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Imipramine with subsequent lithium addition is superior to a similar strategy with fluvoxamine for treatment of severely depressed inpatients. Both strategies were well tolerated.
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FVX had a modest effect on the pharmacokinetics of ATX and 4-hydroxyatomoxetine-O-glucuronide. The presence or absence of any clinical consequences associated with this pharmacokinetic drug-drug interaction needs to be established in future studies.
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The antidepressants citalopram, nefazodone and sertraline have relatively low interaction potential with warfarin; fluoxetine and fluvoxamine relatively high. Carbamazepine appears to reduce warfarin's anticoagulant effect. Other antipsychotics, antidepressants and anxiolytics have only a theoretical risk of interaction. Lithium, gabapentin, sulpiride and amisulpride are predominantly renally excreted and so are not likely to interact with warfarin.
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This paper reviews the published literature on the use of selective serotonin reuptake inhibitors (SSRIs) for the treatment of symptoms associated with autistic disorder and other pervasive developmental disorders (PDDs) in both children and adults. To date, placebocontrolled studies of SSRIs have involved only fluvoxamine (in children and adults) and fluoxetine (in children). Open-label and retrospective studies of all other SSRIs in PDDs have also been published that suggest effectiveness. Despite these positive reports, there continues to be questions about the tolerability and appropriate dosing of SSRIs in children with PDDs. Because of the limited number of placebo-controlled studies, definitive conclusions about the role SSRIs should play in the clinical treatment of children with PDDs cannot be drawn. Larger, placebo-controlled studies of SSRIs are needed to guide clinical treatment.
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The purpose of this pharmacokinetic study was to investigate the dose-dependent inhibition of model substrates for CYP2D6, CYP2C19 and CYP1A2 by four marketed selective serotonin reuptake inhibitors (SSRIs): citalopram, fluoxetine, fluvoxamine and paroxetine.
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to determine the prevalence of depressive disorders in medical inpatients in Izhevsk, the capital of the Udmurt Republic, a region in Russia, and to identify associated factors.
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Our results suggest that NR1D1 does not play a major role in the therapeutic response to fluvoxamine in Japanese MDD patients. However, because our sample was small, a replication study using another population and a larger sample will be required for conclusive results.
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Fifty-nine inpatients who met the DSM-III-R criteria for major depression with psychotic features were treated with fluvoxamine for 6 weeks. Patients were assessed at baseline and weekly thereafter with the Hamilton Depression Rating Scale and the Dimensions of Delusional Experience rating scale.
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After the advent of SSRI, antidepressants in low doses and in combination with neuroleptic treatment entered into use in clinical practice. The indication is the depression that may overlap with schizophrenic disorder.
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Sudden gains are common in treatments for OCD and are predictive of treatment outcome and follow-up. Sudden gains mark a distinct trajectory of response to treatment for OCD. Individuals with sudden gains greatly improve during treatment and maintain their gains during follow-up, whereas individuals without sudden gains improve to a significantly lesser extent. Thus, treatment planning and development can benefit from considering sudden gains and the intra-individual course of improvement.
