Use Of Reboxetine Research Articles

Gut Microbiome Alteration after Reboxetine Administration in Type-1 Diabetic Rats.

Antidepressants are drugs commonly used in clinical settings. However, there are very limited studies on the effects of these drugs on the gut microbiota. Herein, we evaluated the effect of reboxetine (RBX), a selective norepinephrine (noradrenaline) reuptake inhibitor (NRI), on gut microbiota in both diabetic and non-diabetic rats. This is the first report of relation between reboxetine use and the gut microbiota to our knowledge. In this study, type-1 diabetes induced by using streptozotocin (STZ) and RBX was administered to diabetic rats and healthy controls for 14 days. At the end of the treatment, stool samples were collected. Following DNA extraction, amplicon libraries for the V3-V4 region were prepared and sequenced with the Illumina Miseq platform. QIIME was used for preprocessing and analysis of the data. As a result, RBX had a significant effect on gut microbiota structure and composition in diabetic and healthy rats. For example, RBX exposure had a pronounced microbial signature in both groups, with a low Firmicutes/Bacteroidetes ratio and low Lactobacillus levels. While another abundance phylum after exposure to RBX was Proteabacteria, other notable taxa in the diabetic group included Flavobacterium, Desulfovibrionaceae, Helicobacteriaceae, Campylobacterales, and Pasteurellacae when compared to the untreated group.

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Catechol-O-methyltransferase (COMT) metabolizes catecholamines in the prefrontal cortex (PFC). A common polymorphism in the COMT gene (COMT val158met) has pleiotropic effects on cognitive and emotional processing. The met allele has been associated with enhanced cognitive processing but impaired emotional processing relative to the val allele. We genotyped healthy, white men in relation to the COMT val158met polymorphism. They were given a single 4 mg dose of the selective noradrenaline reuptake inhibitor (NRI) reboxetine or placebo in a randomized, double-blind between-subjects model and then completed an emotional memory task 2 hours later. We included 75 men in the study; 41 received reboxetine and 34 received placebo. In the placebo group, met/met carriers did not demonstrate the usual memory advantage for emotional stimuli that was observed in val carriers. Reboxetine restored this emotional enhancement of memory in met/met carriers, but had no significant effect in val carriers. We studied only men, thus limiting the generalizability of our findings. We also relied on self-reported responses to screening questions to establish healthy volunteer status, and in spite of the double-blind design, participants were significantly better than chance at identifying their intervention allocation. Emotional memory is impaired in healthy met homozygotes and selectively improved in this group by reboxetine. This has potential translational implications for the use of reboxetine, which is currently licensed as an antidepressant in several countries, and edivoxetine, a new selective NRI currently in development.

A Case of Profound Weight Loss Secondary to use of Reboxetine

Reboxetine is a selective norepinephrine re-uptake inhibitor used in the treatment of depression. The studies testing the effects of reboxetine on body weight have demonstrated that reboxetine reduces body weight and reboxetine found to be superior to placebo in reducing antipsychotic-induced weight gain. To date there are only a few cases in the literature of reboxetine use in adults resulting in profound weight loss. We present an unusual case report of a patient who experienced a marked weight loss with reboxetine treatment, regained weight after its withdrawal and experienced marked weight loss after re-challenge with reboxetine.

A Case of Profound Weight Loss Secondary to use of Reboxetine

A Case of Profound Weight Loss Secondary to use of Reboxetine

The Declining Use of Reboxetine in Years 2000 to 2006

The Declining Use of Reboxetine in Years 2000 to 2006

Efficacy of Reboxetine in the Treatment of Attention-Deficit/Hyperactivity Disorder in Boys With Intolerance to Methylphenidate

Attention-deficit/hyperactivity disorder (ADHD) is the most common neurobehavioral disorder of childhood. Principal treatment options for ADHD today include the psychostimulants, mainly methylphenidate (MPH). However, approximately 30% to 50% of children and adults with ADHD either do not respond to or do not tolerate treatment with stimulants. In this 8-week open-label, MPH-controlled, parallel group design study, we investigate the efficacy of reboxetine, a new selective norepinephrine reuptake inhibitor, in the treatment of boys with ADHD with a history of intolerance to MPH therapy. Twenty-seven outpatient boys, aged 6 to 16 years, diagnosed with ADHD, participated in the study. Those with a history of intolerance to MPH therapy were assigned to treatment with reboxetine (2-8 mg/d), and the rest were assigned to treatment with MPH (10-20 mg/d) as the control group. The primary outcome measure for this study was the change in rating scores on the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, ADHD Scale (DAS) that was assessed at baseline and at 8 weeks. At the end of 8 weeks, both reboxetine and MPH treatment regimens resulted in significant improvement in ADHD symptoms. The change in the reduction in the total DAS score and the DAS subscale scores between the reboxetine group and the MPH group was not statistically significant in any of the scores. Although preliminary, results of this study indicate that the use of reboxetine, a new selective norepinephrine reuptake inhibitor, in the treatment of ADHD could increase treatment options available for children who have shown intolerance or who are unresponsive to MPH.

