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)

Escitalopram is the recently marketed S-enantiomer of the widely used antidepressant citalopram. Data from intentional overexposure to this medication are limited. Twelve-lead electrocardiogram (ECG) effects from racemic citalopram have been described; however, the present report is the first, to the best of the authors' knowledge, that describes all the reported abnormalities in a single patient receiving escitalopram. A 52-year-old man with a history of depression treated with escitalopram 10 mg/day, extended-release morphine 30 mg/day and zopiclone 15 mg/day was found unconscious at his home. He was known to have attempted suicide three weeks previously. Partially emptied bottles of escitalopram, morphine, oxycodone, zopiclone, lorazepam and diazepam were found close to the patient. He was transferred to the emergency department, where airway management and other supportive care were initiated. The patient was transferred to the intensive care unit. The initial 12-lead ECG demonstrated junctional rhythm at 48 beats/min, a wide complex escape (145 ms) with right bundle branch morphology and a prolonged corrected QT interval at 650 ms. Cardiac monitoring was undertaken. No ventricular arrhythmias or torsade de pointes were detected. No specific treatment for shortening the QT was implemented. Another 12-lead ECG performed 48 h later demonstrated sinus tachycardia with a normal corrected QT, normal PR interval and normal QRS duration. The effects of the overdose of escitalopram on the ECG and its interactions with other drugs are reviewed.
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PMID:Corrected QT interval prolongation after an overdose of escitalopram, morphine, oxycodone, zopiclone and benzodiazepines. 1861 5

Clinical studies indicate that addition of bupropion to selective serotonin (5-HT) reuptake inhibitors (SSRIs) provides incremental benefit over SSRI monotherapy in depression. This study was designed to investigate the effects of co-administration of bupropion with escitalopram on the firing rate of 5-HT and norepinephrine (NE) neurons in anesthetized rats. Escitalopram (10 mg/kg/day x 2 days), given via subcutaneously (s.c.) implanted minipumps, decreased the firing of 5-HT and NE neurons by 70% and 55%, respectively. The firing of 5-HT neurons, unlike that of NE neurons, recovered after the 14-day escitalopram regimen. Bupropion, injected once daily (30 mg/kg/day, s.c. x 2 days), did not increase 5-HT firing but decreased that of NE by 55%. After 14 days of repeated bupropion administration, 5-HT firing was increased by 50%, and NE firing was back to baseline. Co-administration of escitalopram and bupropion doubled 5-HT firing after 2 and 14 days, whereas NE neurons were inhibited by 60% after 2 days, but partially recovered after 14 days. The responsiveness of 5-HT(1A) autoreceptors was significantly attenuated in the combination-treated rats after 2 days, indicating an early desensitization. These results provide support for contributions from 5-HT and NE mechanisms for enhanced effectiveness of combination of SSRI and bupropion treatment.
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PMID:Electrophysiological effects of the co-administration of escitalopram and bupropion on rat serotonin and norepinephrine neurons. 1871 44

A decision analytical model was used to compare expected health outcomes and costs of treating patients with major depression using new selective serotonin reuptake inhibitor (SSRI) escitalopram versus the other SSRI fluoxetine and the serotonin norepinephrine reuptake inhibitor (SNRI) venlafaxine. The primary health outcome measure was an overall treatment success, defined as a remission (Montgomery-Asberg Depression Rating Scale (MADRS) < or = 12), achieved over the 6 months of treatment. Estimated costs consisted of those directly related to treatment (drug acquisition costs, costs of psychiatric visits, hospital outpatient visits, hospitalization, and electroconvulsive therapy) and indirect costs associated with productivity lost due to depression. Clinical input parameters for the economic analyses were derived from published literatures. Resource utilization estimates were obtained from a survey of psychiatrists, while medical treatment patterns were determined from focus groups participated consisting from both general and family practitioners and psychiatrists. Unit costs (including daily cost of patient's absence from work due to depression) were obtained from the standard sources. The unit cost of hospitalization was derived based on the average of factual service rates charged by the local hospital. The results show that escitalopram is more effective and less costly compared to fluoxetine and venlafaxine. Treatment using escitalopram produced the best-expected success rate and the lowest expected per patient cost. Escitalopram earned a savings of Baht 2,002 and Baht 1,768 compared to fluoxetine and venlafaxine respectively over a six-month period.
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PMID:The treatment of major depressive disorders (MDD) in Thailand using escitalopram compared to fluoxetine and venlafaxine: a pharmacoeconomic evaluation. 1883 55

