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Erectile dysfunction (ED) affects as many as 30 million men and their partners in the United States. Although clinicians now recognize that as many as 80% of cases of ED are organic in origin, psychological issues remain important for the ED patient.
Erectile dysfunction (ED) has been the most neglected complication of diabetes. It is a common abnormality that affects more than 20 million American men. The prevalence of ED in the general population between the ages of 40 to 70 years is 52%. In men with diabetes, it ranges from 35% to 75%, and occurs at an earlier age. There have been several advances in the understanding of the physiologic and biochemical mechanisms controlling penile erections. Improved techniques in diagnoses and treatment of impotence have given the male with diabetes some hope in the management of this prevalent and emotionally disturbing complication.
Erectile dysfunction (ED) is defined as the consistent or recurrent inability of a man to attain and/or maintain a penile erection sufficient for sexual activity (2nd International Consultation on Sexual Dysfunction-Paris, June 28th-July 1st, 2003). Following the discovery and introduction of sildenafil, research on the mechanisms underlying penile erection has had an enormous boost and many preclinical and clinical papers have been published in the last 5 years. This review is structured in order to give the reader an overview of the clinical and preclinical data available on the peripheral regulation of and the mediators involved in human penile erection. The most widely accepted risk factors for ED are discussed. The article is focused on human data, and the safety and effectiveness of the 3 commercially available Phosphodiesterase-5 (PDE5) inhibitors used to treat ED are also discussed.
Diagnosis of erectile dysfunction (ED) now largely rests on the medical, sexual, and psychosocial history of the patient, ideally involving the man's partner. The medical history is crucial because ED is associated with so many common disorders and their treatment. A range of validated questionnaires may be used in taking the history. They can provide an objective and systematic record. The history helps identify whether the ED is largely physical or psychogenic. In particular, gradual onset suggests a physical cause, and sudden onset suggests a psychogenic cause. Physical examinations are not usually necessary. Taking blood pressure and physical examination of the genitals for signs of Peyronie's disease and hypogonadism may be helpful. Laboratory tests that identify diabetes (glycosylated haemoglobin), hyperlipidaemia (lipids), and hypogonadism (testosterone) may identify causes of ED. A range of specialized investigations, such as ultrasound and nocturnal penile tumescence and rigidity assessment, is also available, but is not used routinely in most patients with ED.
Pharmacotherapy of erectile dysfunction comprises oral and local application of drugs. Today, Yohimbin is the only drug listed for this indication. Yohimbin acts via central alpha-receptor blockade and showed a significant effect in a recent double blind study compared to placebo. The centrally acting substances Apomorphin and Trazodone were also tested for their potential use with Apomorphin showing promising results. The orally active phosphodiesterase-V inhibitor Sildenafil acts predominantly on the peripheral side; broad clinical studies demonstrated a significant effect of the drugs compared to placebo. For local use, intraurethral (MUSE) and intracavernous applications are available with PGE1 being the drug the most widely used for the moment. Since many different drugs with various modes of action and different modes of application are being developed at the moment, future pharmacological treatments will allow a more refined approach towards an individually adapted regimen.
Erectile dysfunction (ED) is commonly experienced in men with diabetes mellitus. Vascular endothelial growth factor (VEGF) has been extensively documented for its pathogenic significance in different complications of diabetes. We hypothesized that expressions of VEGF, its receptors and its signaling pathway Akt may be drastically altered in diabetic penile tIssues and their alterations may modulate penile expression of the molecules that are believed to play a role in diabetic ED. Otsuka Long-Evans Fatty (OLETF) rats, a type II (non-insulin-dependent) diabetes mellitus, were used at the insulin-resistant stage of type II diabetes (20 weeks of age). We determined protein and mRNA expressions of VEGF, its receptors, Akt, nitric oxide synthase isoforms, and apoptosis-related molecules in the penis using immunohistochemistry, Western blotting, in situ hybridization, and real-time quantitative PCR analyses. The penile sections were also submitted to the Tdt-mediated dUTP nick end labeling assay for apoptosis. OLETF rats showed marked reductions in penile expression of VEGF, its two receptors and Akt. In OLETF rat penises, endothelial and neuronal nitric oxide synthase isoforms were expressed less abundantly. Furthermore, while anti-apoptotic markers, Bcl-2 and phosphorylated Bad, were down-regulated, pro-apoptotic markers, active caspase-3 and Bax, were up-regulated, resulting in the appearance of apoptotic cells in the penile tIssues of OLETF rats. The VEGF signaling system would work less well in diabetic penile tIssues as a result of the reduced expression, leading to diminished endothelial production of nitric oxide and apoptosis-related erectile tIssue damage. We propose that the abnormalities of the VEGF signaling system in the penis may play a role in the pathophysiology of diabetic ED.
