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1.
Psiquiatr. biol. (Ed. impr) ; 26(3): 113-115, sept.-dic. 2019. tab
Artigo em Espanhol | IBECS | ID: ibc-ET5-449

RESUMO

INTRODUCCIÓN: El síndrome serotoninérgico es un cuadro clínico debido a altos niveles de serotonina. Está causado por el uso de uno o varios fármacos con actividad serotoninérgica de forma concomitante. Su diagnóstico es clínico y se lleva a cabo según criterios diagnósticos. CASO CLÍNICO: Paciente de 65años en seguimiento de larga evolución por trastorno afectivo bipolar con reciente instauración de tratamiento con amitriptilina. En urgencias se observa temblor distal, ataxia, bradipsiquia, desorientación temporoespacial, discinesia orolingual, miocolonías oculares y diaforesis. Se descartan posibles etiologías causantes del cuadro. RESULTADOS: Apareció un síndrome serotoninérgico tras la instauración de amitriptilina. No fueron necesarias medidas invasivas de soporte. Se retiró el tratamiento con psicofármacos y se instauraron progresivamente aquellos sin actividad serotoninérgica. CONCLUSIONES: No es necesario el uso concomitante de varios fármacos serotoninérgicos, sino que puede aparecer este síndrome con el uso de un fármaco instaurado de forma brusca


INTRODUCTION: Serotoninergic syndrome is a clinical disorder due to high levels of serotonin. It is caused by the concomitant use of one or several drugs with high serotoninergic activity. Its diagnosis is clinical, and is made following some diagnostic criteria. CLINICAL CASE: The case concerns a 65 year-old patient on long-term follow due to a bipolar affective disorder, and who recently started treatment with amitriptyline. In the Emergency Department, distal tremor was observed, as well as ataxia, bradypsychia, time-space orientation, orolingual dyskinesia, ocular myoclonus, and diaphoresis. Possible aetiological causes of the syndrome were ruled. RESULTS: A serotoninergic syndrome appeared after starting amitriptyline treatment. Invasive support measures were not necessary. The treatment with psychiatric drugs was withdrawn and gradually started with those without serotoninergic activity. CONCLUSIONS: The concomitant use of several serotoninergic drugs is not necessary, although this syndrome can appear with the use of a suddenly introduced drug


Assuntos
Humanos , Feminino , Pessoa de Meia-Idade , Idoso , Síndrome da Serotonina/induzido quimicamente , Transtorno Bipolar/tratamento farmacológico , Amitriptilina/efeitos adversos , Síndrome da Serotonina/diagnóstico , Serotoninérgicos/administração & dosagem , Índice de Gravidade de Doença , Inibidores de Captação de Serotonina/uso terapêutico
3.
A A Pract ; 13(11): 420-422, 2019 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-31577540

RESUMO

Perioperative serotonin syndrome has been associated with a number of medications and herbal supplements. We report a patient who developed serotonin syndrome immediately after an endoscopic procedure in which the preoperative use of black seed oil appears to have played a role in stimulating the syndrome. Black seed oil has not been previously reported in association with perioperative serotonin syndrome. Anesthesia professionals should be aware that patients taking black seed oil supplements may develop serotonin syndrome postoperatively.


Assuntos
Óleos Vegetais/efeitos adversos , Síndrome da Serotonina/induzido quimicamente , Adulto , Endoscopia , Humanos , Masculino , Naloxona/uso terapêutico , Período Perioperatório , Óleos Vegetais/química , Síndrome da Serotonina/tratamento farmacológico
5.
J Forensic Sci ; 64(6): 1950-1952, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31643086

RESUMO

4-bromo-2,5-dimethoxyphenethylamine (2C-B) is a designer drug. In Europe, 2C-B is easily obtained and used for recreational purposes. It is known for its stimulating effects similar to those of 3,4-methylenedioxymethamphetamine, although in higher doses it has more hallucinogenic effects. Here, we report a case of 2C-B ingestion, confirmed by liquid chromatography-tandem mass spectrometry, in an 18-year-old man. The neurological consequences were severe, including the development of serotonin syndrome and severe brain edema. Supportive therapy resulted in a stable condition, although, after several months, the patient still suffered from severe neurological impairment due to the drug-induced toxicity. This case showed that 2C-B could not be identified with the drugs of abuse screening routinely used in Dutch hospitals. The use of 2C-B carries many risks, with potentially profound neurological damage, that both consumers and healthcare physicians are unaware of.


