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.

Peripheric edema could be caused by various medical conditions as well as pharmacologic agents such as antihypertensives, nonsteroidal antiinflamatory drugs, endocrine agents and immunotherapies. Olanzapine is an atypical antipsychotic that is widely prescribed for the treatment of schizophrenia and bipolar affective disorder. Most common adverse reactions of olanzapine are weight gain, postural hypotension, constipation, dizziness, akathisia, sedation. Peripheral edema was reported as an infrequent side effect, which affected 3% of the olanzapine treated patients. In this report, we aim to draw attention of psychiatrists on this rare adverse effect by presenting a 56-year-old case, who applied to our hospital with severe depressive and obsessive-compulsive symptoms and hospitalized because of suicide risk. Before psychiatric admission, he wasn’t taking any medication. He was diagnosed as major depression with psychotic features and obsessive-compulsive disorder. He was started on olanzapine 10 mg/day, quetiapine 300 mg/day and fluoxetine 40 mg/day. Two weeks after initiation of olanzapine, he was found to have bilateral pedal edema without ulceration and temperature change but minimal redness was observed. He had no history suggestive of cardiac, renal and liver dysfunction or allergic reaction against to any drug that could explain his existing edema. Possible medical conditions which may cause edema were ruled out by laboratory tests and physical examination. Olanzapine was stopped immediately and the therapy was modified to risperidone 1 mg/day. After discontinuation of olanzapine, edema was gradually resolved within two weeks. Because olanzapine associated edema has been seen rarely, it could be overlooked by psychiatrists in comparison to its more common side effects. Although it shows self-limited and benign course, patients may feel discomfort and their compliance to treatment may decrease. Also, it may interfere with differential diagnosis of other medical conditions which may cause edema. In conclusion, we suggest that patients should be observed carefully for edema during olanzapine treatment.