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The in vivo pharmacokinetic interaction between two selective serotonin reuptake inhibitors (SSRI) (fluvoxamine, fluoxetine) and tricyclic antidepressants (TCAs) (amitriptyline, clomipramine) or neuroleptics (haloperidol, cyamemazine, levomepromazine, propericiazine) was assessed in 29 in-patients. They were phenotyped twice with dextromethorphan and mephenytoin: first in steady state conditions while under treatment with TCAs or neuroleptics; and also 10 days after an associated treatment with fluvoxamine (150 mg day(-1)) or fluoxetine (20 mg day(-1)). A clear and statistically significant increase in the mean urinary metabolic ratio (MR) of dextromethorphan/dextrorphan and in the mean mephenytoin S/R ratio (S/R) was seen with the fluvoxamine and fluoxetine treatment. The mean MR increased from 0.13 to 0.27 (P<0.01) with fluoxetine and from 0.34 to 0.84 with fluvoxamine (P<0.05). The (dextromethorphan) 'extensive metabolizer' phenotype switched to the 'poor metabolizer' phenotype in six patients by the 10-day fluoxetine treatment, and in two patients by the fluvoxamine treatment. The mean S/R increased from 0.24 to 0.34 (P<0.05) with fluoxetine, and from 0.33 to 0.58 (P<0.002) with fluvoxamine. These results are in agreement with the observed modification of TCA plasma levels after the SSRI association. During fluvoxamine treatment, amitriptyline and clomipramine plasma levels (P<0.06 both) tendentially increased, and those of demethylclomiprarnine decreased (P<0.06). Fluoxetine addition lead to a significant increase (P<0.02) of the desmethylclomipramine plasma levels. Fluvoxamine induced a moderate augmentation of the plasma levels of haloperidol and its reduced metabolite and no change in the plasma levels of cyamemazine and levomepromazine. But patients treated with neuroleptics are to few to draw any firm conclusion. This study suggests, that fluoxetine and fluvoxamine differ in their interaction with the metabolism of some other basic psychotropic drugs, by a mechanism which implies CYP2D6 and CYPmeph and possibly other isoformes of cytochrome P-450. Moreover, the interactions produced varied with the TCA prescribed.
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Fluvoxamine is a potent and selective serotonin reuptake inhibitor (SSRI) that has little or no effect on other monoamine reuptake mechanisms. Relative to other SSRIs, fluvoxamine is a weak inhibitor of cytochrome P450 (CYP) 2D6, a moderate inhibitor of CYP2C19 and CYP3A4 and a potent inhibitor of CYP1A2. In randomised, double-blind trials. fluvoxamine 100 to 300 mg/day for 6 to 10 weeks significantly reduced symptoms of obsessive-compulsive disorder (OCD) compared with placebo. Response rates of 38 to 52% have been reported with fluvoxamine, compared with response rates of 0 to 18% with placebo. In patients with OCD, fluvoxamine had similar efficacy to that of clomipramine and, in smaller trials, the SSRIs paroxetine and citalopram and was significantly more effective than desipramine. Maintenance therapy with fluvoxamine may reduce the likelihood of relapses in up to 67% of patients with OCD. Fluvoxamine < or = 300 mg/day for 6 to 8 weeks was as effective as imipramine in patients with panic disorder, and significantly more effective than placebo. In addition, treatment with fluvoxamine < or = 300 mg/day for > or = 8 weeks improved symptoms of social phobia (social anxiety disorder), post-traumatic stress disorder (PTSD), pathological gambling, compulsive buying, trichotillomania, kleptomania, body dysmorphic disorder, eating disorders and autistic disorder. Large trials comparing the efficacy of fluvoxamine and other SSRIs in patients with anxiety disorders are warranted. Fluvoxamine is generally well tolerated; in postmarketing studies, nausea was the only adverse event occurring in >10% of patients with less commonly reported events including somnolence, asthenia, headache, dry mouth and insomnia. Fluvoxamine is associated with a low risk of suicidal behaviour, sexual dysfunction and withdrawal syndrome. Fewer anticholinergic or cardiovascular events are associated with fluvoxamine than tricyclic antidepressants. Although comparative data are lacking, the tolerability profile of fluvoxamine appears to be broadly similar to those of other SSRIs.
Agomelatine (Valdoxan) is licensed by the European Medicines Agency for the treatment of major depressive episodes in adults. The objective of this review was to consider how the drug should be used in clinical practice in particular starting, stopping and switching to and from the drug.
