UMLS:C0011570 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This open-label multicentre semi-naturalistic study in Finland assessed the impact of educational information on efficacy of 16-week treatment with escitalopram (5-20 mg/day) in a patient population suffering from depression. Patients were randomized single blind to receive educational information (n=79) or no information (n=78) in addition to open-label escitalopram treatment. Patients were assessed using the Montgomery-Asberg Depression Rating Scale (MADRS), Clinical Global Impression - Severity and - Improvement (CGI-S and CGI-I), Patient Global Evaluation (PGE), and Hopkins Symptom Checklist (SCL-90) scales. Tolerability was assessed by the incidence of adverse events (AEs). A total of 132 (84%) out of 157 patients completed the study, with similar completer rates in both groups. There was no statistically significant effect of educational information on the efficacy of escitalopram treatment, as measured by MADRS, CGI and PGE. Mean MADRS total score was 25.3 at baseline, corresponding to moderate to severe depression, and decreased to 7.9 at the end of the treatment for both groups. The response rate (> or = 50% reduction in MADRS total score from baseline) was 80% at the end of treatment for both groups. The clinical relevance of the improvement was seen in CGI-I and PGE scores and there was a strong correlation between the two scales, indicating agreement by both patients and investigators. AEs were mostly mild and transient and 11 patients (7.0%) dropped out of the study due to AEs, with similar incidence in both groups. Escitalopram was effective and well tolerated in the treatment of depression over a 16-week period in a semi-naturalistic setting, and an additional effect of educational information could not be shown, possibly due to the high response to treatment.
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PMID:The influence of educational information on depressed outpatients treated with escitalopram: a semi-naturalistic study. 1745 25

Escitalopram, the active (S)-enantiomer of citalopram, has been approved in many countries throughout the world for the treatment of depression and anxiety disorders. It is more potent and selective than citalopram in inhibiting serotonin re-uptake in the CNS, and less potent than various other selective serotonin re-uptake inhibitors in relation to other transporter proteins and receptors: in particular, it is six times less potent than citalopram in binding to the histamine H1 and muscarinic receptors. Escitalopram has favourable pharmacokinetics: it is rapidly absorbed, has a bioavailability of 80% and is not affected by food intake. It has little potential for drug interactions: it has low protein binding and, as it is metabolised by three CYP isozymes, any impairment in the activity of one is unlikely to have a significant effect on metabolic clearance. Caution is necessary only when it is coadministered with drugs metabolised by CYP2D6, such as metoprolol, or administered to the elderly or patients with severe hepatic or renal impairment. The multiple-dose pharmacokinetics of oral escitalopram are proportional at a range of doses including its therapeutic doses. Escitalopram is approved for the treatment of a number of anxiety disorders. It seems to be well tolerated and induces few or no discontinuation symptoms, and may be considered a first-line agent for the pharmacotherapy of obsessive-compulsive disorder, generalised anxiety disorder, panic disorder and social phobia. Further studies are needed to define its activity in impulse control disorders.
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PMID:The use of escitalopram beyond major depression: pharmacological aspects, efficacy and tolerability in anxiety disorders. 1791 59

Despite the prevalence of multisomatoform disorder (MSD), there are few controlled trials of its pharmacotherapy. The aim of this study was to compare the efficacy and safety of escitalopram (10-20 mg/day) with that of placebo in treating patients with MSD over a 12-week period. Fifty-one outpatients aged from 18 to 65 years, with multiple medically unexplained symptoms, were recruited. The primary efficacy measure was a change on the Patient Health Questionnaire-15 scores from baseline to endpoint. Secondary efficacy endpoints included the Clinical Global Impression-Improvement score, the psychic and somatic subscales of the Hamilton Anxiety Scale, Montgomery-Asberg Depression Rating Scale, the Visual Analogue Pain Rating Scale, the Scale for the Assessment of Illness Behaviour and the Sheehan Disability Scale. On the primary analysis of covariance, escitalopram-treated patients had significantly greater reductions in Patient Health Questionnaire scores (P<0.0001) compared with placebo at week 12. Significant separation from placebo occurred from week 6 onwards. Escitalopram was superior to placebo on all secondary outcome endpoints, with the exception of the Scale for the Assessment of Illness Behaviour. The medication was well tolerated. In conclusion, in this 12-week, randomized, placebo-controlled study, escitalopram (10-20 mg/day) was both effective and well tolerated in the treatment of patients with MSD. Compared with placebo, escitalopram was associated with lower symptom scores, increased response and remission rates, and improved functioning.
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PMID:Escitalopram in the treatment of multisomatoform disorder: a double-blind, placebo-controlled trial. 1809 May 7

