Serotonin transporter promoter region polymorphisms do not influence treatment response to escitalopram in patients with major depression

Maron, Eduard; Tammiste, Anu; Kallassalu, Kristi; Eller, Triin; Vasar, Veiko; Nutt, David; Metspalu, Andres

doi:10.1016/j.euroneuro.2009.01.010

Cited by 62 publications

(34 citation statements)

References 20 publications

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“…In contrast, some researchers have reported that the s/s genotype or s-allele is associated with good treatment response to SSRI, especially in Asian populations [7,8] . Others could not find any significant association between 5-HTTLPR and treatment response to SSRI [5] . The discrepancy between those findings and our results may stem from the following.…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 99%

“…Corroboration by other researchers and meta-analysis also support these findings [4] . However, there also exist negative findings [5] . Moreover, in Asian studies, the direction of the effect of the 5-HTTLPR polymorphism on treatment response to SSRI indicated contradictory results.…”

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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“…163 These findings are generally well replicated in studies involving white popu lations, 120,[164][165][166][167][168][169][170][171][172][173][174][175] although opposite or inconsistent findings have also been reported. [176][177][178][179][180] On the other hand, studies involving Asian populations usually report conflicting results: some studies reported that the short 5-HTTLPR allele was associated with better outcomes, [181][182][183][184] some found no effect of 5-HTTLPR genotype on treatment efficacy 121,185,186 and some reported that the long 5-HTTLPR allele was associated with better outcomes. 83,[187][188][189][190][191] Interestingly, Lotrich and colleagues 192 recently reported that paroxetine blood concentration was positively associated with HAM-D response in a sample of elderly patients, but this association was found to be significant only in carriers of the short allele.…”

Section: Comtmentioning

confidence: 96%

Pharmacogenetics of antidepressant response

Porcelli

Drago

Fabbri

et al. 2011

J Psychiatry Neurosci

156

103

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87Personalized medicine -the adaptation of therapies based on an individual's genetic and molecular profile -is one of the most promising aspects of modern medicine. The identification of the relation between genotype and drug response, including both the therapeutic effect and side effect profile, is expected to deeply affect medical practice. In this paper, we review the current knowledge about the genes related to antidepressant treatment response and provide methodologic proposals for future studies. We have mainly focused on genes associated with pharmacodynamics, for which a list of promising genes has been identified despite some inconsistency across studies. We have also synthesized the main results for pharmacokinetic genes, although so far they seem less relevant than those for pharmaco dynamic genes. We discuss possible reasons for these inconsistent findings and propose new study designs.

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“…Relatively fewer studies genotyped the triallelic locus and they did not support a substantial role of the polymorphism on antidepressant efficacy (Fabbri et al 2013a). Several pharmacogenetic studies (Perlis et al 2003;Murphy et al 2004;Popp et al 2006;Hu et al 2007;Smits et al 2007;Maron et al 2009) and one meta-analysis (Kato and Serretti 2010) reported that the S allele may also be a risk factor for the development of SSRI-induced side effects in Caucasian populations, though not for sexual dysfunction (Bishop et al 2009;Strohmaier et al 2011).…”

Section: Genetic Polymorphismsmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Fabbri

Hosák

Mößner

et al. 2016

The World Journal of Biological Psychiatry

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Major depressive disorder (MDD) is a heritable disease with a heavy personal and socio-economic burden. Antidepressants of different classes are prescribed to treat MDD, but reliable and reproducible markers of efficacy are not available for clinical use. Further complicating treatment, the diagnosis of MDD is not guided by objective criteria, resulting in the risk of under-or overtreatment. A number of markers of MDD and antidepressant response have been investigated at the genetic, epigenetic, gene expression and protein levels. Polymorphisms in genes involved in anti-depressant metabolism (cytochrome P450 isoenzymes), antidepressant transport (ABCB1), glucocorticoid signalling (FKBP5) and serotonin neurotransmission (SLC6A4 and HTR2A) were among those included in the first pharmacogenetic assays that have been tested for clinical applicability. The results of these investigations were encouraging when examining patient-outcome improvement. Furthermore, a nine-serum biomarker panel (including BDNF, cortisol and soluble TNF-a receptor type II) showed good sensitivity and specificity in differentiating between MDD and healthy controls. These first diagnostic and response-predictive tests for MDD provided a source of optimism for future clinical applications. However, such findings should be considered very carefully because their benefit/cost ratio and clinical indications were not clearly demonstrated. Future tests may include combinations of different types of biomarkers and be specific for MDD subtypes or pathological dimensions.

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Serotonin transporter promoter region polymorphisms do not influence treatment response to escitalopram in patients with major depression

Cited by 62 publications

References 20 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

Pharmacogenetics of antidepressant response

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

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