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The aim of the present study was to investigate differences in discontinuation time among antidepressants and total antidepressant discontinuation rate of patients with depression over a 6 month period in a naturalistic treatment setting.
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In the present study, the potency and selectivity of escitalopram, R-fluoxetine, and all of the other currently available selective serotonine reuptake ihibitors were compared for binding affinity at the human serotonin, norepinephrine, and dopamine transporters and several select neurotransmitter receptors using radioligand binding assays.
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The conditioned place preference and the defensive burying paradigms were used to measure the behavioral responses that occur 1 week following cocaine withdrawal.
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Recent large double-blind, placebo-controlled trials have indicated that sertraline is an effective and well-tolerated treatment for posttraumatic stress disorder (PTSD). The avoidance/numbing symptom cluster improved the most significantly with sertraline, but significant improvements were also noted for the intrusive/reexperiencing and arousal symptom clusters. Smaller double-blind, placebo-controlled trials have also indicated that fluoxetine is an effective treatment for PTSD. Multiple small, open studies with other selective serotonin reuptake inhibitors and newer antidepressants indicate that these medications show some promise. Older studies indicate some efficacy for tricyclic antidepressants, and monoamine oxidase inhibitors are a reasonable choice, particularly for intrusive/reexperiencing symptoms.
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Data from peer-reviewed publications (1975-2007) of controlled, crossover design, pharmacodynamic studies on SAD medications in healthy volunteers were analysed. The number of objective psychometrics for each drug/dose level at all time points after dosing, and of instances of statistically significant impairment of cognitive function, enabled calculation of drug-induced cognitive impairment. The magnitude of impairment between drugs was compared using proportional impairment ratios (PIRs).
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The aim of this study was to extract the factors possibly associated with sertraline treatment response and elucidate their interactions and extent of influence.
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To assess the efficacy, safety, and tolerability of escitalopram in the treatment of PTSD.
Cholestatic itch is a feature of numerous hepatobiliary disorders such as primary biliary cirrhosis, primary sclerosing cholangitis, the inherited form of cholestasis, and intrahepatic cholestasis of pregnancy. Although undervalued by physicians, cholestatic itch can be a source of great discomfort to the patient and significantly affects quality of life. Many pruritogens such as bile salts, opioids, serotonin, and histamine have been implicated in the pathogenesis of cholestatic itch, but no causative link has ever been established. Recent findings indicate that the potent neuronal activator lysophosphatidic acid and autotaxin, the enzyme forming lysophosphatidic acid, may be key elements in its pathogenesis. Treatment options for patients with cholestatic itch include the anion exchange resin cholestyramine, bile acid ursodeoxycholic acid, PXR agonist rifampicin, opioid antagonist naltrexone, and the serotonin inhibitor sertraline. These drugs can be used as a stepwise therapeutic approach. The body of evidence for many of these options, however, is not very robust. Patients who do not respond to medical therapy can be candidates for interventional measures, such as albumin dialysis, plasmapheresis, or nasobiliary drainage, or certain experimental approaches such as UVB phototherapy. Research over the past decade has elucidated many of the receptors and neuropeptides involved in itch sensation and transmission; it is hoped that in the future this will lead to the development of novel antipruritic medication for cholestatic itch.
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Previous studies suggest that selective serotonin reuptake inhibitors (SSRIs) are effective when used alone in the treatment of unipolar depression with psychotic features. The purpose of the present study was to examine the response to sertraline for patients with and without psychotic features using standard criteria such as recovery and remission.
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We proposed to assess the oxidant/antioxidant status, lipid peroxidation and nitric oxide (NO) in untreated fibromyalgia (FM) patients and controls. The effect of amitriptyline (A, 20 mg daily) and sertraline (S, 100 mg daily) treatment on patients' superoxide dismutase (SOD), xanthine oxidase (XO), adenosine deaminase (ADA) enzyme activities, thiobarbituric acid reactive substances (TBARS) and NO levels was investigated. Thirty female patients with primary FM and age-matched 16 healthy female controls were included. Patients received an 8-week course of treatment with either A or S. FM patients had higher serum levels of TBARS (particularly malondialdehyde) and lower levels of nitrite compared to controls whereas enzyme activities were similar. A and S significantly improved Fibromyalgia Impact Questionnaire (FIQ) pain scores, Hamilton anxiety and depression rating scales. But neither A nor S had significant effects on measured oxidative stress parameters, except SOD activity that was significantly reduced after S treatment. Total myalgic scores negatively correlated with XO activity, and depression scales negatively correlated with levels of TBARS. Our results indicate that patients with FM are under oxidative stress. These findings represent a rationale for further research assessing the effect of free radical scavengers or antioxidant agents like vitamins and omega-3 fatty acids on peripheral and central mechanisms in FM.
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The effects of embryonic and larval exposure to environmentally relevant (ng/L) concentrations of common antidepressants, fluoxetine, sertraline, venlafaxine, and bupropion (singularly and in mixture) on C-start escape behavior were evaluated in fathead minnows (Pimephales promelas). Embryos (postfertilization until hatching) were exposed for 5 d and, after hatching, were allowed to grow in control well water until 12 d old. Similarly, posthatch fathead minnows were exposed for 12 d to these compounds. High-speed (1,000 frames/s) video recordings of escape behavior were collected and transferred to National Institutes of Health Image for frame-by-frame analysis of latency periods, escape velocities, and total escape response (combination of latency period and escape velocity). When tested 12 d posthatch, fluoxetine and venlafaxine adversely affected C-start performance of larvae exposed as embryos. Conversely, larvae exposed for 12 d posthatch did not exhibit altered escape responses when exposed to fluoxetine but were affected by venlafaxine and bupropion exposure. Mixtures of these four antidepressant pharmaceuticals slowed predator avoidance behaviors in larval fathead minnows regardless of the exposure window. The direct impact of reduced C-start performance on survival and, ultimately, reproductive fitness provides an avenue to assess the ecological relevance of exposure in an assay of relatively short duration.
