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As many as 45% of patients with major depression also meet diagnostic criteria for bipolar (BP) II disorder. Although the use of a concurrent mood-stabilizing drug has been suggested in treating BP II depression, antidepressant monotherapy has received less attention. The efficacy and safety of venlafaxine were examined in 17 BP II (mean+/-SD; age, 41+/-14 years) versus 31 unipolar (UP) (45+/-14 years) patients with major depression. Minimum pretreatment Hamilton Rating Scale for Depression (HAM-D21) score was > or = 20. After a 1-week placebo lead-in, patients were randomly assigned to receive double-blind treatment with once- versus twice-daily venlafaxine dosing starting at 37.5 mg daily and increasing up to 225 mg daily. Patients were evaluated weekly for efficacy using the HAM-D21, the Montgomery-Asberg Depression Rating Scale (MADRS), and the Clinical Global Impression (CGI) Scale. We observed a similar overall efficacy in BP and UP patients by 6 weeks of treatment (p = not significant). However, we also observed a more rapid reduction of HAM-D21 (p < 0.03) and MADRS (p < 0.02) scores by week 2 of treatment in BP patients who completed the entire trial. No episodes of venlafaxine-induced "manic switch" were observed in either patient group. In conclusion, our preliminary findings suggest that short-term, 6-week venlafaxine treatment may be a safe and effective antidepressant monotherapy for BP II major depression.
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In the overall population (placebo: n=1,116; desvenlafaxine: n=1,834), adverse events resulted in discontinuations in 3% of placebo-treated patients and 12% of desvenlafaxine-treated patients; in the subset of fixed-dose studies, the rates were 4% with placebo and increased with desvenlafaxine dose (50 mg/day: 4%; 400 mg/day: 18%). The most common treatment-emergent adverse event was transient nausea that was generally mild to moderate. The most common sexual dysfunction associated with desvenlafaxine treatment was erectile dysfunction in men (7% vs 1% with placebo) and anorgasmia in women (1% and 0%). One desvenlafaxine-treated patient died of a completed suicide; there were four suicide attempts (three desvenlafaxine, one placebo) and eight cases of suicidal ideation (five desvenlafaxine, three placebo) during the on-therapy period. Small but statistically significant changes in mean blood pressure occurred at all desvenlafaxine doses; clinically meaningful changes were observed in 1% of placebo-treated patients and 2% of desvenlafaxine-treated patients. Desvenlafaxine was associated with small but statistically significant mean changes in laboratory assessments, particularly lipid and liver enzyme elevations, and electrocardiograms; few cases of these changes were clinically relevant.
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Venlafaxine provided significantly greater improvement in the MADRS scores after 4 days and in the HAM-D scores after 1 week than did placebo. Response rate (based on a 50% decrease in MADRS scores) was 65% (30 of 46 patients) for venlafaxine and 28% (13 of 47 patients) for placebo. Significantly more placebo-treated patients (40%; N = 19) than venlafaxine-treated patients (9%; N = 4) discontinued treatment early because of lack of efficacy. Nausea and sweating were the most common events, occurring at a significantly higher rate in the venlafaxine group.
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Fluoxetine and venlafaxine decreased suicidal thoughts and behavior for adult and geriatric patients. This protective effect is mediated by decreases in depressive symptoms with treatment. For youths, no significant effects of treatment on suicidal thoughts and behavior were found, although depression responded to treatment. No evidence of increased suicide risk was observed in youths receiving active medication. To our knowledge, this is the first research synthesis of suicidal thoughts and behavior in depressed patients treated with antidepressants that examined the mediating role of depressive symptoms using complete longitudinal person-level data from a large set of published and unpublished studies.
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Twelve women provided hair samples of which nine samples were long enough to analyze the first and third trimesters along with the postpartum period. Citalopram, venlafaxine, fluoxetine and sertraline were the antidepressants studied. In the citalopram group, a statistically significant difference existed between the citalopram:norcitalopram ratio when the first trimester was compared to the postpartum period (0.89+/-0.26 versus 1.4+/-0.24 respectively, p=0.022). A statistically significant difference also existed between the third trimester and the postpartum period for the citalopram group (0.9+/-0.14 and 1.4+/-0.24 respectively, p=0.048). No other statistically significant differences were found.
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With the addition of the latest antidepressant medications, the clinician may now choose antidepressants with little liability for drug-drug interactions. Venlafaxine and mirtazapine are associated with a lower risk of clinically significant drug interactions than SSRIs. Nefazodone is a potent inhibitor of CYP3A4 and therefore may not be suitable for all patient populations. It is, however, a much weaker CYP2D6 inhibitor than the SSRIs. More studies are needed to assess more accurately and precisely the risk of such untoward drug-drug interactions with these novel antidepressants, particularly in more diverse ethnic patient populations.