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Some selective serotonin reuptake inhibitors (SSRIs) have recently been approved for the treatment of anxiety disorders such as obsessive-compulsive disorder, panic disorder and social anxiety disorder, and they are considered first-line treatment for anxiety disorders in Japan as well as in other countries. Previous clinical studies have suggested that the 5-HT2C receptors in subjects with anxiety disorders are hypersensitive. We recently reported that chronic treatment with fluvoxamine or paroxetine desensitized 5-HT2C receptor function. The desensitization of 5-H T2C receptor function has also been reported with other SSRIs and is considered to be a common mechanism of action of SSRIs in the treatment of anxiety disorders. In addition, some studies have suggested that 5-HT2A receptors and 5-HTIA receptors participate in anxiety disorders and the therapeutic mechanism. Both clinical studies and animal studies have indicated that the amygdala plays an essential role in anxiety and fear response. Thus, it may be important to elucidate functional changes in these 5-HT receptor subtypes in brain regions including the amygdala under the chronic administration of SSRIs to understand the anxiolytic mechanism of SSRIs.
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Fluvoxamine is a well-known selective serotonin reuptake inhibitor (SSRI); Despite its anti-inflammatory effect, little is known about the precise mechanisms involved. In our previous work, we found that IP administration of fluvoxamine produced a noticeable anti-inflammatory effect in carrageenan-induced paw edema in rats. In this study, we aimed to evaluate the effect of fluvoxamine on the expression of some inflammatory genes like intercellular adhesion molecule (ICAM1), vascular cell adhesion molecule (VCAM1), cyclooxygenases2 (COX2), and inducible nitric oxide synthase (iNOS).
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Children with ADHD/ANX have a response rate to stimulants for ADHD that is comparable with that of children with general ADHD. The benefit of adding FLV to stimulants for ANX remains unproven.
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A simple, fast, selective and very sensitive capillary GC-MS method for the simultaneous determination of five antidepressant drugs is described. Fluoxetine, fluvoxamine, citalopram, sertraline and paroxetine belong to the newest and most important drug group termed selective serotonin reuptake inhibitors. Imipramine was used in this method as an internal standard for quantification. Optimum parameters for GC separation were investigated, i.e., flow rate, column head pressure, injector temperature, injection splitless conditions and oven temperature program. MS detection was performed in SIM mode to increase the sensitivity. Stability of the solutions, linear concentration range, accuracy, precision, LOD, LOQ (3.6-41.5 mg/L) and specificity were examined in the presence of excipients for checking the reliability of this method. The robustness was evaluated with a matrix of 15 experiments (seven factors and three levels) using Plackett-Burman fractional factorial experimental design, and Youden and Steiner statistical treatment. The method was applied to the analysis of these antidepressants in nearly all their pharmaceutical formulations, obtaining recoveries between 98.1% and 102.7% with regard to the claimed values.
Venlafaxine is efficacious for the treatment of hot flashes and depression and safe to use in combination with tamoxifen. Gabapentin is also efficacious in treating tamoxifen-induced hot flashes and, since it does not interact with cytochrome P450 system, is likely safe to use in patients using tamoxifen. Desvenlafaxine and pregabalin may be alternatives to venlafaxine and gabapentin, respectively, although desvenlafaxine has not yet been studied in this population. Paroxetine, fluoxetine and bupropion are strong CYP2D6 inhibitors which should be avoided in tamoxifen users. Fluvoxamine and nefazodone both inhibit CYP3A, which could potentially affect the metabolism of tamoxifen. Clonidine can be an alternative agent but may carry significant side effects. Evidence of medicinal products for the treatment of tamoxifen-induced hot flashes is equivocal at best.
A longitudinal, retrospective study using electronic prescription data from a Dutch sick fund, ZAO Zorgverzekeringen.
To test the hypothesis that the antidepressant effects of total sleep deprivation (TSD) are linked to the serotonergic and/or noradrenergic system the authors carried out a double-blind study (fluvoxamine versus maprotiline) in 42 inpatients with endogenous depression (ICD). Patients were randomized to a four-week treatment with either fluvoxamine (100-300 mg/day) or maprotiline (100-300 mg/day). In addition, patients underwent a TSD procedure before and after one week of antidepressant medication. There was a statistically significant reduction of depression ratings (HDRS) in both the fluvoxamine and maprotiline group. The day-1 response to TSD before antidepressive medication was not associated with a clear relationship to the outcome after four weeks of treatment with either fluvoxamine or maprotiline. On the other hand, the day-2 response to TSD was significantly correlated with a good outcome to subchronic treatment with maprotiline. Furthermore, the results of the authors' data suggest that a favorable short-term outcome of TSD may be connected to antidepressants enhancing the serotonergic neurotransmission. The global comparison between fluvoxamine and maprotiline revealed that the group of patients treated with fluvoxamine had a significantly higher efficiency index (CGI) than the maprotiline group; fluvoxamine was rated to be tolerated excellently in 70% of the patients whereas this percentage was only 43% in the maprotiline group. There was also significantly more vertigo and dry mouth in the maprotiline group whereas the fluvoxamine group was rated to have significantly more sleep disturbances during the trial.
