Specific Effects of Escitalopram on Neuroendocrine Response

This study has been completed.
Sponsor:
Collaborator:
H. Lundbeck A/S
Information provided by:
Queen's University
ClinicalTrials.gov Identifier:
NCT00150527
First received: September 6, 2005
Last updated: February 4, 2009
Last verified: February 2009

September 6, 2005
February 4, 2009
September 2005
December 2006   (final data collection date for primary outcome measure)
The effect of the drugs on serum cortisol and ACTH following a single dose of each drug. [ Time Frame: 4hrs ] [ Designated as safety issue: No ]
Not Provided
Complete list of historical versions of study NCT00150527 on ClinicalTrials.gov Archive Site
Side effects following a single dose of the drug [ Time Frame: 4hrs ] [ Designated as safety issue: No ]
Not Provided
Not Provided
Not Provided
 
Specific Effects of Escitalopram on Neuroendocrine Response
Specific Effects of Escitalopram on Neuroendocrine Response

Citalopram, a selective serotonin reuptake inhibitor (SSRI), is used as a neuroendocrine probe in human subjects to assess serotonin (5-hydroxytryptamine; 5-HT) function as reflected in prolactin and plasma cortisol release. Citalopram is a racemic mixture of equal parts of the S(+) and R(-) enantiomers. The S(+) form ("escitalopram") has been identified as being the active isomer and inhibitor of serotonin reuptake and consequently antidepressant activity is associated almost exclusively with the S-enantiomer. Escitalopram has been shown to be approximately twice as potent as citalopram at the primary, high-affinity binding site on the human serotonin transporter. Interestingly, investigations have suggested an antagonistic interaction of the R- and S-enantiomer at an allosteric binding site on the serotonin transporter. This antagonism has been shown in animal studies where the addition of R-citalopram to escitalopram treatments significantly counteracts the antidepressant and anti-anxiolytic effects of escitalopram. From these clinical and experimental data, the researchers can anticipate that escitalopram would increase cortisol and prolactin in the neuroendocrine challenge paradigm more effectively than citalopram.

See above.

Observational
Observational Model: Cohort
Time Perspective: Prospective
Not Provided
Not Provided
Non-Probability Sample

Normal healthy people

Healthy
  • Drug: Citalopram
    40 mg, pill, single dose
    Other Name: Celexa
  • Drug: Escitalopram
    20 mg, pill, single dose
    Other Name: unknown
  • Drug: Dexamethasone
    1 mg, pill, single dose
    Other Name: unknown
  • Behavioral: Cold Pressor Test
    single test
    Other Name: unknown
Not Provided
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
8
December 2007
December 2006   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • The age range will be restricted to between 18 and 59 years of age.
  • Subjects must be fit and have no history of significant illness.
  • Subjects must have no risk factors for HIV or viral hepatitis.
  • Subjects must be non-smokers, free of medication, and consume alcoholic and caffeinated beverages in moderation.
  • Subjects must also be in good psychological health with no history of psychiatric illness.

Exclusion Criteria:

  • Personal history of psychiatric illness, habitual smoking, illicit or prescription drug use, high intake of alcohol (>10 drinks/week) or caffeine (>500 mg caffeine/day), shift work, pregnancy, personal or familial history of seizures, significant medical illness or treatment in the last six months, significant physical or laboratory abnormalities, or current use of a weight loss diet.
  • Women entering the study must be on a reliable form of birth control, i.e., tubal ligation, hysterectomy, oral contraceptives, abstinence, or vasectomy in partner.
Both
18 Years to 59 Years
Yes
Contact information is only displayed when the study is recruiting subjects
Canada
 
NCT00150527
ESCIT001
No
Dr. Nicholas Delva, Dalhousie University
Queen's University
H. Lundbeck A/S
Principal Investigator: Nicholas J Delva, MD Queen's University
Queen's University
February 2009

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP