Hyperprolactinemia and erectile dysfunction

Hyperprolactinemia from a pituitary adenoma is a rare cause of erectile dysfunction. Men with erectile dysfunction who are found to have a low testosterone level should have a measurement of their prolactin level. Treatment consists of lowering the prolactin level by medication or surgery, or both. Bromocriptine, a dopamine agonist, is efficacious in lowering elevated prolactin levels and can simultaneously shrink these pituitary tumors. With large tumors, transphenoidal surgery may be used to debulk/remove the tumor. Post-treatment prolactin levels can be used to monitor the efficacy of treatment.     

Sexual dysfunction among Ghanaian men presenting with various medical conditions

Background  

Several medical conditions can affect and disrupt human sexuality. The alteration of sexuality in these medical conditions often hinder effective communication and empathy between the patients and their sexual partners because of cultural attitudes, social norms and negative feelings such as anxiety and guilt. Validated and standardized sexual inventories might therefore help resolve this problem. The objective of this cross-sectional study was to obtain data on the prevalence of male sexual dysfunction (SD) among Ghanaians with various medical conditions residing in Kumasi.     

Nonpharmacologic treatment of erectile dysfunction

Nonpharmacologic treatment for erectile dysfunction (ED) includes sex therapy, the use of vacuum erection devices, penile prosthesis implantation, and penile vascular surgery. Sex therapy is indicated for psychogenic ED and is at times a useful adjunct for other treatments in men with mixed psychogenic and organic ED. Vacuum erection devices produce usable erections in over 90% of patients; however, patient and partner acceptability is an issue. Three-piece inflatable penile prostheses create flaccidity and an erection that comes close to that which occurs naturally. Penile vascular surgery has shown greatest efficacy in young men with vasculogenic ED resulting from pelvic or perineal trauma.     

Relationship between testosterone and erectile dysfunction

Although erectile function is clearly androgen dependent, is it just as clear at what level of testosterone erectile dysfunction (ED) begins? Does the decline in testosterone that occurs with aging always produce ED? Are exogenous androgens the answer to ED? The answers range from clear to complex.     

Diabetes,obesity, and erectile dysfunction

Background: Diabetes mellitus (DM) and obesity affect large parts of the population in the United States and around the world. These disorders are among the most common risk factors for erectile dysfunction (ED), because of their effects on the vasculature and the hormonal milieu.Objective: This article reviews the current literature on the connection between DM, obesity, and ED.Methods: Using the search terms erectile dysfunction, endothelial dysfunction, hypogonadism, diabetes, and obesity, a systematic review of the available literature in the PubMed database was conducted. Relevant English-language publications (to August 2008) were identified.Results: ED is highly prevalent in men with both DM and obesity, and may act as a harbinger for cardiovascular disease (CVD) in this high-risk population. In addition to male hypogonadism and macrovascular disease, endothelial dysfunction is central to the connection between the metabolic syndrome and ED. Conversely, improved glycemic control and weight loss have been found to improve erectile function.Conclusion: ED is very prevalent in men with DM and obesity. It is increasingly being recognized as an early clinical indicator and motivator for patients with CVD. The role of pharmacologic ED treatments in improving endothelial function is currently being investigated.     

Managing concomitant cardiac disease and erectile dysfunction

Early studies of peak heart rates and blood pressure during coitus led physicians to believe that sexual activity represents a significant risk to patients with cardiovascular disease. Subsequent studies indicated, however, that the heart rate during coitus was no higher than the rate during unaccustomed physical exercise or associated with anger. The absolute risk of myocardial infarction (MI) in a patient with a history of MI has been found to be 10 per million per hour, and the doubling of this risk in the 2 hours following coitus has a negligible impact on annual risk. Coronary artery disease (CAD) is a powerful indicator of the presence of erectile dysfunction (ED), and the risk factors for ED are similar to those for CAD. Studies of sildenafil citrate use in patients with a history of cardiovascular disease have found sildenafil to be safe and effective, except for an absolute contraindication in the concomitant use of nitrates. Physicians should become familiar with the clinical guidelines for classifying ED patients with a history of cardiovascular disease as high risk, intermediate or indeterminate risk, and low risk. The guidelines permit physicians MIlow risk while deferring the resumption of sexual activity among higher risk patients pending further evaluation.     

