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Investigation of Genetic Predictors of the Response to Selective Serotonin Re-Uptake Inhibitors Treatment

Investigation of Genetic Predictors of the Response to Selective Serotonin Re-Uptake Inhibitors (SSRI) Treatment in individuals suffering from major depression

Status
Completed
Phases
Phase 4
Study type
Interventional
Source
ANZCTR
Registry ID
ACTRN12609000295246
Enrollment
135
Registered
2009-05-18
Start date
2006-12-01
Completion date
Unknown
Last updated
2020-01-13

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

None listed

Brief summary

The antidepressant medications are among the most commonly prescribed pharmacological agents in patients with mood and anxiety disorder. Despite recent advances in antidepressant pharmacotherapy, there is a pressing need for substantial optimization and improvment of outcome of pharmacotherapy of psychiatric disorders by providing individualized and science-based treatment guidelines. Besides it is rather difficult in clinical practice to predict, which patient will response to a certain pharmacological treatment well and which one less so. Putative predictors of response to antidepressant include demographic and clinical characteristics, personality traits, biological markers and psychophysiological features. Recently the research studies shown that divergences in antidepressant efficacy may be related to genetic variations of patients. The pharmacogenetic studies have multiplied in recent decade due to the impact that such studies may have in everyday clinical practice once reliable predictors could be identified. The pharmacogenetic research using new deoxyribonucleic acid (DNA) microarray-based technology can reasonably be expected to contribute to the prediction of likelihood of treatment response and risk of development of adverse side effects in individual patients in case of antidepressant treatment. By reducing costly treatment failures and the likelihood of serious adverse events, pharmacogenetic testing may help to improve the treatment possibilities for chronic diseases, reduce the burden prescription drug costs, and lower the costs of drug development. The further detailed investigation of peripheral gene expression profiles may help to identify responsible genes that underlie the process of development of affective disorders and open novel horizons for understanding molecular mechanisms of psychopharmacological treatment.

Interventions

escitalopram in doses 10-20mg per day, during 12 weeks, oral administration

Sponsors

Tartu University
Lead SponsorUniversity

Study design

Allocation
Non-randomised trial
Intervention model
Single group
Primary purpose
Treatment
Masking
Open (masking not used)

Eligibility

Sex/Gender
All
Age
18 Years to 70 Years
Healthy volunteers
No

Inclusion criteria

Both genders Major Depression diagnosis according to Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria At severity of depression of at least moderate as indicated by a Montgomery-Asberg's Depression Rating Scale (MADRS) total score of 22 or higher Only secondary current comorbid anxiety disorder

Exclusion criteria

Bipolar disorder Psychotic disorder or features Current eating disorders Mental retardation Any pervasive developmental disorder or cognitive disorder Alcohol or drug abuse-related disorders within 12 months prior to baseline Acute infections, neurological or any other unstable general disorders, serious suicide risk, formal behaviour therapy, or systematic psychotherapy, pregnancy or breastfeeding A history of hypersensitivity or non-response to escitalopram

Outcome results

None listed

Source: ANZCTR · Data processed: Feb 4, 2026