To evaluate the tolerability and response to escitalopram in Indian patients with major depression, over an 8-week open-label multicentric study was carried out among 18-65 years old Indian patients suffering from DSM IV major depressive disorder with Montgomery-Asberg depression rating scale (MADRS) total score> or =22. Patients received a fixed dose of escitalopram 10 mg daily for 2 weeks, followed by flexible dose of 10 to 20 mg daily for 6 weeks. Patients were evaluated for depression and rated on MADRS score and clinical global impressions-severity (CGI-S) and--improvement (CGI-I) scores. They were monitored for treatment-emergent adverse effects. A total of 119 patients were enrolled and 103 completed the trial. There was a decrease from baseline in the MADRS total score after one week of treatment continuing until 8 weeks. By week 8, 76.9% patients had responded to treatment (> or =50% or more reduction of MADRS total score). A similar pattern of improvement to that seen with the MADRS total score was seen with CGI-S and CGI-I scores. Escitalopram was well tolerated, with only 2 patients (1.7%) withdrawing from the study due to adverse events. There were no serious adverse events.
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PMID:An open-label multicentric study of the tolerability and response to escitalopram treatment in Indian patients with major depressive disorder. 1817 88

Escitalopram is the S-enantiomer of the selective serotonin reuptake inhibitor (SSRI) citalopram, which contains equal amounts of the S- and R-forms in a racemic mixture. Escitalopram is the most selective SSRI, with almost no significant affinity to other tested receptors. It has been demonstrated that it is escitalopram that carries the therapeutic potential of citalopram, and has statistically superior and clinically relevant properties compared with citalopram. Escitalopram is at least as effective in the treatment of depression and anxiety as other SSRIs, as well as venlafaxine, bupropion and duloxetine. Owing to multiple metabolic degrading pathways, the clinically relevant interactions of escitalopram with other drugs are minimal. Compared with other antidepressants, escitalopram is generally better tolerated, its onset of action is relatively fast, and its use may have cost-effectiveness and cost-utility advantages. Escitalopram is an effective first-line option in the management of patients with major depression, including severe forms, and various anxiety disorders.
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PMID:Escitalopram for the treatment of major depression and anxiety disorders. 1841 57

Recent studies have implicated brain-derived neurotrophic factor (BDNF) in the pathophysiology of depression and the activity of antidepressant drugs. Serum BDNF levels are lower in depressed patients, and increase in response to antidepressant medication. However, how BDNF responds to different classes of antidepressant drugs is unknown. We assessed serum BDNF levels in 21 patients with major depressive episode treated with sertraline, escitalopram, or venlafaxine and 20 healthy controls. Serum samples were collected between 10 a.m. and 12 p.m. at baseline, 5 weeks, and 6 months of treatment. BDNF levels were measured via immunoassay. The severity of symptoms and response to treatment were assessed by the Hamilton rating scales for depression (HRSD). Baseline serum BDNF levels were significantly lower in depressed patients compared to controls. Sertraline increased BDNF levels after 5 weeks and 6 months of treatment. Venlafaxine increased BDNF levels only after 6 months. Escitalopram did not affect BDNF levels at either time point. A significant negative association was found between percentage increase in BDNF levels and percentage decreased in HRSD scores after 6 months of treatment. In conclusion, these results suggest that different antidepressant drugs have variable effects on serum BDNF levels. This is true even though the three different drugs were equally effective in relieving symptoms of depression and anxiety.
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PMID:Changes in BDNF serum levels in patients with major depression disorder (MDD) after 6 months treatment with sertraline, escitalopram, or venlafaxine. 1851 Oct 76

