Serotonin transporter gene polymorphism associated with short-term treatment response to venlafaxine

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Abstract

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-sberg 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. Copyright © 2010 S. Karger AG.

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Lee, S. H., Choi, T. K., Lee, E., Seok, J. H., Lee, S. H., Lee, H. S., & Kim, S. J. (2010). Serotonin transporter gene polymorphism associated with short-term treatment response to venlafaxine. Neuropsychobiology, 62(3), 198–206. https://doi.org/10.1159/000319362

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