Post-hoc pooled analysis of data from two 6-month randomised controlled trials in patients with major depressive disorder (MDD) revealed superior efficacy and tolerability of escitalopram when compared with paroxetine. Escitalopram (n=394) produced a significantly (p<0.01) greater mean treatment difference of 2.0 points in primary endpoints, judged using the Montgomery-Asberg Depression Rating Scale (MADRS) total score, compared with paroxetine (n=383). Significant differences were also observed in Clinical Global Impression (CGI)--severity (escitalopram, 2.1; paroxetine, 2.4; p<0.01) and CGI--improvement (escitalopram, 1.8; paroxetine, 2.0: p<0.01). In the sub-group of severely depressed patients (baseline MADRS> or = 30), escitalopram showed further improved efficacy compared with paroxetine in all scores. This analysis supports previous observations of superior efficacy and tolerability of long-term escitalopram treatment (10 to 20 mg/day) compared with paroxetine (20 to 40 mg/day). Escitalopram is a good therapeutic option for the long-term treatment of MDD, particularly in severely depressed patients.
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PMID:Superiority of escitalopram to paroxetine in the treatment of depression. 1918 67

Obsessive-compulsive disorder (OCD) is a common and severe neuropsychiatric disorder treated by both behavioral and pharmacologic techniques. Despite the availability of treatments for OCD, including the selective serotonin reuptake inhibitors (SSRIs), many OCD patients have an inadequate response to current treatments. As such, additional approaches to the management of OCD are required. A potential but little studied treatment for OCD is the SSRI escitalopram. Escitalopram is the S-enantiomer of citalopram, the preparation containing both S and R enantiomers of citalopram. Not only is escitalopram the most selective of the SSRIs, it is also devoid of R-citalopram, which may interfere with the effects of the S enantiomer. Escitalopram appears to be effective in depression and several anxiety disorders, including social anxiety disorder and generalized anxiety disorder, conditions in which it also appears reasonably well tolerated. Enantiomeric specificity, high serotonin reuptake selectivity, comparatively good tolerability and favorable pharmacokinetics, and preliminary evidence of efficacy in OCD suggest a potential role for the use of escitalopram in the treatment of OCD. Nevertheless, additional work including evaluating the use of escitalopram with behavioral interventions and in long-term treatment of OCD is needed to clarify its overall role in managing OCD.
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PMID:An emerging role for escitalopram in the treatment of obsessive-compulsive disorder. 1930 May 74

Escitalopram (ES-CIT) is a widely used, highly specific antidepressant. Until now there has been very little evidence on how this drug under pathological conditions affects an important feature within the pathophysiology of stress-related disorders such as depression: the endogenous neurotrophins. By using a well-characterized rat model in which chronic stress induces depressive-like behavior, the levels of neurotrophins brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) were determined in representative brain regions and serum using a highly sensitive improved fluorometric two-site ELISA system. There was a significant increase of BDNF in the left and right cortices after stress treatment (twofold increase) that was reversed by application of ES-CIT. An ES-CIT-dependent NGF reduction in stressed rats was detectable in the right cortex only (P = 0.027). The left hippocampus revealed significantly higher amounts of BDNF (2.5-fold increase) protein than the right hippocampus. These interhemispheric differences were unrelated to stress or ES-CIT treatment in all animals. BDNF and NGF of the frontal cortex, cerebellum, and serum did not change between the study groups. There was a negative correlation between body weight and serum BDNF, independent of stress or ES-CIT treatment. In conclusion, BDNF and NGF show substantial changes in this rodent model of chronic social stress, which is susceptible to antidepressant treatment with ES-CIT and therefore may constitute a neurobiological correlate for the disease.
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PMID:Effects of escitalopram on the regulation of brain-derived neurotrophic factor and nerve growth factor protein levels in a rat model of chronic stress. 1936 Sep 2

Severe forms of depression are a major therapeutic concern for psychiatrists. According to Health Authority recommendations, they require the systematic initiation of treatment with active drugs, and they respond less well to placebos than the less severe forms. Escitalopram, which is the most active enanthiomer of the racemic compound (citalopram), is tolerated well at the doses indicated in the marketing authorisation (10 to 20mg per day) and it is particularly effective in the severe forms of depression. Several studies have compared escitalopram to another specific serotonin recapture inhibitor (SSRI) in severe depression. In a 24-week study, 20mg per day of escitalopram, compared to 40mg per day paroxetin, demonstrated significantly greater efficacy (p<0.05) on the primary criterion (modification of the total MADRS score between inclusion and the end of the study). In this same study, the difference in favour of escitalopram increased in parallel with the increase in initial severity. In a grouped analysis of three studies versus citalopram, the superior efficacy of escitalopram also increased in parallel with the initial severity. The antidepressants, combined serotonin recapture inhibitors and noradrenalin (SRINA), might, in theory, be more effective than the SRI because of their broader mode of action. Recent data on escitalopram have invalidated this fact. In a study comparing 20mg per day of escitalopram to 225mg per day of venlafaxine during eight weeks in severely depressed patients (MADRS>30), escitalopram led to a significantly enhanced improvement (p<0.05). A grouped analysis of two similarly designed studies showed that the difference in favour of escitalopram increased at the same time as the initial severity increased. An analysis of two studies comparing 10 to 20mg per day of escitalopram to 60mg per day of duloxetine in severely depressed patients, revealed the superior efficacy of escitalopram in the sub-sample of severely depressed patients (p<0.01), with significant superiority on each of the 10 items of the MADRS taken singly. Despite the limits of regrouped analyses, all these results underline the fact that escitalopram is at least as effective as the comparators, and notably compared to the two SRINA studied, in the severe forms of depression.
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PMID:[Severe forms of depression: the efficacy of escitalopram]. 1939 84

