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Marcel D Waldinger

Publications and source records attributed to Marcel D Waldinger.

26 records · Page 2Linked to original sources
PubMed2005

On-demand SSRI treatment of premature ejaculation: pharmacodynamic limitations for relevant ejaculation delay and consequent solutions.

INTRODUCTION: Recently, the idea has emerged that on-demand use of serotonin reuptake inhibitors (SSRIs), particularly short half-life, should be equally effective in delaying ejaculation as daily SSRI treatment of premature ejaculation. AIM: To provide evidence that SSRI-induced ejaculation delay is mainly dependent on pharmacodynamic properties of the drug and hardly on pharmacokinetic factors, and that combined SSRI administration with specific 5-hydroxytryptamine (5-HT) receptor antagonism leads acutely to stronger ejaculation delay than acute SSRI monoadministration. METHODS: We performed a detailed analysis of serotonin neurotransmission and reviewed animal studies with 5-HT(1A) receptor antagonists. In addition, we critically reviewed existing on-demand SSRI treatments publications and the current debate on a definition of premature ejaculation. MAIN OUTCOME MEASURES: Intravaginal ejaculation latency time (IELT). RESULTS: Acute SSRI administration leads to only a mild or no increase of 5-HT neurotransmission and concomitant stimulation of postsynaptic 5-HT receptors. Existing on-demand SSRI treatment studies suffer from methodological insufficiencies, and the reported high-fold increases of ejaculation time contradict with neuropharmacological insights from serotonin metabolism. Animal studies show that SSRI coadministration with 5-HT(1A) receptor antagonists significantly increases the ejaculation time acutely compared to acute SSRI monoadministration. CONCLUSION: On-demand SSRI treatment has less ejaculation-delaying effects than daily SSRI treatment. SSRIs with a short half-life are likely leading to much less ejaculation delay than current registered SSRIs. Combined use of SSRIs with 5-HT(1A) receptor antagonists increases the likelihood of clinically relevant ejaculation delay after on-demand treatment. On-demand SSRIs with short half-life that insufficiently delay ejaculation in men with IELTs less than 1 minute should be called ejaculation-delaying drugs rather than drugs against premature ejaculation.

Animals↗
PubMed2004

On-demand treatment of premature ejaculation with clomipramine and paroxetine: a randomized, double-blind fixed-dose study with stopwatch assessment.

OBJECTIVE: To investigate the degree of ejaculation delay induced by on-demand treatment with 20 mg paroxetine and 25 mg clomipramine and to assess the type and severity of non-sexual side-effects of treatment at the day of and the day after treatment with these drugs. METHOD: A randomized, double-blind, fixed-dose, on-demand study in 30 men with lifelong premature ejaculation was performed. During a 1-month baseline period and a 4-week drug treatment period patients assessed the intravaginal ejaculation latency time (IELT) at home with a stopwatch. Only men with an IELT <1 min were randomly assigned to drug treatment. Patients assessed the drug coitus interval time (DCIT) and used the UKU side effect scale questionnaire at baseline, the day of and the day after intercourse. RESULTS: On-demand treatment with 25 mg clomipramine, with a mean DCIT of 5.14 h, led to a 4.05 (95%CI: 3.26-5.02) fold-increase of the IELT. On-demand treatment with 20 mg paroxetine, with a mean DCIT of 5.39 h, led to a 1.41 (95%CI: 1.22-1.63) fold-increase of the IELT. Both drugs had a high incidence of non-sexual side effects at the coitus day and the next day. At the day of coitus paroxetine led to significant sleepiness and yawning compared to clomipramine. At the day after coitus clomipramine induced significant nausea compared to paroxetine. CONCLUSION: On-demand treatment with 25 mg clomipramine led to a clinical relevant ejaculation delay. In contrast, 20 mg paroxetine had no clinical relevant ejaculation delay in men with lifelong premature ejaculation with an IELT of less than 1 minute. Both drugs exert mostly mild yet annoying non-sexual side effects both at the coitus day and the next day.

Adolescent↗
PubMed2004

Utility of selective serotonin reuptake inhibitors in premature ejaculation.

The introduction of selective serotonin reuptake inhibitors (SSRIs) has revolutionized our understanding of the treatment of premature ejaculation. Lifelong premature ejaculation may be a neurobiological phenomenon, namely part of a biological variability of the intravaginal ejaculation latency time in men. Animal studies support this view, and an animal model for premature and delayed ejaculation has recently been developed. It is proposed that drug treatment of premature ejaculation should consist of 5-hydroxytryptamine (5-HT)2c receptor stimulation and/or 5-HT1A receptor inhibition. A meta-analysis of 35 daily treatment studies with selective serotonin reuptake inhibitors (SSRIs) and clomipramine demonstrated comparable efficacy of clomipramine with the SSRIs sertraline and fluoxetine in delaying ejaculation, whereas the efficacy of the SSRI paroxetine was greater than all other SSRIs and clomipramine. It is postulated that acute treatment with SSRIs, including those with short half-lives, will not produce an ejaculation delay equivalent to that induced by daily treatment of SSRIs.