Role of duplex scanning in the diagnosis of erectile dysfunction

A total of 110 patients aged 34-74 years who complained of erectile dysfunction (ED) were examined. A control group of 9 patients without complaints of ED was formed to determine the normal condition. Baseline ultrasonography was followed by scanning after intracavernous administration of a vasoactive drug to whose use 59 individuals contended to. In the control group, the variation of PSV values was in the range of 23-59 cm/sec. Among the patients with complaints of ED, the baseline study has indicated normal PSV values in both cavernous arteries in 21 cases of the 110 patients; in the other patients, the baseline cavernous arterial blood flow, such as that in the great arteries, was less than 30 cm/sec. Summing up the data of observations of 59 patients undergone erectile stimulation has ascertained that that 20, 34, and 4 patients were diagnosed as having the isolated arterial form of ED, the arteriovenous form, and venous form, respectively; there was no evidence for the form of vascular genesis in 1 patient. Ultrasonography, including color duplex scanning with Doppler energy flow mapping, and B-mode before and after erectile stimulation with intracavernous administration of an E1-prostaglandin drug, makes it possible to assess the contribution of the vascular component to the pathogenesis of erectile dysfunction.     

Postprostatectomy erectile dysfunction: the role of penile rehabilitation

Radical prostatectomy has become the gold standard for the treatment of prostate cancer in patients who have a longer than 10-year life expectancy. Surgical treatment has led to severe quality-of-life issues in these patients, especially urinary incontinence and erectile dysfunction (ED). This article reviews the etiology and pathophysiology of postprostatectomy ED, and current management strategies for these patients.     

Improved erectile function after Rho-kinase inhibition in a rat castrate model of erectile dysfunction

Androgens are reported to act as strong modulators of erectile function influencing both nitric oxide and vasoconstrictor signaling. Castration results in a depressed erectile response that is associated with a loss of nitric oxide production and increased responsiveness to constrictive agents. The increased vasoconstrictor response may be a result of an active RhoA/Rho-kinase signaling pathway. We report here results of studies designed to test the hypothesis that inhibition of the Rho-kinase pathway restores erectile function in a castrate model by relaxing the smooth muscle. Mean arterial (MAP) and corpus cavernosal (CCP) pressures were monitored during intracavernosal injection of the Rho-kinase inhibitor Y-27632. Castration reduced the maximal erectile response (CCP/MAP) by 33%, and testosterone replacement restored the response (intact, 0.736 +/- 0.040; castrate, 0.492 +/- 0.022; testosterone, 0.681 +/- 0.073). Injection of Y-27632 increased CCP in all experimental groups; it also left shifted the voltage response curve and increased the maximal CCP/MAP response (intact, 0.753 +/- 0.091; castrate, 0.782 +/- 0.081; testosterone treated, 0.894 +/- 0.033). Y-27632 dose dependently relaxed phenylephrine-stimulated cavernosal tissues. Cavernosal tissues showed increased RhoA and Rho-kinase protein levels after castration. Our data support the hypothesis that an active Rho/Rho-kinase pathway contributes to the reduced erectile response after castration due to an upregulation of RhoA/Rho-kinase protein levels and that inhibition of this pathway may serve as an effective treatment for erectile dysfunction.     

Novel azulene derivatives for the treatment of erectile dysfunction

Based on the dopamine D₄ receptor partial agonist FAUC 3019, a series of azulenylmethylpiperazines was synthesized and affinities for the monoaminergic GPCRs including dopamine, serotonin, histamine and α-adrenergic receptor subtypes were determined. Ligand efficacies of the most promising test compounds revealed the N,N-dimethylaminomethyl substituted azulene 11 to be the most potent D₄ partial agonist (EC₅₀ = 0.41 nM). This candidate was investigated for its ability to promote penile erection. Applying an in vivo animal model, test compound 11 turned out to stimulate penile erection in male rats with superior potency in low concentrations when compared to apomorphine.     

Oral and non-oral combination therapy for erectile dysfunction

An estimated 30 million men in the United States suffer from varying degrees of erectile dysfunction. Increasing age and comorbidities are likely to increase the number of men who are initially refractory or become refractory to phosphodiesterase (PDE)-5 inhibitors, the most popular oral therapy. Combination therapy, a concept well proved in other areas of medicine, is therefore of increasing importance. Combination oral and non-oral (intracavernosal injection and intraurethral application) therapies have been shown to salvage monotherapy. The early introduction of combination therapy has been shown to expedite both the return of natural function and PDE-5 inhibitor responsiveness in post-prostatectomy patients with no reports of serious adverse events. Larger controlled studies are needed to corroborate those encouraging findings.