In the medication of depression, the antidepressants such as selective 5-HT reuptake inhibitors (SSRIs) and a 5-HT and NA reuptake inhibitor (SNRI) are mainly in use in Japan. However, remission rates for SSRI or SNRI are 60% or less. This means that there are still many patients with treatment-resistant depression (TRD). Meanwhile it is considered that the DA nerve system plays an important role for recovery from troublesome feelings and a sense of aimlessness in life in patients with TRD. Recently, new generation antidepressants under development in Japan (escitalopram, duloxetine, mirtazapine, and bupropion) are expected as an option in the medical treatment of TRD. We introduce the pharmacological (focusing on the DA nerve system) and clinical data on these new antidepressants and their putative positioning of each antidepressant. Escitalopram is a stronger and safer SSRI with an earlier onset of action. The antidepressant effect of duloxetine is considered stronger than that of other SNRIs. Mirtazapine is an antagonist of alpha2, 5-HT2A, and 5-HT2C receptors and promotes releases of NA, 5-HT, and DA. Clinically, mirtazapine shows an earlier onset of action and a sedative effect. Bupropion is a DA and NA reuptake inhibitor, and is considered useful to activate DA neurons.
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PMID:[Mechanism of action of new generation antidepressants under development in Japan: focusing on dopamine neurotransmission]. 1966 59

There is evidence that some antidepressant drugs are beneficial in the prophylaxis of migraine. Previous reports have shown that migraine patients may respond to various antidepressant agents used for prophylactic therapy. The main purpose of this study was to compare the efficacy of antidepressants from 2 different groups (venlafaxine vs escitalopram) on people who had migraine headache without depression or anxiety. In this prospective study, we evaluated the headache diaries of 93 patients who were being treated with venlafaxine (n = 35) and escitalopram (n = 58). At the end of the 3-month period, patients were reassessed, and those with marked differences in attack frequency, duration, intensity (with visual analog scales), lost work-day equivalent index, and migraine disability assessment questionnaire were compared. There was a clear reduction in headache frequency (P < 0.0001), duration (P < 0.0001), and severity (P < 0.0001) in the venlafaxine group. In addition, there was a significant improvement in daily work performance during headaches (P < 0.0001). In the escitalopram group, monthly headache frequency (P < 0.026), duration (P < 0.002), and intensity (P < 0.027) all decreased significantly, although not to the same extent as with venlafaxine. After the third month of venlafaxine and escitalopram treatment, most of the patients (82.8% vs 96.5%) were seen to have moved to the minimal or infrequent migraine disability assessment group. According to our findings, venlafaxine and escitalopram are both effective in the prophylaxis of migraine headache without depression and anxiety. This effect was independent of mood disorder. Escitalopram should be the first choice because of its fewer side effects, but venlafaxine may be used if escitalopram is found to be insufficient.
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PMID:Escitalopram and venlafaxine for the prophylaxis of migraine headache without mood disorders. 1966 78

Area-specific and stimulation-dependent changes of human brain activation by selective serotonin reuptake inhibitors (SSRI) are an important issue for improved understanding of treatment mechanisms, given the frequent prescription of these drugs in depression and anxiety disorders. The aim of this neuroimaging study was to investigate differences in BOLD-signal caused by administration of the SSRIs escitalopram and citalopram using pharmacological functional magnetic resonance imaging (pharmaco-fMRI). Eighteen healthy subjects participated in a placebo-controlled, randomized, double-blind study in cross-over repeated measures design. Each volunteer performed facial emotional discrimination and a sensorimotor control paradigm during three scanning sessions. Citalopram (20 mg/d), escitalopram (10 mg/d) and placebo were administered for 10 days each with a drug-free period of at least 21 days. Significant pharmacological effects on BOLD-signal were found in the amygdala, medial frontal gyrus, parahippocampal, fusiform and middle temporal gyri. Post-hoc t-tests revealed decreased BOLD-signal in the right amygdala and left parahippocampal gyrus in both pharmacological conditions, compared to placebo. Escitalopram, compared to citalopram, induced a decrease of BOLD-signal in the medial frontal gyrus and an increase in the right fusiform and left parahippocampal gyri. Drug effects were concentrated in brain regions with dense serotonergic projections. Both escitalopram and citalopram attenuated BOLD-signal in the amygdala and parahippocampal cortex to emotionally significant stimuli compared to control stimuli. We believe that reduced reactivity in the medial frontal gyrus found for escitalopram compared to citalopram administration might explain the response differences between study drugs as demonstrated in previous clinical trials.
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PMID:Area-specific modulation of neural activation comparing escitalopram and citalopram revealed by pharmaco-fMRI: a randomized cross-over study. 1983 14


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