Relationship between the serotonin receptor 1A polymorphism with treatment response to escitalopram in patients with major depresive disorder

Hun Soo Chang, In Kwang Choi, Hwa Young Lee, Yoo Jung Jeong, Bohye Kim, Min-Soo Lee

Research output: Contribution to journalArticle

Abstract

Objective: Serotonin 1A receptor (HTR1A) is a candidate molecule for influencing the pathophysiology of major depressive disorder (MDD) and clinical responses to antidepressant treatment. Among polymorphisms of the HTR1A gene, -1019C>G (rs6295) is reportedly a biologically functional polymorphism associated with response to antidepressant treatment. The aim of this study was to determine the relationship between the HTR1A-1019C>G polymorphism and the response to escitalopram in patients with MD. Method: Eighty Korean patients were examined using the Structured Clinical Interview for DSM-IV Axis I disorders and took escitalopram at a daily dose of 5 to 40 mg. Clinical symptoms were evaluated using the 21-item Hamilton Depression Rating (HAM-D) scale during 8 weeks of treatment. The genotypes were determined using HpyCH4 IV digestion following polymerase chain reaction. Results: The proportion of G-allele carriers was 25.0% in responders, which was lower than that in non-responders (53.9%) at 1 week of escitalopram treatment (OR = 0.28, P = 0.030). In allelic analysis, the frequency of the G allele was significantly lower in responders at 1 week than in non-responders (12.5% versus 31.7%, respectively; OR = 0.29, P = 0.029). Similarly, the ratio of HAM-D score at 1 week to the baseline score in C-allele carriers was 67.6% ± 2.42%, which was significantly lower than the ratio of 75.8% ± 2.74% in patients possessing the G allele (P = 0.027). Conclusions: Although this study is preliminary and has several limitations, our results suggest that HTR1A- 1019C>G may be a genetic marker predicting the response to escitalopram treatment.

Original languageEnglish
Pages (from-to)148-154
Number of pages7
JournalClinical Neuropsychiatry
Volume10
Issue number3-4
Publication statusPublished - 2013 Oct 10

Fingerprint

Citalopram
Receptor, Serotonin, 5-HT1A
Alleles
Antidepressive Agents
Depression
Therapeutics
Major Depressive Disorder
Genetic Markers
Gene Frequency
Diagnostic and Statistical Manual of Mental Disorders
Digestion
Genotype
Interviews
Polymerase Chain Reaction
Genes

Keywords

  • Escitalopram
  • Major depressive disorder
  • Serotonin receptor 1A
  • Single-nucleotide polymorphism
  • Treatment response

ASJC Scopus subject areas

  • Psychiatry and Mental health

Cite this

Relationship between the serotonin receptor 1A polymorphism with treatment response to escitalopram in patients with major depresive disorder. / Soo Chang, Hun; Choi, In Kwang; Lee, Hwa Young; Jeong, Yoo Jung; Kim, Bohye; Lee, Min-Soo.

In: Clinical Neuropsychiatry, Vol. 10, No. 3-4, 10.10.2013, p. 148-154.

Research output: Contribution to journalArticle

Soo Chang, Hun ; Choi, In Kwang ; Lee, Hwa Young ; Jeong, Yoo Jung ; Kim, Bohye ; Lee, Min-Soo. / Relationship between the serotonin receptor 1A polymorphism with treatment response to escitalopram in patients with major depresive disorder. In: Clinical Neuropsychiatry. 2013 ; Vol. 10, No. 3-4. pp. 148-154.
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abstract = "Objective: Serotonin 1A receptor (HTR1A) is a candidate molecule for influencing the pathophysiology of major depressive disorder (MDD) and clinical responses to antidepressant treatment. Among polymorphisms of the HTR1A gene, -1019C>G (rs6295) is reportedly a biologically functional polymorphism associated with response to antidepressant treatment. The aim of this study was to determine the relationship between the HTR1A-1019C>G polymorphism and the response to escitalopram in patients with MD. Method: Eighty Korean patients were examined using the Structured Clinical Interview for DSM-IV Axis I disorders and took escitalopram at a daily dose of 5 to 40 mg. Clinical symptoms were evaluated using the 21-item Hamilton Depression Rating (HAM-D) scale during 8 weeks of treatment. The genotypes were determined using HpyCH4 IV digestion following polymerase chain reaction. Results: The proportion of G-allele carriers was 25.0{\%} in responders, which was lower than that in non-responders (53.9{\%}) at 1 week of escitalopram treatment (OR = 0.28, P = 0.030). In allelic analysis, the frequency of the G allele was significantly lower in responders at 1 week than in non-responders (12.5{\%} versus 31.7{\%}, respectively; OR = 0.29, P = 0.029). Similarly, the ratio of HAM-D score at 1 week to the baseline score in C-allele carriers was 67.6{\%} ± 2.42{\%}, which was significantly lower than the ratio of 75.8{\%} ± 2.74{\%} in patients possessing the G allele (P = 0.027). Conclusions: Although this study is preliminary and has several limitations, our results suggest that HTR1A- 1019C>G may be a genetic marker predicting the response to escitalopram treatment.",
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T1 - Relationship between the serotonin receptor 1A polymorphism with treatment response to escitalopram in patients with major depresive disorder

