SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Erectile dysfunction (ED) is defined as a temporary or permanent inability to obtain or maintain erection sufficient for satisfactory sexual intercourse. ED is not considered to be a genuine disease, it is rather a symptom accompanying other systemic diseases. Almost 52 per cent of men claim erectile dysfunction of different degree, however, only 5-10 per cent of them would confirm their handicap.
Erectile dysfunction is a disorder with multifactorial causes. The pathophysiological origin can be severe general disease. Consequently each patient has to undergo a general diagnostic procedure so that severe disease is not missed. The diagnostic work-up of erectile dysfunction follows a three-step scheme of increasing invasiveness. The non-invasive step is the most important. These investigations comprise taking an extensive general history including a detailed sexual history, psychological diagnosis, physical examination, and laboratory tests. The semi-invasive procedures include the intracavernous injection test, colour-coded duplex sonography and optional neurophysiological examinations. The invasive investigations include dynamic infusion pharmacological cavernosography and cavernosometry, and penile angiography. The extensiveness of the diagnostic procedures should be adapted to the complexity of the history and the therapeutic expectations. However, if there is any suspicion of a severe disease remaining undiagnosed, the diagnostic procedures should be adequately comprehensive.
Erectile dysfunction has an organic etiology in most cases, with vascular disease the single most common cause. In addition to a thorough history and physical examination, clinical evaluation may include hormonal assessment, diabetes screening, nocturnal tumescence testing and color Doppler flow studies of the penile vasculature. Therapy for erectile dysfunction has progressed rapidly during the past decade, with alternatives including hormone supplements, vacuum constriction devices, penile self-injection therapy and penile prostheses. The majority of patients and their partners report satisfactory results with these treatments.
Erectile dysfunction (ED) may be caused by abnormalities of intracavernous penile structures. In order to investigate whether specific proteins could be identified that might be related to ED, the composition of structural proteins in cavernous tissues of patients with ED was compared to that of normal cavernous tissues by gel electrophoresis. Increased expression of a 68-kDa nonionic detergent extraction-resistant protein was demonstrated in tissues of more than half of the patients with vasculogenic ED, whereas only one out of nine normal cavernous tissues showed the same phenomenon. Increased expression was not related to a specific type of vascular insufficiency, aging, or diabetic constituency. Histochemical and immunochemical studies revealed that the increased amount of the 68-kDa protein is not merely the result of a surplus of nervous, smooth muscle, or elastic tissues. Furthermore, antibodies specific for 68-kDa neurofilament and 62- to 67.5-kDa tropoelastin did not recognize the 68-kDa protein on Western blots. The possibility that the 68-kDa protein may help us understand the etiology of certain cases of erectile dysfunction is discussed.
Erectile dysfunction (ED) is a common medical condition affecting over 20 m men in the United States. Efficacious medical therapy for the treatment of erectile dysfunction has been available since the early 1980s and can be divided into local pharmacotherapy and systemic therapy. Alprostadil, a synthetic form of prostaglandin E1, is a useful local pharmacotherapeutic agent for the treatment ED. Alprostadil is presently available for administration as an intracavernosal injection or an intraurethral suppository. Local alprostadil therapy is effective at restoring the ability to participate in intercourse in up to 70% of men with ED. The principle side-effects of alprostadil are local, with few systemic reactions. The mechanism of alprostadil, its efficacy in clinical trials and side-effects are examined to outline the utility of alprostadil for the treatment of ED.
Erectile dysfunction (ED), defined by the Impotence-NIH Consensus Conference as the "persistent inability to achieve and/or maintain erection sufficient for satisfactory sexual activity" affect more than 100 million men worldwide, at particular severity levels. The global prevalence of ED is estimated to affect about 10%, but has been found to increase significantly with age (39% in men 40 years of age and 67% at 70 years of age). In men aged 40 to 70 years, the severe ED prevalence increased of three folds, 5 to 15%. In order to evaluate the efficacy and tolerance of sildenafil, it was conducted a national open, multicentre study on a portuguese population affected by ED. Subjects under ambulatory treatment were recruited in Psychiatry/Sexology Clinical units and Urology/Andrology. The results of the study carried out on a group of 62 men with ED, demonstrate that sildenafil was effective in the recovering of erectile function, increasing the number of attempts to sexual activity and improving their success rates (mainly in severe dysfunction). Fifty one patients treated with sildenafil, at the end of the study referred a global improvement in their erections (92.2%). Doses of 50 mg and 100 mg sildenafil were used and were well tolerated and also effective in the treatment of this pathology (70% and 69% respectively). Being this study a flexible dose one and taking into consideration that the final dose used was found the more suitable to the patients, can be concluded that 43.1% of the patients elected dose of 50 mg whereas 56.9% elected the maximum prescribed dose of 100 mg. Over and above global efficacy experimented by patients, a significant improvement in the sexual activity with partners was occurred. These results make possible a final conclusion--in the studied patients group affected by Erectile Dysfunction, aside from associated somatic pathology, sildenafil use provided a remarkable clinical profit, in what concerns global efficacy, by erectile function mechanisms improvement, concerning patients sensitivity of improvement, occurring in the major part of them, being these of high importance to the lifting up of their self-esteem.