Restless legs syndrome as side effect of second generation antidepressants

Although of clinical interest, the question is still not fully answered whether antidepressants (AD) can cause or exacerbate restless legs syndrome (RLS). The literature provides contradictory information. This study addresses this problem for the class of second generation AD. In four neurological offices, all patients treated for the first time with an AD were prospectively observed with regard to the question of whether RLS occurred or pre-existing RLS worsened as a result of the medication. Because initial treatment in the participating offices is mainly executed with “modern” selective AD, the study was restricted to these drugs (fluoxetine, paroxetine, citalopram, sertraline, escitalopram, venlafaxine, duloxetine, reboxetine, and mirtazapine). In 9% of patients, RLS was recorded as a side effect related to the administration of AD. The frequency of this side effect varied among the drugs. The problem is most pronounced with mirtazapine provoking or deteriorating RLS in 28% of patients. By contrast, no case occurred during use of reboxetine. As for the other AD, the rate of newly occurred and deteriorated RLS, ranged from 5% to 10%. Typically, RLS occurred during the initial days of treatment.

Reboxetine Use in the Treatment of Attention-Deficit/Hyperactivity Disorder

Journal of Child and Adolescent PsychopharmacologyVol. 16, No. 6 Letters to the EditorReboxetine Use in the Treatment of Attention-Deficit/Hyperactivity DisorderHalime T. Çak and Füsun Çuhadaroğlu ÇetinHalime T. ÇakSearch for more papers by this author and Füsun Çuhadaroğlu ÇetinSearch for more papers by this authorPublished Online:4 Jan 2007https://doi.org/10.1089/cap.2006.16.803AboutSectionsPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail "Reboxetine Use in the Treatment of Attention-Deficit/Hyperactivity Disorder." , 16(6), pp. 803–804FiguresReferencesRelatedDetailsCited byA systematic review of reboxetine for treating patients with attention deficit hyperactivity disorder21 November 2014 | Nordic Journal of Psychiatry, Vol. 69, No. 4Efficacy of reboxetine in adults with attention-deficit/hyperactivity disorder: A randomized, placebo-controlled clinical trial11 February 2011 | Human Psychopharmacology: Clinical and Experimental, Vol. 25, No. 7-8 Volume 16Issue 6Dec 2006 InformationCopyright 2006, Mary Ann Liebert, Inc.To cite this article:Halime T. Çak and Füsun Çuhadaroğlu Çetin.Reboxetine Use in the Treatment of Attention-Deficit/Hyperactivity Disorder.Journal of Child and Adolescent Psychopharmacology.Dec 2006.803-804.http://doi.org/10.1089/cap.2006.16.803Published in Volume: 16 Issue 6: January 4, 2007PDF download

Transfer of reboxetine into breastmilk, its plasma concentrations and lack of adverse effects in the breastfed infant

To investigate the transfer of reboxetine into milk, the absolute and relative infant doses via milk and to assess plasma concentrations and adverse unwanted effects in the breastfed infant. Multiple samples of blood and milk were obtained over a dose interval at steady-state from four women who were taking reboxetine for postnatal depression. Drug concentrations in plasma and milk were measured by high performance liquid chromatography and milk/plasma ratio (M/P), absolute infant dose and relative infant dose were estimated by standard methods. Their four, breastfed, infants were also examined clinically, and a blood sample was taken for drug analysis. The median (range) dose taken by the women was 6 (4-10) mg/day. There was no significant difference in reboxetine concentration between paired fore-and hind-milk samples. The mean (95% CI) M/P was 0.06 (0.03, 0.09). Absolute infant dose was 1.7 (0.7, 2.4) microg/kg/day for reboxetine while the relative infant dose was 2.0% (1.3, 2.7%). Three of the infants met normal developmental milestones and no adverse effects were seen in any infant. The fourth infant had developmental problems that were not associated with the maternal reboxetine therapy. The concentrations of reboxetine in plasma from the four infants were <4 microg/l, 2.6 microg/l, 2.3 microg/l and 5 microg/l, respectively. The study suggests that reboxetine use by lactating women is safe for the breastfed infant. Nevertheless, our study had only four mother/baby pairs, and each decision to breastfeed should always be made on the basis of an individual risk/benefit analysis.

