Search

We report a case of a hospitalised patient who developed probable serotonin toxicity shortly after the initiation of linezolid in whom the selective serotonin reuptake inhibitor (SSRI) escitalopram had been recently discontinued. On day 2 of linezolid administration, the patient reported severe anxiety and was observed to have full body jerking and twitching motions without mental status change. Notably, the patient was concomitantly receiving the antidepressant, trazodone and the benzodiazepine, clonazepam possibly affecting the severity and manifestations of serotonin toxicity. Linezolid was discontinued after 5 days and the patient's symptoms resolved. Serotonin toxicity can present with an array of symptoms and be life threatening if left unrecognised. This report highlights the clinical lessons that discontinuation of an SSRI upon initiation of linezolid does not eliminate the risk of serotonin toxicity and that other concomitant medications may worsen or improve some of the symptoms lending delay and uncertainty to the diagnosis., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2018. No commercial re-use. See rights and permissions. Published by BMJ.)

As the number of patients receiving a left ventricular assist device increases, physicians must always keep in mind that several conditions can present with non-specific symptoms, such as fever, tachypnoea and confusion. We herein report the case of a left ventricular assist device patient who developed a life-threatening condition with acute hyperthermia, confusion and extremities' clonus and muscle spasms. The patient was diagnosed with serotonin syndrome, attributed to the coadministration of 2 commonly prescribed medications (citalopram and omeprazole). This case highlights that a significant proportion of left ventricular assist device patients is treated with serotonergic agents that may predispose them to the appearance of serotonin syndrome, a potentially life-threatening condition.

Background: Serotonin syndrome is a rare but potentially fatal complication of drugs that have effects on central nervous system serotonin. It is characterized by sudden onset of altered mental status, increased neuromuscular activity, and autonomic instability., Case Report: The authors reported a case of serotonin syndrome associated with combined therapy of monoamine oxidase-B inhibitors and selective serotonin reuptake inhibitor A 77-year-old Thai man had been taking escitalopram for depression for three years. He presented with high-grade fever and confusion two days after taking rasagiline for Parkinson's disease. He also had agitation, hallucination, and behavioral change. Escitalopram and rasagiline were discontinued but his renal function worsened, turning to acute kidney injury. He was diagnosed as serotonin syndrome., Conclusion: This is the first case report of serotonin syndrome due to combination of escitalopram and rasagiline used.

Unlabelled: Metaxalone has only recently been associated with serotonin syndrome. The mechanism of action of this centrally acting muscle relaxant is unknown; however, the observation of serotonin syndrome in patients with metaxalone overdose suggests a role in the serotonergic pathway., Case Report: (Case 1) A 29-year-old woman with overdose of metaxalone presented to the emergency department with altered mental status, seizure-like activity, hyperthermia, rigidity in the lower extremities, myoclonus, and hyperreflexia. Vital signs on arrival include blood pressure of 168/80 mmHg, heart rate of 208 beats per minute (bpm), respirations of 20/min, a temperature of 41.6° C rectally, and room air oxygen saturation of 97%. She was intubated and sedated with benzodiazepines, and actively cooled. Serum paroxetine concentration was 23 (therapeutic range: 20-200) ng/mL, and serum metaxalone concentration was 31 mcg/mL (peak plasma concentrations average 0.9 mcg/mL at 3.3 h following a single oral dose of 400 mg). (Case 2) A 27-year-old man presented to the emergency department with altered mental status, rigidity in his lower extremities, myoclonus, and hyperreflexia. Vital signs on arrival include blood pressure of 158/131 mmHg, heart rate of 126 bpm, respiratory rate of 20 breaths per minute, and temperature of 37.2°C, with oxygen saturation of 98% on room air. His medication list included metaxalone and escitalopram. He was managed aggressively with IV boluses of diazepam, in total 80 mg, in the emergency department. Serum escitalopram concentration was 24 ng/mL with a therapeutic range of 21-64 ng/mL, and serum metaxalone concentration was 58 mcg/mL., Conclusion: These two cases suggest that at supratherapeutic concentrations metaxalone has serotonergic effects. Severe serotonin toxicity may result from metaxalone abuse in individuals using a selective serotonin reuptake inhibitor therapeutically.