Erectile dysfunction (ED) is a prevalent health condition with significant psychosocial impacts, yet the causal role of age at first sexual intercourse (AFS) remains unclear. This study investigated the causal effect of AFS on the risk of ED using Mendelian randomization (MR) and Bayesian methods. Five traditional 2-sample MR analyses and 5 Bayesian MR analyses were performed using genome-wide association studies summary statistics from European populations. Sensitivity analyses included MR Egger regression, MR-pleiotropy residual sum and outlier, and Cochran Q-test. In mixed-sex cohorts (Groups 1 and 2), inverse variance weighted results demonstrated significant protective effects: odds ratio (OR) = 0.626, θ = -0.469, P = 2.73 × 10-6 for Group 1 and OR = 0.617, θ = -0.483, P = 3.56 × 10-5 for Group 2. The analyses for male-specific cohorts (Groups 3-10) showed weaker but consistent effects. For Group 3, OR = 0.643, θ = -0.442, P = .010. For Group 4, some instrumental variables associated with confounders were removed. The result became statistically insignificant: OR = 0.680, θ = -0.385, P = .064. For Group 5, the instrument selection criteria were relaxed and significance was retained: OR = 0.695, θ = -0.364, P = .016. For Groups 6 to 10, Bayesian MR was used to strengthen the inferences. In particular, for Group 8, which has a strongly informed prior, a posterior mean θ = -0.358 and a 95% credible interval (-0.575, -0.136) were obtained. This study provides evidence supporting a causal protective effect of later AFS on ED risk. While traditional MR analyses in male-specific cohorts yielded suggestive results, Bayesian MR analyses, which allow for the integration of prior evidence, provided more precise estimates and strengthened the causal inference. These findings may inform future sexual health policies. Strengths include the use of male-specific cohorts and Bayesian enhancement for weak instruments. Limitations include reliance on European-ancestry data and inability to stratify ED subtypes.
Erectile dysfunction (ED) is defined as the consistent inability to obtain or maintain an erection for satisfactory sexual relations. An estimated 20-30 million men suffer from some degree of sexual dysfunction. The past 20 years of research on erectile physiology have increased our understanding of the biochemical factors and intracellular mechanisms responsible for corpus cavernosal smooth muscle contraction and relaxation, and revealed that ED is predominantly a disease of vascular origin. Since the advent of sildenafil (Viagra), there has been a resurgence of interest in ED, and an increase in patients presenting with this disease. A thorough knowledge of the physiology of erection is essential for future pharmacological innovations in the field of male ED.
Erectile dysfunction (ED), assessed clinically by tools such as the International Index of Erectile Function (IIEF), affects millions of men across the world. Around 10-25% of men of all ages are affected rising to 20-45% in older age groups. Different definitions of ED and selection of different patient populations account for much of the variability reported in epidemiological surveys. Ageing populations in the developed world and growing populations in the developing world make it likely that the prevalence of ED will increase in the future. ED affects quality of life, and the condition may result in outcomes such as anxiety and withdrawal from a relationship. The condition remains a source of embarrassment for many men and health professionals, and it remains under-reported, under-recognized, and undertreated. Adequate medical assessment and intervention are needed to address ED.
Erectile dysfunction (ED) is a common condition with a significant deleterious effect on the quality of life. The prevalence rate of ED is about 20-45% and its incidence in western countries has been evaluated from 25 to 30 cases per 1000 person year. Risk factors of ED are ageing, diabetes, and cardiovascular, uro-genital, psychiatric and any chronic diseases. Smoking, hormonal factors and some drugs may be associated with ED. Modifications of risk factors must be initiated before the age of 50 to prevent ED occurrence. Two thirds of men with ED report embarrassment when discussing this problem with a physician and less than 25% ask for medical advice. As a symptom of endothelial dysfunction, ED may be considered a premonitory sign of coronary or peripheral vascular disease and diabetes.
Erectile dysfunction (ED) is often the first clinical sign of endothelial dysfunction and may precede overt cardiovascular diseases. Bone marrow-derived endothelial progenitor cells migrate into the peripheral circulation to promote endothelial repair. The number of circulating progenitor cells is reduced in patients with cardiovascular risk factor. The objective of our study was to determine the number of these cells in patients with ED both with and without cardiovascular risk factors. These subjects have lower number of circulating progenitor cells, confirming the existence of an endothelial dysfunction and supplying the evidence that ED may be the first symptom of an endothelial damage.