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These results indicate that the co-administration of 5-HT2 receptor agonists with paroxetine and venlafaxine may provide a powerful tool for enhancing the clinical efficacy of these antidepressants.
The relationship between Panic Disorder (PD) and dissociation is well known. In this study we aimed to investigate whether or not dissociative experiences affect the response to PD drug treatment. For this purpose, standart dose of venlafaxine was preferred for treatment. 63 patients with PD were included in the study. Venlafaxine treatment with increasing dose was administered to each patient during a 10-week period. The Panic Disorder Severity Scale (PDSS) and the Dissociation Questionnaire (DIS-Q) were applied to the patients at the beginning of the study. Patients were divided into two groups based on DIS-Q scores. PDSS was applied again to both groups at the end of 10-week treatment. No difference between sociodemographic data and PDSS scores of two groups - patients with low DIS-Q scores (<2.5) and high DIS-Q scores (>2.5) - was found at the beginning. At the end of the study, a significant decrease in PDSS scores measured in both groups was detected. However, the decrease in PDSS score for the group with lower DIS-Q score was at a higher percentage (z=-3.822, p=0.0001). These results depict that dissociative symptoms accompanying PD affect psychopharmacological treatment in a negative way. Reevaluation of dissociative symptoms at the beginning and end of treatment would help in planning personal therapy.
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Venlafaxine proved to be very efficient, well tolerated and safe in the treatment of depression occurring after cerebrovascular incidents to the subjects in this study.
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To determine the feasibility and safety of aripiprazole augmentation for incomplete response to sequential selective serotonin reuptake inhibitor (SSRI) and serotonin-norepinephrine reuptake inhibitor (SNRI) pharmacotherapy in late-life depression.
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The study aimed to evaluate the clinical response to venlafaxine in social phobia in 12 patients who were non-responders to selective serotonin reuptake inhibitors, and to assess how the response could be influenced by the comorbidity in Axis II with avoidant personality disorder (APD). The duration of the study was of 15 weeks using open flexible doses regimen in individuals with or without concomitant APD. The venlafaxine dose ranged from 112.5 mg/day to 187.5 mg/day. Venlafaxine improves social phobia and/or APD symptomatology, as demonstrated by decreasing Liebowitz Social Anxiety Scale total scores (P < 0.05). In fact, venlafaxine significantly reduced the avoidant behaviour and specific sociophobic aspects, while notably improving the depression dimension and the basic anxiety symptoms. With regard to tolerability, the profile of venlafaxine was satisfactory with the main side-effects being nausea, headache and anxiety.
All clinical trials that were available prior to submission for publication were reviewed. Preliminary trials and unpublished reports were not reviewed.
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Studies have been conducted for six antidepressants: fluoxetine, sertraline, paroxetine, moclobemide, venlafaxine, and nefazodone, using the technique of prescription-event monitoring. Patients were identified using incident dispensed prescription data. Questionnaires were sent to patients' general practitioners six months after the date of first prescription. Questionnaires asked for date of birth, sex, indication for prescribing each drug, and all events entered in the patients' records after the date of first prescription.
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We studied the efficacy of venlafaxine in treatment-resistant depressions of the borderline level. Thirty patients, aged from 23 to 63 years, with non-psychotic depressions were examined. Due to the absence of the effect of the previous treatment, they were treated with venlafaxine in dosage 75-150 mg/day during 35 weeks. The positive response was seen in 19 (63,7%) patients. The drug was well-tolerated.
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We identified 15,441 single-agent exposures. Seizures occurred in 313 cases. The most prevalent pharmaceuticals were mefenamic acid (51 of the 313 cases), citalopram (34), trimipramine (27), venlafaxine (23), tramadol (15), diphenhydramine (14), amitriptyline (12), carbamazepine (11), maprotiline (10), and quetiapine (10). Antidepressants were involved in 136 cases. Drugs with a high seizure potential were bupropion (31.6%, seizures in 6 of 19 cases, 95% CI: 15.4-50.0%), maprotiline (17.5%, 10/57, 95% CI: 9.8-29.4%), venlafaxine (13.7%, 23/168, 95% CI: 9.3-19.7%), citalopram (13.1%, 34/259, 95% CI: 9.5-17.8%), and mefenamic acid (10.9%, 51/470, 95% CI: 8.4-14.0%). In adolescents (15-19y/o) 23.9% (95% CI: 17.6-31.7%) of the cases involving mefenamic acid resulted in seizures, but only 5.7% (95% CI: 3.3-9.7%) in adults (≥ 20y/o; p < 0.001). For citalopram these numbers were 22.0% (95% CI: 12.8-35.2%) and 10.9% (95% CI: 7.1-16.4%), respectively (p = 0.058). The probability of seizures with mefenamic acid, citalopram, trimipramine, and venlafaxine increased as the ingested dose increased.
