China
Africa
Explore chapters and articles related to this topic
Pharmacology of Opioids
Published in Pamela E. Macintyre, Stephan A. Schug, Acute Pain Management, 2021
Pamela E. Macintyre, Stephan A. Schug
As noted earlier, the main active metabolite of tramadol is O-desmethyltramadol (M1), which is excreted by the kidney. M1 is a more potent μ-receptor agonist than tramadol itself, thereby contributing to its analgesic efficacy. The formation of M1 depends on the enzyme CYP2D6, therefore, in poor metabolizers the analgesic effect of tramadol may be reduced. Conversely, in ultrarapid metabolizers, opioid-related effects will be increased (Owusu Obeng et al, 2017), including the risk of OIVI, especially in patients with renal impairment (Faria et al, 2018). It is possible that the risk of serotonin syndrome is increased in patients who are poor metabolizers as serotonin reuptake inhibition may be promoted (Faria et al, 2018).
Treatment of Psychological Disorders
Published in Mohamed Ahmed Abd El-Hay, Understanding Psychology for Medicine and Nursing, 2019
The selective serotonin reuptake inhibitors (SSRIs) increase serotonin levels by blocking its reuptake. These involve fluoxetine, paroxetine, sertraline, fluvoxamine, citalopram, and escitalopram. Common side effects of SSRIs include nausea, trouble sleeping, nervousness, tremors, and sexual problems. Co-prescription of SSRIs with other serotonergic drugs and especially MAOIs can lead to serotonin syndrome. This is characterized by a classic triad of mental status changes, neuromuscular abnormalities, and autonomic hyperactivity. These include anxiety, agitation, confusion, hyperreflexia, clonus, tremors, myoclonus, rigidity, increased heart rate, flushing, hyperthermia, and excessive sweating. Death can occur in severe cases of serotonin syndrome.
Disorders
Published in Jonathan P Rogers, Cheryl CY Leung, Timothy RJ Nicholson, Pocket Prescriber Psychiatry, 2019
Jonathan P Rogers, Cheryl CY Leung, Timothy RJ Nicholson
Serotonin syndrome is an acute and potentially life-threatening reaction to antidepressants involving autonomic dysfunction, neuromuscular disturbance and altered mental status (see p. 389, refer ‘Serotonin Syndrome’ in ‘Drug toxicity syndromes’ in ‘Emergencies’ chapter).
Ginsenoside Re attenuates 8-OH-DPAT-induced serotonergic behaviors in mice via interactive modulation between PKCδ gene and Nrf2
Published in Drug and Chemical Toxicology, 2023
Eun-Joo Shin, Ji Hoon Jeong, Bao-Trong Nguyen, Naveen Sharma, Cuong Ngoc Kim Tran, Seung-Yeol Nah, Yi Lee, Jae Kyung Byun, Sung Kwon Ko, Hyoung-Chun Kim
The 5-HT1A receptor agonist (±)-8-hydroxy-dipropylaminotetralin (8-OH-DPAT) has been well-recognized to elicit ‘traditional serotonin syndrome behaviors’ (Haberzettl et al.2013). Serotonin syndrome is a serious disorder/toxic state due to the excessive serotonergic function in the brain, most commonly after the overdose of antidepressants or after the combination of several neuropsychiatric prescriptions (Boyer and Shannon 2005). Serotonin syndrome has become a common health problem, reflecting the frequent application of drugs that activate serotonergic transmission (Isbister et al.2004). Serotonin syndrome can be induced by an excess of serotonin (5-hydroxytryptophan, 5-HT) precursor or receptor agonists, increased release of 5-HT, or reduced 5-HT reuptake or metabolism (Kalueff et al.2008). Indeed, increased prescription of antidepressants (i.e., selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs)) augmented the incidence of serotonin syndrome (Boyer and Shannon 2005, Isbister and Buckley 2005). Therefore, it is highly important that sustained exposure to antidepressant drugs has the potential to cause serotonin syndrome.
The serotonin toxidrome: shortfalls of current diagnostic criteria for related syndromes
Published in Clinical Toxicology, 2022
Angela L. Chiew, Nicholas A. Buckley
A syndrome of serotonin “hyperstimulation” called serotonin syndrome was initially described in the 1960s [1]. Since these early descriptions and the proposal of diagnostic criteria, there have been increasing reports of serotonin syndrome with an expanding list of drugs implicated. The true incidence of serotonin syndrome is unknown, and this relates to the challenges that still arise with diagnosis and offending agents. However, the incidence is very much higher if those without “hyperstimulation” but with multiple minor side effects of serotonergic agents are diagnosed as having serotonin syndrome. The term serotonin syndrome is also used to describe moderate to severe serotonin toxicity. A syndrome is a group of signs and symptoms characterizing a group of patients, but this can be done whether or not there is a clear mechanism (e.g., Down’s syndrome versus Chronic Fatigue Syndrome). The use of the term “serotonin syndrome” in settings without a clear serotonergic pathophysiological mechanism is all too common. Using clinical symptom/sign criteria to identify possible cases is only useful when other likely diagnoses are excluded. Identifying novel agents that cause serotonin syndrome from such criteria is only possible if the signs are pathognomonic or at least extremely specific.
Lasmiditan: an additional therapeutic option for the acute treatment of migraine
Published in Expert Review of Neurotherapeutics, 2021
Daniele Martinelli, Vito Bitetto, Cristina Tassorelli
Another relevant issue is the tolerability of lasmiditan in subjects who are on concomitant preventive treatments, given the fact that all oral preventive antimigraine drugs have a central effect. Particular attention is needed for patients using drugs that interfere with the serotonin pathway for the potential risk of serotonin syndrome. Moreover, two other common conditions require special consideration: firstly, the concomitant intake of alcohol or other central nervous system depressant drugs, due to the possibility of a synergistic effect on vigilance. Secondly, caution is advised in subject who are being treated pharmacologically for heart rate control due to the potential additive effect of lasmiditan in decreasing the heart rate. Clinical studies are needed to verify whether caution has to become contraindication because of drug-to-drug interaction.