Our library of drug research abstracts drawn from the medical literature is updated on a regular schedule, and you can be assured that new remeron research articles will be listed here shortly after becoming available to us.
Related Sponsors
Medical research on remeron
Employing mirtazapine to aid benzodiazepine withdrawal.
Singapore Med J. 2008 Jun; 49(6): e166-7
Chandrasekaran PK
Insomnia and depression are frequently encountered in patients during withdrawal from substances. While there are no approved medications for treating them, off-label attempts to address these phenomena with mirtazapine have shown some promising results. This case describes the use of mirtazapine as an aid in benzodiazepine withdrawal and its potential benefits in alleviating insomnia and depression in a 32-year-old man. It was found to ameliorate sleep myoclonus that was thought to be associated with his withdrawal syndrome. It is hoped this report will generate interest and stimulate further research in this area of psychopharmacology.
Progressive multifocal leukoencephalopathy.
Curr Treat Options Neurol. 2008 May; 10(3): 178-85
Aksamit AJ
Treatment of progressive multifocal leukoencephalopathy (PML) in a patient with exogenous immunosuppression starts with discontinuation of immunosuppressive medication. The restored host immunity will clear JC virus, the cause of PML, from the brain via cell-mediated immune mechanisms. Patients with solid-organ transplants will lose the transplanted organ, however, and patients who have autoimmune disorders may experience exacerbation of their underlying disease. These factors need to be weighed against the potentially fatal nature of PML. If the patient's immunosuppression is AIDS-related, highly active antiretroviral therapy (HAART) should be initiated if it has not previously been used. If the patient is already receiving HAART, the therapy should be changed to optimize treatment, with the goals of a nondetectable HIV viral load and normalization or near normalization of the CD4 count. For non-AIDS PML patients, daily intravenous cytosine arabinoside for 5 days can be offered if the patient is not pancytopenic and can tolerate a chemotherapeutic agent. For AIDS patients with PML or failing non-AIDS patients with neurologic deterioration, cidofovir can be considered. These therapies can be offered if neurologic stabilization satisfies the quality-of-life goals for the patient. For patients intolerant of other therapies or unsuited to them, oral mirtazapine or risperidone can be considered. The safety of these agents has been established in the treatment of psychiatric disease, but their efficacy has not yet been proven. Small interfering RNA (siRNA) therapy holds the promise of specific antiviral therapy, but delivery methods, safety, and efficacy are yet to be established.
Effects of antidepressants on mRNA levels of antioxidant enzymes in human monocytic U-937 cells.
Prog Neuropsychopharmacol Biol Psychiatry. 2008 Jun 4;
Schmidt AJ, Heiser P, Hemmeter UM, Krieg JC, Vedder H
Alterations of antioxidant enzyme activities have been described in a number of psychiatric disorders including major depression. Subsequently, the present study examined the effects of different types of antidepressants (desipramine, imipramine, maprotiline and mirtazapine) in different concentrations (10(-5), 10(-6) and 10(-7) M) on the mRNA levels of various enzymes of the antioxidant system, including both intracellular superoxide dismutase isoforms, glutathione peroxidase and catalase as well as several enzymes of the glutathione metabolism in monocytic U-937 cells after short- and long-term treatment (2.5 and 24 h) via RT-PCR. Results indicated mainly short-term decreases in the mRNA levels of antioxidant enzymes after treatment with these substances in all the concentrations used. In addition, after long-term treatment, significant increases in the mRNA levels were seen in the cases of Cu, Zn superoxide dismutase, gamma-glutamyl-cysteine synthetase, glutathione-S-transferase and glutathione reductase, including the impacts of all the antidepressants used in concentrations of 10(-6) M and 10(-7) M. Based on the large number of significant effects of all types of antidepressants tested on various antioxidant enzymes, we suggest that antioxidant enzymes may represent important targets in the course of antidepressive treatment.
Successful antidepressive treatment with mirtazapine following lung transplantation.
