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Zh Nevrol Psikhiatr Im S S Korsakova. 2008; 108(6): 43-46
Tarasova SV, Amelin AV, Skoromets AA
Efficacy of antidepressants fluvoxamine, amitriptyline and transcranial electrostimulation of the brain in the treatment of chronic daily headache has been studied. Amitriptyline had the highest effect in dosage 50 mg daily but was not well tolerated by patients that resulted in that only 50% of them finished the study. Fluvoxamine had high efficacy and good tolerability in the treatment of chronic daily headache and medication overuse headache. Small dosages of amitriptyline and fluvoxamine potentiated the analgesic effect of transcranial electrostimulation of the brain. The combination of antidepressants with transcranial electrostimulation of the brain alleviated the negative effect of the withdrawal of overused analgesics and may be recommended for out-patient use.
Fluvoxamine in the treatment of anxiety disorders.
Neuropsychiatr Dis Treat. 2005 Dec; 1(4): 289-99
Irons J
Fluvoxamine is a selective-serotonin reuptake inhibitor (SSRI) that has proved effective in large double-blind, randomized, controlled trials involving patients with social anxiety disorder (SAD), obsessive-compulsive disorder (OCD), and panic disorder. Improvements have also been demonstrated in patients with post-traumatic stress disorder, as well as those with a range of obsessive-compulsive spectrum disorders including binge eating disorder, bulimia nervosa, pathological gambling, and body dysmorphic disorder. Several well controlled studies have confirmed the efficacy of fluvoxamine in children and adolescents with OCD, SAD, and other anxiety disorders, and it was the first SSRI to be registered for the treatment of OCD in children. Fluvoxamine is well tolerated. In common with other SSRIs, the most frequently reported adverse event is nausea. Fluvoxamine does not cause sedation or cognitive impairment and is associated with a low risk of sexual dysfunction, suicidality, and withdrawal reactions. It is safe in overdose and has no significant effect on body weight or cardiovascular parameters.
Neuropsychiatr Dis Treat. 2005 Dec; 1(4): 287
Devane CL
J Pharm Biomed Anal. 2008 May 8;
Barri T, Trtić-Petrović T, Karlsson M, Jönsson JA
The technique equilibrium sampling through membrane (ESTM) was extended to measuring the free drug concentration in solutions of drug and protein. Bjerrum and Scatchard plots were employed for characterizing individual drug binding to pure human blood proteins. Four drugs were investigated as a model system: fluvoxamine and ropivacaine which dominantly bind to alpha-acid glycoprotein (AGP), and R,S-ibuprofen and S-ketoprofen which highly bind to human serum albumin (HSA). The level of drug binding to AGP and HSA relied on drug and protein concentrations. Bjerrum and Scatchard plots revealed high affinity constants (K(a)) at low protein concentration. Both Bjerrum and Scatchard plots of fluvoxamine and ropivacaine binding to AGP showed one specific binding site (n(1)=1) with ropivacaine K(a) value close to 5 times higher than the K(a) of fluvoxamine at 22.9muM AGP concentration. Bjerrum plots of ketoprofen and ibuprofen gave total number of binding sites or bound molecules of 6-7, which did not depend on the drug or protein concentration. Scatchard plots of ketoprofen and ibuprofen exhibited two binding sites (n(1) and n(2)) at 0.15muM and 0.75muM HSA concentrations. On one hand, at 0.15muM HSA, ketoprofen and ibuprofen were bound to site I at n(1)=1.2 and n(1)=1.0, respectively. However, at 0.75muM HSA, ketoprofen and ibuprofen were bound to site I at n(1)=1.2 and n(1)=1.9, respectively. On the other hand, site II, at 0.15muM HSA, interacted with ketoprofen and ibuprofen at n(2)=5.6 and 6.7, respectively. However, at 0.75muM HSA, site II interacted with ketoprofen at n(2)=7.4 and ibuprofen at n(2)=6.2. It would be concluded that, upon mixing ketoprofen and ibuprofen in a HSA solution, a ketoprofen-ibuprofen interaction would most likely occur at site II in HSA.
Efficacy, tolerability and side-effect profile of fluvoxamine for major depression: meta-analysis.
J Psychopharmacol. 2008 Jun 18;
Omori IM, Watanabe N, Nakagawa A, Akechi T, Cipriani A, Barbui C, McGuire H, Churchill R, Furukawa TA
Abstract Fluvoxamine, one of the oldest selective serotonin reuptaking inhibitors, is commonly prescribed to patients with major depression. Several studies have reviewed the efficacy and tolerability of fluvoxamine for the treatment of major depression. However, these reviews are outdated, have not been systematic and/or suffered from several methodological weaknesses. We conducted a systematic review to synthesize the best available evidence on the efficacy of fluvoxamine for adult patients suffering from major depression in comparison with other active antidepressive agents. Relevant randomized controlled trials were identified through a comprehensive search. The primary outcome was a relative risk of response, and the secondary outcome was a relative risk of remission. Tolerability and side-effect profile were also examined. Fifty-three trials were included. There were no large differences between fluvoxamine and any other antidepressants in terms of efficacy and tolerability. There is evidence of differing side effect profiles, especially when comparing gastrointestinal side effects between fluvoxamine and tricyclics. Clinicians should focus on practically or clinically relevant differences including those in side-effect profiles.
