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Ten outpatients with OCD participated in the study. Functional magnetic resonance imaging (fMRI) was performed before and after treatment. Stroop and symptom provocation tasks were administered during fMRI. Each patient was randomly allocated to receive either pharmacotherapy with fluvoxamine 200 mg/day (n = 4) or behavior therapy (n = 6) for 12 weeks.
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Fluvoxamine is a better antidepressant drug in comparison with nortriptyline as it causes a less impairment of psychomotor functions.
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Seven Japanese patients on maintenance hemodialysis who were comorbid with mild depression were medicated with 50 mg/day fluvoxamine maleate for 28 days. Effectiveness was obtained in four out of seven patients (57%). The plasma fluvoxamine concentrations were examined in three patients. The plasma fuvoxamine concentration decreased by 22% by hemodialysis. There is a tendency for the dialyzed rate of fluvoxamine to become lower if the plasma albumin concentration is higher. The half-life of fluvoxamine was possibly shortened more in the patient with hypoalbuminaemia. The plasma fluvoxamine concentration reached a steady state 8 days after the start of medication and thereafter. The time required to reach steady state was lengthened when compared with the results in normal Japanese volunteers.
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Tegafur, an anticancer prodrug, is bioactivated to 5-fluorouracil (5-FU) mainly by cytochrome P450 (P450) enzymes. The conversion from tegafur into 5-FU catalyzed by human liver microsomal P450 enzymes was investigated. In fourteen cDNA-expressed human P450 enzymes having measurable activities, CYP1A2, CYP2A6, CYP2E1, and CYP3A5 were highly active in catalyzing 5-FU formation at a tegafur concentration of 100 microM. Kinetic analysis revealed that CYP1A2 had the highest V(max)/K(m) value and that the V(max) value of CYP2A6 was high in 5-FU formation. In human liver microsomes, the activities of 5-FU formation from 10 microM, 100 microM, and 1 mM tegafur were significantly correlated with both coumarin 7-hydroxylation (r = 0.83, 0.86, and 0.74) and paclitaxel 6 alpha-hydroxylation (r = 0.77, 0.62, and 0.85) activities, respectively. Coumarin efficiently inhibited the 5-FU formation activities from 100 microM and 1 mM tegafur catalyzed by human liver microsomes that had high coumarin 7-hydroxylation activity. On the other hand, furafylline, fluvoxamine, and quercetin, as well as coumarin, showed inhibitory effects in liver microsomes that had high catalytic activities of 5-FU formation. The other P450 inhibitors examined showed weak or no inhibition in human liver microsomes. Polyclonal anti-CYP1A2 antibody, monoclonal anti-CYP2A6, and anti-CYP2C8 antibodies inhibited 5-FU formation activities to different extents in those two microsomal samples. These results suggest that CYP1A2, CYP2A6, and CYP2C8 have important roles in human liver microsomal 5-FU formation and that the involvement of these three P450 forms differs among individual humans.
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Recombinant cytochrome P450 (P450) phenotyping, different approaches for estimating fraction metabolized (f(m)), and multiple measures of in vivo inhibitor exposure were tested for their ability to predict drug interaction magnitude in dogs. In previous reports, midazolam-ketoconazole interaction studies in dogs have been attributed to inhibition of CYP3A pathways. However, in vitro phenotyping studies demonstrated higher apparent intrinsic clearances (CL(int,app)) of midazolam with canine CYP2B11 and CYP2C21. Application of activity correction factors and isoform hepatic abundance to liver microsome CL(int,app) values further implicated CYP2B11 (f(m) >or= 0.89) as the dog enzyme responsible for midazolam- and temazepam-ketoconazole interactions in vivo. Mean area under the curve (AUC) in the presence of the inhibitor/AUC ratios from intravenous and oral midazolam interaction studies were predicted well with unbound K(i) and estimates of unbound hepatic inlet inhibitor concentrations and intestinal metabolism using the AUC-competitive inhibitor relationship. No interactions were observed in vivo with bufuralol, although significant interactions with bufuralol were predicted with fluoxetine via CYP2D and CYP2C pathways (>2.45-fold) but not with clomipramine (<2-fold). The minor caffeine-fluvoxamine interaction (1.78-fold) was slightly higher than predicted values based on determination of a moderate f(m) value for CYP1A1, although CYP1A2 may also be involved in caffeine metabolism. The findings suggest promise for in vitro approaches to drug interaction assessment in dogs, but they also highlight the need to identify improved substrate and inhibitor probes for canine P450s.
