ABSTRACT
Premature ejaculation (PE), as one of the most common male sexual dysfunctions, has a serious negative impact on the sexual satisfaction of the patients and their sexual partners. Lifelong PE is a most common type and a current focus of research as well. The etiology and pathogenesis of this disease are not yet clear and genetic factors are considered to be closely related to lifelong PE. Studies show that the 5-hydroxytryptamine transporter (5-HTT) gene plays an important role in the development and progression of lifelong premature ejaculation and the 5-HTT-linked polymorphic region (5-HTTLPR) has attracted much attention in recent years. This article presents an overview on the correlation between 5-HTTLPR and lifelong PE.
Subject(s)
Adult , Humans , Male , Ejaculation , Polymorphism, Genetic , Premature Ejaculation , Genetics , Serotonin Plasma Membrane Transport Proteins , GeneticsABSTRACT
<p><b>Objective</b>To investigate the correlation between the premature ejaculation diagnostic tool (PEDT) and International Index of Erectile Function-15 (IIEF-15) in different types of premature ejaculation (PE).</p><p><b>METHODS</b>We performed a cross-section survey among 352 PE patients received in the andrology clinic from December 2014 to December 2015 and 104 healthy men from the health examination center using basic demographic information (as on age, height, weight, education status, occupation, income, etc.), PEDT results, and IIEF-15 scores of the subjects.</p><p><b>RESULTS</b>The PE patients had remarkably higher PEDT and lower IIEF-15 scores than the healthy men (P<0.01). The PEDT score of the PE patients was negatively correlated with their total IIEF-15 score as well as with the scores in the domains of erectile function, sexual intercourse satisfaction, and overall satisfaction after adjusted for age (P<0.01). The patients with acquired PE (APE) showed a lower IIEF-15 score than those with lifelong PE (LPE) (P<0.01). The PEDT score of the APE patients was correlated negatively with the total IIEF-15 score (r=－0.391, P<0.01) and the scores in the domains of erectile function (r=－0.362, P<0.01) and overall satisfaction (r=－0.621, P<0.01), but not correlated with intercourse satisfaction, sexual orgasm, or sexual desire. The PEDT score of the LPE group was correlated negatively with intercourse satisfaction (r=－0.286, P<0.05) but not correlated with either the total IIEF-15 score or the scores in the domains of erectile function, overall satisfaction, sexual orgasm, or sexual desire.</p><p><b>CONCLUSIONS</b>PE patients have a higher PEDT score and a lower IIEF-15 score than normal males. The PEDT score of APE patients is significantly correlated with the total IIEF-15 score, while that of LPE patients is correlated not with the total IIEF-15 score but with intercourse satisfaction.</p>
Subject(s)
Adult , Humans , Male , Middle Aged , Andrology , Case-Control Studies , Coitus , Psychology , Cross-Sectional Studies , Erectile Dysfunction , Libido , Penile Erection , Physiology , Personal Satisfaction , Premature Ejaculation , Diagnosis , Surveys and QuestionnairesABSTRACT
<p><b>OBJECTIVE</b>To observe the effificacy and safety of Qiaoshao Formula (, QSF) on patients with lifelong premature ejaculation (LPE) of Gan (Liver) depression and Shen (Kidney) defificiency syndrome.</p><p><b>METHODS</b>A total of 60 LPE patients were randomly divided into treatment (QSF) and control (dapoxetine) groups. The treatment group received QSF twice a day and the control group received dapoxetine 1 to 2 h prior to planned sexual intercourse for 4 weeks. The outcomes included intra-vaginal ejaculation latency time (IELT), premature ejaculation diagnostic tool (PEDT), clinical global impression of change (CGIC), scores of Chinese medicine symptoms (CMSS), sex life satisfaction (SLS) and adverse events (AEs).</p><p><b>RESULTS</b>In the treated group, the median IELT was 3 min vs. 1.5 min before and after treatment (P<0.05). PEDT in the treated group was reduced to 11.76±1.68 from 15.83±2.30 after treatment (P<0.05). Besides, patient's SLS was improved from 1.30±0.05 to 6.30±0.04 (P<0.05), and spouse's SLS was increased from 1.30±0.to 6.10±0.06 (P<0.05); CMSS was decrease from 14.86±3.02 to 9.62±2.87 (P<0.05). In addition, no significant AE was observed in both groups.</p><p><b>CONCLUSION</b>QSF may be effective and safe on LPE patients with Gan depression and Shen defificiency syndrome.</p>
Subject(s)