Erectile dysfunction (ED) is a highly prevalent and often under-treated condition. Erection is basically a spinal reflex that can be initiated by recruitment of penile afferents but also by visual, olfactory and imaginary stimuli. The generated nervous signals will influence the balance between contractile and relaxant factors, which control the degree of contraction of penile corporal cavernosal smooth muscles and, thus, determine the erectile state of the penis. The different steps involved in neurotransmission, impulse propagation and intracellular transduction of neural signals may be changed in different types of ED. Recent studies have revealed important roles for the small GTPase RhoA and its effector, Rho-kinase in regulating cavernosal smooth muscle tone. The RhoA/Rho-kinase pathway modulates the level of phosphorylation of the myosin light chain, mainly through inhibition of myosin phosphatase, and contributes to agonist-induced Ca(2+)-sensitization in smooth muscle contraction. Changes in this pathway may contribute to ED in various patient subgroups (e.g. hypertension, diabetes, hypogonadism). This review summarizes the importance of Rho-kinase signaling in the erectile response and introduces the evidence pointing to RGS-containing Rho-guanine nucleotide exchange factors (GEFs) as critical mediators of RhoA-GTPase activation in cavernosal smooth muscle and its possible compartmentalization in the caveolae. In addition, we suggest that the design of selective inhibitors of these GEFs might represent a novel class of pharmacological agents to treat ED.
Erectile dysfunction (ED), more commonly known as impotence, is, along with men's health in general, a neglected subject. In this article, the author highlights reasons why ED may occur, the treatments available and why professionals should encourage men to discuss this problem.
Erectile dysfunction (ED) is a common male sexual dysfunction. Some ED patients who do not respond to any nonsurgical therapy will eventually be candidate for penile prostheses. This paper introduces the characteristics and application of inflatable penile prosthesis made in China.
Erectile dysfunction may affect one in 10 men as they age. The publicity surrounding the introduction of Viagra has led to more men coming forward for treatment for ED. Specialist urology nurses have the communication and counselling skills necessary to provide quality care to this patient group.
Erectile dysfunction (ED) profoundly affects the quality of life. The prevalence of ED in renal transplant recipients is reported by high as 50% to 60%. We evaluated the efficacy and safety of vardenafil in these patients with ED as well as its effects on graft function and on cylosporine or tacrolimus concentrations. Thirty-nine recipients with ED and serum creatinine values<2 mg/dL were treated with vardenafil. ED was assessed using the self-administered International Index of Erectile Function (IIEF). ED was diagnosed by using penile color-Doppler ultrasonography and intracavernosal injection. Vardenafil efficacy was assessed by readministering the IIEF questionnaire after 4 weeks of therapy. Serum creatinine levels, creatinine clearances, and cyclosporine/tacrolimus concentrations were measured before and after vardenafil therapy. Twenty-one recipients with ED served as placebo controls and 15 without ED as another control group. The IIEF scores improved from 12.80+/-3.5 to 26.46+/-2.4 in vardenafil-treated patients with ED (P<.001). Renal function and cyclosporine/tacrolimus concentrations did not change with vardenafil therapy. Side effects were observed in 7 (18%) patients: headache in three, palpitations in one, flushing in two, and dyspepsia in one. This study demonstrated that ED improved with vardenafil in renal transplant recipients with ED. For 4 weeks vardenafil therapy was free of side effects. Renal function tests did not change. Also, no dose change in immunosuppressive drugs was required during 4 weeks of verdanafil therapy.
Erectile dysfunction (ED) arises as a result of a collision of circumstances among any of a number of factors (e.g., risk factors, causes, probable associations), each with its own primary power to affect the outcome. Furthermore, each of the components has its own timing as part of a complex effort of compensation and adjustment that often obscures the individual details. In the end, ED results from a failure of local tissues or systemic supply and control structures. The power of any individual "cause" to degrade erectile function is an important but as-yet unquantified property. The power of a small abnormality over a long or critical period (e.g., organogenesis), or many small contributions, or multiple risk factors will certainly be greater than the sum of the individual elements. Without a full quantitation of pathways and their potential influence, one can compare the importance of causative factors only in limited ways. Not surprisingly, it is the presence of a multiplicity of unidentified or poorly understood causative factors that accounts in large measure for the current inability to cure and prevent ED. There are two other important properties of a putatively causative factor for ED--reversibility and preventability--and these are strongly influenced by the time of onset and the duration of impact. Thus, a critical understanding that comes from recognizing the importance of the temporal associations of component factors is that the causes of ED in an individual may be guessed at but cannot be fully disclosed by an analysis of a "snapshot" of the disease taken at the time of diagnosis.
Erectile dysfunction (ED) is defined as the inability to attain and/or maintain penile erection sufficient for satisfactory sexual performance. ED is a highly prevalent health problem with considerable impact on the quality of life of men and their partners. Although the treatment of ED with oral phosphodiesterase type V (PDE5) inhibitors is effective in a wide range of individuals, it is not efficacious in all patients. The failure of PDE5 inhibitors happens mainly in men with diabetes, non-nerve sparing radical prostatectomy, and high disease severity. Therefore, improved therapies based on a better understanding of the fundamental issues in erectile physiology and pathophysiology have recently been proposed. Here, we summarize studies on ED treatment using gene and stem cell therapies. Adenoviral-mediated intracavernosal transfer of therapeutic genes, such as endothelial nitric oxide synthase (eNOS), calcitonin gene-related peptide (CGRP), superoxide dismutase (SOD), and RhoA/Rho kinase and mesenchymal stem cell-based cell and gene therapy strategy for the treatment of age- and diabetes-related ED are the focus of this review.