Prog Neuropsychopharmacol Biol Psychiatry. 2008 Jun 20;
Fusar-Poli P, Martinelli V, Hobson R, Politi P
Neuropsychiatr Dis Treat. 2005 Mar; 1(1): 59-68
Lavergne F, Berlin I, Gamma A, Stassen H, Angst J
The purpose of this open multicenter study of 4771 patients with a DSM-IV diagnosis of Major Depressive Episode was to analyse the response to mirtazapine in general practice and primary care. Patients with a baseline score of at least 20 on the Montgomery-Asberg Depression Rating Scale (MADRS) were treated with mirtazapine for 6 weeks (30 mg/day) and clinically assessed by their psychiatrists at weekly intervals through the MADRS and Clinical Global Improvement (CGI) rating scales. The data analysis was carried out on an "intent-to-treat" basis to collect outcome information on all patients. Our results suggested that the efficacy of the antidepressant effect relates to a nonspecific process. Nearly all patients (95%) showed at least slight improvement at the end of the observation period, while the response to treatment was independent of the clinical forms of depression. In particular, all measures of efficacy displayed the maximum change within the first 2 weeks of treatment, with further improvement occurring at much slower rates. Significant improvement within the first 2 weeks of treatment was highly predictive of the final response, and can serve as a guideline for clinicians when deciding about increased dosage, augmentation, or change of medication in unresponsive patients. Detailed analyses of individual MADRS items showed that mirtazapine's pharmacological profile, unlike selective serotonin reuptake inhibitors, led relatively quickly to a significant reduction of suicidal thoughts, a fact of particular clinical relevance.
Neuropsychiatr Dis Treat. 2005 Mar; 1(1): 3-7
Pinder RM
Noradrenaline has long played a key role in the way the etiology of depression is conceptualized and in the mechanism of action of many current antidepressants. Tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), serotonin-noradrenaline reuptake inhibitors (SNRIs), selective noradrenaline reuptake inhibitors (NRIs), the noradrenergic and specific serotonergic antidepressant (NaSSA) mirtazapine, and many atypicals, like mianserin and bupropion, influence, at least in part, central noradrenergic function. Enhancement of noradrenergic function may be particularly helpful in patients with melancholia. However, while noradrenaline will continue to be a target for research into the etiology and treatment of depression, it is unlikely that antidepressants acting solely on noradrenaline will be pursued.
Neuroimaging of mirtazapine enantiomers in humans.
Psychopharmacology (Berl). 2008 Jun 20;
Smith DF, Hansen SB, Jakobsen S, Bender D, Audrain H, Ashkanian M, Stork BS, Minuzzi L, Hall H, Rosenberg R
INTRODUCTION: Mirtazapine is a racemic antidepressant with a multireceptor profile. Previous studies have shown that the enantiomers of mirtazapine have different pharmacologic effects in the brain of laboratory animals. MATERIALS AND METHODS: In the present study, we used positron emission tomography (PET) and autoradiography to study effects of (R)- and (S)-[(11)C]mirtazapine in the human brain. Detailed brain imaging by PET using three methods of kinetic data analysis showed no reliable differences between regional binding potentials of (R)- and (S)-[(11)C]mirtazapine in healthy subjects. RESULTS: Autoradiographic studies carried out in whole hemispheres of human brain tissue showed, however, that (R)- and (S)-mirtazapine differ markedly as inhibitors of [(3)H]clonidine binding at alpha(2)-adrenoceptors. CONCLUSION: The multireceptor binding profiles of mirtazapine enantiomers, along with individual differences between subjects, may preclude PET neuroimaging from demonstrating reliable differences between the regional distribution and binding of (R)- and (S)-[(11)C]mirtazapine in the living human brain.
Estimating the effects of co-medications on plasma olanzapine concentrations by using a mixed model.