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The incidence of cardiovascular events did not differ among duloxetine initiators relative to other antidepressant comparators or those with untreated depression but was higher than those without depression, suggesting that depression itself (or associated morbidities) may affect the risk of cardiovascular events.
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In a randomized double-blind study, we compared six patients who received venlafaxine along with their usual treatment (zuclopenthixol and/or clonazepam) with seven patients who received placebo plus usual care. Irritability, hyperactivity/noncompliance, and overall clinical improvement were measured after 2 and 8 weeks, using validated clinical scales.
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All 81 patients from a 12-week double-blind randomized controlled trial (RCT) comparing venlafaxine with nortriptyline were asked to participate in a 3 year follow-up study. Thirty-two patients who did not achieve remission during the RCT, entered an open sequential treatment protocol and were treated with augmentation with lithium, switch to a monoamine oxidase inhibitor or ECT.
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Thirty-six OCD patients (based on DSM-IV criteria) who had not responded to at least 1 adequate SRI trial conducted in our outpatient clinic were treated from January 2000 through April 2004 with CBT, incorporating exposure and ritual prevention. The therapy was conducted in a naturalistic setting and manualized guidelines were adapted to each patient. Pharmacologic treatment underwent no changes during the trial period. Outcome measures included the Yale-Brown Obsessive Compulsive Scale, the Clinical Global Impressions-Severity of Illness scale, and the Global Assessment of Functioning scale. The primary outcome measure was a rating of "much improved" or "very much improved" on the Clinical Global Impressions-Improvement scale (CGI-I).
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Interindividual differences in the pharmacokinetics of venlafaxine, a new antidepressant, were shown during early clinical trials in Japan. Venlafaxine is metabolized mainly by CYP2D6 to an active metabolite, O-desmethylvenlafaxine (ODV). Therefore, the influence of the CYP2D6 genotypes on venlafaxine pharmacokinetics was examined in a Japanese population.
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There is a need to identify clinically useful biomarkers in major depressive disorder (MDD). In this context the functional connectivity of the orbitofrontal cortex (OFC) to other areas of the affect regulation circuit is of interest. The aim of this study was to identify neural changes during antidepressant treatment and correlates associated with the treatment outcome. In an exploratory analysis it was investigated whether functional connectivity measures moderated a response to mirtazapine and venlafaxine. Twenty-three drug-free patients with MDD were recruited from the Department of Psychiatry and Psychotherapy of the Ludwig-Maximilians University in Munich. The patients were subjected to a 4-wk randomized clinical trial with two common antidepressants, venlafaxine or mirtazapine. Functional connectivity of the OFC, derived from functional magnetic resonance imaging with an emotional face-matching task, was measured before and after the trial. Higher OFC connectivity with the left motor areas and the OFC regions prior to the trial characterized responders (p<0.05, false discovery rate). The treatment non-responders were characterized by higher OFC-cerebellum connectivity. The strength of response was positively correlated with functional coupling between left OFC and the caudate nuclei and thalami. Differences in longitudinal changes were detected between venlafaxine and mirtazapine treatment in the motor areas, cerebellum, cingulate gyrus and angular gyrus. These results indicate that OFC functional connectivity might be useful as a marker for therapy response to mirtazapine and venlafaxine and to reconstruct the differences in their mechanism of action.
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Tramadol (Ultram, Ultracet) is a centrally acting synthetic opioid with analgesic efficacy comparable to codeine. Antinociception is attributed to low but effective affinity for the mu-opioid receptor (μ), as well as reuptake inhibition of the monoamines norepinephrine (NE) and serotonin (5HT). Dual action antidepressants mirtazapine (Remeron), duloxetine (Cymbalta), and most notably venlafaxine (Effexor), which tramadol is closely related to in structure, also inhibit NE and 5HT reuptake. These medications are proven effective antidepressants and this shared monoaminergic action resulted in the research of tramadol as a potential treatment for depression. The present article intends to substantiate the use of tramadol in this manner by analyzing several decades of research which is presented as an illustration of neuronal theories, as well as lab work and case studies of both the supporting ideas and potential hazards. Finally, the article promotes the benefits of acute action in comparison to modern antidepressants and the documentation of low abuse rates while maintaining an object view of the risks, most notably, the risk for addiction from agonist action on μ-receptors.
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Eighteen patients with major depression and 25 healthy controls underwent a lumbar puncture; CSF samples were withdrawn and assayed for IL-1, IL-6, TNFα, BDNF, and NPY levels. Patients with depression were then entered into an 8-week treatment protocol and had repeated lumbar puncture procedures post-treatment.