Research and Clinical Trials on Escitalopram (Lexapro, Cipralex)

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By Dr Greg Mulhauser

This list of current clinical research trials on Escitalopram (Lexapro, Cipralex) is followed by a short set of abstracts from the most recent research articles published on the drug.

Article Contents

Escitalopram (Lexapro, Cipralex) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Escitalopram (Lexapro, Cipralex).

 

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Current Research Literature on Escitalopram (Lexapro, Cipralex)

Here are abstracts for some of the latest research articles to have appeared on Escitalopram (Lexapro, Cipralex):

Are typical starting doses of the selective serotonin reuptake inhibitors sub-optimal? A meta-analysis of randomized, double-blind, placebo-controlled, dose-finding studies in major depressive disorder.

World J Biol Psychiatry. 2010 Mar; 11(2 Pt 2): 300-7
Papakostas GI, Charles D, Fava M
The purpose of this meta-analysis is to examine the relationship between selective serotonin reuptake inhibitor (SSRI) starting dose and treatment outcome in major depressive disorder (MDD). Medline/Pubmed, EMBASE, the Cochrane database, as well as a number of online clinical trial registries were searched for double-blind, placebo-controlled, fixed-dose trials comparing different starting doses of SSRIs for MDD. Data from nine trials (n=2340) were combined using a random-effects model. Patients randomized to receive the usual starting dose (10 mg escitalopram; 20 mg fluoxetine, paroxetine, citalopram; 50 mg sertraline and fluvoxamine) were less likely to respond than patients who received higher starting doses (RR=0.9; P=0.04; response rate 50.8 vs. 54.8%). The rate of discontinuation due to adverse events was lower among the usual starting dose group (9.8%) compared to the higher starting dose group (16.5%).Initiating treatment with SSRIs at doses higher than those typically used in clinical trials/settings is associated with higher response rates but also higher rates of discontinuation due to intolerance. Developing treatment strategies allowing clinicians to deliver higher initial SSRI doses while enhancing the tolerability of treatment may represent an alternative approach to improving the efficacy of treatment of MDD.

Interaction between serotonin transporter gene variants and life events predicts response to antidepressants in the GENDEP project.

Pharmacogenomics J. 2010 Mar 9;
Keers R, Uher R, Huezo-Diaz P, Smith R, Jaffee S, Rietschel M, Henigsberg N, Kozel D, Mors O, Maier W, Zobel A, Hauser J, Souery D, Placentino A, Larsen ER, Dmitrzak-Weglarz M, Gupta B, Hoda F, Craig I, McGuffin P, Farmer AE, Aitchison KJ
There is substantial inter-individual variation in response to antidepressants, and genetic variation may, in part, explain these differences. For example, there is evidence to suggest that variation in the serotonin transporter gene (SLC6A4) predicts response to selective serotonin reuptake inhibitors (SSRIs). Environmental factors such as the occurrence of stressful life events before treatment may also be important. One prior report suggests that both factors interact in predicting response to antidepressants. GENDEP, a prospective part-randomized pharmacogenomics trial, collected longitudinal data on the outcome of 811 patients with major depression undergoing treatment with either an SSRI (escitalopram) or a tricyclic antidepressant (nortriptyline). Life events experienced over 6 months preceding treatment were measured using a List of Threatening Experiences Questionnaire, and several polymorphisms in the serotonin transporter gene (SLC6A4) have been genotyped including the serotonin transporter-linked polymorphic region (5-HTTLPR). Stressful life events were shown to predict a significantly better response to escitalopram but had no effect on response to nortriptyline. Variation in the 5-HTTLPR and another polymorphism in the gene, STin4, significantly modified these effects. Gene-environment interactions including life events may therefore be important not only in the aetiology of depression, but also in predicting response to antidepressant medication.The Pharmacogenomics Journal advance online publication, 9 March 2010; doi:10.1038/tpj.2010.14.

Melatonin inhibits serotonin transporter activity in intestinal epithelial cells.

