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2008, Urology Journal
International Journal of Impotence Research
Safety and efficacy of citalopram in the treatment of premature ejaculation: a double-blind placebo-controlled, fixed dose, randomized study2006 •
International Urology and Nephrology
Sertraline in the treatment of premature ejaculation: A double-blind placebo controlled study1998 •
International Urology and Nephrology
Duloxetine, dual serotonin and norepinephrine reuptake inhibitor, versus paroxetine, selective serotonin reuptake inhibitor, in the treatment for premature ejaculation2015 •
The Journal of Sexual Medicine
The Effects of Citalopram and Fluoxetine on Sexual Behavior in Healthy Men: Evidence of Delayed Ejaculation and Unaffected Sexual Desire. A Randomized, Placebo-Controlled, Double-Blind, Double-Dummy, Parallel Group Study2008 •
2008 •
Clinical Neuropharmacology
Comparison of Dapoxetine Versus Paroxetine in Patients With Premature Ejaculation: A Double-blind, Placebo- controlled, Fixed-dose, Randomized Study.2006 •
Purpose: To compare the efficacy and safety of dapoxetine, paroxetine, and placebo for the oral pharmaco-therapy of premature ejaculation. Materials and Methods: Three hundred forty potent men with premature ejaculation were recruited to this study. Patients were randomly assigned to receive 60 mg dapox-etine (group 1, n = 115), or 20 mg paroxetine (group 2, n = 113) or placebo (group 3, n = 112) orally daily during a 12-week period for each agent. The efficacy of the 3 treatments was assessed every 2 weeks during treatment and at the end of study using responses to International Index of Erectile Function (IIEF), intravaginal ejaculatory latency time (IELT) evaluation, mean intercourse satisfaction domain, mean weekly coitus episodes and adverse drug effects. Results: At the end of the 12-week treatment with dapox-etine, paroxetine, and placebo, the mean IELT was increased from 38, 31 and 34 seconds to 179, 370 and 55 seconds, respectively (P = 0.01 in group 1 and P = 0.001 in group 2). Baseline mean intercourse satisfaction domain values of International Index of Erectile Function of 10, 11, and 11 reached 14, 17 and 12 at the end of the 12-week treatment in groups 1, 2, and 3 respectively (P = 0.03 in groups 1, 2). The mean weekly intercourse episodes increased from pretreatment values of 1.4, 1.3, and 1.3 to 2.2, 2.5 and 1.4, for dapoxetine, paroxetine and placebo, respectively (P = 0.04 in groups 1, 2). The incidence of adverse effects with dapoxetine and paroxetine was significantly higher (P = 0.04 in groups 1, 2) compared to that of placebo. Conclusions: Paroxetine appears to provide significantly better results in terms of IELT and intercourse satisfaction versus dapoxetine. Each treatment was well tolerated.
Journal of Clinical Psychopharmacology
Once-daily high-dose pindolol for paroxetine-refractory premature ejaculation: a double-blind, placebo-controlled and randomized study.2008 •
Purpose: To evaluate the efficacy and safety of pindolol 7.5 mg/d in delaying of ejaculation in paroxetine-refractory patients. Materials and Methods: Eighty-six married men (mean age, 33 years) with premature ejaculation unresponsive to paroxetine 20 mg/d given for 2 months or longer were randomized to receive 7.5 mg pindolol (n = 44) (group 1) (PXT + POL) or placebo (n = 42) (group 2) (PXT + PBO) for 6 weeks, while continuing paroxetine. After 6 weeks, all patients received paroxetine and placebo and were followed for 3 further weeks in a single-blind manner. Pretreatment evaluation included history and physical examination, mean intravaginal ejaculatory latency time (IELT), International Index of Erectile Function (IIEF), and Meares-Stamey test. The efficacy of 2 treatments was assessed every 1 week during treatment and, at the end of study, using responses to IIEF, IELT evaluation, mean intercourse satisfaction domain, mean weekly coitus episodes, and adverse drug effects. Results: Seventy-seven (89.5%) completed the whole treatment schedule. At the end of 6-week treatment period, the IELT after paroxetine-pindolol and paroxetine-placebo gradually increased from mean 48 and 41 seconds to approximately 188 and 58 seconds, respectively (P = 0.001). The mean weekly intercourse episodes increased from pretreatment values of 1.5 