Research and Clinical Trials on Citalopram (Celexa, Cipramil, Seropram)

By Dr Greg Mulhauser
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This list of current clinical research trials on Citalopram (Celexa, Cipramil, Seropram) is followed by a short set of abstracts from the most recent research articles published on the drug.

Article Contents

Citalopram (Celexa, Cipramil, Seropram) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Citalopram (Celexa, Cipramil, Seropram).

 

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Current Research Literature on Citalopram (Celexa, Cipramil, Seropram)

Here are abstracts for some of the latest research articles to have appeared on Citalopram (Celexa, Cipramil, Seropram):

Discriminative stimulus properties of the "atypical" antidepressant, mirtazapine, in rats: a pharmacological characterization.

Psychopharmacology (Berl). 2008 Aug 16;
Dekeyne A, Millan MJ
RATIONALE: Though interoceptive properties of antidepressants have been described, discriminative stimulus (DS) properties of mirtazapine, which does not affect monoamine reuptake, remain uncharacterized. OBJECTIVES: The objectives of the study are to train rats to recognize a mirtazapine DS, then perform substitution studies with other antidepressants and drugs acting at sites occupied by mirtazapine. MATERIALS AND METHODS: Using a two-lever, fixed-ratio 10 schedule, rats were trained to discriminate mirtazapine (2.5 mg/kg, i.p.) from saline. RESULTS: Sessions, 63 +/- 8, were necessary to reach the criterion for 14 rats that all subsequently recognized (100%) mirtazapine at the training dose. Mirtazapine blocks serotonin (5-HT)(2C) receptors, and the 5-HT(2C) antagonists, SB242,084, SB243,213 and S32006, revealed dose-dependent and full (>/=80%) substitution at doses of 2.5, 2.5, and 0.63 mg/kg, respectively. By contrast, the 5-HT(2A) antagonists, MDL100,907 and SR46349-B, the 5-HT(2B) antagonist, SB204,741, and the 5-HT(3) antagonist, ondansetron, showed no significant substitution. Though mirtazapine indirectly recruits 5-HT(1A) receptors, the 5-HT(1A) agonists, buspirone and 8-OH-DPAT, did not substitute. Mirtazapine blocks alpha(2)-adrenoceptors, but several alpha(2)-adrenoceptor antagonists (yohimbine, RX821,002 and atipamezole) failed to substitute. Despite blockade by mirtazapine of histamine H(1) receptors, no substitution was seen with the selective H(1) antagonist, pyrilamine. Finally, the selective noradrenaline reuptake inhibitor, reboxetine (0.16), fully substituted for mirtazapine, whereas the 5-HT/noradrenaline reuptake inhibitors, duloxetine and S33005, several 5-HT reuptake inhibitors (citalopram, fluvoxamine, and paroxetine) and the dopamine reuptake inhibitors, bupropion and GBR12,935, did not substitute. CONCLUSION: Mirtazapine elicits a DS in rats for which selective antagonists at 5-HT(2C) receptors display dose-dependent substitution, whereas drugs acting at other sites recognized by mirtazapine are ineffective.

Clinically relevant pharmacokinetic drug interactions with second-generation antidepressants: An update.

Clin Ther. 2008 Jul; 30(7): 1206-27
Spina E, Santoro V, D'Arrigo C
Background: 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 >/=1 CYP isozyme. Objective: The goal of this article was to review the current literature on clinically relevant pharmacokinetic drug interactions with second-generation antidepressants. Methods: A search of MEDLINE and EMBASE was conducted for original research and review articles published in English between January 1985 and February 2008. Among the search terms were drug interactions, second-generation antidepressants, newer antidepressants, SSRIs, SNRIs, fluoxetine, paroxetine, fluvoxamine, sertraline, citalopram, escitalopram, venlafaxine, duloxetine, mirtazapine, reboxetine, bupropion, nefazodone, pharmacokinetics, drug metabolism, and cytochrome P450. Only articles published in peerreviewed journals were included, and meeting abstracts were excluded. The reference lists of relevant articles were hand-searched for additional publications. Results: Second-generation antidepressants differ in their potential for pharmacokinetic drug interactions. Fluoxetine and paroxetine are potent inhibitors of CYP2D6, fluvoxamine markedly inhibits CYP1A2 and CYP2C19, and nefazodone is a substantial inhibitor of CYP3A4. Therefore, clinically relevant interactions may be expected when these antidepressants are coadministered with substrates of the pertinent isozymes, particularly those with a narrow therapeutic index. Duloxetine and bupropion are moderate inhibitors of CYP2D6, and sertraline may cause significant inhibition of this isoform, but only at high doses. Citalopram, escitalopram, venlafaxine, mirtazapine, and reboxetine are weak or negligible inhibitors of CYP isozymes in vitro and are less likely than other second-generation antidepressants to interact with co-administered medications. Conclusions: Second-generation antidepressants are not equivalent in their potential for pharmacokinetic drug interactions. Although interactions may be predictable in specific circumstances, use of an antidepressant with a more favorable drug-interaction profile may be justified.

Serotonin transporter gene polymorphisms in patients with chronic tension-type headache: A preliminary study.