Prog Neuropsychopharmacol Biol Psychiatry. 2008 May 7;
Botts S, Diaz FJ, Santoro V, Spina E, Muscatello MR, Cogollo M, Castro FE, de Leon J
The purpose of this study was to estimate the effect sizes of drug interactions on plasma olanzapine concentrations while adjusting for potentially confounding factors such as smoking. The estimation was performed by using a mixed model, data from a series of previously published studies of lamotrigine, oxcarbazepine, topiramate, and mirtazapine, and unpublished data from patients under clinical therapeutic drug monitoring (TDM). The total sample included 163 adult patients (age >/=18 years) who provided both steady-state plasma olanzapine concentrations and smoking information. They provided a total of 360 olanzapine concentrations (1 to 11 measures per patient). Smoking and concomitant carbamazepine or lamotrigine use were found to have significant effects on median plasma olanzapine concentrations. The effects of lamotrigine on plasma olanzapine concentrations were modified by smoking. After adjusting for olanzapine dose and carbamazepine intake, plasma olanzapine concentrations were 10% lower in non-smokers who were taking lamotrigine than in non-smokers who were not taking lamotrigine; olanzapine concentrations were 35% higher in smokers who were taking lamotrigine than in smokers who were not taking lamotrigine; olanzapine concentrations were 41% lower in smokers who were not taking lamotrigine than in non-smokers who were not taking lamotrigine; and olanzapine concentrations were 11% lower in smokers who were taking lamotrigine than in non-smokers who were taking lamotrigine. After adjusting for olanzapine dose and taking carbamazepine, the correction factor comparing smokers taking lamotrigine versus non-smokers who were not taking lamotrigine was 1.3. Gender, age, and concomitant use of mirtazapine, valproic acid, lamotrigine, topiramate, lorazepam, citalopram or oxcarbazepine did not have significant effects on olanzapine concentrations. The main limitation of this clinical design is the unavoidable substantial "noise" that characterizes (uncontrolled) clinical environments, which may make it difficult to detect the effects of some variables. Other limitations were the small sample size of some drug sub-samples and the lack of testing for plasma olanzapine metabolites.
Sleep. 2008 Jun 1; 31(6): 824-31
Marshall NS, Yee BJ, Desai AV, Buchanan PR, Wong KK, Crompton R, Melehan KL, Zack N, Rao SG, Gendreau RM, Kranzler J, Grunstein RR
OBJECTIVE: Mirtazapine is an a2A antagonist and mixed 5-HT2/5-HT3 antagonist that has been proposed as a potential treatment for obstructive sleep apnea (OSA). A small, randomized, controlled trial has previously found an approximate halving in the severity of OSA with daily doses of 4.5 and 15 mg. We aimed to confirm and extend these findings in 2 randomized placebo-controlled, proof-of-concept trials. METHODS: Two randomized, double-blind, placebo-controlled trials of mirtazapine for OSA (apnea-hypopnea index 10-40/h). Study 1: 3-way crossover, dose-finding study testing the self-administration of mirtazapine (7.5, 15, 30, and/or 45 mg) or placebo 30 minutes prior to bedtime for 2 weeks at each dose. Twenty patients were randomly assigned to 1 of 6 different dose-sequence groups, with each patient exposed to a maximum of 3 doses. Study 2: 3-arm, randomized, parallel-group trial of mirtazapine at 15 mg or mirtazapine 15 mg + Compound CD0012 or placebo for 4 weeks in 65 patients with OSA. RESULTS: Two patients withdrew from Study 1 after complaints of unacceptable lethargy. Fifteen patients were withdrawn from study 2, 7 after complaints of unacceptable lethargy or other side-effects. No measurement of sleep apnea improved due to mirtazapine in either study. Weight gain was significantly greater on mirtazapine than on placebo in both trials. CONCLUSIONS: Mirtazapine did not improve sleep apnea in either trial. Mirtazapine caused weight gain, which may further worsen OSA. Therefore, mirtazapine is not recommended for the treatment of OSA.
Severe tramadol addiction in a 61 year-old woman without a history of substance abuse.
Int J Immunopathol Pharmacol. 2008 April-June; 21(2): 475-476
Pollice R, Casacchia M, Bianchini V, Mazza M, Conti CM, Roncone R
We describe here the first case of Tramadol addiction and withdrawal in an elderly female patient in apparently good physical health. We report successful treatment with mirtazapine and clonidine. We believe that patients must be advised to take Tramadol regularly and to stop gradually especially after long treatment periods; moreover physicians must consider the potential physical dependence when they prescribe Tramadol for pain. Hence, we are observing some patients who continue to take Tramadol in order to achieve a feeling of well-being, even though their pain is controlled after disease regression. Finally, the establishing of an evidence-based Tramadol detoxification protocol would be highly desirable.