Assuntos
Edema Encefálico/induzido quimicamente , Drogas Desenhadas/efeitos adversos , Dimetoxifeniletilamina/efeitos adversos , Convulsões/induzido quimicamente , Síndrome da Serotonina/induzido quimicamente , Adolescente , Cromatografia Líquida , Humanos , Masculino , Transtornos Relacionados ao Uso de Substâncias/complicações , Espectrometria de Massas em Tandem
7.
Medicine (Baltimore) ; 98(13): e15057, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30921235

RESUMO

RATIONALE: Takotsubo cardiomyopathy (TC) is characterized by transient left ventricular dysfunction. We describe a patient with stroke who presented with TC caused by serotonin syndrome (SS) following the administration of serotonergic and dopaminergic agents. PATIENT CONCERNS: A 55-year-old man with stroke was administered venlafaxine, tianeptine, ropinirole, carbidopa/levodopa, bromocriptine, and methylphenidate during rehabilitation. The patient presented with clinical features of SS (mental confusion, agitation, hyperhidrosis, chills, rigidity, and tachycardia), which persisted over 24 hours. The day after his SS symptoms disappeared, the patient's blood pressure decreased, and he developed tachycardia. DIAGNOSES: Echocardiography revealed an extensively akinetic apical segment and a severely hypokinetic midventricular segment of the left ventricle with basal hyperkinesia. The ejection fraction was reduced to 38%, and he was diagnosed with TC by the cardiologist. INTERVENTIONS: He was administered oxygen at 8 to 10 L/minutes via a Venturi mask, and norepinephrine bitartrate was administered intravenously. Hydration was maintained with normal saline infusion. OUTCOMES: Following appropriate management of TC, the patient was hemodynamically stable with significant recovery of his left ventricular wall motion. LESSONS: Prognosis of TC is usually favorable; however, it could be fatal in some cases. Clinicians should be aware of the potential development of TC in patients with stroke presenting with SS following the administration of serotonergic and dopaminergic agents.


Assuntos
Síndrome da Serotonina/induzido quimicamente , Inibidores da Recaptação de Serotonina e Norepinefrina/efeitos adversos , Acidente Vascular Cerebral/tratamento farmacológico , Cardiomiopatia de Takotsubo/induzido quimicamente , Humanos , Masculino , Pessoa de Meia-Idade
8.
World Neurosurg ; 126: 261-263, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30898741

RESUMO

BACKGROUND: Serotonin syndrome (SS) is a common disease entity and could result in death if missed. The incidence of SS is underestimated due to misdiagnosis of many cases, especially the ones with less severe presentation. Many medications have been depicted as the source of SS. We present a case of SS in a patient who received intravenous tramadol and oral gabapentin as pain management after spine surgery. CASE DESCRIPTION: A 66-year-old man was admitted to our outpatient clinic with walking difficulties for 2 months. He was neurologically intact. However, he had neurologic claudication. He was on insulin, telmisartan-hydrochlorothiazide, amlodipine, and albuterol before the surgery, and these drugs were continued after the surgery. After he was diagnosed with lumbar spinal stenosis, he underwent total laminectomies of L3 and L4 and bilateral transpedicular screw placement from L1 to L5. He received tramadol 100 mg once daily intravenously and gabapentin 300 mg thrice daily orally after the spine surgery. He became confused, aggressive, and agitated during his stay in the hospital postoperatively. He became frustrated with even his children and wife. He started receiving haloperidol and quetiapine after psychiatry consultation. Because he worsened immediately after quetiapine and haloperidol, his medications were ceased in a step-by-step manner (first, tramadol and second, gabapentin). He became stable in a few hours, and his symptoms have improved since then. CONCLUSIONS: Physicians treating spine patients should be alert about SS in patients using both tramadol and gabapentin.


