الفهرس 
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Abstract
Background: One of the most common male sexual dysfunctions is premature ejaculation (PE), which may lead to problems in sexual relationship and infertility. Many factors can contribute in this disorder (psychological and biological factors) causing either primary or acquired (PE), but most of them are not evidence based. Hormones have a central role in ejaculation control, thus pathological hormonal levels may directly or indirectly affect the ejaculatory control. Therefore, this study aimed to detect any association between dihydrotestosterone/estradiol ratio and testosterone/estradiol ratio in a cohort of premature ejaculatory dysfunction patients. Methods: a prospective case-control study was conducted on 104 men recruited from Mansoura University Hospitals Andrology outpatient clinic. They were divided into two groups, PE patients’ group (which classified into two subgroups; primary lifelong PE patients’ group and acquired PE patients’ group) and control group. Results: -The serum levels of DHT did not differ significantly between both primary PE and secondary PE and the control group. DHT levels was significantly higher in secondary PE compared to primary PE groups.There was lack of correlation between serum DHT and IELT .Serum DHT failed to discriminate between PE and healthy subjects in our study.Meanwhile, There was significant higher level of E2 among both primary and secondary PE compared with the control group.E2 was significantly higher in those with ED, prostatitis plus ED when compared to those without (p = 0.009, < 0.001 respectively). E2 level showed good AUC (AUC = 0.802) suggesting the ability of this hormone to discriminate between PE and healthy subjects at a cutoff value of 2.9 ng/dl. Both TT/E2 and DHT/E2 ratios were significantly lower in both primary and secondary PE compared with the control group. Both TT/E2 and DHT/E2 ratios were significantly lower in those associated with ED, prostatitis plus ED compared with those without suggesting that lower TT/E2 and DHT/E2 ratios may have a role in these conditions. DHT/E2 showed fair AUC (AUC = 0.749) and TT/E2 showed poor AUC (AUC = 0.666,) in discrimination between PE and normal controls. Conclusions: imbalance between androgens and estradiol may have a role in PE. Larger studies are required to verify these results and to understand how sex hormones affect PE and verify its clinical significance.