and 1.5 to 2.7 and 1.7, for groups PXT + POL and PXT + PBO, respectively (P = 0.01). Baseline mean intercourse satisfaction domain values of IIEF 12 and 11 reached to 16 and 11 at 6-week treatment in PXT + POL and PXT + PBO groups, respectively (P = 0.01). Upon discontinuing pindolol, all outcome measures returned to baseline values rapidly. The incidence of side effects with paroxetine-pindolol was significantly higher (P = 0.04). Conclusions: These findings support that a single high dose of pindolol (7.5 mg) is an effective augmentation strategy in paroxetine-refractory patients. (J Clin Psychopharmacol 2008;28:39-44) N ormal ejaculation function relies on the coordination of neurogenic, psychologic, relational, and sociocultural factors. Premature ejaculation (PE) is the most frequent sexual complaint in men. 1 Psychopharmacotherapy for PE was initiated when delayed ejaculation was encountered as a side effect of antidepressants more than 40 years ago. 2 Premature ejaculation can be treated effectively with selective serotonin reuptake inhibitors (SSRIs). A meta-analysis showed a rank order of efficacy, with paroxetine exerting the strongest effect on ejaculation. 3 However, treatment outcome with SSRIs for PE is not universally successful. 4 In addition, despite significant fold increase of intravaginal ejaculatory latency time (IELT) from baseline in some patients, they still have IELT time less than 2 minutes. The emotional burden of PE is very clear. Any PE patients may lack self-esteem with performance anxiety and feelings of shame and inferiority. Five-hydroxytryptamine (5-HT or serotonin) is involved in ejaculatory control. 5-HT is probably the most widely studied neurotransmitter implicated in mediating ejaculation. To date, three 5-HT receptor subtypes (5-HT 1A , 5-HT 1B , and 5-HT 2C) have been postulated to mediate 5-HT's modulating activity on ejaculation. 5 Waldinger et al 6 reported that activation of the 5HT 2C receptors delays ejaculation, whereas activation of the 5HT 1A receptors speeds up ejaculation response. The 5-HT 1B receptor agonist anpirtoline delays ejaculation in rats. 7 5-HT 1A autoreceptors have Bbraking[ effect on 5-HT-mediated function. In addition, it has been reported that buspirone, an anxiolytic with 5-HT 1A partial agonist properties, is effective in the treatment of SSRI-related PE. 8 Experimental studies have demonstrated that SSRIs, such as fluvoxamine or citalopram, increase the extracellular concentration of 5-HT at synaptic terminals, proximity of cell bodies, and dendrites of 5-HT neurones in the raphe nucleus. 9 Activation of the 5-HT 1A autoreceptors inhibits 5-HT neurone firing and, hence, 5-HT release in terminal synapses. 10 Therefore, weak or delay of clinical SSRIs effects might be due to feedback inhibition of 5HT release. 11 If this were true, pharmacological blockade of 5-HT 1A autoreceptors should mimic the effect of autoreceptor desensitization and improve the effects of SSRIs. Pindolol has 5-HT 1A auto-receptor antagonist properties. 12 Pindolol blocks 5-HT 1A autoreceptors in the dorsal raphe nuclei and potentiates the increase in 5-HT transmission induced by SSRIs. There has been considerable interest in the development of new pharmacological approaches aimed at enhancing the therapeutic action of SSRIs in PE. We examined the effectiveness of a pindolol-paroxetine combination in patients with PE Original Contribution
Central European Journal of Urology
Comparison of the treatment efficacies of paroxetine, fluoxetine and dapoxetine in low socioeconomic status patients with lifelong premature ejaculationJournal of Clinical Psychopharmacology
Once-Daily High-Dose Pindolol for Paroxetine-Refractory Premature Ejaculation2008 •