Although antidepressant medications are effective in about 50-70% of patients with major depressive disorder (MDD), they have a delayed onset of therapeutic effect. This latency is one of the current major limitations of these medications, in that it prolongs the impairments associated with depression, leaves patients vulnerable to an increased risk of suicide, increases the likelihood that a patient will prematurely discontinue therapy, and increases medical costs associated with severe depression. It is becoming increasingly clear that differences may exist between antidepressants and some evidence suggests that some antidepressant agents may begin to work faster than others. Escitalopram, duloxetine, venlafaxine, and mirtazapine have shown statistically significant differences in some measures of antidepressant action within the first two weeks of treatment, both in placebo-controlled trials and in head-to-head comparisons with other antidepressants. Results of the current review should be regarded with certain important limitations in mind. First, differences in times to onset of antidepressant response have been shown in clinical efficacy studies not specifically designed to detect differences in onset of action (post-hoc analysis). Second, results observed in 'pure' clinical trial samples should not be directly generalized to the real clinical practice since it has been proven in clinical settings that less than one in seven depressed patients would be eligible to participate in antidepressant clinical trials. For instance, depressed patients who are suicidal or who score higher than 30 on the 17-item HAM-D are excluded from antidepressant clinical trials. Third, caution is warranted when applying these findings to clinical populations with more severe depressions with respect to the fact that among clinical populations, severity of depression coincides with comorbidity, including such psychiatric disorders as anxiety disorders, personality disorders and substance abuse. In addition, the magnitudes of the size-effects of antidepressants versus placebo are clearly higher in severely depressed patients. Fourth, specific items on depression rating scales may induce greater antidepressant/placebo differences. For instance, the 17-item HAM-D contains three questions pertaining to sleep. It questions the fact that earlier onset may appear not only via a specific antidepressant effect but also via a non-specific effect on anxiety, sleep, physical pain or other accessory symptoms. Thus, current data do not clearly support claims that one drug reduces the symptoms of depression faster than another, though the existing literature suggests that escitalopram displays some superiority in terms of rapidity of action. Given the potential benefits of early-acting antidepressant treatments, the possibility of superior speed of onset of escitalopram presented here merits further study in adequately designed, prospective clinical trials. A definitive demonstration of early onset of action awaits the results of appropriately designed and powered clinical studies, which may include (1) a prospective definition of early onset of action, (2) more focused assessments of core emotional symptoms and cognitive deficits of depression by using specific and sensitive tools, (3) a data-analytic approach capable of capturing the dynamic nature of symptomatic change (for example, survival analysis), and (4) strategies to minimize biases and heterogeneity of response.
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PMID:[Antidepressants and their onset of action: a major clinical, methodological and pronostical issue]. 1851 54

Pooled analyses have shown that escitalopram has superior effectiveness versus all comparators, including selective serotonin reuptake inhibitors and venlafaxine. Recent studies have compared escitalopram with duloxetine. Data from two randomized, double-blind studies that compared escitalopram (10-20 mg/day) and duloxetine (60 mg/day) were pooled and analysed for all patients and for the subsample of severely depressed patients [baseline Montgomery-Asberg Depression Rating Scale (MADRS) score > or =30]. Escitalopram (n=280) was superior to duloxetine (n=284) with respect to mean change from baseline in MADRS score at weeks 1, 2, 4 and 8 with a mean treatment difference at week 8 of 2.6 points (P<0.01). Similar results were seen for severely depressed patients, with a mean treatment difference of 3.7 points (P<0.01). Response and remission rates at week 8 were significantly higher for patients treated with escitalopram [response 67.1% for escitalopram compared with 53.2% for duloxetine, P<0.001; remission (MADRS< or =12) 54.3% for escitalopram compared with 44.4% for duloxetine, P<0.05]. The numbers needed to treat based on response and remission rates, in favour of escitalopram, were 8 and 11, respectively, for all patients (6 and 7, respectively, for severely depressed patients). Significantly fewer (P<0.001) patients (all cause and owing to adverse events) withdrew from the escitalopram group. This pooled analysis shows that over an 8-week treatment period, escitalopram (10-20 mg/day) is superior in both effectiveness and tolerability compared with duloxetine (60 mg/day).
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PMID:Escitalopram and duloxetine in the treatment of major depressive disorder: a pooled analysis of two trials. 1854 55