Br J Pharmacol. 2008 May 19;
Geldof M, Freijer JI, van Beijsterveldt L, Langlois X, Danhof M
Background and purpose:The pharmacokinetic-pharmacodynamic (PK-PD) correlation of fluvoxamine 5-HT transporter (SERT) occupancy was determined in rat frontal cortex ex vivo.Experimental approach:Rats (n=47) with permanent arterial and venous cannulas received a 30 min intravenous infusion of fluvoxamine (1 or 7.3 mg kg(-1)). At various time points after dosing, brains were collected for determination of fluvoxamine concentration and SERT occupancy. In addition, the time course of fluvoxamine concentration in plasma was determined up to the time of brain collection. In a separate study (n=26), the time course of fluvoxamine concentration in brain extracellular fluid (ECF) and plasma was determined. The results of the investigations were interpreted by nonlinear mixed effects modelingKey results:Highest SERT occupancy was reached at the first time point (10 or 15 min) and maintained for 1.5 and 7 h after 1 and 7.3 mg kg(-1), respectively. Thereafter, SERT occupancy decreased linearly at a rate of 8% h(-1). SERT occupancy could be directly related to plasma, brain ECF and brain tissue concentrations by a hyperbolic function (B(max) model). Maximal SERT occupancy (B(max)) was 95%. Estimated concentrations at half-maximal SERT occupancy (EC(50)) in plasma, ECF and brain tissue were 0.48, 0.22 and 14.8 ng mL(-1) respectively. The minimum value of the objective function decreased 12 points for ECF and brain tissue concentrations relative to plasma (P
Pharmacopsychiatry. 2008 May; 41(3): 81-91
Diaz FJ, Santoro V, Spina E, Cogollo M, Rivera TE, Botts S, Leon J
AIM: The purpose of this study was to estimate the effect sizes of drug interactions on plasma clozapine concentrations, adjusting for potentially confounding factors such as smoking. METHODS: The estimation was performed by using a mixed model, and a combination of unpublished (N=83) and published (N=172) data that included patients taking phenobarbital, valproic acid, fluvoxamine, fluoxetine, paroxetine, sertraline, citalopram and reboxetine, and patients not taking co-medications. RESULTS: The 255 patients provided a total of 415 steady-state trough plasma clozapine concentrations. Each patient provided 1 to 15 measures of plasma clozapine concentrations. Total plasma clozapine concentration, defined as the sum of plasma clozapine and norclozapine concentrations, was also investigated. A random intercept linear model of the natural log of plasma clozapine concentration with the natural log of dose and other variables as independent variables was built. The model confirmed that phenobarbital induces clozapine metabolism (effect size, E=-28%), and that fluoxetine (E=+42%), fluvoxamine (E=+263%) and paroxetine (E=+30%) inhibit it. Valproic acid appeared to inhibit clozapine metabolism in non-smokers (effect size, E=+16%), whereas it appeared to induce clozapine metabolism in smokers (E=-22%). The effect sizes of smoking on plasma clozapine concentration were -20% in patients not taking valproic acid, and -46% in patients taking valproic acid. Thus, smoking induces clozapine metabolism, and this induction may be stronger when the patient is taking valproic acid. The effect sizes allowed the computation of clozapine dose-correction factors for phenobarbital, 1.4 [95% confidence interval, CI, (1.1, 1.7)]; paroxetine, 0.77 (0.67, 0.89); fluoxetine, 0.70 (0.64, 0.78); fluvoxamine, 0.28 (0.22, 0.35); and valproic acid [0.86 (0.75, 1.0) in non-smokers, and 1.3 (0.96, 1.73) in smokers]. Sertraline, reboxetine and citalopram had no obvious effects. DISCUSSION: The results for total plasma clozapine concentrations are similar to those for plasma clozapine concentrations. The main limitations of this study were that the computed effect sizes reflect only the doses and treatment-durations of the co-medications studied, and that the substantial "noise" of the clinical environment may make it difficult to detect the effects of some variables, particularly those with small effect sizes. Gender was not significant probably due to its relatively small effect size in the studied population, and age was not significant probably due to the limited age variability. CONCLUSION: This article contributes to the clozapine literature by describing a possible interaction between taking valproic acid and smoking, which modifies plasma clozapine concentrations, by estimating the effect sizes of other compounds on plasma clozapine concentrations after correcting for confounders, and by providing dose-correction factors for clinicians.