Assuntos
Analgésicos/efeitos adversos , Gabapentina/efeitos adversos , Dor Pós-Operatória/tratamento farmacológico , Síndrome da Serotonina/induzido quimicamente , Tramadol/efeitos adversos , Idoso , Analgésicos/uso terapêutico , Gabapentina/uso terapêutico , Humanos , Laminectomia , Masculino , Fusão Vertebral , Estenose Espinal/cirurgia , Tramadol/uso terapêutico
9.
Clin Neuropharmacol ; 42(3): 103-104, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30844852

RESUMO

BACKGROUND: We report on the serotonin syndrome after an alcohol intake in a patient with major depressive disorder treated with escitalopram and clomipramine. CASE: A 26-year-old male patient with major depressive disorder had been stable on the treatment with escitalopram (20 mg/d) and clomipramine (50 mg/d) for 4 months. He had rarely taken alcohol, especially never with medication. One night after taking these drugs with a can of beer, he developed agitation, disorientation, myoclonus, hyperreflexia, tremor, tachycardia, diaphoresis, and hypertension, fulfilling the criteria for the serotonin syndrome. It was considered that the serotonin syndrome in the present case might be induced by alcohol's pharmacodynamic interaction with escitalopram and clomipramine leading to decreased clearance of extracellular serotonin in the brain and/or pharmacokinetic interaction with clomipramine leading to increased clomipramine levels. CONCLUSIONS: The present case report suggests that there may be an interaction between alcohol and antidepressants resulting in the serotonin syndrome, and clinicians should be aware of this possibility.


Assuntos
Consumo de Bebidas Alcoólicas/efeitos adversos , Citalopram/efeitos adversos , Clomipramina/efeitos adversos , Síndrome da Serotonina/induzido quimicamente , Inibidores de Captação de Serotonina/efeitos adversos , Adulto , Antidepressivos/efeitos adversos , Transtorno Depressivo Maior/tratamento farmacológico , Interações Medicamentosas , Humanos , Masculino
11.
Forensic Sci Med Pathol ; 15(2): 258-261, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30796754

RESUMO

Drugs for the treatment of depressive disorders, including SNRIs (serotonin noradrenaline reuptake inhibitors) venlafaxine and duloxetine, are widely prescribed as they have a high therapeutic to toxicity ratio. In rare cases, adverse effects may be severe, usually due to iatrogenic, accidental or intentional self-overdose that cause the excessive accumulation of serotonin and noradrenaline in synaptic clefts. Lethal intoxication with a combination of venlafaxine and duloxetine (postmortem blood concentrations 24 mg/L and 0.97 mg/L, respectively) without co-ingested substances, comorbidities or injuries that could have an unknown contribution to a fatal outcome is presented for the first time in the following case report, with a comprehensive clinical history, and complete results of the performed analyses. The cause of death was a serotonin syndrome that progressed to death in approximately six hours and 15 min after the suicidal ingestion of venlafaxine and duloxetine. Despite the high therapeutic to toxicity ratio SNRIs, which are reserved for patients with severe forms of depressive disorders and a higher suicidal tendency, they should be cautiously prescribed and handed over in smaller packages to make them easier to follow, and thus avoid accumulation within the patient's reach.


Assuntos
Cloridrato de Duloxetina/envenenamento , Síndrome da Serotonina/induzido quimicamente , Inibidores da Recaptação de Serotonina e Norepinefrina/envenenamento , Cloridrato de Venlafaxina/envenenamento , Adulto , Overdose de Drogas , Cloridrato de Duloxetina/análise , Feminino , Humanos , Inibidores da Recaptação de Serotonina e Norepinefrina/análise , Suicídio , Cloridrato de Venlafaxina/análise
15.
Am J Case Rep ; 19: 1227-1231, 2018 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-30318504

RESUMO

BACKGROUND Serotonin syndrome is a common yet potentially life-threatening condition caused by increased serotonergic activity, usually from serotonergic pharmaceutical agents. Primary features of serotonin syndrome include mental status changes, autonomic hyperactivity, and neuromuscular abnormalities. However, the presentation of serotonin syndrome is often quite variable, leading to its under-diagnosis. CASE REPORT A 50-year-old female with chronic kidney disease on peritoneal dialysis presented to the Emergency Department with severe, diffuse body pain. Over the course of her hospital stay, she developed severe nausea, vomiting, and diarrhea followed by hyperreflexia and inducible clonus. Laboratory studies were remarkable for elevated liver transaminases. Review of her medications revealed several serotonergic agents, including duloxetine, tramadol, and ondansetron. Given her symptoms and the multiple serotonergic agents she was taking, she was diagnosed with serotonin syndrome. Discontinuation of the serotonergic agents led to resolution of her symptoms over the course of 4 days. CONCLUSIONS Our patient's initial presentation of diffuse body pain highlights the variable presentation of serotonin syndrome. Our case also demonstrates the importance of recognizing serotonin syndrome, as the supportive ondansetron we gave to alleviate her nausea and vomiting likely exacerbated her serotonin syndrome.


