Serotonin Transporter Polymorphism (5-HTTLPR) and Citalopram Effectiveness and Side Effects in Children with Depression and/or Anxiety Disorders

Kronenberg, Sefi; Apter, Alan; Brent, David A.; Schirman, Shella; Melhem, Nadine; Pick, Nimrod; Gothelf, Doron; Carmel, Miri; Frisch, Amos; Weizman, Abraham

doi:10.1089/cap.2006.0144

Cited by 69 publications

(65 citation statements)

References 47 publications

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“…Carriers of the s-allele treated with paroxetine exhibit reduced tolerability and higher discontinuation rates compared to l/l homozygotes [10] , and the s-variant was associated with side effects induced by SSRI [11] . Furthermore, the s-allele was shown to identify patients at risk for developing insomnia and agitation with fluoxetine treatment [12] . Other studies reported no association between 5-HTTLPR and adverse effects induced by SSRI [13,14] .…”

Section: Introductionmentioning

confidence: 99%

Serotonin Transporter Gene Polymorphism Associated with Short-Term Treatment Response to Venlafaxine

Lee

Choi

Lee³

et al. 2010

Neuropsychobiology

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Background: Polymorphisms of serotonin transporter, especially serotonin transporter linked promoter region (5- HTTLPR) and serotonin transporter intron 2 variable number tandem repeat (5-HTTVNTR), have been suggested to be associated with treatment response to selective serotonin reuptake inhibitors. However, there have been only few reports of the association between 5-HTTLPR or 5-HTTVNTR and treatment response to venlafaxine. Methods: 84 Korean major depressive disorder patients were included in this study. They were administered 75 mg of venlafaxine XR (extended release) for 1 week and then took 150 mg for the next 3 weeks. All patients were evaluated at baseline and week 4 by the Hamilton Depression Rating Scale (HAM-D), Montgomery-Åsberg Depression Rating Scale (MADRS), Beck Depression Inventory (BDI), Hamilton Anxiety Rating Scale (HAM-A), and Beck Anxiety Inventory (BAI). Results: (1) Treatment response of depressive symptoms (BDI, HAM-D, MADRS) to venlafaxine at week 4 was associated with the non-s/s (l/l and l/s) genotype of 5-HTTLPR; (2) in repeated measures ANOVA, the BDI, MADRS and HAM-A scores decreased more significantly in patients with the non-s/s genotype than in those with the s/s genotype, and (3) multiple regression analyses suggested that the 5-HTTLPR polymorphism is a predictive factor for short-term treatment response to venlafaxine. However, 5-HTTVNTR showed no significant association with treatment response to venlafaxine. Both 5-HTTLPR and 5-HTTVNTR were not associated with side effects of venlafaxine. Conclusion: The 5-HTTLPR non-s/s genotype can be associated with venlafaxine treatment responses. However, further large-scale studies are warranted to confirm this finding.

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Section: Introductionmentioning

confidence: 99%

Serotonin Transporter Gene Polymorphism Associated with Short-Term Treatment Response to Venlafaxine

Lee

Choi

Lee³

et al. 2010

Neuropsychobiology

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“…[23,24] In one study, depressed and anxious youth homozygous for the more functional allele of the serotonin transporter promoter gene are more likely to respond to citalopram. [25] This genotype did not predict response in the TORDIAs, although polymorphisms of the FKBP5 associated with greater glucocorticoid receptor subsensitivity was associated with an increased risk of suicidal events, which were much more common in depressed youth who did not respond to treatment. [26] …”

Section: Pharmacokinetics and Pharmacogeneticsmentioning

confidence: 83%

Treatment-resistant depression in adolescents: review and updates on clinical management

2011

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Treatment-resistant depression (TRD) in adolescents is prevalent and impairing. We here review the definition, prevalence, clinical significance, risk factors, and management of TRD in adolescents. Risk factors associated with TRD include characteristics of depression (severity, level of hopelessness, and suicidal ideation), psychiatric and medical comorbidities, environmental factors (family conflict, maternal depression, and history of abuse), and pharmacokinetics and other biomarkers. Management options include review of the adequacy of the initial treatment, re-assessment for the above-noted factors that might predispose to treatment resistance, switching antidepressants, and augmentation with medication or psychotherapy. Other modalities, such as electroconvulsive therapy, vagal nerve stimulation, and repetitive transcranial magnetic stimulation, are also reviewed.

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“…One study of a pharmacological treatment for paediactric anxiety depression has been reported. The study found the S allele of the 5-HTTLPR is associated with poorer response to citalopram in children and adolescents (Kronenberg et al, 2007). Although the mechanism would be quite different, it is plausible that there could be a similar role for genetic factors in response to CBT.…”

Section: Future Directionsmentioning

confidence: 89%

Genetics

Eley

Zavos

2010

Information Processing Biases and Anxiety

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Serotonin Transporter Polymorphism (5-HTTLPR) and Citalopram Effectiveness and Side Effects in Children with Depression and/or Anxiety Disorders

Abstract: The 5-HTTLPR ss genotype was associated with a poorer clinical response with regard to depressive symptoms as well with fewer reports of agitation. The 5-HTTLPR polymorphism may be a genetic marker of response to citalopram in children and adolescents with depression and/or anxiety.

Cited by 69 publications

References 47 publications

Serotonin Transporter Gene Polymorphism Associated with Short-Term Treatment Response to Venlafaxine

Serotonin Transporter Gene Polymorphism Associated with Short-Term Treatment Response to Venlafaxine

Treatment-resistant depression in adolescents: review and updates on clinical management

Genetics

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