Driving a car is vital for the functional autonomy of patients to take part in activities of daily living. Both psychopathologic symptoms and psychopharmacologic treatment may impair driving ability. This article provides a systematic review of published studies (1980-2011) on commonly prescribed newer antidepressants and driving performance. A total of 21 studies could be included in the review, indicating that there is a lack of controlled patient studies. Investigations on newer antidepressants were frequently undertaken in healthy subjects focusing on acute or subchronic effects of application, predominately in young male participants, with dosages usually given in an ambulatory setting. No data, according to selection criteria, were found with respect to agomelatine, duloxetine, bupropion and viloxazine. There is evidence that the SSRIs (citalopram, escitalopram, fluoxetine, fluvoxamine, sertraline, paroxetine) and the SNRI venlafaxine have no deleterious effects on driving ability. Acute use of mirtazapine does produce impairments that diminish to some degree when given as a nocturnal dose and cannot be seen after repeated dosing in healthy controls. Patients obviously benefit from treatment with newer antidepressants; however, at least a subgroup does not reach performance level of healthy subjects. More patient studies are needed that elaborate specific relationships between clinical subtypes of the illness and response to different antidepressants, considering course and duration of illness, co-morbidities and not least neuropsychological and neurobiological characteristics.
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After the end of a 3-month course of 200 mg/day sertraline, the subjects were interviewed at several time points about their alcohol drinking, if any, using the timeline follow-back method. For 90% of the original study group, mixed effects and generalized estimating equation models were used to compare monthly drinking amounts over a 6-month posttreatment period with drinking amounts in the last month of treatment.
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The Children's Yale-Brown Obsessive Compulsive Scale (CY-BOCS), the National Institute of Mental Health Global Obsessive Compulsive Scale (NIMH GOCS), and the NIMH Clinical Global Impressions of Severity of Illness (CGI-S) and Improvement (CGI-I) rating scales.
Acute estradiol treatment was reported to slow the clearance of serotonin via activation of estrogen receptors (ER)β and/or GPR30 and to block the ability of a selective serotonin reuptake inhibitor (SSRI) to slow serotonin clearance via activation of ERα. In this study, the behavioral consequences of longer-term treatments with estradiol or ER subtype-selective agonists and/or an SSRI were examined in the forced swim test (FST). Ovariectomized rats were administered the following for 2 weeks: estradiol, ERβ agonist (diarylpropionitrile, DPN), GPR30 agonist (G1), ERα agonist (PPT), and/or the SSRI sertraline. Similar to sertraline, longer-term treatment with estradiol, DPN or G1 induced an antidepressant-like effect. By contrast, PPT did not, even though it blocked the antidepressant-like effect of sertraline. Uterus weights, used as a peripheral measure of estrogenic activity, were increased by estradiol and PPT but not DPN or G1 treatment. A second part of this study investigated, using Western blot analyses in homogenates from hippocampus, whether these behavioral effects are accompanied by changes in the activation of specific signaling pathways and/or TrkB. Estradiol and G1 increased phosphorylation of Akt, ERK and TrkB. These effects were similar to those obtained after treatment with sertraline. Treatment with DPN increased phosphorylation of ERK and TrkB, but it did not alter that of Akt. Treatment with PPT increased phosphorylation of Akt and ERK without altering that of TrkB. In conclusion, activation of at least TrkB and possibly ERK may be involved in the antidepressant-like effect of estradiol, ERβ and GPR30 agonists whereas Akt activation may not be necessary.
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After 12 weeks of acute phase treatment in a double-blind, randomized, parallel-group, multi-center trial of sertraline or imipramine, patients with chronic depression (> or = 2 years in major depression, or major depression superimposed on dysthymia) continued study drug for 16 weeks. Initially, 635 patients were randomized to sertraline or imipramine in a 2:1 ratio. Nonresponders after 12 weeks entered a 12-week double-blind crossover trial of the alternate medication. Entry into continuation treatment required at least a satisfactory response (partial remission) to initial or crossover treatment.
This population-based, descriptive study of insured patients (N=54,107) identified people who were 18 years or older, had a claim for MDD, had at least one prescription for an antidepressant medication in 2013, and had continuous insurance coverage during the study period. Prescription claims were evaluated to determine the most commonly prescribed antidepressant medication and most common dose.
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The second-generation antidepressants include selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), and other compounds with different mechanisms of action. All second-generation antidepressants are metabolized in the liver by the cytochrome P450 (CYP) enzyme system. Concomitant intake of inhibitors or inducers of the CYP isozymes involved in the biotransformation of specific antidepressants may alter plasma concentrations of these agents, although this effect is unlikely to be associated with clinically relevant interactions. Rather, concern about drug interactions with second-generation antidepressants is based on their in vitro potential to inhibit > or = 1 CYP isozyme.
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ClinicalTrials.gov identifier: NCT00056472.
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To evaluate this, the single prolonged stress (SPS) model was used in the present study. The SPS rats were administered by AF (at doses of 3.5, 7 and 14.0mg/kg, i.g.) after induction of SPS from days 2-13. After the exposure to SPS, behavioral assessments were conducted, including contextual fear paradigm (CFP), elevated plus-maze test (EPMT), open-field test (OFT). The rats were decapitated at the end of the behavioral tests and levels of allopregnanolone in prefrontal cortex, hippocampus and amygdala were measured by enzyme linked immunosorbent assay (ELISA).