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SSRIs decreased the TNF-alpha-induced endothelial expression of VCAM-1 at concentration range 10(-7) M to 10(-4) M (p<0.05). ICAM-1 expression was decreased in the presence of fluvoxamine and fluoxetine at concentrations from 10(-7) M to 10(-4) M (p<0.05) and in the presence of citalopram at concentrations from 10(-7) M to 10(-5) M (p<0.05). All SSRIs inhibited the TNF-alpha-stimulated adhesiveness to U937 cells at 10(-5) M and 10(-4) M (p<0.05). Compared to baseline, there was a greater reduction in ICAM-1 and VCAM-1 levels post-sertaline than post placebo in heart failure patients (p<0.05).
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The pharmacokinetics of drugs with specific binding sites in the brain needs to be evaluated at these sites. In this study, we measured the time course of the selective serotonin reuptake inhibitor fluvoxamine in the human brain based on serotonin transporter (5-HTT) occupancy by positron emission tomography. Consecutive positron emission tomography scans were performed using [11C]3-amino-4-(2-dimethylaminomethyl-phenylsulfanyl)-benzonitrile before, 5 hours, 26 hours, and 53 hours after 50 mg of fluvoxamine administration in 6 healthy male volunteers (mean, 24.3 +/- 4.8 years). Quantification was performed using the multilinear reference tissue model 2. Mean 5-HTT occupancies were 72.9% +/- 4.9% at 5 hours, 50.3% +/- 11.0% at 26 hours, and 24.7% +/- 15.3% at 53 hours, and plasma concentrations were 13.9 +/- 5.5 ng/mL at 5 hours, 5.1 +/- 3.2 ng/mL at 26 hours, and 1.5 +/- 1.7 ng/mL at 53 hours. The relationship between the plasma concentration of fluvoxamine and 5-HTT occupancy at these different time points was fitted to the law of mass action.
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The number of ADs taken by an individual was negatively correlated with the SS (r=-.074, p=.011). SS did not correlate with demographic features. SS was similar among the four subgroups but their satisfaction reasons differed. Predictors of higher SS (SS=5.0 versus 4.0) were reporting "efficacy" and "fewer side effects" as satisfaction reasons.
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Chronic pain is often intractable to analgesics, and in animals it involves a conditioned nociceptive response (CR) - learned pain. The neural pathways of nociception and olfactory function in the brain overlap. The influence of olfactory stimuli on acute pain has been studied in some depth in animal and human models, but the influence of olfactory stimuli on learned pain has not been understood. We examined the effects of analgesic drugs and olfactory stimulants (preferred or repellent odor) on acute pain, the unconditioned nociceptive response (UCR) and the CR in mice. The CR was provoked by repeated injection of formalin into the hind-paw in animals in the same context, which elicited the typical pain behaviors of paw licking (including biting). The analgesic drugs acetaminophen, fentanyl, gabapentin and fluvoxamine diminished the UCR but did not affect the CR. In contrast, the preferred odor reduced both the UCR and the CR. Our findings suggest that, like chronic pain, the CR is resistant to analgesic drugs and that preferred odor suppress the neural pathways that mediate the CR of pain perception.
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Information regarding the long-term effectiveness of the combination of pharmacotherapy and cognitive-behavioral therapy (CBT) in the treatment of obsessive-compulsive disorder (OCD) is limited. Our study is the first to examine the long-term effectiveness of cognitive therapy (CT) and to compare long-term effectiveness of CT alone, exposure in vivo with response prevention (ERP) alone, and CBT (either CT or ERP) in combination with fluvoxamine in the treatment of OCD.
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Metabolism of clozapine is complex and not fully understood. Pharmacokinetic interactions with other drugs have been described but, in some cases, their mechanism is unknown.
The present study compared the effects of a wide range of 5-hydroxytryptamine (5-HT)-modulating and potential anxiolytic agents in the rat elevated plus-maze using spatiotemporal (i.e., open arm time and entries) and ethologically derived measures (i.e., risk assessment activities and directed exploration). The drugs used were 5-HT1A receptor partial (buspirone and ipsapirone) and full (8-OH-DPAT and flesinoxan) agonists, mixed 5-HT2A/2C receptor antagonists (ritanserin, ketanserin, mianserin, and pirenperone), selective 5-HT3 receptor antagonists (ICS 205-930, MDL 72222, ondansetron, and (RS)-zacopride), and selective (fluoxetine, fluvoxamine, and zimelidine) and nonselective (imipramine) 5-HT reuptake inhibitors. Only buspirone and mianserin produced effects indicative of an anxiolytic-like action on the spatiotemporal measures. However, all 5-HT1A receptor ligands, as well as mianserin, ketanserin, ondansetron, and zacopride, decreased the number of aborted attempts at entry into open arms (risk assessment). In addition, buspirone, mianserin, and zacopride increased head-dipping (directed exploration). Among the 5-HT reuptake inhibitors, zimelidine reduced head-dipping and total entries. The present findings demonstrate that risk assessment responses are sensitive to the action of 5-HT1A receptor ligands, but their modulation by drugs targetting 5-HT2A, 5-HT2C, and 5-HT3 receptors was not convincingly established.