The serotonin toxicity (ST) is a potentially life-threatening adverse drug reaction results from therapeutic drug use, intentional self-poisoning, or inadvertent interactions between drugs. ST can be caused by a single or a combination of drugs with serotonergic activity due to excessive serotonergic agonism on central nervous system and peripheral serotonergic receptors (monoamine oxidase inhibitors, tricyclic antidepressants, SSRIs, opiate analgesics, over-the-counter cough medicines, antibiotics, weight-reduction agents, antiemetics, antimigraine agents, drugs of abuse, H2-antagonist and herbal products). The serotonin toxicity is often described as a clinical triad of mental-status changes (agitation and excitement with confusion), autonomic hyperactivity (diaphoresis, fever, tachycardia, and tachypnea), neuromuscular abnormalities (tremor, clonus, myoclonus, and hyperreflexia) and, in the advanced stage, spasticity; not all of these findings are consistently present. In this article, we describe two cases of ST due to interaction between Citalopram and two CYP2D6 inhibitors: Cimetidine and Topiramate and their clinical resolution after treatment discontinuation.

Case-Report: We report a case of serotonin syndrome caused by interaction between nasal fentanyl, oxycodone and escitalopram. Due to chronic painful episodes with paroxistic level of pain, a 66-year-old patient, treated for prostate adenocarcinoma and bone metastases received an association of major opiate analgesics (oxycodone 120 mg/day for 6 months, and fentanyl nasal spray four puff of 200 microg/puff). After the addition, for mood disorders, of a small dose of escitalopram (5 mg/day), he developed severe serotoninergic features including diaphoresis, night sweating, tremor, diarrhea, visual disorders with mydriasis and weight loss of 8.8 lbs (4 kg). Discontinuation of escitalopram resulted in complete resolution of his symptoms within 48 h except for persistent blurred vision., Discussion: The clinical manifestations of this case meet Sternbach's criteria of serotonin syndrome. Its possible etiologic factors include adverse drug reaction and pharmacodynamic interaction between selective serotonin reuptake inhibitor (SSRI) antidepressant and opioid analgesics. The Naranjo probability scale suggested a probable causality of escitalopram, oxycodone and fentanyl treatment on the serotonin syndrome. Serotonin syndrome occurrence is estimated around 0.04% in the literature with incidence rates between 14 to 16% in voluntary overdose with serotoninergic agents. It is an infrequent syndrome with, most of the time, a mild to moderate clinical expression. Nevertheless, lethal evolution might occur resulting from either monotherapy with serotoninergic agents (eg: SSRI antidepressants) or the combination of several medications that will increase serotoninergic transmission and therefore intra cerebral serotonin levels. Its physiopathology is related to a hyperstimulation of 5-HT(1A) receptors. Its clinical manifestations involve mental status impairment and cognitive disorders, neuromuscular disorders and neurovegetative impairment. The prescription of SSRI antidepressants among patients depressed, and in pain, exhibiting somatic diseases, and who require regimens of major opiate or related analgesics, is not without risk., Conclusion: Clinicians and especially psychiatrists should be aware of possible interaction and the risk of serotonin syndrome when a patient receives a combination of different opioid analgesics and serotonin reuptake inhibitor antidepressants. Improved information and collaboration with somatic and pain specialists and the general practitioners could help reduce the occurrence of this syndrome which can have dreadful consequences. Patients must be informed of such complications, which means that patients should be asked for a history of such events and monitored for serotoninergic adverse events, in order to avoid delays in this diagnosis., (Copyright © 2009 L’Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.)

Background: Serotonin syndrome is an iatrogenic disorder that results from serotonergic overactivity. Severe myoclonus and increased restlessness are hallmarks of the disorder., Methods: We report a case of serotonin syndrome related to poor drug elimination., Results: A 74-year-old white female with moderate to severe Alzheimer's dementia was brought to the emergency department for increasingly aggressive behavior. Upon admission, her risperidone dose was increased and citalopram continued. Several days later, she developed diffuse limb and facial myoclonus, spontaneous clonus, diaphoresis, and fever. Her symptoms completely resolved after discontinuation of these medications., Conclusion: Serotonin syndrome should be considered in the differential when elderly patients present with severe myoclonus. If unrecognized, this syndrome can lead to more severe manifestations including rhabdomyolysis, renal failure, and coma.