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Paroxetine is generally well tolerated by both younger and older individuals and its adverse event profile is consistent with that expected for an SSRI. The tolerability profile of paroxetine in patients with panic disorder appears to resemble that in patients with depression. Headache, nausea, somnolence, dry mouth and insomnia were the most common adverse events among 469 patients with panic disorder who received paroxetine 10 to 60 mg/day in short term clinical trials. The individual incidences for these events ranged from 18 to 25%; however, the incidence of headache in paroxetine-treated patients was the same as that in placebo recipients. (ABSTRACT TRUNCATED)
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Antipyrine biotransformation could be described by Michaelis-Menten kinetics: norantipyrine: maximum rate of metabolite formation (Vmax), 0.91 +/- 0.04 nmol . mg-1 . min-1; Michaelis-Menten constant (Km), 19.0 +/- 0.8 mmol/L; 4-hydroxyantipyrine: Vmax, 1.54 +/- 0.08 nmol . mg-1 . min-1;Km,39.6 +/- 2.5 mmol/L. Antibodies against CYP3A4 inhibited the formation of 4-hydroxyantipyrine by 25% to 65%. LKM-2 antibodies (anti-CYP2C) caused a 75% to 100% inhibition of norantipyrine and a 58% to 80% inhibition of 3-hydroxymethylantipyrine formation. Sulfaphenazole inhibited the formation of 3-hydroxymethylantipyrine and norantipyrine by about 50%. Furafylline and fluvoxamine inhibited norantipyrine, 4-hydroxyantipyrine, and 3-hydroxymethylantipyrine formation by about 30%, 30%, and 50%, respectively. Ketoconazole reduced formation of norantipyrine, 3-hydroxymethylantipyrine, and 4-hydroxyantipyrine by up to 80%. Formation in stable expressed enzymes indicated involvement of CYP1A2, CYP2B6, CYP2C, and CYP3A4 in metabolite formation.
The effect of amitriptyline on hypothalamic-pituitary-adrenocortical (HPA) axis activity was compared with that of fluvoxamine in 38 patients suffering from DMS-IV major depressive disorder. Basal plasma adrenocorticotropic hormone and cortisol levels were determined in the so-called "observation window" of an hour (08:00-09:00 h), and cortisol levels were determined again at 20:00 h. Clinical and biochemical assessments were performed before therapy (T0), at day 14 (T14), and at day 42 (T42) of the course of antidepressant treatment. At T0, neuroendocrine parameters did not differ in patients from those in controls, except for the ratio between cortisol levels at 20:00 h and the mean level of the "window" (ratio F20/F8), which was significantly higher, suggesting a dysregulation of the circadian pattern of cortisol. Although a decrease in the ratio F20/F8 was already apparent at T14 of both treatments, the repeated measures analysis of variance failed to demonstrate a significant variation with time (T0, T14, and T42) and with treatment (amitriptyline and fluvoxamine) for any hormonal measure. At T42, both treated groups showed a similar level of clinical improvement. Our results did not demonstrate any effect of antidepressant therapy on the cortisol circadian rhythm abnormality.
