The incidence of treatment-emergent sexual dysfunction in the acute and continuation phases of the prevention of recurrent episodes of depression with venlafaxine ER for two years (PREVENT) study was assessed. Adult outpatients with recurrent major depressive disorder were randomly assigned to receive venlafaxine extended release (ER; 75-300 mg/day) or fluoxetine (20-60 mg/day). Sexual dysfunction was assessed using items from the 17-item Hamilton Rating Scale for Depression (HAM-D17) and the Inventory of Depressive Symptomatology-Self-Report (IDS-SR). The baseline rates of sexual dysfunction based on the HAM-D17 and IDS-SR items were 57.9% and 48.8%, respectively. The rates of new-onset sexual dysfunction for the venlafaxine ER-treated (44.8%, HAM-D17; 38.4%, IDS-SR) and fluoxetine-treated patients (52.9%, HAM-D17; 50.0%, IDS-SR) were similar; approximately 80% of the cases resolved during treatment. Treatment response was associated with lower rates of new-onset sexual dysfunction compared with nonresponse. The patients who remitted were the least likely to experience sexual dysfunction during antidepressant treatment.
"Thus, the majority of studies examining the drug–related SD during psychiatric treatment were based on the study of antidepressant drugs. It is noteworthy to mention, however, that the identification of treatment–related SD in MD can be difficult, as SD (particularly low sexual desire in women and premature ejaculation in men) is common in the general population, and because SD itself may be a symptom of MD, even in the absence of treatment [19, 20]. "
[Show abstract][Hide abstract] ABSTRACT: Sexual dysfunction (SD) is common in patients taking antipsychotics, and is the most bothersome symptom and adverse drug effect compromising treatment compliance. Mechanisms involved in psychotropics-induced SD are either largely unknown or poorly understood. The aim of this review is to present an updated analysis of SD associated with the use of psychotropic drugs in psychiatric patients.
Contemporary evidence from available studies demonstrates that SD rates are drug-related rather than drug-class specific, and that these rates vary widely. Mechanisms involved in psychotropics-induced SD are either largely unknown or poorly understood. Our understanding of psychotropics-induced SD is limited by the inability to differentiate whether these effects are really drug-induced or due to different inclusion criteria.
Rigorous research, basic and clinical, is needed to understand the exact incidence, severity and mechanisms involved in the development of SD induced by various psychotropic treatment regimens.
Central European Journal of Urology 04/2014; 66(4):466-471. DOI:10.5173/ceju.2013.04.art22
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