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Dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis has been reported in patients with psychotic major depression (PMD), and a higher rate of cortisol hypersecretion is observed in PMD than in nonpsychotic patients. Approximately 19% of patients who meet the criteria for major depressive disorder (MDD) have psychotic features. Accumulated studies have indicated that repeated corticosterone (CORT) injections induce depressive behavioral and neurochemical manifestations in rodents. However, the pharmacological characterization of this model has not been fully established. In the present study, we investigated the pharmacological characteristics of this model. Rats received CORT injections (20 mg/kg, subcutaneously), once per day for 21 consecutive days prior to a behavioral test. The rats were then tested for depressive behavior using a forced swimming test. The repeated CORT injections increased the immobility time in the forced swimming test, indicating an increase in depressive-like behavior. An acute treatment with a glucocorticoid receptor antagonist, mifepristone, counteracted the depressive-like behavior. In contrast, an acute treatment with a selective serotonin reuptake inhibitor (SSRI), fluvoxamine, and a tricyclic antidepressant (TCA), imipramine, did not have any effect on this condition, while a combination of fluvoxamine and risperidone exerted an antidepressant-like effect. This observation is of interest in the light of the clinical findings that a combination of antidepressants and antipsychotics, but not SSRIs and TCAs, is effective for the treatment of patients with PMD. Based on previous findings and the present results, this model could be used as an animal model of PMD and may be useful for evaluating the antidepressant-like potential of compounds targeting the HPA axis.
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On average, fluvoxamine increased the total area under the concentration-time curve [AUC(0- infinity )] of tizanidine 33-fold (range, 14-fold to 103-fold; P =.000002) and the peak plasma concentration 12-fold (range, 5-fold to 32-fold; P =.000001). The mean elimination half-life of tizanidine was prolonged from 1.5 to 4.3 hours (P =.00004) by fluvoxamine. The AUC(0- infinity ) of tizanidine and its increase by fluvoxamine correlated with the caffeine/paraxanthine ratio and its increase, respectively (P <.03). All pharmacodynamic variables revealed a significant difference between the fluvoxamine and placebo phases, eg, in the maximal effects on systolic blood pressure (-35 mm Hg, P =.000009), diastolic blood pressure (-20 mm Hg, P =.00002), heart rate (-4 beats/min, P =.007), Digit Symbol Substitution Test (P =.0003), subjective drug effect (P =.0000001), and drowsiness (P =.0002). In particular, the decrease in systolic blood pressure, to the level of 80 mm Hg or even less, was an alarming finding.
Improving knowledge about the cytochrome p450 system means that potential drug interactions can be predicted. Interactions involving warfarin may be thus avoidable. As many patients who have suffered from a stroke or other thromboembolic events may also develop psychiatric disorder, knowledge about possible interactions with psychotropics is essential for prescribers.
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To determine whether duloxetine is a substrate, inhibitor or inducer of cytochrome P450 (CYP) 1A2 enzyme, using in vitro and in vivo studies in humans.
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The objective of this review was to evaluate the effectiveness of SSRIs in reducing premenstrual syndrome symptoms in women diagnosed with severe premenstrual syndrome.
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Future research should examine the impact of plans' pharmacy management approaches, using patient-level data.
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The mechanism of the attenuation, by serotonin uptake blockers, of the release-inhibiting effect of exogenous serotonin autoreceptor agonists was studied in rabbit brain cortex and rat hypothalamus slices. The slices were preincubated with 3H-serotonin and then superfused and stimulated electrically. In rabbit brain slices stimulated by trains of 4 pulses at 100 Hz, 5-carboxamidotryptamine and 5-methoxytryptamine reduced the evoked overflow of tritium, and their concentration-response curves were not changed by any of three serotonin uptake inhibitors, namely citalopram, fluvoxamine and 6-nitroquipazine. In contrast, when the slices were stimulated by trains of 10 pulses at 0.033 Hz, fluvoxamine shifted the concentration-response curve of 5-methoxytryptamine to the right. Experiments with the autoreceptor antagonist metitepine indicated that little, if any, endogenous autoinhibitory tone developed in the course of trains of 4 pulses/100 Hz, irrespective of the absence or presence of uptake inhibitors, as well as during trains of 10 pulses/0.033 Hz in the absence of uptake inhibitors, whereas marked autoinhibition developed when 10 pulses/0.033 Hz were applied in the presence of fluvoxamine. In rat hypothalamic slices stimulated by trains of 4 pulses at 100 Hz, citalopram also failed to change the concentration-response curve of 5-methoxytryptamine. These results indicate that serotonin uptake blockers attenuate the effect of exogenous autoreceptor agonists by an increase in the biophase concentration of released serotonin and, hence, in endogenous autoinhibitory tone, and not by some direct "molecular link" unrelated to the biophase concentration of released serotonin.