Assuntos
Dor Crônica/etiologia , Inibidores de Captação de Serotonina/efeitos adversos , Dor Crônica/diagnóstico , Feminino , Humanos , Pessoa de Meia-Idade , Síndrome da Serotonina/induzido quimicamente , Síndrome da Serotonina/complicações , Síndrome da Serotonina/diagnóstico
16.
Psychosomatics ; 59(6): 539-546, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-30104021

RESUMO

BACKGROUND: Serotonin syndrome (SS) is a potentially serious side effect of serotonergic drugs. Cases of SS have been reported from the administration of methylene blue (MB), an agent with monoamine oxidase inhibiting properties. To date, the reported cases of MB-induced SS have all been with MB given parenterally. We report a case induced by the initiation of a MB-containing oral agent. METHODS: A case of SS felt to be induced by the initiation of an MB-containing orally-administered urinary analgesic, started in a patient concurrently treated with multiple serotonergic drugs, is presented. A systematic literature review of MB-induced SS follows. The review consisted of searches in MEDLINE databases using the key terms "methylene blue" and "serotonin syndrome". The authors read all abstracts, and articles related to MB and serotonin toxicity; non-associated articles were discarded. Results are summarized. RESULTS: 23 manuscripts were identified, resulting in 50 unique cases of MB-induced SS. The majority of cases were related to peri-operative use of MB in parathyroidectomies or for the treatment of vasoplegic shock. All cases were associated with MB given parenterally. Concurrent treatment with serotonergic antidepressants was described in all 50 cases. Symptoms of SS ranged from mild to severe. One fatality was reported. CONCLUSIONS: Methylene blue can induce SS, felt to be secondary to MAOI properties. Although previous reports have exclusively been associated with MB given via parental administration, our case suggests that SS can be induced by oral administration of MB-containing agents.


Assuntos
Analgésicos/administração & dosagem , Inibidores Enzimáticos/efeitos adversos , Azul de Metileno/efeitos adversos , Síndrome da Serotonina/induzido quimicamente , Neoplasias da Bexiga Urinária/cirurgia , Idoso , Humanos , Masculino
17.
Pharmacotherapy ; 38(9): 888-898, 2018 09.
Artigo em Inglês | MEDLINE | ID: mdl-29972695

RESUMO

STUDY OBJECTIVE: Serotonergic adverse drug events (ADEs) are caused by enhanced intrasynaptic concentrations of 5-hydroxytryptamine (5-HT). No systematic process currently exists for evaluating cumulative 5-HT and off-target toxicity of serotonergic drugs. The primary study aim was to create a Serotonergic Expanded Bioactivity Matrix (SEBM) by using a molecular bioinformatics, polypharmacologic approach for assessment of the participation of individual 5-HT drugs in serotonin syndrome (SS) reports. DATA SOURCES: Publicly available databases including the U.S. Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS), ChEMBL, DrugBank, PubChem, and Kyoto Encyclopedia of Genes and Genomes (KEGG) were queried for computational and pharmacologic data. DESIGN: An in-house bioinformatics TargetSearch program ( http://dxulab.org/software) was used to characterize 71 serotonergic drugs interacting at 13 serotonin receptor subtypes and serotonin reuptake transporter protein (SERT). In addition, off-target interactions at norepinephrine transporter (NET), monoamine oxidase (MAO), and muscarinic receptors were included to define seven polypharmacological drug cohorts. Serotonin syndrome reports for each serotonergic drug were extracted from FAERS by using the Sternbach and Hunter criteria. MEASUREMENTS AND MAIN RESULTS: A proportional reporting adverse drug reaction (ADR) ratio (PRR) was calculated from each drug's total ADEs and SS case reports and aggregated by drug bioactivity cohorts. Triple-receptor interactions had a disproportionately higher number of SS cases using both the Hunter criteria (mean PRR 1.72, 95% CI 1.05-2.39) and Sternbach (mean PRR 1.54, 95% CI 1.29-1.79). 5-Hydroxytryptamine agonists were associated with a significantly lower proportion of SS cases using the Hunter and Sternbach criteria, respectively (mean PRR 0.49, 95% CI 0.17-0.81 and mean PRR 0.49, 95% CI 0.15-0.83). Drugs with disproportionately higher participation in SS vary considerably between the two diagnostic criteria. CONCLUSION: The SEBM model suggests a possible polypharmacological role in SS. Although further research is needed, off-target receptor activity may help explain differences in severity of toxicity and clinical presentation.