Objective: To discuss two cases of life-threatening serotonin toxicity due to a drug interaction between citalopram and fluconazole and to review the pertinent literature., Methods: A Medline search without date limitation was conducted using the terms serotonin syndrome, serotonin toxicity, fluconazole and citalopram., Results and Discussion: Fluconazole inhibits CYP2C19. Citalopram is a substrate for 2C19 and inhibition of its metabolism may result in serotonin toxicity. Serotonin toxicity in oncology patients may not present with the classic constellation of signs typically described in the literature. Delirium may be the only presenting feature. Current level of evidence for treatment of serotonin toxicity is level 4 or 5 (case series and expert opinion). Nevertheless, there is a strong theoretical basis for treating serotonin toxicity in medical patients with a 5H(2A) blocker such as cyproheptadine., Conclusions: Consultation-liaison psychiatrists and oncologists should be aware of this preventable and underrecognized interaction. Citalopram should be stopped or substituted prior to the concurrent administration of fluconazole, and in the event of toxicity, treatment with cyproheptadine has a favorable risk-benefit ratio despite a lack of randomized controlled data to support its use.

Objective: To report a case of serotonin syndrome associated with interaction between fentanyl and citalopram, as evidenced by medication history, clinical features and reversal following discontinuation of fentanyl., Case Summary: A 65-year-old patient chronically treated with the selective serotonin reuptake inhibitor (SSRI) citalopram developed confusion, agitation, tachycardia, tremors, myoclonic jerks and unsteady gait, consistent with serotonin syndrome, following initiation of fentanyl, and all symptoms and signs resolved following discontinuation of fentanyl. Based on the Naranjo probability scale, serotonin syndrome was a probable adverse reaction associated with co-administration of citalopram and fentanyl., Discussion: Serotonin syndrome is a potentially lethal pharmacodynamic interaction between medications that increase serotonergic transmission at the synaptic junction. The development of new pharmacological agents with varied properties and actions has increased the risk of serotonin syndrome as a clinical diagnosis. SSRIs and fentanyl are commonly co-administered, especially in the setting of chronic or malignant pain, as underlying depression may contribute to the pathogenesis of pain., Conclusion: Healthcare professionals should be aware of the possible development of serotonin syndrome as a complication of initiation of fentanyl and other phenylpiperidine opioids in patients treated with SSRIs.

Escitalopram is the newest selective serotonin reuptake inhibitor (SSRI) available for use in the United States. It has been approved for the treatment of major depression and generalized anxiety disorder. It is the S-enantiomer of the SSRI citalopram and is highly serotonin specific as it has minimal effect on the reuptake of dopamine or norepinephrine. It is also a well-tolerated medication, with a side-effect profile comparable to the other SSRIs. While a number of side effects have been seen during escitalopram therapy, such as insomnia, nausea, and increased sweating, there are no reported cases of serotonin syndrome associated with escitalopram therapy to date. We present the case of a 24-year-old woman who developed serotonin syndrome after an increase in her escitalopram to 30 mg/day. We will review the diagnostic criteria of serotonin syndrome and the clinical scenarios in which serotonin syndrome can develop. We will also discuss the proposed treatments and role that polypharmacology may play in the development of this clinical entity.

Serotonin syndrome is a disorder resulting from excess stimulation of serotonin and is associated with drug interaction, single-drug therapy, and overdose. We report a case involving a 32-year-old man who developed sudden agitation, diaphoresis, subjective fever, tremor, and insomnia. These symptoms were related to doubling the dose of citalopram in combination antidepressant therapy. Discontinuation of the agent resulted in early notable clinical resolution after 1 week. This is a rare report of serotonin syndrome induced by citalopram polytherapy. Although serotonin syndrome is rare, clinicians need to recognize it early.