Adult , Humans , Male , Middle Aged , Young Adult , Drugs, Chinese Herbal , Therapeutic Uses , Kidney , Pathology , Liver , Pathology , Personal Satisfaction , Premature Ejaculation , Diagnosis , Drug Therapy , Syndrome , Time Factors , Treatment OutcomeABSTRACT
PURPOSE: To investigate the association between the 5-HT-transporter-gene-linked promoter region (5-HTTLPR) polymorphism and 20-mg paroxetine-induced ejaculation delay in men with lifelong premature ejaculation (LPE). MATERIALS AND METHODS: This was a prospective study of 10 weeks of paroxetine treatment in 54 men with LPE. Intravaginal ejaculation latency time (IELT) was measured by stopwatch. Controls consisted of 92 Caucasian men. All men with LPE were genotyped for the 5-HTTLPR polymorphism. Allele frequencies and genotypes of short (S) and long (L) variants of the polymorphism were compared between patients and controls. Associations between the LL, SL, and SS genotypes and fold increase of mean IELT were investigated. RESULTS: Of the 54 patients, 43 (79.6%) responded to 20-mg paroxetine treatment with an ejaculation delay, whereas 11 patients (20.4%) did not respond; 44%, 18%, and 18% of the patients showed a fold increase in mean IELT of 2-10, 10-20, and more than 20, respectively. Of the 54 men, 14 (25.9%) had the LL genotype, 29 (53.7%) had the SL genotype, and 11 (20.4%) had the SS genotype. In the 92 controls, the LL, SL, and SS genotypes were present in 27 (29.3%), 41 (44.6%), and 24 (26.1%), respectively. No statistically significant differences were found in 5-HTTLPR allelic variations or in 5-HTTLPR gene variations. In all men treated with 20 mg paroxetine, analysis of variance of the natural logarithm of fold increase in the IELT showed no statistically significant difference according to genotype (p=0.83). CONCLUSIONS: The 5-HTTLPR polymorphism is not associated with daily 20-mg paroxetine treatment-induced ejaculation delay in men with LPE.
Subject(s)
Humans , Male , Ejaculation , Gene Frequency , Genotype , Paroxetine , Premature Ejaculation , Promoter Regions, Genetic , Prospective Studies , Serotonin Plasma Membrane Transport Proteins , SerotoninABSTRACT
PURPOSE: Nonresponse to any selective serotonin reuptake inhibitor (SSRI) treatment is rare. In this study, we aimed to investigate ejaculation delay nonresponse to paroxetine treatment in men with lifelong premature ejaculation (PE) who were also known to be nonresponders to other SSRIs. MATERIALS AND METHODS: Five males with lifelong PE who were known nonresponders to paroxetine and other serotonergic antidepressants and eight males with lifelong PE who were specifically recruited were included. Blood sampling occurred 1 month and 1 day before the start of treatment and at the end of three consecutive series of 4 weeks of daily treatment with 10-, 20-, and 30-mg paroxetine, respectively. Blood samples for measurement of leptin and paroxetine were taken at 8:30 AM, 9:30 AM, 10:30 AM, and 11:30 AM, respectively. At 9:00 AM, one tablet of 10-, 20-, or 30-mg paroxetine was taken during the first, second, and third month, respectively. Intravaginal ejaculatory latency time (IELT) was measured with a stopwatch. The main outcome measures were the fold increase in the geometric mean IELT, serum leptin and paroxetine concentrations, body mass index (BMI), 5-HT1A receptor C-1019G polymorphism, and CYP2D6 mutations. RESULTS: Between the 7 paroxetine responders and 6 nonresponders, the fold increase in the geometric mean IELT was significantly different after daily 10-mg (p=0.003), 20-mg (p=0.002), and 30-mg paroxetine (p=0.026) and ranged from 2.0 to 8.8 and from 1.1 to 1.7, respectively. BMI at baseline and at the end of the study was not significantly different between responders and nonresponders. Serum leptin levels at baseline were similar in responders and nonresponders and did not change during treatment. The serum paroxetine concentration increased with increasing dosage and was not significantly different between responders and nonresponders. There was no association between the fold increase in the geometric mean IELT and serum paroxetine levels during the three treatment periods nor between leptin levels during the treatment periods and serum paroxetine levels. For the 5-HT1A receptor C-1019G variation, all responders had the CC genotype and all nonresponders had the GC genotype, respectively. CONCLUSIONS: Complete absence of paroxetine-induced ejaculation delay is presumably related to pharmacodynamic factors and perhaps to 5-HT1A receptor gene polymorphism.
