Plasma serotonin level after 1 day of fluoxetine treatment: a biological predictor for antidepressant response?

Alvarez, Jean‐Claude; Gluck, Nathalie; Fallet, Alain; Grégoire, Anne; Chevalier, Jean-François; Advenier, C.; Spreux‐Varoquaux, Odile

doi:10.1007/s002130050924

Cited by 48 publications

(41 citation statements)

References 20 publications

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“…The effect of SSRIs on plasma serotonin concentrations is not well understood, and published results are contradictory – with some studies reporting decreased plasma serotonin after SSRI treatment 32, 62-65 , while others report increased concentrations 66-69 , which may be due, in part, to the plasma collection method or the platform used to assay serotonin. However, we observed a clear decrease in those concentrations in PGRN-AMPS MDD patients as measured with an LCECA platform – a highly sensitive, quantitative method.…”

Section: Discussionmentioning

confidence: 99%

TSPAN5, ERICH3 and selective serotonin reuptake inhibitors in major depressive disorder: pharmacometabolomics-informed pharmacogenomics

et al. 2016

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Millions of patients suffer from Major Depressive Disorder (MDD), but many do not respond to selective serotonin reuptake inhibitor (SSRI) therapy. We used a pharmacometabolomics-informed pharmacogenomics research strategy to identify genes associated with metabolites that were related to SSRI response. Specifically, 306 MDD patients were treated with citalopram or escitalopram and blood was drawn at baseline, four and eight weeks for blood drug levels, genome-wide single nucleotide polymorphism (SNP) genotyping and metabolomic analyses. SSRI treatment decreased plasma serotonin concentrations (p<0.0001). Baseline and plasma serotonin concentration changes were associated with clinical outcomes (p<0.05). Therefore, baseline and serotonin concentration changes were used as phenotypes for genome wide association studies (GWAS). GWAS for baseline plasma serotonin concentrations revealed a genome-wide significant (p=7.84E-09) SNP clusters on chromosome four 5’ of TSPAN5 and a cluster across ERICH3 on chromosome one (p=9.28E-08) that were also observed during GWAS for change in serotonin at four (p=5.6E-08 and p=7.54E-07, respectively) and eight weeks (p=1.25E-06 and p=3.99E-07, respectively). The SNPs on chromosome four were eQTLs for TSPAN5. Knockdown (KD) and over expression (OE) of TSPAN5 in a neuroblastoma cell line significantly altered expression of serotonin pathway genes (TPH1, TPH2, DDC and MAOA). Chromosome one SNPs included two ERICH3 nonsynonymous SNPs that resulted in accelerated proteasome-mediated degradation. In addition, ERICH3 and TSPAN5 KD and OE altered media serotonin concentrations. Application of a pharmacometabolomics-informed pharmacogenomic research strategy, followed by functional validation, indicated that TSPAN5 and ERICH3 are associated with plasma serotonin concentrations and may play a role in SSRI treatment outcomes.

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Section: Discussionmentioning

confidence: 99%

TSPAN5, ERICH3 and selective serotonin reuptake inhibitors in major depressive disorder: pharmacometabolomics-informed pharmacogenomics

et al. 2016

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“…The blood 5-HT level after 1 day of fluoxetine (one of the typical selective serotonin reuptake inhibitors (SSRIs)) treatment is correlated to the depression degree (P < 0.05). 15 The treatment of Paroxetine (SSRIs) also has the similar effect. 16 In this study, we built a chronic unpredictable mild stress model (CUMS) on rats which mimicked the depression of people and tried to find the relationship between depression behavior and blood 5-HT level.…”

Section: Introductionmentioning

confidence: 99%

Application of a Disposable Screen-Printed Electrode to Depression Diagnosis for Laboratory Rats Based on Blood Serotonin Detection

Liu

et al. 2011

ANAL. SCI.