Reboxetine may cause amenorrhea in female patients

Objective. Reboxetine is a selective noradrenaline reuptake inhibitor (NaRI), a study on the effects of reboxetine on amenorrhea has not been reported in the literature up to now. This report describes a patient with symptoms of amenorrhea which is thought to be caused by reboxetine. Case. A female patient with major depressive disorder was given reboxetine 8 mg/day. She had experienced secondary amenorrhea for 3 months. The patient had no periodic irregularity before reboxetine use, and after reboxetine was discontinued menstruation resumed. After another trial with reboxetine at the optimal dose (8 mg/day, increased gradually), the patient reported amenorrhea again for 2 months. On discontinuing reboxetine, her menstrual cycle became regular again. Discussion. FSH, LH, E2 and prolactin levels were normal in our patient. Because amenorrhea was temporally related with reboxetine trials, we posit that this phenomenon may be due to side effects of reboxetine. This may be due to noraderenergic effects on hormonal function.

Worsening of Borderline Symptoms Under Reboxetine Treatment

Back to table of contents Previous article Next article LetterFull AccessWorsening of Borderline Symptoms Under Reboxetine TreatmentIon Anghelescu, M.D., Britta Jänen, M.D., Frank Schindler, M.D., and Claas-Hinrich Lammers, M.D., Ion AnghelescuSearch for more papers by this author, M.D., Britta JänenSearch for more papers by this author, M.D., Frank SchindlerSearch for more papers by this author, M.D., and Claas-Hinrich LammersSearch for more papers by this author, M.D., Department of Psychiatry, University Medicine Berlin, GermanyPublished Online:1 Nov 2005AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail SIR: Reboxetine, a norepinephrine reuptake inhibitor, is a potent antidepressant for patients with major depressive disorder or dysthymia.1 Borderline patients do not only show symptoms such as self-mutilation, suicidality, dissociative symptoms, aversive tension and instability of mood but also very often depressive symptoms which require a psychopharmacological treatment. Here we report the clinical observation in two patients that the use of reboxetine as an antidepressant in borderline patients does provoke an increase in borderline symptoms such as dissociative symptoms, aversive tension and irritability.Case ReportsMs. A. is a 23-year-old female with the diagnosis of dysthymia who was admitted because of acute suicidality. The diagnoses made over the past few years were borderline personality disorder, cannabis and alcohol abuse, panic disorder with agoraphobia and anorexia nervosa. Her major complaints were affective lability, depersonalisation and concentration difficulties. Self-injuries have occurred for about 7 years, her childhood history was remarkable for sexual abuse by her father. Because of insufficient efficacy and sedation as a side effect the premedication with mirtazapine 30 mg daily was switched to reboxetine, because she refused to take an SSRI. Already with reboxetine 4 mg daily she suffered from severe irritability and aversive tension with increased suicidality and dissociative symptoms, which could also be translated into a visual analogue scale. Three days after discontinuation the symptoms completely remitted.Ms. B. is a 32-year-old female with the diagnosis of a major depressive episode (HDRS-17 of 17 at admission). Her major complaint was sadness and feelings of guilt with insomnia. She was treated with quetiapine (200 mg daily) because of its sedating effects and because of galactorrhea associated with amisulpride intake before. Moreover, she suggested the substitution of venlafaxine, which had caused significant weight gain of about 5 kg in 4 weeks. Therefore, reboxetine was initiated, and increased from 2 to 6 mg daily over 3 days. With this dosage she developed severe affective lability and impulsivity with acute suicidality (HDRS-17: 21). Two days after discontination and switch to 50 mg sertraline she remitted completely from these new symptoms. She then reported—what was denied at the beginning—recurrent states of aversive tension, identity problems and flashback intrusions since the age of 14. This led to the supplementary diagnosis of borderline personality disorder.DiscussionWe report for the first time worsening of borderline symptoms, especially dissociative symptoms and aversive tension, under the treatment with reboxetine in two patients with borderline personality disorder. We interpret this clinical observation as an increased noradrenergic sensitivity with an hyperresponsiveness of the adrenergic system under stimulation. An heightened and dysregulated adrenergic function and a symptom provocation through increase of noradrenergic neurotransmission is a robust finding in patients with post traumatic stress disorder (PTSD).2 Since borderline personality disorder has been conceptualized as a chronic complex PTSD, our clinical observation indicates that noradrenergic hyperresponsitivity is a neurobiological mechanism for borderline symptoms. This observation is supported by the finding of reduction of aversive tension and dissociation by clonidine, an inhibitor of the central noradrenergic system.3References1 Burrows GD, Maguire KP, Norman TR: Antidepressant efficacy and tolerability of the selective norepinephrine reuptake inhibitor reboxetine: a review. J Clin Psychiatry 1998; 59(suppl 14):4-7Google Scholar2 Southwick SM, Bremner JD, Rasmusson A, et al: Role of norepinephrine in the pathophysiology and treatment of posttraumatic stress disorder. Biol Psychiatry 1999; 46:1192–1204Crossref, Medline, Google Scholar3 Philipsen A, Richter H, Schmahl C, et al: Clonidine in acute aversive inner tension and self-injurious behavior in female patients with Borderline personality disorder. J Clin Psychiatry (in press)Google Scholar FiguresReferencesCited byDetailsCited bySocial Cognitive and Affective Neuroscience, Vol. 4, No. 2Psychopharmacology, Vol. 197, No. 1Medications in the treatment of borderline personality disorder 200618 April 2007 | Current Psychiatry Reports, Vol. 9, No. 1Pharmakologische und psycho- therapeutische Behandlung der Borderline-StörungZeitschrift für Psychiatrie, Psychologie und Psychotherapie, Vol. 54, No. 3 Volume 17Issue 4 November 2005Pages 559-560 Metrics PDF download History Published online 1 November 2005 Published in print 1 November 2005

