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Studies report mixed findings regarding antidepressant agents and suicide risks, and few examine suicide deaths. Studies using observational data can accrue the large sample sizes needed to examine suicide death, but selection biases must be addressed. We assessed associations between suicide death and treatment with the 7 most commonly used antidepressants in a national sample of Department of Veterans Affairs patients in depression treatment. Multiple analytic strategies were used to address potential selection biases.
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To determine the efficacy of drug therapies in the treatment of sleep apnoea.
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Selective serotonin reuptake inhibitors are commonly used to treat major depression; however, the percentage of serotonin (5-HT) transporter (5-HTT) sites occupied during clinical dosing is unknown. This study measured the proportion of 5-HTT sites blocked during paroxetine and citalopram treatment of depression and assessed the relationship between serum paroxetine levels and the proportion of 5-HTT sites blocked.
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These data demonstrate that SSRIs differentially inhibit bone cell function via apoptosis. This may explain the mechanisms of bone loss with chronic use and aid clinical choices.
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Paroxetine, a phenylpiperidine derivative, is an antidepressant that selectively inhibits serotonin reuptake. In this study 111 outpatients with major depression diagnosed by DSM-III criteria were treated with either paroxetine or placebo in a 6-week, randomized, double-blind study. Paroxetine was significantly superior to placebo on six of the seven major efficacy variables. Significant differences in favor of paroxetine were apparent by Week 2. Paroxetine was also well tolerated. These results support the efficacy and safety of paroxetine as a treatment for patients with major depression.
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This meta-analysis of placebo-controlled paroxetine trials examines suicidality incidence in adults, focusing on disorder and age as potential risk factors. The findings are put in context with an efficacy meta-analysis of the same trial datasets.
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The study results are consistent with those of previous quality content studies of commercially available English patient drug information leaflets. The results have important implications for patients as access to a reliable source of drug information may prevent harm or limit the suffering from serious adverse drug reactions.
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Sixty depressive FD patients with weight loss were randomly divided into a mirtazapine group (MG), a paroxetine group (PG) or a conventional therapy group (CG) for an 8-wk clinical trial. Adverse effects and treatment response were recorded. The Nepean Dyspepsia Index-symptom (NDSI) checklist and the 17-item Hamilton Rating Scale of Depression (HAMD-17) were used to evaluate dyspepsia and depressive symptoms, respectively. The body composition analyzer was used to measure body weight and fat. Serum hormone levels were measured by ELISA.
The present findings suggest that PMDD women have fluctuating serotonergic function across their menstrual cycles and that the pattern may be different from PMS without PMDD.
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The alpha(2)-adrenoreceptor antagonist mirtazapine, which is also a 5-HT(2), 5-HT(3) and H(1) receptors antagonist and the selective serotonin (5-HT) reuptake inhibitor paroxetine are effective antidepressant drugs which enhance 5-HT neurotransmission via different mechanisms. The present studies were undertaken to determine whether the mirtazapine-paroxetine combination could induce an earlier and/or a greater effect on the 5-HT system than either drug alone. Using in vivo electrophysiological paradigms, the firing activity of dorsal raphe 5-HT neurons was decreased by 70% in rats treated with paroxetine (10 mg/kg/day, s.c.) for 2 days and was back to normal after 21 days. In contrast, a 2-day treatment with mirtazapine (5 mg/kg/day, s.c.) did not alter the firing of 5-HT neurons whereas it was increased by 60% after 21 days of treatment. A low dose of mirtazapine (5 mg/kg/day, s.c.x2 days) failed to offset the decremental effect of paroxetine on the 5-HT neuron firing activity, but a higher dose (10 mg/kg/day, s.c.x2 days) did attenuate the decremental effect of paroxetine. In the dorsal hippocampus, neither mirtazapine (5 mg/kg/day, s.c.) nor a paroxetine (10 mg/kg/day, s.c.) treatment altered the responsiveness of 5-HT(1A) receptors to microiontophoretically-applied 5-HT. Both in controls and in rats treated for 2 days with paroxetine alone, the administration of the 5-HT(1A) antagonist WAY 100635 (25-100 microg/kg, i.v.) did not change the firing activity of dorsal hippocampus CA(3) pyramidal neurons. However, WAY 100635 increased significantly the firing activity of these neurons in rats treated with mirtazapine alone but to a greater extent with both mirtazapine and paroxetine for 2 days. After 21 days of treatment, WAY 100635 increased to a greater degree the firing rate of CA(3) pyramidal neurons in rats which received the combination over rats given either drug alone. It is concluded that the mirtazapine-paroxetine combination shortened the delay in enhancing the tonic activation of postsynaptic 5-HT(1A) receptors and produced a greater activation of the postsynaptic 5-HT(1A) receptors than either drug given alone. The present results suggested that mirtazapine may have a faster onset of action than a SSRI, and that the co-administration of mirtazapine and paroxetine may accelerate the antidepressant response and as well as being more effective than either drug alone.
