Introduction Ejaculatory/orgasmic disorders, common male sexual dysfunctions, include premature ejaculation, inhibited ejaculation, anejaculation, retrograde ejaculation and anorgasmia. Aim To provide recommendations/guidelines concerning state-of-the-art knowledge for management of ejaculation/orgasmic disorders in men. Methods An International Consultation in collaboration with the major urology and sexual medicine associations assembled over 200 multidisciplinary experts from 60 countries into 17 committees. Committee members established specific objectives and scopes for various male and female sexual medicine topics. The recommendations concerning state-of-the-art knowledge in the respective sexual medicine topic represent the opinion of experts from five continents developed in a process over a 2-year period. Concerning the Disorders of Ejaculation/Orgasm in Men Committee, there were nine experts from six countries. Main Outcome Measure Expert opinion was based on grading of evidence-based medical literature, widespread internal committee discussion, public presentation and debate. Results Premature ejaculation management is dependent upon etiology. When secondary to ED, etiology-specific treatment is employed. When lifelong, initial pharmacotherapy (SSRI, topical anesthesia, PDE5 inhibitors) is appropriate. When associated with psychogenic/relationship factors, behavioral therapy is indicated. When acquired, pharmacotherapy and/or behavioral therapies are preferred. Retrograde ejaculation, diagnosed with spermatozoa and fructose in centrifuged post-ejaculatory voided urine, is managed by education, patient reassurance, pharmacotherapy or bladder neck reconstruction. Men with anejaculation or anorgasmia have a biologic failure of emission and/or psychogenic inhibited ejaculation. Men with age-related penile hypoanesthesia should be educated, reassured and be instructed in revised sexual techniques which maximize arousal. Conclusions More research is needed in understanding management of men with ejaculation/orgasmic dysfunction.

Patients with primary premature ejaculation have penile hypersensitivity, which provides further implications for an organic basis of premature ejaculation.

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Patients with premature ejaculation have hypersensitivity and hyperexcitability of the glans penis, which may give rise to uncontrolled ejaculation and are believed to be organic implications for premature ejaculation.

Patients with primary premature ejaculation have penile hypersensitivity, which provides further implications for an organic basis of premature ejaculation.

Icariin and icariside II (ICA II), 2 active components isolated from herba epimedii, have a closely structural relationship. There is evidence that icariin may be useful in the treatment of erectile dysfunction (ED); however, the study on the therapeutic efficacy of ICA II on ED is currently scant. We investigated the effects of ICA II on improving erectile function of rats with streptozocin-induced diabetes. Fifty 8-week-old Sprague-Dawley rats were randomly distributed into normal control and diabetic groups. Diabetes was induced by a onetime intraperitoneal injection of streptozocin (60 mg/kg). Three days later, the diabetic rats were randomly divided into 4 groups including a saline-treated placebo arm and 3 ICA II-treated models (1, 5, and 10 mg/kg/d). After 3 months, penile hemodynamics was measured by cavernous nerve electrostimulation (CNE) with real time intracorporal pressure assessment. Penises were harvested with subsequent histological examination (picrosirius red stain, Hart elastin stain, and immunohistochemical stain) and Western blots to explore the expression of the nitric oxide-cyclic guanosine monophosphate (NOcGMP) and transforming growth factor b1 (TGFb1)/Smad2 signaling pathways. Diabetes significantly attenuated erectile responses to CNE. Diabetic rats had decreased corpus cavernosum smooth muscle/collagen ratio and endothelial cell content relative to the control group. The ratio of collagen I to III was significantly lower in the corpora of diabetic rats; furthermore, cavernous elastic fibers were fragmented in the diabetic animals. Neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase, and vascular endothelial growth factor were expressed at lower levels in the diabetic group; ICA II-treated diabetic rats had higher expression in the penis relative to placebo-treated diabetic animals. Both the TGFb1/Smad2/connective tissue growth factor (CTGF) signaling pathway and apoptosis were down-regulated in the penis from ICA II-treated rats. ICA II treatment attenuates diabetes-related impairment of penile hemodynamics, likely by increasing smooth muscle, endothelial function, and nNOS expression. ICA II could alter corpus cavernosum fibrous-muscular pathological structure in diabetic rats, which could be regulated by the TGFb1/Smad2/CTGF and NO-cGMP signaling pathways.

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Objectives: SS-cream is a topical agent made from the extracts of natural products for treating premature ejaculation (PE). To determine the optimal clinical dosage of SS-cream on PE, we investigated the safety and ef®cacy of SS-cream with various doses. A double blind, randomized placebo controlled clinical study was performed. Methods: Fifty patients completed the study. Mean age of the patients was 37.1 AE 1.0 y and mean ejaculatory latency was 1.35 AE 0.07 min. Sexual satisfaction rate of both the partner and patient was 16.2%. Each patient was instructed to apply the different cream (placebo, SS-cream 0.05, 0.10, 0.15, 0.20 g) on glans penis 1 h before sexual intercourse in random fashion. The ejaculatory latency was measured by stop watch and the satisfaction rate of both partner and patient was also recorded two times in the screening period and after the application of each test drugs. Clinical ef®cacy was considered if ejaculatory latency was prolonged more than 2 min and sexual satisfaction rate increased more than 20% than that of pretest values. Results: The mean ejaculatory latencies were signi®cantly prolonged after using various test drugs (placebo 2.27 AE 0.32, SS-cream 0.05 g 4.47 AE 0.81, 0.10 g 5.34 AE 0.79, 0.15 g 6.22 AE 0.87, 0.20 g 11.06 AE 1.17 min, respectively). Clinical ef®cacies evaluated by ejaculatory latency were placebo 18%, SS-cream 0.05 g 30%, 0.10 g 60%, 0.15 g 54%, 0.20 g 84%, respectively. The satisfaction rate was also signi®cantly increased dose-dependently (placebo 26%, SS-cream 0.05 g 60%, 0.10 g 70%, 0.15 g 78%, 0.20 g 90%, respectively). A side effect such as local mild burning sensation was noted in 35/250 times (14%) and no adverse effect on sexual function and no systemic side effects were observed. From the result of logistic regression analysis on clinical ef®cacy, the ED 50 of SScream was obtained as 0.10 g. SS-cream 0.20 g was effective in 84% without any serious systemic side effects. Conclusion: From the above results, our conclusions are that SS-cream is effective on the treatment of PE with a few local side effects and that clinical optimal dose of SS-cream is 0.20 g.