J Pineal Res. 2010 Mar 4;
Matheus N, Mendoza C, Iceta R, Mesonero JE, Alcalde AI
Gastrointestinal serotonin (5-HT) and melatonin are two closely related neuromodulators which are synthesised in the enterochromaffin cells of the intestinal epithelium and which have been shown to be involved in the physiopathology of the gastrointestinal tract. The effects of 5-HT depend on 5-HT availability which is, in part, modulated by the serotonin transporter (SERT). This transporter provides an efficient 5-HT uptake after release and is expressed in the membrane of the enterocytes. Although the origin and effects of 5-HT and melatonin are similar, the interrelationship between them in the gastrointestinal tract is unknown. The main aim of this study was to determine whether melatonin affects SERT activity and expression, and, if so, to elucidate the mechanisms involved. Caco-2 cell line was used to carry out the study as these cells have been shown to endogenously express SERT. The results showed that melatonin inhibits SERT activity by affecting both V(max) and kt kinetic constants although SERT synthesis or intracellular trafficking did not appear to be affected. The melatonin effect seemed to be independent of melatonin receptors MT(1) and MT(2) and protein kinase C and cAMP intracellular pathways. Our results suggest that the inhibition of SERT might be due to a catalytic effect of melatonin on the allosteric citalopram-sensitive site in SERT. This study shows, for the first time, that melatonin modulates SERT activity, thus demonstrating the feedback system between melatonin and the serotoninergic system in the gastrointestinal tract.

Salvage use of citalopram for treatment of fluoxetine-resistant premature ejaculation in recently married men: a prospective clinical trial.

Urol J. 2010; 7(1): 40-4
Dadfar MR, Baghinia MR
Introduction: A wide variety of therapeutic modalities have been tried for treatment of premature ejaculation. Selective serotonin reuptake inhibitors are from the latest and most effective medical agents. Among these drugs, fluoxetine hydrochloride has been used for some years in our institutions with considerable drug untoward effects and significant failure rates. We tried to salvage treatment process by using citalopram in fluoxetine-resistant patients. Materials and Methods: In a prospective clinical trial, we used citalopram hydrobromide as a salvage agent in 16 newly married men with premature ejaculation who experienced a history of unsuccessful treatment with fluoxetine hydrochloride. Intravaginal ejaculation latency time (IVELT) was recorded by a stopwatch before and after the treatment, and a 5-stage visual scale was designed and used to compare patients' sexual satisfaction levels during the 1-month treatment period. Results: The IVELT and sexual satisfaction levels both significantly improved after citalopram prescription. The mean measured IVELT was 0.388 +/- 0.212 minutes before the treatment, which increased to 4.313 +/- 2.886 minutes after the treatment. The reported drug untoward effects were mild. Citalopram was ineffective only in 1 patient, which was discontinued after 4 weeks. Conclusion: Our study showed that citalopram is effective and safe in the treatment of premature ejaculation in newly married men after failed treatment with fluoxetine.

Effect of escitalopram on the processing of emotional faces.

Braz J Med Biol Res. 2010 Mar 5;
Alves-Neto WC, Guapo VG, Graeff FG, Deakin JF, Del-Ben CM
Serotonin has been implicated in the neurobiology of depressive and anxiety disorders, but little is known about its role in the modulation of basic emotional processing. The aim of this study was to determine the effect of the selective serotonin reuptake inhibitor, escitalopram, on the perception of facial emotional expressions. Twelve healthy male volunteers completed two experimental sessions each, in a randomized, balanced order, double-blind design. A single oral dose of escitalopram (10 mg) or placebo was administered 3 h before the task. Participants were presented to a task composed of six basic emotions (anger, disgust, fear, happiness, sadness, and surprise) that were morphed between neutral and each standard emotion in 10% steps. Escitalopram facilitated the recognition of sadness and inhibited the recognition of happiness in male, but not female faces. No drug effect on subjective measures was detected. These results confirm that serotonin modulates the recognition of emotional faces, and suggest that the gender of the face can have a role in this modulation. Further studies including female volunteers are needed.

 

This page was last reviewed by Dr Greg Mulhauser, Sunday, 31 January 2010.

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