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No exact and digital diagnostic methods for depression have been found. In this study, we prepared a 5-HT biosensor based on screen-printed electrode and applied it to a rat depression model caused by chronic unpredictable mild stress (CUMS). During CUMS, the blood 5-HT and the depression behavior of the depressed rats and the rats treated by antidepressants were recorded. The correlation coefficient of 5-HT was 0.9966 (0 -4 × 10 -6 M) on the sensor. Results demonstrated that 5-HT level of the depressed rats declined while the depression behavior was aggravated. Fluoxetine (20 mg/kg) and lentinan (10, 20 mg/kg) mildly elevated 5-HT level and slowly regulated the behavior. Mifepristone (20 mg/kg) and Rhizoma Coptidis water extract (10, 20, 100 mg/kg) quickly reversed 5-HT level and the depression behavior. This sensor can accurately test blood 5-HT and might be applied to rapid diagnosis for depression and evaluation of antidepressants effect.

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“…Alvarez et al studied the effects of therapy with fluoxetine and clomipramine for 12 weeks. They found both drugs had no difference in effect on the platelet inositol phosphate but the platelet activity was normalized among patients who responded to the antidepressant treatment 36 . In a study of depressed patients with CHD, reduced platelet activity occurred in patients treated with paroxetine for 6 weeks but not in patients treated with nortriptyline.…”

Section: Discussionmentioning

confidence: 98%

“…Several studies have indicated that SSRIs reduce elevated platelet activities, which may or may not occur in treatment with other kinds of antidepressants 8, 36–38 . Alvarez et al studied the effects of therapy with fluoxetine and clomipramine for 12 weeks.…”

Section: Discussionmentioning

confidence: 99%

Responses of mental stress–induced myocardial ischemia to escitalopram treatment: Background, design, and method for the Responses of Mental Stress Induced Myocardial Ischemia to Escitalopram Treatment trial

Jiang

Velázquez

Samad

et al. 2012

American Heart Journal

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Background Mental stress induced myocardial ischemia (MSIMI) is common in patients with clinically stable coronary heart disease (CHD) and is associated with poor outcomes. Depression is a risk factor of MSIMI. The Responses of Mental Stress Induced Myocardial Ischemia to Escitalopram Treatment (REMIT) trial investigates whether selective serotonin reuptake inhibitor (SSRI) treatment can improve MSIMI. The rationale and outline of the study are described. Method In this single center randomized clinical trial, adult patients with clinically stable CHD are recruited for baseline mental and exercise stress testing assessed by echocardiography. Additionally, psychometric questionnaires are administered and blood samples are collected for platelet activity analysis. Patients who demonstrate MSIMI, defined by new abnormal wall motion, ejection fraction reduction ≥8%, and/or development of ischemic ST change in electrocardiogram during mental stress testing, are randomized at a 1:1 ratio to escitalopram or placebo for 6 weeks. Approximately 120 patients with MSIMI are enrolled in the trial. The stress testing, platelet activity assessment and psychometric questionnaires are repeated at the end of the 6-week intervention. The hypothesis of the study is that SSRI treatment improves MSIMI via mood regulation and modification of platelet activity. Conclusion The REMIT study examines the effect of SSRI on MSIMI in vulnerable CHD patients and probes some potential underlying mechanisms.

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Plasma serotonin level after 1 day of fluoxetine treatment: a biological predictor for antidepressant response?

Abstract: These preliminary data show that fluoxetine and norfluoxetine might influence 5-HT peripheral venous blood parameters and that plasma 5-HT after 1 day of treatment might be a biological predictor for antidepressant response.

Cited by 48 publications

References 20 publications

TSPAN5, ERICH3 and selective serotonin reuptake inhibitors in major depressive disorder: pharmacometabolomics-informed pharmacogenomics

TSPAN5, ERICH3 and selective serotonin reuptake inhibitors in major depressive disorder: pharmacometabolomics-informed pharmacogenomics

Application of a Disposable Screen-Printed Electrode to Depression Diagnosis for Laboratory Rats Based on Blood Serotonin Detection

Responses of mental stress–induced myocardial ischemia to escitalopram treatment: Background, design, and method for the Responses of Mental Stress Induced Myocardial Ischemia to Escitalopram Treatment trial

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