Erectile dysfunction (ED) management in the following 3-5 years will be dominated by substances targeting the L-arginine-NO-guanylate cyclase-cGMP-PDE-5 pathway, resulting in an intracellular elevation of the cGMP concentrations. Promising alternatives to the PDE-5 inhibitors, such as guanylate cyclase activators and Rho-kinase inhibitors, may also effectively compliment a PDE-5 inhibitor. Intranasal application of the melanocortin agonist PT 141 (Melanotan II) seems to be promising. As scheduled sexual activities are not preferred by the majority of couples, the future of ED-therapy will focus on drugs with a 1-2 day long efficacy window, or a daily bedtime application of low dosage agents which result in nocturnal reoxygenation of the cavernous bodies and in turn in functional improvement. Elevation of the cGMP levels and improvement of endothelial function as a result of this approach also promises benefits in cardiovascular diseases and in LUTS.
Nine men with chronic erectile dysfunction (three primary, six secondary) who had no regular sexual partner were treated in two 12-session all-male psychoeducational therapy groups. Treatment intervention addressed specific factors which inhibited adequate sexual function with a focus on coping skills to overcome those factors. Pre, post, and follow-up behavioral self-report data and responses on a goal attainment scale questionnaire indicated that the treatment groups were successful for five men with secondary and one man with primary erectile dysfunction. Subjective report and pre- and posttreatment fantasy productions to TAT cards for the first group indicated that all men significantly improved their attitudes about sexuality and their sexual self-concept. The results suggest that this is a viable, cost-effective treatment for secondary erectile dysfunction, but not for primary erectile dysfunction unless supplementary individual therapy is provided.
The pharmacological treatment of erectile dysfunction has taken central importance among therapeutic approaches for this increasingly recognized, widespread disorder. In the past decade and a half, the specialty of erectile dysfunction management has witnessed an enormous growth in basic scientific interest which has been translated impressively to the clinical arena. Discoveries of regulatory mechanisms involved in penile erection have been garnered both at peripheral neurologic and end organ levels and at central brain and spinal cord levels. These discoveries along with ongoing investigations in the field provide a firm foundation for implementing exciting and effective erectile dysfunction pharmacotherapies both now and in the future. The purpose of this report is to review the current trends and new directions in the pharmacotherapy of erectile dysfunction.
PURPOSE: Published studies on the epidemiology of erectile dysfunction and the physiology/ pathophysiology of erectile function are reviewed. MATERIALS AND METHODS: A literature search of more than 400 studies of the epidemiology and pathophysiology of impotence and erectile dysfunction published during the last 3 decades was conducted and the most pertinent articles are discussed. RESULTS: It has been estimated that the prevalence of erectile dysfunction of all degrees is 52% in men 40 to 70 years old, with higher rates in those older than 70 years. Erectile dysfunction has a significant negative impact on quality of life. Risk factors for erectile dysfunction include aging, chronic illnesses, various medications and cigarette smoking. A nitric oxide/cyclic guanosine monophosphate mechanism has an important role in mediating the corporal smooth muscle relaxation necessary for erectile function. Other mechanisms involving neuropeptides, gap junctions and ion channels also may modulate corporal smooth muscle tone. Erectile dysfunction can be due to vasculogenic, neurogenic, hormonal and/or psychogenic factors as well as alterations in the nitric oxide/cyclic guanosine monophosphate pathway or other regulatory mechanisms, resulting in an imbalance in corporal smooth muscle contraction and relaxation. CONCLUSIONS: Erectile dysfunction is a common condition associated with aging, chronic illnesses and various modifiable risk factors. Normal penile erection is a hemodynamic process that is dependent on corporal smooth muscle relaxation mediated by parasympathetic neurotransmission, nitric oxide, and possibly other regulatory factors and electrophysiological events. As more knowledge is gained of the physiology and regulatory factors that mediate normal erectile function, the mechanisms involved in the pathophysiology of erectile dysfunction should be further elucidated.