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As part of a double-blind, placebo-controlled trial, 128 children (mean age, 10.8 years; range, 6-17) with DSM-IV anxiety disorders (i.e., social, separation, and generalized anxiety) were assessed by expert clinicians on 16 SSs using the Pediatric Anxiety Rating Scale.
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The effects of 5-hydroxytryptamine (5-HT) and sumatriptan were investigated on isolated guinea pig gallbladder strips. While 0.1 microM-50 mM of 5-HT exhibited contractile and/or relaxant effects in quiescent preparations, the same concentrations of sumatriptan did not. On the other hand, carbachol-precontracted tissues were relaxed by the same amounts of 5-HT and sumatriptan in a concentration-dependent manner. The relaxant responses to 5-HT were not antagonized or changed by tetrodotoxin, indomethacin, capsaicin, NG-nitro-L-arginine (L-NOARG), GR55562 [(+/-)-propranolol, 3-[3-(N,N-dimethylamino)propyl 1-4-hydroxy-N-[4-(pyridin-4-yl)phenyl]benzamide , S(-)-propranolol, methysergide, ketanserin. tropisetron, GR 113808 ([1-[2-(methylsulphonylamino)ethyl -4-piperidinyl]methyl-1-methyl-1H-indole-3-carboxylate maleate salt). pargyline, and fluvoxamine. The relaxant responses to sumatriptan were antagonized by GR55562 but not by S(-)-propranolol. These results suggest that 5-HT and sumatriptan cause relaxation in carbachol-precontracted isolated guinea pig gallbladder strips by yet undefined mechanisms.
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The administration of tryptophan (Trp)-free amino acid mixtures to depressed patients responding to serotonin [5-hydroxytryptamine (5-HT)] uptake inhibitors (SSRIs) worsens their clinical state. This procedure reduces Trp availability to brain and thus impairs 5-HT synthesis. We have examined the influence of Trp depletion on extracellular 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) concentrations in the rat brain using in vivo microdialysis. The treatment with the SSRI fluvoxamine significantly increased 5-HT content in dialysates from frontal cortex, as compared with control rats (10.2 +/- 2.7 vs. 3.1 +/- 0.4 fmol per fraction), whereas 5-HIAA was unaffected. Food deprivation for 20 h reduced dialysate 5-HT content to almost control values in fluvoxamine-treated rats (10.2 +/- 2.7 vs. 4.3 +/- 0.6 fmol per fraction) but did not alter dialysate 5-HIAA content (7.8 +/- 0.4 vs. 7.2 +/- 0.5 pmol per fraction). The administration of Trp-free amino acid mixtures to fluvoxamine-treated rats significantly attenuated the release of 5-HT in frontal cortex (approximately 50%) and, to a lesser extent, in the midbrain raphe nuclei. This effect was more marked in rats not deprived from food before the experiments (67% reduction of dialysate 5-HT content in frontal cortex) and was absent in control rats (treated with saline). In contrast, dialysate 5-HIAA was markedly affected by Trp depletion in all groups, including controls (65-75% reductions). These data show that the administration of an amino acid mixture with the same composition and dose (in milligrams per kilogram of body weight) as those inducing a severe mood impairment in depressed patients reduces 5-HT and 5-HIAA concentrations in brain dialysates. The reduction of 5-HT release, however, occurs only in animals previously treated with the antidepressant fluvoxamine for 2 weeks, which would be consistent with a marked reduction of 5-HT-mediated transmission in treated depressed patients but not in healthy controls.
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Overdose deaths from antidepressants have not decreased over the last 15 years. A trend away from prescribing drugs with a higher fatal toxicity index in favour of those with a lower index, would reduce the number of deaths from antidepressant poisoning.