Animals↗
PubMed2003

Antidepressants and ejaculation: a double-blind, randomized, fixed-dose study with mirtazapine and paroxetine.

A double-blind, fixed-dose study in healthy men with lifelong early ejaculation was performed to evaluate potential differences in their effects on ejaculation latency, between clinically relevant doses of the selective serotonin reuptake inhibitor paroxetine and the noradrenergic and specific serotonergic antidepressant mirtazapine. Twenty-four men with an intravaginal ejaculation latency time (IELT) less than 1 minute were randomly assigned to paroxetine (20 mg/d) or mirtazapine (30 mg/d) for a period of 6 weeks; half the dosage was given in the first week. During the preceding 1-month baseline and 6-week treatment period, intravaginal ejaculation latency times were measured at home using a stopwatch procedure. The trial was completed by 18 men. Analysis of variance revealed a between-group difference in the development of the delay in intravaginal ejaculation latency time over time (P < 0.001); the intravaginal ejaculation latency time after paroxetine and mirtazapine gradually increased from 15 to 119 s and from 23 to 28 s, respectively, after 6 weeks. Paroxetine 20 mg/d exerted a strong delay (maximum 5.7-fold increase), whereas mirtazapine 30 mg/d did not delay ejaculation (0.9-fold increase). These results confirm earlier findings that paroxetine, but not mirtazapine, significantly delays orgasm and ejaculation in men with early ejaculation, whereas mirtazapine is devoid of any effect on it.

Adolescent↗
PubMed2002

The selective serotonin re-uptake inhibitors fluvoxamine and paroxetine differ in sexual inhibitory effects after chronic treatment.

RATIONALE: The selective serotonin re-uptake inhibitors (SSRIs) delay orgasm and ejaculation in men. In men with rapid ejaculation it was shown that, of the SSRIs, paroxetine exerted the strongest delay in ejaculation and fluvoxamine the weakest. OBJECTIVES: In the present study, we compared the acute and chronic effects of fluvoxamine and paroxetine on sexual behavior in the male rat in order to compare their differential inhibitory effects on sexual behavior. METHODS: During a 4-week period, 48 male Wistar rats, selected on the basis of their sexual performance, were repeatedly tested for sexual behavior. All male rats received vehicle (saline, n=12), fluvoxamine (30 mg/kg, n=12), or paroxetine (10 mg/kg, n=12) daily for 2 weeks. Sexual behavioral tests were performed on days 1 (acute), 7, and 14. RESULTS: After acute oral administration, fluvoxamine and paroxetine did not inhibit sexual behavior. After 7 days and 14 days treatment, fluvoxamine mildly inhibited certain parameters of sexual behavior but ejaculation was never delayed. In contrast, paroxetine, after 7 days and particularly after 14 days treatment, strongly inhibited sexual behavior, including ejaculation. CONCLUSIONS: These results strongly concur with clinical data, suggesting that paroxetine, but not fluvoxamine, delays ejaculation. Because fluvoxamine does not delay ejaculation it may serve as an optimal treatment for depressive illness when sexual side effects, such as a delayed ejaculation, are undesired. The mechanisms whereby paroxetine and fluvoxamine, both being selective serotonin uptake inhibitors, differentially inhibit sexual behavior are unclear.

Animals↗
PubMed2002

The neurobiological approach to premature ejaculation.

PURPOSE: Data showing the neurobiological background of rapid ejaculation was reviewed. In addition, new hypotheses to integrate clinical symptomatology, psychopharmacotherapy and psychotherapy of rapid ejaculation with brain function are provided. MATERIALS AND METHODS: A computerized MEDLINE search, and manual bibliographic review of cross-references and neurobiological animal studies were performed. These reports were analyzed, summarized and compared with the studies performed by the author. RESULTS: The literature on premature ejaculation published between 1887 and 2001 was reviewed. It appeared that the various psychological hypotheses and psychotherapies have not adequately been investigated. In contrast, psychopharmacological treatment studies, animal research data and stopwatch assessments in men with rapid (premature) ejaculation indicate that lifelong rapid ejaculation is a neurobiological phenomenon related to central serotonergic neurotransmission and likely influenced by hereditary factors. CONCLUSIONS: Basic and clinical psychopharmacological studies suggest that premature ejaculation is a not a psychological disturbance but a neurobiological phenomenon.

Animals↗
PubMedDate not supplied

Postorgasmic illness syndrome: two cases.

We describe the symptoms of a postejaculatory syndrome in two men with spontaneous ejaculations. The syndrome consists of severe fatigue, intense warmth, and a flulike state, with generalized myalgia. These symptoms occur rapidly after ejaculation and only disappear after 4 to 7 days. The symptoms are so severe that sexual activity is avoided. The cluster of symptoms is named postorgasmic illness syndrome (POIS). To date, no explanation has been offered for the etiology and pathogenesis of the symptoms, and the prevalence is unknown. Both cases are presented to draw attention to this syndrome for further research regarding etiology, pathogenesis, and treatment.

Adult↗