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This study shows a significant increase in the risk of developing vaginal candidiasis following the use of the antibiotics studied (ciprofloxacin, ofloxacin, norfloxacin, cefixime, azithromycin and fosfomycin) compared with that after taking the antidepressants fluvoxamine, fluoxetine, paroxetine, sertraline, venlafaxine and nefazodine in these PEM studies.
In the early 1970s, a number of observers hypothesized that there had been an increase in mild depression in the United State. Interest in mild depression had increased in the world. One manifestation of that interest was the decision in previous official Nomenclatures of WHO and APA to create separate category for affective disorders in the DSM-III. Patients of mild depression complain mainly of physical symptom, for example, headache, lumbago, abdominal pain, dizziness, sleep disturbance, appetite loss. Early internal treatment of mild depression consists of three factors, rest, antidepressants and psychosocial supports. Up to date, the first choice of antidepressants in SSRI. SSRI has antidepressive effect and less side effect than TCA.
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The behavioural effects of selective serotonin reuptake inhibitors (paroxetine, sertraline, citalopram, fluvoxamine, fluoxetine) and reference compounds (N,N'-di(o-tolyl)guanidine, haloperidol, 3-(3-hydroxyphenyl)-N-(l-propyl)piperidine and chlorpromazine) were studied for their ability to produce dystonia and torticollis following direct micro injection into the left red nucleus of the rat, an area of the brain containing a high density of sigma2 receptors but relatively devoid of biogenic amine receptors. Each animal was monitored for abnormalities in posture and movement for a period of 30 min and then sacrificed 40 min following drug administation. Only fluvoxamine (100 nmol) and fluoxetine (100 nmol) elicited acute dystonic behaviour (1-5 min). The onset of dystonia was accompanied by facial spasticity, vacuous chewing movements and grooming behaviour which reflected the extent of dystonia. The dystonic behaviour following the direct intrarubal injection of fluvoxamine and fluoxetine suggest the possible activation of sigma2 receptors while citalopram, sertraline and paroxetine were without effect. The results of this study support the role of sigma2 receptors in the regulation and control of movement and coordination and provides preliminary evidence to suggest the in vivo activity of sigma receptors by fluoxetine and fluvoxamine.
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Thirty patients, 26 women and 4 men, with drug-resistant depression were enrolled in the study. The subjects from Group No. I (14 patients) were given fluvoxamine and treated with weak variable magnetic field using the VIOFOR JPS device; the subjects from Group No. II (16 patients) were also given fluvoxamine but they were treated with the VIOFOR JPS device in placebo mode. Changes in depressive symptoms were estimated with the 21-point Hamilton Depression Scale (HDRS), Montgomery-Asberg Depression Scale (MADRS) and Beck Depression Inventory (BDI) questionnaire.
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Six subjects completing clinical treatment with fluvoxamine were enrolled in the study. Spectroscopic quantification of whole brain fluvoxamine concentrations and chromatographic determination of plasma fluvoxamine levels were performed serially for up to 10 days after drug withdrawal. Psychiatric evaluation to assess withdrawal symptoms was also done at each scanning session.
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This article reviews new developments of pharmacotherapy in obsessive-compulsive disorder (OCD) and OC spectrum disorders of the past five years. New developments primarily involved the ex-tension of evidence of efficacy of serotonin reuptake inhibitors(SRIs), the use of atypical antipsychotics in addition to SRIs for treatment refractory patients, the combination of pharmacotherapy with behavior therapy, and studies assessing predictors of response. Today, frontline pharmacological treatment of OCD still consists of drugs with potent serotonin reuptake inhibition proper-ties. In case of non-response, treatment options comprise adding another drug, increasing the dose, switching drugs, or changing the mode of delivery.
At a clinical level, it could be useful to underline dopamine-dependent characteristics of some SSRI-related side effects. This approach would allow clinicians the opportunity to search other dopamine-dependent side effects systematically. At a pharmacologic level, this approach could stimulate the development of molecules with a "corrective" function on dopamine-dependent side effects of SSRIs by facilitating dopaminergic neurotransmission.
