RELATIONSHIP BETWEEN THE SEROTONIN RECEPTOR 1A POLYMORPHISM WITH TREATMENT RESPONSE TO ESCITALOPRAM IN PATIENTS WITH MAJOR DEPRESSIVE DISORDER
- Authors
- Chang, Hun Soo; Choi, In-Kwang; Lee, Hwa-Young; Jeong, Yoo-Jung; Kim, Bohye; Lee, Min-Soo
- Issue Date
- Jun-2013
- Publisher
- Giovanni Fioriti Editore s.r.l.
- Keywords
- serotonin receptor 1A; escitalopram; major depressive disorder; single-nucleotide polymorphism; treatment response
- Citation
- Clinical Neuropsychiatry, v.10, no.3-4, pp 148 - 154
- Pages
- 7
- Journal Title
- Clinical Neuropsychiatry
- Volume
- 10
- Number
- 3-4
- Start Page
- 148
- End Page
- 154
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/13677
- ISSN
- 1724-4935
- 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 MDD. 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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