AU - Soo Chang, Hun

AU - Choi, In Kwang

AU - Lee, Hwa Young

AU - Jeong, Yoo Jung

AU - Kim, Bohye

AU - Lee, Min-Soo

PY - 2013/10/10

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N2 - Objective: Serotonin 1A receptor (HTR1A) is a candidate molecule for influencing the pathophysiology of major depressive disorder (MDD) and clinical responses to antidepressant treatment. Among polymorphisms of the HTR1A gene, -1019C>G (rs6295) is reportedly a biologically functional polymorphism associated with response to antidepressant treatment. The aim of this study was to determine the relationship between the HTR1A-1019C>G polymorphism and the response to escitalopram in patients with MD. Method: Eighty Korean patients were examined using the Structured Clinical Interview for DSM-IV Axis I disorders and took escitalopram at a daily dose of 5 to 40 mg. Clinical symptoms were evaluated using the 21-item Hamilton Depression Rating (HAM-D) scale during 8 weeks of treatment. The genotypes were determined using HpyCH4 IV digestion following polymerase chain reaction. Results: The proportion of G-allele carriers was 25.0% in responders, which was lower than that in non-responders (53.9%) at 1 week of escitalopram treatment (OR = 0.28, P = 0.030). In allelic analysis, the frequency of the G allele was significantly lower in responders at 1 week than in non-responders (12.5% versus 31.7%, respectively; OR = 0.29, P = 0.029). Similarly, the ratio of HAM-D score at 1 week to the baseline score in C-allele carriers was 67.6% ± 2.42%, which was significantly lower than the ratio of 75.8% ± 2.74% in patients possessing the G allele (P = 0.027). Conclusions: Although this study is preliminary and has several limitations, our results suggest that HTR1A- 1019C>G may be a genetic marker predicting the response to escitalopram treatment.

AB - Objective: Serotonin 1A receptor (HTR1A) is a candidate molecule for influencing the pathophysiology of major depressive disorder (MDD) and clinical responses to antidepressant treatment. Among polymorphisms of the HTR1A gene, -1019C>G (rs6295) is reportedly a biologically functional polymorphism associated with response to antidepressant treatment. The aim of this study was to determine the relationship between the HTR1A-1019C>G polymorphism and the response to escitalopram in patients with MD. Method: Eighty Korean patients were examined using the Structured Clinical Interview for DSM-IV Axis I disorders and took escitalopram at a daily dose of 5 to 40 mg. Clinical symptoms were evaluated using the 21-item Hamilton Depression Rating (HAM-D) scale during 8 weeks of treatment. The genotypes were determined using HpyCH4 IV digestion following polymerase chain reaction. Results: The proportion of G-allele carriers was 25.0% in responders, which was lower than that in non-responders (53.9%) at 1 week of escitalopram treatment (OR = 0.28, P = 0.030). In allelic analysis, the frequency of the G allele was significantly lower in responders at 1 week than in non-responders (12.5% versus 31.7%, respectively; OR = 0.29, P = 0.029). Similarly, the ratio of HAM-D score at 1 week to the baseline score in C-allele carriers was 67.6% ± 2.42%, which was significantly lower than the ratio of 75.8% ± 2.74% in patients possessing the G allele (P = 0.027). Conclusions: Although this study is preliminary and has several limitations, our results suggest that HTR1A- 1019C>G may be a genetic marker predicting the response to escitalopram treatment.

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