Profound weight loss associated with reboxetine use in a 44‐year‐old woman

We report a case of significant weight loss experienced by a 44-year-old Caucasian woman treated with reboxetine. She was treated with this drug at 12 mg daily for a total duration of 11 months. During the corresponding period her body mass index (BMI) decreased from a baseline of 21.4 kg m(-2) to a low of 16.8 kg m(-2). Withdrawal of the drug led to a full recovery of her BMI. The strongest evidence linking reboxetine to this woman's weight loss laid in the fact that the re-introduction of the drug subsequently caused a similar negative impact in her BMI.

Adjunctive use of reboxetine in schizophrenia

Background. – Schizophrenia is frequently complicated by depressive or negative symptoms that respond only moderately to treatment with antipsychotic drugs. Reboxetine is a novel antidepressant, which inhibits the reuptake of norepinephrine. We sought to study the efficacy and tolerability of the adjunctive use of reboxetine in a cohort of schizophrenic patients with prominent depressive or negative symptoms. Methods. – Sixteen schizophrenic inpatients were recruited for this study. All subjects received 4–8 mg of reboxetine/day while the antipsychotic medication (typical antipsychotics = 4; atypical antipsychotics = 12) was continued. All subjects underwent a standardized assessment including PANSS, CGI, HAMD, and CDSS before and after treatment with reboxetine (mean 26 ± 17 d). Results. – All subjects tolerated treatment with reboxetine. Adverse effects were mild and did not require discontinuation of reboxetine. All clinical scores (PANSS 93.1 vs. 63.1; CGI 5.4 vs. 4.1; HAMD 20.4 vs. 8.1; CDSS 12.5 vs. 4.6) improved significantly under adjunctive treatment with reboxetine (all P < 0.01). Conclusion. – The adjunctive use of reboxetine in schizophrenic patients was safe and well-tolerated. Our results suggest that the adjunctive use of reboxetine may be an effective treatment for depressive and negative symptoms in schizophrenia.

Adjunctive use of reboxetine in schizophrenia

Adjunctive use of reboxetine in schizophrenia

Reboxetine: a pharmacologically potent, selective, and specific norepinephrine reuptake inhibitor

Background: Reboxetine is a potent antidepressant, with efficacy comparable to that of imipramine, desipramine, and fluoxetine, and has improved side-effect profile. The basis of its efficacy and improved tolerability is sought through studies of reboxetine in a number of pharmacological models of depression. Methods: Pharmacological selectivity for uptake systems was defined by uptake and binding assays for the three monoamine uptake sites. Specificity was determined in 39 different receptor and 6 enzyme assays. In vivo selectivity was defined by measurement of neuronal firing rates in the locus coeruleus, dorsal raphe, and substantia nigra. Reserpine-induced blepharospasm and hypothermia, clonidine-induced hypothermia, defined reboxetine’s in vivo pharmacology. Reboxetine’s antidepressant potential was evaluated behaviorally by the tail-suspension test, forced swimming, and the DRL 72 operant responding test. Results: Reboxetine is a potent, selective, and specific norepinephrine reuptake inhibitor (selective NRI) as determined by both in vitro and in vivo measurements. Unlike desipramine or imipramine, reboxetine has weak affinity (Ki > 1000 nmol/L) for muscarinic, histaminergic H1, adrenergic α 1, and dopaminergic D 2 receptors. In vivo action of reboxetine is entirely consistent with the pharmacological action of an antidepressant with preferential action at the norepinephrine reuptake site. Reboxetine showed an antidepressant profile in all tests of antidepressant activity used. Significant decreases in immobility were observed in the tail suspension test and behavioral despair test. Increased efficiency in responding was observed in the DRL 72 test. Conclusions: Reboxetine is a potent, selective, and specific noradrenergic reuptake inhibitor. It has a superior pharmacological selectivity to existing tricyclic antidepressants and selective serotonin reuptake inhibitors when tested in a large number of in vitro and in vivo systems. Given the pharmacological profile, reboxetine is expected to be a selective and potent tool for psychopharmacological research. The use of reboxetine in the clinic will also help clarify the role norepinephrine plays in depression.