Assuntos
Polifarmacologia , Serotoninérgicos/efeitos adversos , Síndrome da Serotonina/induzido quimicamente , Biologia Computacional , Bases de Dados de Produtos Farmacêuticos , Humanos , Modelos Biológicos
18.
Arch Toxicol ; 92(8): 2457-2473, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29916050

RESUMO

Drugs may cause serotonin toxicity by a number of different mechanisms including inhibition of serotonin uptake and metabolism, increased serotonin synthesis and release, activation of serotonin receptors, and inhibition of cytochrome P450 oxidases. Some drug interactions involving opioids can increase intrasynaptic levels of serotonin, and opioid analgesic drugs are now recognized as being involved in some cases of serotonin toxicity especially if administered in conjunction with other serotonergic medications including monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and tricyclic antidepressants. In March 2016, the FDA issued a Drug Safety Communication concerning the association of the entire class of opioid pain medicines with serotonin toxicity. Reports of the involvement of individual opioids particularly tramadol, tapentadol, meperidine, methadone, oxycodone, fentanyl, and dextromethorphan are reviewed. While relevance to human serotonin toxicity of animal models, including many studies on rat brain synaptosomes, is questionable, important insights have recently been forthcoming from research utilizing 5-HT receptors, serotonin transporter (SERT), and knockout mice. In studies with human SERT-transfected human HEK293 cells, the synthetic opioids tramadol, meperidine, methadone, tapentadol, and dextromethorphan inhibited SERT, but fentanyl and a number of phenanthrenes including morphine and hydromorphone did not. Receptor ligand-binding assays revealed interaction of fentanyl with 5-HT1A receptors and interaction of meperidine, methadone, and fentanyl with 5-HT2A receptors. Although the opioids most often associated with serotonin toxicity in humans inhibit human SERT in vitro, fentanyl and oxycodone are not inhibitory even though their clinical involvement has been reported. This suggests some SERT-independent effects on the serotonin system in vivo. Heightened clinician awareness of the possibility of serotonin toxicity among patients taking opioids and serotonergic antidepressants is called for.


Assuntos
Analgésicos Opioides/efeitos adversos , Modelos Animais , Síndrome da Serotonina/induzido quimicamente , Serotonina/metabolismo , Animais , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Interações Medicamentosas , Humanos , Síndrome da Serotonina/metabolismo
20.
Am J Med ; 131(11): 1382.e1-1382.e6, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-29752906

RESUMO

Tramadol is commonly prescribed for pain control because it presents a lower risk for addiction and respiratory depression compared to other opioids. However, tramadol's serotonin and norepinephrine reuptake inhibitory effects result in a unique adverse effect profile. Two such adverse events are serotonin syndrome and seizures. The prevalence of tramadol-induced serotonin syndrome and seizures is modest in the general population, but if left untreated, the morbidity and mortality can be high; therefore, prompt recognition and management is essential. Various risk factors such as medical comorbidities, use or abuse of supratherapeutic doses of tramadol, and concomitant administration of proconvulsant serotonergic cytochrome P-450 inhibitors will help clinicians identify individuals at an elevated risk for serotonin toxicity and seizures. Serotonin syndrome and seizures can be effectively treated by administering benzodiazepines, providing supportive care, and discontinuing tramadol and other contributing agents. Cyproheptadine should be administered in moderate to severe cases of serotonin syndrome. Our objective is to summarize the literature on the pharmacology, epidemiology, risk factors, clinical presentations, and evidence-based management of tramadol-related seizures and serotonin syndrome.


Assuntos
Analgésicos Opioides/efeitos adversos , Convulsões/induzido quimicamente , Síndrome da Serotonina/induzido quimicamente , Tramadol/efeitos adversos , Anticonvulsivantes/uso terapêutico , Humanos , Fatores de Risco , Síndrome da Serotonina/complicações , Síndrome da Serotonina/diagnóstico , Síndrome da Serotonina/tratamento farmacológico
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