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Paroxetine, an antidepressant with a high affinity for serotonin (5-HT) re-uptake sites, is a potential tracer of these sites. We determined the kinetic properties of [3H]paroxetine in rat brain in vivo. Relative to [14C]iodo-antipyrine, the brain uptake index (BUI) of [3H]paroxetine was 60-70%. The unidirectional blood clearance of [3H]paroxetine were 0.05-0.12 ml g-1 min-1, lower than expected from the BUI values. The steady state volume of distribution was 3.5 ml hg-1 in the diencephalon and 1.8 ml g-1 in the cerebellum, suggesting a binding potential of unity. Autoradiographs at four hours after [3H]paroxetine injection (300 microCi, i.p.) revealed heterogeneous binding consistent with the calculated binding potentials. Binding was nearly absent from cerebellum and was highest in the dorsal raphe, superior colliculus, dorsal hypothalamus, and entorhinal cortex, but did not reach equilibrium in four hours of tracer circulation. The specific binding relative to vermis was displaced by pretreatment with fluoxetine (10 mg/kg, i.p.).
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Of 20,906 children who initiated antidepressant therapy, 16,774 (80%) had no previous antidepressant use. During the first year of use, we observed 266 attempted and 3 completed suicides, which yielded an event rate of 27.04 suicidal acts per 1000 person-years (95% confidence interval [CI]: 23.9-30.5 suicidal acts per 1000 person-years). There were no meaningful differences in the rate ratios (RRs) comparing fluoxetine with citalopram (RR: 0.97 [95% CI: 0.54-1.76]), fluvoxamine (RR: 1.05 [95% CI: 0.46-2.43]), paroxetine (RR: 0.80 [95% CI: 0.47-1.37]), and sertraline (RR: 1.02 [95% CI: 0.56-1.84]). Tricyclic agents showed risks similar to those of selective serotonin reuptake inhibitors (RR: 0.92 [95% CI: 0.43-2.00]).
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The urinary concentration ratio of dextromethorphan:dextrorphan (interpreted as an in vivo index of CYP2D6 activity) was determined for each subject before and after the 8 days of receiving SSRIs. Plasma SSRI trough concentrations were measured on days 6-9. The CYP2D6 genotype was determined in a subject with an undetectable paroxetine concentration. Inhibition of CYP2D6 correlated significantly with plasma concentrations of paroxetine and fluoxetine. In contrast, no significant correlations emerged between CYP2D6 inhibition and plasma concentrations of sertraline or fluvoxamine. The subject with an undetectable paroxetine concentration was found to carry at least three functional CYP2D6 genes.
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Several studies have suggested that neurokinin-1 (NK1) receptor antagonists may have therapeutic potential as novel antidepressant drugs. To test these compounds preclinically, gerbils have become one of the preferred species in that they demonstrate close NK1 receptor homology with humans and bind NK1 antagonists with higher affinity than rats and mice. The intent of the present study was to determine whether the forced-swim test (FST), one of the most commonly used animal tests of antidepressant-like activity, could be adapted for use with the gerbil. Critical factors in the establishment of this assay included swim tank diameter, weight, and sex of the animals tested. Pharmacological validation of the FST using standard antidepressant compounds (eg fluoxetine, paroxetine, desipramine) resulted in decreased immobility time during the test, indicative of an antidepressant-like effect. Similar to results reported for the rat and mouse FST, the antipsychotic drug haloperidol increased immobility, whereas the psychostimulant, amphetamine decreased immobility, and anxiolytic drugs (eg buspirone) had no effect. Investigation into the locomotor effects of all compounds tested was consistent with previous reports in other species, with the exception of paroxetine, which produced hyperactivity at therapeutically effective doses in gerbils. In addition to standard antidepressants, NK1 antagonists (L-733060, MK-869, and CP-122721) all reduced immobility in the gerbil FST without affecting locomotor activity. Overall, these results suggest that the gerbil is an ideal species for use in the FST, and that this paradigm may have predictive validity for identifying novel antidepressant compounds.
