Rasagiline and venlafaxine: The serotonin syndrome

2017 ◽  
Vol 41 (S1) ◽  
pp. S759-S759
Author(s):  
A. Rodriguez Campos ◽  
L. Rodríguez Andrés ◽  
G. Medina Ojeda ◽  
L. Gallardo Borge ◽  
E. Rybak Koite

Rasagiline is a highly potent irreversible monoamine oxidase (MAO)-B inhibitor, antiparkinsonian drug that may be used with caution in patients treated with antidepressant drugs because of the possible appearance of severe adverse effects. It is presented the case report of a woman treated with rasagiline and venlafaxine that presents confusion and a serotonin syndrome. Pathogenesis, physiopathology and treatment are discussed. Growing evidence suggests that Parkinson disease and depression are linked. Antidepressant drugs and PD treatment should be used with caution because of possible drug interaction.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Author(s):  
Abdullah Aboukarr ◽  
Mirella Giudice

<p>ABSTRACT</p><p>Background: Monoamine oxidase B (MAO-B) inhibitors are used to treat the motor symptoms of Parkinson disease. Depression is commonly associated with Parkinson disease, and selective serotonin reuptake inhibitors (SSRIs) are often used for its management. Tertiary sources warn that the combination of MAO-B inhibitors and SSRIs can result in increased serotonergic effects, leading to serotonin syndrome.</p><p>Objective:To explore the mechanism, clinical significance, and management of this potential drug interaction through a review of the supporting evidence.</p><p>Data Sources: PubMed, MEDLINE (1946 forward), Embase (1947 forward), PsycINFO (1806 forward), and International Pharmaceutical Abstracts (1970 forward) were searched on February 4, 2017. Study Selection and Data Extraction: Studies and case reports describing aspects of the potential interaction between MAO-B inhibitors and SSRIs in patients with Parkinson disease and published in English were identified by both title and abstract.</p><p>Data Synthesis: The search identified 8 studies evaluating the potential interaction between SSRIs and the MAO-B inhibitors selegiline and rasagiline. The largest, a retrospective cohort study of 1504 patients with Parkinson disease, found no cases of serotonin syndrome with coadministration of rasagiline and an SSRI. A survey of 63 investigators in the Parkinson Study Group identified 11 potential cases of serotonin syndrome among 4568 patients treated with the combination of selegiline and antidepressants (including SSRIs). In addition, 17 case reports describing the onset of serotonin syndrome with coadministration of an SSRI and either selegiline or rasagiline were identified. Following discontinuation or dose reduction of one or both of the agents, the symptoms of serotonin syndrome gradually resolved in most cases, with none being fatal.</p><p>Conclusions: According to the literature, serotonin syndrome occurs rarely, and the combination of SSRI and MAO-B inhibitor is well tolerated. Therefore, SSRIs and MAO-B inhibitors can be coadministered, provided that their recommended doses are not exceeded and the SSRI dose is kept at the lower end of the therapeutic range. Among the SSRIs, citalopram and sertraline may be preferred.</p><p>RÉSUMÉ</p><p>Contexte : Les inhibiteurs de la monoamine oxydase B (MAO-B) sont employés dans le traitement des symptômes moteurs de la maladie de Parkinson, maladie à laquelle la dépression est souvent associée et fréquemment traitée à l’aide d’inhibiteurs sélectifs de la recapture de la sérotonine (ISRS). Des sources tertiaires mettent en garde contre la combinaison d’inhibiteurs de la MAO-B et d’ISRS car elle peut mener à une augmentation des effets sérotoninergiques, dégénérant en un syndrome sérotoninergique.</p><p>Objectif : Chercher à connaître le mécanisme, la signification clinique et la prise en charge de cette potentielle interaction médicamenteuse en procédant à une revue des preuves à l’appui.</p><p>Sources des données : Les bases de données PubMed, MEDLINE (depuis 1946), Embase (depuis 1947), PscyINFO (depuis 1806), et International Pharmaceutical Abstracts (depuis 1970) ont été interrogées le 4 février 2017.</p><p>Sélection des études et extraction des données : Des études et des observations cliniques, publiées en anglais, portant sur des aspects de la potentielle interaction entre les inhibiteurs de la MAO-B et les ISRS chez les patients atteints de la maladie de Parkinson ont été repérées par une recherche ciblant les titres et les résumés.</p><p>Synthèse des données : La recherche a permis de trouver 8 études analysant la potentielle interaction entre les ISRS et deux inhibiteurs de la MAO-B : la sélégiline et la rasagiline. La plus importante d’entre elles, une étude de cohorte rétrospective sur 1504 patients atteints de la maladie de Parkinson, n’a relevé aucun cas de syndrome sérotoninergique en présence d’une prise concomitante de rasagiline et d’un ISRS. Une enquête auprès de 63 chercheurs dans le Parkinson Study Group a permis de relever 11 potentiels cas de syndrome sérotoninergique chez 4568 patients traités avec une combinaison de sélégiline et d’antidépresseurs (notamment des ISRS). De plus, 17 observations cliniques qui décrivaient un début de syndrome sérotoninergique en présence d’une prise concomitante d’un ISRS et de sélégiline ou de rasagiline ont été recensées. Suivant la réduction de la posologie ou l’interruption d’un ou des deux médicaments, les symptômes du syndrome sérotoninergique se sont graduellement résolus dans la plupart des cas, et il n’y a eu aucune mortalité.</p><p>Conclusions : Selon la documentation, le syndrome sérotoninergique est rare et la combinaison d’ISRS et d’inhibiteurs de la MAO-B est bien tolérée. Ainsi, les deux types d’inhibiteurs peuvent être administrés conjointement pourvu que l’on ne dépasse pas la posologie recommandée et que la dose d’ISRS demeure dans le bas de l’intervalle thérapeutique. Parmi les ISRS, il peut être préférable d’employer le citalopram ou la sertraline.</p>