A Double-Blind, Placebo-Controlled and Randomized Study Mohammad Reza Safarinejad, MD Purpose: To evaluate the efficacy and safety of pindolol 7.5 mg/d in delaying of ejaculation in paroxetine-refractory patients. Materials and Methods: Eighty-six married men (mean age, 33 years) with premature ejaculation unresponsive to paroxetine 20 mg/d given for 2 months or longer were randomized to receive 7.5 mg pindolol (n = 44) (group 1) (PXT + POL) or placebo (n = 42) (group 2) (PXT + PBO) for 6 weeks, while continuing paroxetine. After 6 weeks, all patients received paroxetine and placebo and were followed for 3 further weeks in a single-blind manner. Pretreatment evaluation included history and physical examination, mean intravaginal ejaculatory latency time (IELT), International Index of Erectile Function (IIEF), and Meares-Stamey test. The efficacy of 2 treatments was assessed every 1 week during treatment and, at the end of study, using responses to IIEF, IELT evaluation, mean intercourse satisfaction domain, mean weekly coitus episodes, and adverse drug effects. Results: Seventy-seven (89.5%) completed the whole treatment schedule. At the end of 6-week treatment period, the IELT after paroxetine-pindolol and paroxetine-placebo gradually increased from mean 48 and 41 seconds to approximately 188 and 58 seconds, respectively (P = 0.001). The mean weekly intercourse episodes increased from pretreatment values of 1.5 and 1.5 to 2.7 and 1.7, for groups PXT + POL and PXT + PBO, respectively (P = 0.01). Baseline mean intercourse satisfaction domain values of IIEF 12 and 11 reached to 16 and 11 at 6-week treatment in PXT + POL and PXT + PBO groups, respectively (P = 0.01). Upon discontinuing pindolol, all outcome measures returned to baseline values rapidly. The incidence of side effects with paroxetine-pindolol was significantly higher (P = 0.04). Conclusions: These findings support that a single high dose of pindolol (7.5 mg) is an effective augmentation strategy in paroxetine-refractory patients. (J Clin Psychopharmacol 2008;28:39-44) N ormal ejaculation function relies on the coordination of neurogenic, psychologic, relational, and sociocultural factors. Premature ejaculation (PE) is the most frequent sexual complaint in men. 1 Psychopharmacotherapy for PE was initiated when delayed ejaculation was encountered as a side effect of antidepressants more than 40 years ago. 2 Premature ejaculation can be treated effectively with selective serotonin reuptake inhibitors (SSRIs). A meta-analysis showed a rank order of efficacy, with paroxetine exerting the strongest effect on ejaculation. 3 However, treatment outcome with SSRIs for PE is not universally successful. 4 In addition, despite significant fold increase of intravaginal ejaculatory latency time (IELT) from baseline in some patients, they still have IELT time less than 2 minutes. The emotional burden of PE is very clear. Any PE patients may lack self-esteem with performance anxiety and feelings of shame and inferiority. Five-hydroxytryptamine (5-HT or serotonin) is involved in ejaculatory control. 5-HT is probably the most widely studied neurotransmitter implicated in mediating ejaculation. To date, three 5-HT receptor subtypes (5-HT 1A , 5-HT 1B , and 5-HT 2C) have been postulated to mediate 5-HT's modulating activity on ejaculation. 5 Waldinger et al 6 reported that activation of the 5HT 2C receptors delays ejaculation, whereas activation of the 5HT 1A receptors speeds up ejaculation response. The 5-HT 1B receptor agonist anpirtoline delays ejaculation in rats. 7 5-HT 1A autoreceptors have Bbraking[ effect on 5-HT-mediated function. In addition, it has been reported that buspirone, an anxiolytic with 5-HT 1A partial agonist properties, is effective in the treatment of SSRI-related PE. 8 Experimental studies have demonstrated that SSRIs, such as fluvoxamine or citalopram, increase the extracellular concentration of 5-HT at synaptic terminals, proximity of cell bodies, and dendrites of 5-HT neurones in the raphe nucleus. 9 Activation of the 5-HT 1A autoreceptors inhibits 5-HT neurone firing and, hence, 5-HT release in terminal synapses. 10 Therefore, weak or delay of clinical SSRIs effects might be due to feedback inhibition of 5HT release. 11 If this were true, pharmacological blockade of 5-HT 1A autoreceptors should mimic the effect of autoreceptor desensitization and improve the effects of SSRIs. Pindolol has 5-HT 1A auto-receptor antagonist properties. 12 Pindolol blocks 5-HT 1A autoreceptors in the dorsal raphe nuclei and potentiates the increase in 5-HT transmission induced by SSRIs. There has been considerable interest in the development of new pharmacological approaches aimed at enhancing the therapeutic action of SSRIs in PE. We examined the effectiveness of a pindolol-paroxetine combination in patients with PE Original Contribution
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