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Selective serotonin reuptake inhibitors (SSRIs) are neurologically active drugs that can contaminate surface waters and have the potential to negatively affect aquatic organisms. In this investigation, the 48-h acute toxicity of mixtures (binary and quaternary) of four common SSRIs (fluoxetine [Prozac], sertraline [Zoloft], paroxetine [Paxil], and citalopram [Celexa]) were determined in the daphnid Ceriodaphnia dubia. Logistic regression was used to model mortality data and to investigate the applicability of concentration addition and independent action models to explain observed mortality. The concentrations estimated to induce 50% mortality in 48 h for the individual SSRIs sertraline, fluoxetine, paroxetine, and citalopram were 0.48 to 0.66, 1.23 to 1.84, 2.23 to 3.57, and 10.47 to 14.53 microM, respectively. Concentration addition was a better predictor of mixture effects than independent action and suggested that the tested SSRIs have a similar mechanism of action. Results indicate that environmental hazard assessments should be conservative and consider that acutely toxic effects in aquatic organisms can be additive for each SSRI in a mixture.
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After the treatment, 43 cases in our study had increased their ejaculation latency time, enhanced the quality of their sexy lives and their wives', and had significant difference compared with pre-treatment(P < 0.001). They had good effects on improving premature ejaculation after taking Seroxat (11.26 +/- 5.79) days; and after having stopped taking seroxat for (20.94 +/- 8.04) days, the situation of premature ejaculation in 32 cases were as same as that of before. There were seven cases whose sexuality and oomph increased, and two cases whose sexuality were decreased. A few patients had constipation, dry in mouth, insomnia and itch in skin, after taking the drugs.
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To assess whether the combination of psychological therapy and pharmacotherapy provides a more efficacious treatment for PTSD than either of these interventions delivered separately.
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The aim of this review was to critically appraise the existing literature with a particular focus on identifying methodological issues associated with studying outcomes following the use of selective serotonin reuptake inhibitors (SSRIs) during pregnancy. Existing studies evaluating outcomes following prenatal SSRI exposure suffer from a number of important methodological limitations that should be taken into account when interpreting their results. The contradictory results obtained from prospective and retrospective cohort studies and case-control studies could be accounted for by dissimilarity between study populations, selection bias, detection bias, confounding, or differences in underlying maternal illness, data sources used, exposure classification, follow-up and statistical power/analysis. Only a small number of studies actually account for underlying maternal illness and how this may lead to adverse pregnancy outcomes. Even when such information is available, studies that include data on maternal illness have small sample sizes, limiting the statistical power to identify statistically and clinically relevant associations. Pregnancy outcomes may be confounded by the higher incidence of smoking, alcohol consumption and substance abuse frequently encountered amongst those suffering from depression, factors that are often insufficiently controlled for. While evidence of associations between prenatal SSRI exposure and adverse pregnancy outcomes are conflicting, there is an urgent need to evaluate how the particular SSRI used, the dose, timing and duration of use, genetics (maternal, paternal and/or fetal), concomitant medication use, maternal characteristics and underlying maternal illness all interact to alter pregnancy outcomes.
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Many studies have reported both a gender difference in the rates of depression and its treatment by using any of the widely used antidepressant drug groups. Some studies suggest that females respond more poorly to tricyclic antidepressants than males and appear to respond better to selective serotonin reuptake inhibitors (SSRI). There is no study investigating the analgesic/antinociceptive effects of antidepressant drugs on the basis of gender difference. In this study, we aimed to investigate the antinociceptive effect of paroxetine on the basis of gender difference.
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This study is a pre-registration trial of generic duloxetine that was approved by the China Food and Drug Administration (approval number: 2006L01603).
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A sensitive HPLC method was developed and validated for the determination of sildenafil concentrations in rat plasma (200 μL) using a liquid-liquid extraction procedure and paroxetine as an internal standard. In order to eliminate interferences and improve the peak shape, a back-extraction into an acidic solution was utilized. Chromatographic separation was achieved on a cyanopropyl bonded-phase column with a mobile phase composed of 50 m m potassium dihydrogen phosphate buffer (pH 4.5) and acetonitrile (75:25, v/v), pumped at the flow rate of 1 mL/min. A UV detector was set at 230 nm. A calibration curve was constructed within a concentration range from 10 to 1500 ng/mL. The limit of detection was 5 ng/mL. The inter- and intra-day precisions of the assay were in the ranges 2.91-7.33 and 2.61-6.18%, respectively, and the accuracies for inter- and intra-day runs were within 0.14-3.92 and 0.44-2.96%, respectively. The recovery of sildenafil was 85.22 ± 4.54%. Tests confirmed the stability of sildenafil in plasma during three freeze-thaw cycles and during long-term storage at -20 and -80°C for up to 2 months. The proposed method was successfully applied to a pharmacokinetic study in rats.
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A prospective study type crossover was designed with 14 patients. Grupo A: 7 patient received paroxetine 20 mg/d by three weeks followed by paroxetine 20 mg 4-6 hours before the intercourse by three weeks. Group B: the other 7 patients received the same scheme but replacing by placebo. Later to three weeks of therapy suspension, crossover was made.