

Xiao

et al. 2024

Clinical Case Reports

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Key Clinical MessageLinezolid is a potent oxazolidinone for the treatment of various gram‐positive bacterial infections. However, the drug can cause potential adverse reactions such as thrombocytopenia, hyperlactacidemia and serotonin syndrome, which warrant consideration by the medical team when planning treatment. The existing literature has reported some adverse reactions caused by linezolid, but most of these are based on clinical characteristics and simple treatment measures. Two cases of linezolid overdose resulting in thrombocytopenia, hyperlactacidemia and serotonin syndrome are presented, which were successfully managed with therapeutic drug monitoring. A dose adjustment strategy was adopted to safely and effectively mitigate linezolid‐related adverse events.

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Serotonin syndrome: Preventing, recognizing, and treating it

Abstract: As the use of serotonergic agents to treat depression has increased, so too has the incidence of serotonin syndrome. We identify the common agents implicated in serotonin syndrome and the clinical tools to diagnose, manage, and prevent serotonergic toxicity.

Cited by 93 publications

References 32 publications

Toxic Leukoencephalopathy in a Teenager Caused by the Recreational Ingestion of 25I-NBOMe: A Case Report and Review of Literature

Toxic Leukoencephalopathy in a Teenager Caused by the Recreational Ingestion of 25I-NBOMe: A Case Report and Review of Literature

Pathophysiology of Depression: Molecular Regulation of Melatonin Homeostasis – Current Status

Adverse reactions caused by high serum concentration of linezolid: Two case reports and literature review

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