2017 ◽  
Vol 41 (S1) ◽  
pp. S700-S700
Author(s):  
M. Preve ◽  
A. Ruccia ◽  
R. Traber ◽  
R.A. Colombo

IntroductionSerotonin syndrome is a potential adverse reaction to drugs increasing serotoninergic activity in the nervous system, some of them being frequently prescribed, such as antidepressant drugs. The association of myoclonus, diarrhea, confusion, hypomania, agitation, hyperreflexia, shivering, in-coordination, fever and diaphoresis, when patients are treated with serotoninergic agents, could constitute a “serotonin syndrome”. The purpose of this report is to review the clinical evidence of serotonin syndrome with SSRIs augmentation of amisulpride. We propose two case report and literature review.MethodWe conducted a systematic review of the literature with the principal database (PubMed, Enbase, PsychInfo) and we present two case report [1,2].ResultsWe describe two different case report with SSRIs augmentation of amisulpride.Discussion and conclusionTo our knowledge this is no report about the emergence of serotonin syndrome due to the use of SSRIs augmentation of amisulpride. Serotonin syndrome symptoms include high body temperature, agitation, increased reflexes, tremor, sweating, fever, dilated pupils, and diarrhea. Further research is warranted to replicate our clinical and qualitative observations and, in general, quantitative studies in large samples followed up over time are needed. Methodological limitations, clinical implications and suggestions for future research directions are considered.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2013 ◽  
Vol 27 (1) ◽  
pp. 71-78 ◽  
Author(s):  
Susie H. Park ◽  
Robin C. Wackernah ◽  
Glen L. Stimmel

Background: There is a warning associated with all serotonergic antidepressants and its concomitant use with tramadol due to the concern for a drug–drug interaction resulting in serotonin syndrome (SS). The prescribing of antidepressants with tramadol may be unnecessarily restricted due to fear of causing this syndrome. Objectives: There are 3 objectives of this review. To (1) review case reports of SS associated with the combination of tramadol and antidepressant drugs in recommended doses, (2) describe the mechanisms of the drug interaction, and (3) identify the potential risk factors for SS. Methods: Case reports of SS associated with tramadol and antidepressants were identified via Cochrane Library, PubMed, and Ovid (through October 2012) using search terms SS, tramadol, antidepressants, fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, escitalopram, venlafaxine, desvenlafaxine, duloxetine, mirtazapine, milnacipran, trazodone, vilazodone, and bupropion. Cases involving monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants were excluded. Results: Nine articles were identified describing 10 cases of suspected SS associated with therapeutic doses of tramadol combined with an antidepressant. Mechanisms of the drug–drug interactions involve pharmacodynamic, pharmacokinetic, and possible pharmacogenetic factors. Conclusions: Review of the available case reports of tramadol combined with antidepressant drugs in therapeutic doses indicates caution in regard to the potential for SS but does not constitute a contraindication to their use. Tramadol is only contraindicated in combination with MAOIs but not other antidepressants in common use today. These case reports do suggest several factors associated with a greater risk of SS, including increased age, higher dosages, and use of concomitant potent cytochrome P450 2D6 inhibitors. Tramadol can be safely combined with antidepressants; however, monitoring and counseling patients are prudent when starting a new serotonergic agent or when doses are increased.


2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Mi-mi Zhou ◽  
Si-yuan Jing ◽  
Yue Chen

The dosing of anti-Parkinson drugs is considered as the optimal control of the symptoms of PD, and increasing the dose of drugs is a common method to treat the aggravate state of PD. However, this is a case of PD elderly patient who had nephritic syndrome, with an increase in the dose, the symptoms did not get improved,but a series of other adverse effects appeared.