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The aim of the present study was to test a possible effect of the A218C tryptophan hydroxylase (TPH) gene variant on the antidepressant activity of fluvoxamine in a sample of major and bipolar depressives, with or without psychotic features. Two hundred and seventeen inpatients were treated with fluvoxamine 300 mg and either placebo or pindolol in a double blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. TPH allelic variants were determined in each subject by using a PCR-based technique. No significant finding was observed in the overall sample as well as in the pindolol group, while TPH*A/A was associated with a slower response to fluvoxamine treatment in subjects not taking pindolol (P = 0.001). This effect was independent from the previously reported influence of 5-HTTLPR polymorphism. If confirmed, these results may shed further light on the genetically determined component of the response to pharmacological treatments, thus helping the clinician to individualize each patient's therapy according to their genetic pattern.
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In major depressive disorder (MDD), treatment persistence is critical to optimize symptom remission, functional recovery, and health care costs. Desvenlafaxine tends to have fewer drug interactions and better tolerability than other MDD drugs; however, its use has not been assessed in the real world.
We found an association between rs6465084 in GRM3 and MDD in the allele-wise analysis after Bonferroni's correction (P-value=0.0371). However, we did not find any association between GRM3 and BP or the fluvoxamine therapeutic response in MDD in the allele/genotype-wise analysis. We also did not detect any association between GRM2 and MDD, BP or the fluvoxamine therapeutic response in MDD in the allele/genotype-wise or haplotype-wise analysis.
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The subjects for the present study were 37 patients (20 and 17 patients with mood and anxiety disorders, respectively), meeting a diagnosis of DSM-IV. Each subject gave informed consent for the research involved in this study. Presence and severity of the serotonin-related symptoms were determined by Sternbach's criteria and the JSSS, respectively.
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No studies have been specifically oriented toward evaluating the effect of drugs on AG; in the available studies, the improvement of AG might have been the consequence of the reduction of panic attacks. Before developing a "true" psychopharmacology of AG it is crucial to clarify its definition. There may be several potential mechanisms involved, including fear-learning processes, balance system dysfunction, high light sensitivity, and impaired visuospatial abilities, but further studies are warranted.
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Omeprazole is mainly metabolized by the polymorphic cytochrome P450 (CYP) 2C19. The inhibitory effect of fluvoxamine, an inhibitor of CYP2C19 as well as CYP1A2, on the metabolism of omeprazole was compared between different genotypes for CYP2C19.
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In psychopharmacology, treatment with psychotropic drugs is often suboptimal, mainly because of the high interindividual variability in pharmacokinetic properties. Therapeutic drug monitoring (TDM) can be a valuable tool for monitoring the individual effects of a prescribed dosage in a patient, and it facilitates antipsychotic treatment by increasing the effectiveness and safety of drugs and by reducing treatment costs. The aim of this study was to develop and validate an ultrafast liquid chromatography (UFLC) method with tandem mass spectrometric detection for the measurement of 16 antipsychotics and antidepressants in human plasma samples for TDM or other applications.
Brain serotonin plays a crucial role in the regulation of food intake and body weight homeostasis. Previous data suggest an interaction with corticotropin-releasing hormone (CRH). To further examine the interaction between these neurotransmitters, the selective serotonin reuptake-inhibitor (SSRI) fluvoxamine was given intraperitoneally in fa/fa Zucker rats with and without the CRH-receptor-antagonist alpha-helical CRH administered intracerebroventricularly (i.c.v.). The saline treated animals gained weight. Fluvoxamine led to a significant weight loss while not affecting food intake. Furthermore, insulin levels in this animal model were reduced following fluvoxamine administration. These effects were antagonized by alpha-helical CRH and are thus most likely mediated via CRH or CRH-like peptides.
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200 inpatients treated for the first time with fluvoxamine were prospectively evaluated for the occurrence of a serotonin syndrome over a period of 8200 treatment days. Retrospective follow-up data of outpatient treatment covered 8891 days.
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The authors studied 19 outpatients with major depressive disorder using prolactin response to d-fenfluramine as a measure of central serotonergic functioning. Testing of patients was conducted just before and right after 8 weeks of treatment with either fluoxetine (n = 10) or fluvoxamine (n = 9) as part of a randomized, double-blind treatment trial. Blood samples for prolactin were collected prior to administration of d-fenfluramine (0.5 mg/kg) and then over the next 5 hours.