Escitalopram has shown some different pharmacologic properties compared to its racemic molecule, citalopram. When comparing with venlafaxine, similar efficacy of this drug was observed, notably when considering the frequency of responders [50% of decrease on the Montgomery and Asberg Depression rating Scale (MADRS)] and the frequency of remitters (MADRS<12), even when the doses of both drugs were increased up to 20 mg per day for escitalopram and 225 mg per day for venlafaxine. In addition, a recent study conducted by Jonas et al. (2006) [Jonas J, Bose A, Alexopoulos G, et al. Double blind comparison of escitalopram and duloxetine in the acute treatment of Major Depressive Disorder 45th Annual Meeting of the American College of Neuropsychopharmacology December 2006] suggested a better efficacy of escitalopram in comparison to duloxetine. When considering severe major depressive episodes, the efficacy of escitalopram compared to noradrenalin and serotonin reuptake inhibitors (NaSRI) could be superior, with a more important rate of remitters in the escitalopram group. Regarding the tolerance of both types of drugs, the percentage of patients who withdrew the drug for side-effects would be higher in patients on venlafaxine. This increase in frequency of side-effects has been observed in different studies conducted with venlafaxine and duloxetine. All these data highlight the advantages of escitalopram in the treatment of major depressive episodes and escitalopram has, therefore, obtained marketing approval in France with some specific mentions in favour of this drug.
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PMID:[Escitalopram versus serotonin reuptake inhibitors]. 1855 50

Despite limited understanding of the pathophysiology of depression and the underlying mechanisms mediating antidepressant effects, there are several efficient treatments. The anhedonia symptoms of depression are characterized by decreased motivation and drive and imply possible malfunctioning of the mesolimbic dopamine system, whereas cognitive deficits might reflect decreased plasticity in hippocampus. In female Flinders Sensitive Line (FSL) rats, a model of depression, we compared the effects of three long-term antidepressant treatments: voluntary running, escitalopram and the combination of both on antidepressant-like behaviour in the Porsolt swim test (PST), and on regulation of mRNA for dopamine and neuropeptides in striatal dopamine pathways and brain-derived neurotrophic factor (BDNF) in hippocampus. Escitalopram diet attenuated running behaviour in FSL rats but not in non-depressed controls rats. In the PST the running group had increased climbing activity (noradrenergic/dopaminergic response), whereas the combination of escitalopram and running-wheel access increased swimming (serotonergic response). Running elevated mRNA for dynorphin in caudate putamen and BDNF in hippocampus. The combined treatment down-regulated D1 receptor and enkephalin mRNA in accumbens. Escitalopram alone did not affect behaviour or mRNA levels. We demonstrate a novel behavioural effect of escitalopram, i.e. attenuation of running in 'depressed' rats. The antidepressant-like effect of escitalopram was dependent on the presence of a running wheel, but not actual running indicating that the environment influenced the antidepressant effect of escitalopram. Different patterns of mRNA changes in hippocampus and brain reward pathways and responses in the PST by running and escitalopram suggest that antidepressant-like responses by running and escitalopram are achieved by different mechanisms.
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PMID:Housing conditions modulate escitalopram effects on antidepressive-like behaviour and brain neurochemistry. 1857 Jul 3

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