Neurol India. 2008 Apr-Jun; 56(2): 156-60
Akcali A, Tataroglu C, Erdal E, Aydin N, Pehlivan S
Background and Objectives: This study is designed to understand the pathophysiology of one of the most serious health problems, chronic tension-type headache (CTTH). Two polymorphic sites in serotonin transporter protein gene attracted much interest. These are: the variable number of tandem repeats (VNTR) and 5'-flanking promoter region (5-HTTLPR). Materials and Methods: VNTR and 5-HTTLPR polymorphisms were investigated in 126 CTTH patients and 138 healthy control subjects. The patients were being treated with amitripytyline or citalopram or sertraline (SSRI). The polymerase chain reaction (PCR) method was used to investigate the polymorphisms in the serotonin transporter protein gene. Results: There were no statistically significant results based on the 5-HTTLPR gene alleles, however, STin 2.12/12 genotype and STin 2.12 allele were seen to predominate the control group. In order to investigate the combined effect of the two polymorphic loci on the 5-HTT gene expression, samples were separated into nine groups. Genotypes (S/S-12/10) and (L/S-12/10) displayed statistically significant frequency in the CTTH group than in the control group. No significant differences were noticed between the 5-HTTLPR and VNTR haplotype groups and success in treatment. Conclusion: It is possible to make reliable comparisons and hypothesis about the homozygous and/or heterozygous presence of S and STin 12/10 alleles which may be in interaction with CTTH. On the other hand, the presence of homozygous L and STin12 alleles may play a protective role against CTTH. It is also possible that heterogeneity among diseases showing the same clinical research will require a lot of effort for individual identification.

Does the Duration of Index Episode Affect the Treatment Outcome of Major Depressive Disorder? A STAR*D Report.

J Clin Psychiatry. 2008 Jul 29; e1-e11
Gilmer WS, Gollan JK, Wisniewski SR, Howland RH, Trivedi MH, Miyahara S, Fleck J, Thase ME, Alpert JE, Nierenberg AA, Warden D, Fava M, Rush AJ
OBJECTIVE: This article aims to identify baseline sociodemographic and clinical characteristics associated with the duration of the index major depressive episode (MDE) and to assess the effect of the current MDE duration on response and remission rates with up to 14 weeks of citalopram. METHOD: Eligible participants met DSM-IV criteria for nonpsychotic major depressive disorder, scored >/= 14 on the 17-item Hamilton Rating Scale for Depression (HAM-D-17), and were not resistant to adequate antidepressant treatment in the current episode. The first patient was enrolled in July 2001 and the last visit for the last patient in follow-up was in March 2006. The evaluable sample (N = 2851) was divided into 4 groups based on the index MDE duration at study entry: acute (/= 42 months, N = 394). These 4 groups were compared in terms of baseline sociodemographic and clinical characteristics and treatment outcomes. Citalopram was generally begun at 20 mg/day and raised to 40 mg/day by weeks 2 through 4 and to 60 mg/day (final dose) by weeks 4 through 6. Logistic regression models with adjusted post hoc analyses were used to control for associated baseline characteristics. Response was defined as >/= 50% reduction in baseline 16-item Quick Inventory of Depressive Symptomatology-Self-Report (QIDS-SR-16) scores at exit. Remission was defined as

Selecting among second-step antidepressant medication monotherapies: predictive value of clinical, demographic, or first-step treatment features.

Arch Gen Psychiatry. 2008 Aug; 65(8): 870-80
Rush AJ, Wisniewski SR, Warden D, Luther JF, Davis LL, Fava M, Nierenberg AA, Trivedi MH
CONTEXT: Little is known about selecting among second-step medications for major depressive disorder after intolerance or lack of remission with an initial selective serotonin reuptake inhibitor. OBJECTIVE: To determine whether sociodemographic, clinical, or first-step treatment features predict remission with or intolerance overall or differentially to any 1 of 3 second-step medications after an unsatisfactory outcome with citalopram hydrobromide. DESIGN: An equipoise stratified randomized study. Participants were recruited from July 17, 2001, through April 20, 2004. SETTING: Public or private sector primary care (n = 18) and psychiatric care (n = 23) settings across the United States. PARTICIPANTS: Representative outpatients aged 18 to 75 years with nonpsychotic major depressive disorder (N = 727). INTERVENTIONS: Sustained-release bupropion hydrochloride was started at 150 mg/d and incrementally increased to 400 mg/d. Sertraline hydrochloride was started at 50 mg/d and incrementally increased to 200 mg/d. Extended-release venlafaxine hydrochloride was started at 37.5 mg/d and incrementally increased to 375 mg/d. MAIN OUTCOME MEASURES: The 16-item Quick Inventory of Depressive Symptomatology, Self-Rated and the Frequency, Intensity, and Burden of Side Effects Rating. RESULTS: Remission was more likely among participants who were white, employed, cohabiting or married, or privately insured or who had prior intolerance to citalopram or at least a response to citalopram, and no prior suicide attempts. Remission was less likely among participants with concurrent generalized anxiety, obsessive-compulsive, panic, or posttraumatic stress disorders; social phobia; anxious or melancholic features; or more severe depression. Intolerance was less likely for Hispanic participants, but more likely for participants with previous suicide attempts or intolerance to citalopram. Participants with concurrent substance use were less likely to remit (odds ratio, 0.37) and more likely not to tolerate extended-release venlafaxine. Intolerance to citalopram was associated with intolerance to sertraline (P = .04). CONCLUSIONS: Clinical, demographic, and treatment history were of little value in recommending 1 medication vs another as a second-step treatment for major depressive disorder. Participants most likely to remit in the second step had less Axis I psychiatric disorder comorbidity, less social disadvantage, and at least a response to citalopram in the first step. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00021528.

 

This page was last reviewed by Dr Greg Mulhauser, Friday, 4 July 2008.

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