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In total, 120 patients were recruited. No statistically significant difference was detected regarding age, gender, types of cancer, KPS between two groups of patients (P> 0.05). Baseline pain score of patients with moderate pain in treatment and control group was 4.9±0.8 and 5.1±0.8, respectively; and decreased to 1.8±1.1 and 1.2±1.1 after treatment, respectively. Pain intensity was significantly reduced in the treatment group (P =0.028). Average daily consumption of oxycodone prolonged- release tablets was (54.0±19.6) mg and (44.7± 18.7) mg respectively, which is lower in treatment grpup than in control group, but the difference was not statistically significant (P=0.065). Baseline pain score of patients with severe pain in treatment and control groups were 8.3±1.1 and 8.3±1.1, respectively; and pain intensity after treatment decreased to 2.9±1.0 and 2.3±1.0. Pain intensity was significantly reduced in the treatment group, with statistical significance (P =0.026). Average daily consumption of oxycodone prolonged-release tablets was (132.0±42.2) mg and (110.7±33.9) mg, respectively, which is lower in treatment group than in control group, and the difference was statistically significant (P=0.035). In terms of quality of life, patients in treatment group had better performance status, daily activity, mood, and sleep than that in control group (P < 0.05). Patients in two groups had similar side effects, eg., constipation, nausea/vomiting, lethargy, dizziness, itchy skin, dysuria, and ataxia. Lower incidence of nausea/vomiting, lethargy, was obtained from patients in treatment than in control group, while significant low constipation was observed in treatment than in control group (35.0% vs 49.2%, P=0.026).
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In this case, unlike those previously reported, hyponatremia recurred 16 months after a different SSRI was initiated. The Naranjo probability scale indicates a probable relationship between recurrent hyponatremia and paroxetine. The mechanism of SSRI-induced hyponatremia is multifactorial.
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In our sample, 48.7% of the patients presented a recurrence within the first 2 years of treatment. Bupropion appears less effective in long-term treatment of MDD than the other compared antidepressants, with exception of fluoxetine (p = 0.09), amitriptyline (p = 0.13), fluvoxamine (p = 0.83), venlafaxine (p = 0.5), and trazodone (p = 0.58). Fluvoxamine appears to be less effective than citalopram (p = 0.036), paroxetine (p = 0.037), clomipramine (p = 0.05), sertraline (p = 0.011), and duloxetine (p = 0.024).
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Duloxetine is a potent and selective inhibitor of serotonin and norepinephrine reuptake with weak activity on dopamine reuptake. Enzymes involved in duloxetine metabolism are cytochrome P450 isoenzymes (CYP) CYP1A2 and to a lesser extent CYP2D6 whereas the selective serotonin reuptake inhibitor Fluvoxamine is known to be a potent inhibitor of CYP1A2. Changes in plasma levels of duloxetine revealing pharmacokinetic interactions with fluvoxamine, clinical effects and adverse effects of adding fluvoxamine in thirteen patients with a steady-state duloxetine treatment by intraindividual comparisons were analyzed in this retrospective survey. Patients had been treated with duloxetine under steady-state conditions until fluvoxamine was added. Plasma duloxetine levels were measured at steady state of different daily doses due to lacking experience with the combination of DLX and FLX. Adding 25 mg of fluvoxamine (FLX) per day to a steady-state treatment with 30 mg of duloxetine (DLX) in 8 patients led to an average increase of duloxetine plasma levels that was 3-fold with a magnitude of 50-506%. Our findings indicate that duloxetine plasma levels can be enhanced by a potent CYP1A2 inhibition by FLX and that DLX, even in higher plasma levels, seems to be well tolerated. The use of combined treatments, however, underscores the importance of understanding pharmacokinetic interactions.
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This new validated method fulfills all criteria for TDM and was successfully applied in the routine TDM of antipsychotics and antidepressants at the First Affiliated Hospital of Kunming Medical University.
We used the following methods for this study: (1) determination of enzyme kinetics for antipyrine metabolite formation in human liver microsomes, (2) inhibition studies with antibodies and inhibitors, and (3) formation of metabolites by stable expressed human P450 enzymes.
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Pharmacotherapy for mood disorders during pregnancy is often complicated by pregnancy-related pharmacokinetic changes and the need for dose adjustments. The objectives of this review are to summarize the evidence for change in perinatal pharmacokinetics of commonly used pharmacotherapies for mood disorders, discuss the implications for clinical and therapeutic drug monitoring (TDM), and make clinical recommendations.