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The advent of the selective serotonin reuptake inhibitors (SSRIs) is generally considered to have improved the treatment of depression. Head-to-head trials comparing SSRIs to each other have shown little difference in efficacy among agents. The main differences between the SSRIs relate to safety and tolerability profiles, reflecting the fact that the SSRIs possess significant and variable secondary pharmacological properties. This heterogeneity contributes to clinically relevant differences that clinicians are increasingly using to select antidepressant treatment more closely appropriate to specific patient populations and circumstances. This review assesses the place of fluvoxamine amongst the SSRIs in the context of current issues and concerns with drug therapy. Fluvoxamine has a proven efficacy and safety profile in treating elderly patients with depression. The beneficial effects of fluvoxamine in obsessive-compulsive disorder (OCD) are also well documented. On the other hand, its σ1-receptor binding profile may account for the observed high level of efficacy in psychotic depression and may explain the benefit of fluvoxamine in treating depression comorbid with anxiety/stress. There is no definitive evidence that suicide risk is higher with SSRIs than with other antidepressants or nonpharmacological treatments and postmarketing surveillance indicates that fluvoxamine is not associated with a higher level of suicidality.
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Selective serotonin [5-hydroxytryptamine (5-HT)] reuptake inhibitors (SSRIs) and the 5-HT noradrenaline reuptake inhibitor, venlafaxine, are mainstays in treatment for depression. The highly specific actions of SSRIs of enhancing serotonergic neurotransmission appears to explain their benefit, while lack of direct actions on other neurotransmitter systems is responsible for their superior safety profile compared with tricyclic antidepressants. Although SSRIs (and venlafaxine) have similar adverse effects, certain differences are emerging. Fluvoxamine may have fewer effects on sexual dysfunction and sleep pattern. SSRIs have a cardiovascular safety profile superior to that of tricyclic antidepressants for patients with cardiovascular disease; fluvoxamine is safe in patients with cardiovascular disease and in the elderly. A discontinuation syndrome may develop upon abrupt SSRI cessation. SSRIs are more tolerable than tricyclic antidepressants in overdose, and there is no conclusive evidence to suggest that they are associated with an increased risk of suicide. Although the literature suggests that there are no clinically significant differences in efficacy amongst SSRIs, treatment decisions need to be based on considerations such as patient acceptability, response history and toxicity.
Our results demonstrate a low affinity of fluvoxamine and a very high affinity of mirtazapine for the human brain H₁R in vivo. This study provides a basis for investigating the efficacy of new-generation antidepressants in central histamine systems.
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A man who complained of chronic anal idiopathic pruritus was treated with citalopram (Seropram(R)) 10 mg b.i.d. Six days after the beginning of the antidepressive treatment, he developed an extensive papular and purpuric erythema with keratinocytes necrosis and dermal leucocytoclastic vasculitis. Cutaneous lesions remained for several weeks, as the half-life of citalopram is very long (33 to 36 hours) but did not relapse. A women developed painful papular and purpuric erythema mainly located in sun-exposed sites, during therapy with paroxetine (Deroxat(R)) 20 mg b.i.d., which had been introduced one month before to treat depression. Cutaneous lesions healed spontaneously in 2 weeks after the discontinuation of paroxetine and with sun avoidance and didn't relapse.
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Compulsive buying behaviour has recently received long overdue attention as a clinical issue. Aim of this report is to describe treatment of two female patients diagnosed with compulsive buying disorder in comorbidity with binge eating disorder. In both cases, criteria for diagnosing of other axis I or axis II disorder were not present. Fluvoxamine was used in pharmacotherapy, and psychodynamic psychotherapy as a psychotherapeutical approach. We conclude that fluvoxamine and psychodynamic psychotherapy may be effective in treatment of compulsive buyers in comorbidity with binge eating disorder.
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The most common SSs at baseline were restlessness (74%), stomachaches (70%), blushing (51%), palpitations (48%), muscle tension (45%), sweating (45%), and trembling/shaking (43%). Older children (age 12 and older) reported more SSs than younger children, boys and girls reported similar numbers of SSs, and SSs were higher among children with than without generalized anxiety disorder. SSs were significantly and positively correlated with anxiety severity, impairment, and global functioning. Pre-/postreductions in SSs were statistically significant in both PBO and FLV conditions; however, FLV was superior to PBO in reducing SSs.