Subject(s)
Adolescent , Adult , Aged , Humans , Male , Middle Aged , Young Adult , Body Mass Index , Cytochrome P-450 CYP2D6/genetics , Leptin/blood , Mutation , Paroxetine/administration & dosage , Polymorphism, Genetic , Premature Ejaculation/drug therapy , Receptor, Serotonin, 5-HT1A/genetics , Risk Factors , Selective Serotonin Reuptake Inhibitors/administration & dosage , Time Factors , Treatment OutcomeABSTRACT
PURPOSE: Nonresponse to any selective serotonin reuptake inhibitor (SSRI) treatment is rare. In this study, we aimed to investigate ejaculation delay nonresponse to paroxetine treatment in men with lifelong premature ejaculation (PE) who were also known to be nonresponders to other SSRIs. MATERIALS AND METHODS: Five males with lifelong PE who were known nonresponders to paroxetine and other serotonergic antidepressants and eight males with lifelong PE who were specifically recruited were included. Blood sampling occurred 1 month and 1 day before the start of treatment and at the end of three consecutive series of 4 weeks of daily treatment with 10-, 20-, and 30-mg paroxetine, respectively. Blood samples for measurement of leptin and paroxetine were taken at 8:30 AM, 9:30 AM, 10:30 AM, and 11:30 AM, respectively. At 9:00 AM, one tablet of 10-, 20-, or 30-mg paroxetine was taken during the first, second, and third month, respectively. Intravaginal ejaculatory latency time (IELT) was measured with a stopwatch. The main outcome measures were the fold increase in the geometric mean IELT, serum leptin and paroxetine concentrations, body mass index (BMI), 5-HT1A receptor C-1019G polymorphism, and CYP2D6 mutations. RESULTS: Between the 7 paroxetine responders and 6 nonresponders, the fold increase in the geometric mean IELT was significantly different after daily 10-mg (p=0.003), 20-mg (p=0.002), and 30-mg paroxetine (p=0.026) and ranged from 2.0 to 8.8 and from 1.1 to 1.7, respectively. BMI at baseline and at the end of the study was not significantly different between responders and nonresponders. Serum leptin levels at baseline were similar in responders and nonresponders and did not change during treatment. The serum paroxetine concentration increased with increasing dosage and was not significantly different between responders and nonresponders. There was no association between the fold increase in the geometric mean IELT and serum paroxetine levels during the three treatment periods nor between leptin levels during the treatment periods and serum paroxetine levels. For the 5-HT1A receptor C-1019G variation, all responders had the CC genotype and all nonresponders had the GC genotype, respectively. CONCLUSIONS: Complete absence of paroxetine-induced ejaculation delay is presumably related to pharmacodynamic factors and perhaps to 5-HT1A receptor gene polymorphism.