1994 ◽  
Vol 28 (6) ◽  
pp. 732-735 ◽  
Author(s):  
Mark A. Graber ◽  
T. Brent Hoehns ◽  
Paul J. Perry

OBJECTIVE: To report a serious drug interaction possibly occurring with the monoamine oxidase inhibitor phenelzine and the selective serotonin reuptake inhibitor sertraline. CASE SUMMARY: A 61-year-old woman with treatment-refractory major depressive disorder was being treated unsuccessfully with lithium, phenelzine, thioridazine, and doxepin. Sertraline 100 mg/d was added to the patient's therapy. Within three hours of ingesting the first dose, the patient experienced a dramatic increase in her temperature, pulse, and respirations along with labile blood pressure, and symptoms of rigidity, diaphoresis, shivering, and decreased sensorium. The patient was transported to the emergency room and treated with diazepam 10 mg iv, followed by midazolam 10 mg iv for control of rigidity. She was also intubated. The patient then experienced precipitous falls in her blood pressure and respiratory rate. Ice packs combined with a cooling blanket and dantrolene 80 mg iv were administered to control fever and rigidity, respectively. She had an initial working diagnosis of neuroleptic malignant syndrome, which was later changed to serotonin syndrome. Dantrolene was continued for 72 hours at which time the patient was extubated and transferred to a psychiatric unit. CONCLUSIONS: Selective serotonin reuptake inhibitor antidepressants should not be combined with monoamine oxidase inhibitor antidepressants because of the risk of serotonin syndrome.


2016 ◽  
Vol 33 (S1) ◽  
pp. S631-S631
Author(s):  
M. García Moreno ◽  
A. De Cós Milas ◽  
L. Beatobe Carreño ◽  
B. Poza Cano

IntroductionAutistic disorder (AD) is a neuropsychiatric disorder that often presents significant disruptive symptoms such as irritability, aggression and self-injury in addition to impairment of social skills and communication. These symptoms interfere both individuals with AD and their families and social environment.ObjectiveShow paliperidone effect in behavioural symptoms in AD.MethodsLiterature review about behavioural symptoms in AD and paliperidone effect in its treatment, followed by a case report of clinical improvement after treatment with paliperidone in a patient with autism. Agitation subscale Aberrant Behavior Checklist (ABC-I) scores was compared prior and 4 weeks after paliperidone treatment, and clinical improvement was assessed with Clinical Global Impression-Improvement Scale (CGI-I).ResultsAlthough risperidone has been one of the most studied atypical antipsychotic to treat this symptoms, its use should be limited in order to avoid extrapyramidal and metabolic symptoms. Paliperidone – the major metabolite of risperidone – has shown effectiveness in the treatment of behavioral symptoms in patients with autism, even in subjects with a prior ineffective trial of risperidone. Our patient, 21-years-old male with AD and significant disruptive symptoms was treated with paliperidone 9 mg/day. We observed a 20-points reduction in ABC-I scores 4 weeks later, with most significant improvement in items like auto-agression, heteroaggressivity, irritability and slams. CGI-I scores showed a much better improvement, and no significant adverse effects appeared.ConclusionsPaliperidone is an effective and safe treatment in behavioral symptoms associated to AD, with reduction in ABC-I subscale scores. More studies are needed to confirm our data.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2017 ◽  
Vol 41 (S1) ◽  
pp. S755-S755
Author(s):  
R. Landera Rodríguez ◽  
M. Juncal Ruiz ◽  
R. Martín Gutiérrez ◽  
M. Gómez Revuelta ◽  
I. Madrazo del Río Hortega ◽  
...  

IntroductionClozapine, is widely prescribed for treatment of refractory schizophrenia, but its use may be limited by potentially serious adverse effects. The most feared complication remains agranulocytosis [absolute neutrophil count (ANC) < 500/mm3], which occurs in 1% of patients. Guidelines recommend immediate cessation until the granulocyte count normalizes, but little is known about the subsequent treatment and the possibility of restoring clozapine.ObjectivesTo know procedures that allow clozapine rechallenge after induced agranulocytosis in refractory schizophrenia.MethodsWe present a clinical case of agranulocytosis and evolution after simple reinstitution of clozapine.ResultsA 38-year-old woman diagnosed refractory schizophrenia. After 10 years with clozapine (300 mg/day), we find neutropenia (ANC 1420/mm3) in a monthly control blood count with progression to agranulocytosis (ANC 460/mm3) in the following month. We suspend clozapine and started olanzapine (20 mg/day) with restoration of haematological values in a period of one month. The patient had psychotic decompensation at two months after the change with lack of response to different psychopharmacological strategies for five months. According to the hematology department we decided to re-introduce clozapine (200 mg/day) in combination with olanzapine with complete clinical remission. Between the 3rd and 9th week after rechallenge we observe a progressive decline in ANC, while remaining within the range of normal. From the 9th week and in the last 6 months neutrophil counts remained stable.ConclusionsAlthough, more research is needed to establish the safety to rechallenge of clozapine after agranulocytosis, it must be an alternative to consider when other treatment strategies fail.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2016 ◽  
Vol 12 (01) ◽  
pp. 58-61
Author(s):  
Nantawan Tinroongroj ◽  
Apichard Sukonthasarn

2021 ◽  
pp. 379-383
Author(s):  
Meghan L. McPhie ◽  
Kevin Y.M. Ren ◽  
J. Michael Hendry ◽  
Sonja Molin ◽  
Thomas Herzinger

Tattoos have become increasingly popular worldwide making adverse effects from tattoos a growing concern. In our report, we present a 51-year-old man who developed an unusual allergic reaction to the red ink portions of his tattoos that coincided with the initiation of ledipasvir/sofosbuvir treatment for his hepatitis C. Clinical and histological features were consistent with a delayed-type hypersensitivity reaction to red ink.


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