In a randomized, placebo-controlled, two-phase cross-over study, ten healthy volunteers took either 100 mg fluvoxamine or matched placebo orally once daily for 5 days. On day 6, 10 mg buspirone was taken orally. Plasma concentrations of buspirone and its active metabolite, 1-(2-pyrimidinyl)-piperazine (1-PP), were measured up to 18 h and the pharmacodynamic effects of buspirone up to 8 h.
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Fluvoxamine is the selective serotonin re-uptake inhibitor with the largest database in the treatment of obsessive-compulsive disorder, a severe, and often chronic, anxiety disorder associated with substantial impairment in functioning. The selective serotonin re-uptake inhibitors represent a first-line treatment in patients with obsessive-compulsive disorder. These agents work primarily by blocking the re-uptake of serotonin into the presynaptic nerve terminal, which is believed to be mediated by their effects on the serotonin transport system. In the last two decades, the anti-obsessional effect of fluvoxamine has been tested in several double-blind, placebo-controlled and active-comparison studies, demonstrating its superior efficacy over obsessions and compulsions compared with non-serotonergic antidepressants (i.e., desipramine) and equal efficacy to clomipramine (a tricyclic antidepressant with potent serotonin re-uptake inhibition) and other selective serotonin re-uptake inhibitors (paroxetine and citalopram). However, compared with clomipramine, the selective serotonin re-uptake inhibitor fluvoxamine showed fewer side effects and better tolerability. This reflects the poor affinity of this compound for adrenergic, muscarinic, cholinergic or histaminergic receptors.
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Electroencephalogram sleep measures over a 4-week period were obtained on 35 inpatients with major depression (unipolar) who received either fluvoxamine or desipramine in a randomized double-blind trial. Fluvoxamine showed immediate rapid eye movement (REM) sleep suppression and an alerting effect on sleep continuity measures. In contrast, desipramine administration was associated with REM suppression and sleep continuity improvement. The "alerting" quality of fluvoxamine, similar to other serotonergic antidepressants, appears to be unrelated to a lack of clinical efficacy, but may be related to persistent REM sleep suppression. However, it is premature to comment on the serotonin specificity for REM sleep.
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The purpose of this study was to assess the efficacy of fluvoxamine in the treatment of binge-eating disorder. Binge-eating disorder is a newly described eating disorder characterized by recurrent episodes of binge eating but without purging behaviors. Uncontrolled reports have suggested that serotonin selective reuptake inhibitors (SSRIs) may be effective in treating this disorder.
A gas chromatographic-mass spectrometric (GC-MS) screening procedure was developed for detection of selective serotonin reuptake inhibitors (SSRIs) in urine as part of a systematic toxicological analysis procedure. After acid hydrolysis of one aliquot of urine, another aliquot was added. The mixture was then liquid-liquid extracted at pH 8-9, acetylated, and GC separated. Using mass chromatography with the ions m/z 58, 72, 86, 173, 176, 234, 238, and 290, the possible presence of SSRIs and/or their metabolites could be indicated. The identity of positive signals in such mass chromatograms was confirmed by comparison of the peaks underlying full mass spectra with the reference spectra recorded during this study. The overall recoveries of citalopram, sertraline, and paroxetine ranged between 60 and 80%, and those of fluoxetine and fluvoxamine, which were destroyed during acid hydrolysis, were between 40 and 45%. The coefficients of variation were less than 10-20%, and the limit of detection was at least 100 ng/mL (signal-to-noise ratio = 3). This method allowed the detection of therapeutic concentrations of citalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline in human urine samples.
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Selective serotonin reuptake inhibitors can be added to clozapine therapy in order to treat remaining negative symptoms and obsessive compulsive symptoms. The present case report describes a 44-year-old man exhibiting extremely elevated plasma levels of clozapine after the addition of fluvoxamine, up to 4160 mcg/l. The elevated plasma levels of clozapine, which were discovered 6 months after the SSRI was added, is likely to be caused by a drug-drug interaction. Clozapine is a substrate of CYP 1A2 and is predominantly metabolised in the liver. Of the SSRIs, fluvoxamine is one of the most potent inhibitors of the isoenzyme CYP 1A2. This case serves to emphasise the need for continuous attention to drug-drug interactions, especially when they might be easily overlooked due to the lack of clear symptoms.
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It was concluded that adding magnetostimulation to pharmacological therapy results in a progressive, significant reduction of intensification of depression symptoms.
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Fluvoxamine was synthesized from 4-trifluoromethylbenzonitrile by the steps of Grignard reaction, hydrolysis and oximation.