Abstract

Aim and Objective: Escitalopram (SCT) shows an antidepressant effect due to its mechanism of increasing the serotonin level by inhibiting the serotonin transporter protein (5HTT). 5HTT is encoded by solute carrier family 6 member 4 gene (SLC6A4) in the brain. Recognition of SCT plasma level of patients and pharmacodynamics of individuals during SCT treatment will increase the expected response to the treatment and reduce the adverse effects. This study aims to determine the effect of SLC6A4 promoter long/short polymorphism and the SCT plasma level of patients on the response to treatment during the SCT drug therapy. Materials and Methods: Blood and plasma samples of 30 major depressive patients using 20 mg SCT for 8 weeks between the ages of 18 and 65 were analyzed to determine SCT plasma level and SLC6A4 promoter polymorphism. The treatment response level was determined by using the Hamilton Depression Rating Scale at patient files. Results: SCT plasma level of the nine patients with LL polymorphism was found to be in the range of 13.40–63.36 ng/mL. For 13 patients with LS polymorphism, SCT plasma level was found to be in the range of 2.93–57.48 ng/mL. For eight patients with SS polymorphism, the SCT plasma level was found to be in the range of 0.95–49.32 ng/mL. Conclusion: When the association between SCT plasma level and response to the drug treatment was examined, we had significant results to show that SCT level affected the response to treatment, especially in the LS group, as well as the SLC6A4 promoter variation. This study may lead to a more profound understanding of rational drug therapy as well as to a careful application of pharmacogenetics in psychiatry..

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