Life Sci. 2008 Jun 4; 82(23-24): 1169-74
Nomura K, Castanon-Cervantes O, Davidson A, Fukuhara C
Alterations in circadian rhythm generation may be related to the development of mood disorders. Although it has been reported that the most popular antidepressant, selective serotonin reuptake inhibitors (SSRIs) affect circadian phase, no data are available that describe the effects of SSRIs on other circadian parameters (period, amplitude and damping rate) in dissociated cells. In the present study we used real-time monitoring of bioluminescence in rat-1 fibroblasts expressing the Period1-luciferase transgene, and that in Period1-luciferase transgenic mouse suprachiasmatic nucleus (SCN) explants, in order to characterize the effects of SSRI on circadian oscillator function in vitro. We found that mRNA of the serotonin transporter (SERT), a target of SSRIs, was expressed in rat-1 fibroblasts. Sertraline, fluoxetine, fluvoxamine, citalopram and paroxetine all significantly shortened the period of Period1-bioluminescence rhythms in rat-1 fibroblasts. The amplitude was reduced by sertraline, and the damping rate was decreased by sertraline, fluoxetine, flvoxamine and paroxetine. The effect of sertraline was dose-dependent, and it also shortened the circadian period in the SCN. SERT is associated with lipid microdomains, which are required for efficient SERT activity. Indeed, cholesterol chelating reagent methyl-beta-cyclodextrin significantly reduced the period and the amplitude in rat-1 fibroblasts. Furthermore, lipid binding reagent xylazine significantly reduced the period. In summary our data present evidence that SSRIs affect circadian rhythmicity. The action of SSRIs is likely mediated by suppression of SERT activity. A better understanding of the relationship between mental illness and biological timing may yield new insight into disease etiology and avenues for treatment.
J Clin Psychopharmacol. 2008 Jun; 28(3): 325-8
Suzuki Y, Fukui N, Sawamura K, Sugai T, Watanabe J, Ono S, Inoue Y, Ozdemir V, Someya T
Therapeutic drug monitoring studies of selective serotonin reuptake inhibitor (SSRI) antidepressants thus far failed to identify a clear concentration-response relationship in major depression. Majority of the previous studies defined clinical response as 50% or greater reduction from baseline in depression rating scale scores. Because many patients who meet these criteria still present symptoms associated with functional impairment, there is a need to consider "remission" as an alternative end point in concentration-response analyses of SSRIs. The present 12-week prospective study investigated the relationship between fluvoxamine (an SSRI) plasma concentration and remission in outpatients with depression. We used a flexible dose titration study designed to mimic clinical practice within the therapeutic dose range of fluvoxamine (25-200 mg/d). Receiver operating characteristics (ROC) curve was computed to determine the optimal fluvoxamine plasma concentration for remission using 269 concentration data obtained from 80 patients. Analysis of the ROC curve from the entire study sample did not reveal a fluvoxamine concentration significantly predicting remission. By contrast, ROC analysis specifically in patients with moderate to severe depression (N = 51; baseline 17-item Hamilton Rating Scale for Depression score > or = 20) found a fluvoxamine concentration of 61.4 ng/mL as a significant predictor of remission. In conclusion, therapeutic drug monitoring may be useful for rational titration and individualization of fluvoxamine dose and predicting remission in patients with moderate to severe depression, who may presumably display lesser placebo component in pharmacodynamic response.
Additive effects of combined application of multiple HERG blockers.
J Cardiovasc Pharmacol. 2008 Jun; 51(6): 549-52
Margulis M, Sorota S
Pro-arrhythmia by noncardiac drugs has become an important safety concern in the pharmaceutical industry. The most common underlying mechanism for induction of arrhythmias by noncardiac drugs is off-target block of the native cardiac repolarizing current, IKr. The pore-forming subunit of IKr is encoded by the human ether-a-go-go related gene (hERG), and in vitro measurements of hERG activity has become a standard component of drug safety evaluations. hERG/IKr channels are blocked by a wide array of different chemical series; therefore, patients could be exposed to multiple blockers. There are few published studies addressing whether multiple blockers will exert independent actions on hERG channels. Whole cell patch clamp was used to evaluate the potential for cooperative effects when 2 hERG blocking agents were applied simultaneously. Cisapride, quinidine, fluvoxamine, and BeKm-1 were selected as representative agents binding to: (1) hydrophobic residues in the inner vestibule (cisapride and quinidine, the most frequent sites of interaction), (2) an extracellular segment near the pore (BeKm-1) or, (3) an unknown site (fluvoxamine). No synergistic blocking actions were seen. In some cases block was slightly less than additive. On balance, the results are consistent with additive and independent actions with simultaneous application of 2 hERG blockers.