PURPOSE: The prevalence and severity of erectile dysfunction in patients with hypertension need to be further evaluated. We evaluate medical and hypertension status, and erectile function in patients with hypertension. MATERIALS AND METHODS: The International Index of Erectile Function, which is a detailed questionnaire, including well established components to evaluate patient medical history, hypertension status and erectile dysfunction, was mailed to 476 male patients of the outpatient Hypertension Center of Columbia Presbyterian Medical Center. RESULTS: The questionnaire was completed by 104 (22.3%) patients, and mean age was 62.2 years (range 34 to 75). Of the patients 84.8% were sexually active and 68. 3% had various degrees of erectile dysfunction, which was mild in 7. 7%, moderate in 15.4% and severe in 45.2%. Compared to the general population of erectile dysfunction cases in the literature our study population with hypertension had a higher incidence of severe erectile dysfunction. Although correlations of antihypertensive medications with incidence of erectile dysfunction did not reach statistical significance, there was a clear trend with patients treated with diuretics and beta-blockers having the highest incidence and those treated with alpha-blockers having the lowest incidence of erectile dysfunction. CONCLUSIONS: In addition to the observation that erectile dysfunction is more prevalent in patients with hypertension than in an age matched general population, our study shows that it is more severe in those with hypertension than in the general population.
Organic causes of erectile dysfunction with androgen deficiency may be associated with aging, systemic illness, and a number of specific endocrine disorders stemming from pituitary, thyroid, and adrenal dysfunction. Central hypogonadism is the main mechanism in the majority. Erectile dysfunction in diabetes mellitus is caused by chronic complications due to poor metabolic control. Diagnosis and management of these disorders are discussed, as is the need for tight glycemic control in men with diabetes.
To establish a mouse model for the study of venoocclusive erectile dysfunction, we investigated erectile function in wild-type (WT), castrated (CAST), and castrated mice receiving immediate testosterone replacement (TEST). Adult C57BL6 mice ( approximately 30 g) underwent electrical stimulation of the cavernous nerve in vivo (parameters: 16 Hz frequency, 5 ms duration, 4V stimulatory voltage) with intracavernosal pressure (ICP) monitoring. A total of 55 mice (5 WT, 25 CAST, and 25 TEST) were evaluated. CAST and TEST (5.0 mg/pellet, 60-day release) mice were divided into groups of 5 and evaluated at 24 hours, 72 hours, 1 week, 2 weeks, and 4 weeks. Penile tissue was immunohistochemically stained for alpha-actin (marker for smooth muscle cells) and CD-31 (marker for endothelial cells). Stained slides were analyzed using Image Pro-plus software. In secondary studies, a Doppler flow meter was employed to evaluate penile blood flow. ICP measurements (mm Hg) were significantly decreased in CAST mice at 24 hour-, 72 hour-, 1 week-, 2 week-, and 4-week time points compared with WT mice (41.9 +/- 14.9, 19.1 +/- 4.2, 17.5 +/- 8.2, 14.2 +/- 4.4, and 10.0 +/- 3.8, respectively, vs 50.2 +/- 2.8), but TEST animals maintained or had an increase in ICP in comparison with WT mice (48.0 +/- 1.4, 52.3 +/- 1.3, 60.8 +/- 7.6, 80.5 +/- 2.1, and 81.5 +/- 1.2, respectively). Mean systemic arterial pressure remained approximately 80 mm Hg irrespective of treatment. CAST mouse penis specimens revealed decreased alpha-actin and CD-31 immunoreactivity only at the 4-week interval, compared with WT and TEST specimens. Doppler ultrasound flow rates (centimeter per second), taken before, during, and immediately after cavernous nerve stimulation, were WT 45.4 +/- 7.3, 30.6 +/- 5.2, 55.3 +/- 8.2 vs CAST (2 weeks) 22.2 +/- 2.5, 25.0 +/- 1.5, 23.1 +/- 2.0 vs TEST (2 weeks) 30.5 +/- 6.5, 25.7 +/- 2.0, 45.2 +/- 4.5. This prominently showed that intrapenile flow was not reduced normally during erectile stimulation in CAST mice. This is the first described mouse model of castration-induced veno-occlusive erectile dysfunction. Erectile response abnormalities as measured by ICP and Doppler ultrasound studies in CAST mice may be attributed to hypogonadal effects on erectile tissue function. Morphologic changes in the cavernosal tissue of CAST mice coincide with these abnormalities to some extent. This study defines an androgen-dependent mechanism of veno-occlusive erectile function in the mouse. The castrated mouse model can be applied in future studies of veno-occlusive erectile dysfunction.
Patients with erectile dysfunction, who admitted to 4 different urological centres in Turkey were evaluated in terms of aetiological factors to establish the aetiology of erectile dysfunction in our population and compare it with the data derived from Western communities. After the history, physical examination, psychological evaluation and laboratory testing, a clinical diagnosis was established as primarily psychogenic, organic, or mixed aetiology. Mean patient age was 43.5 years (range 17 to 69), and 9 of the patients were unmarried. Of the patients 53 had vascular risk factors, and 10 reported a history of alcohol abuse. Eleven patients were using drugs that might interfere with the disorder. In this multicentral study of 115 impotent men, an organic cause was found in 43%, psychogenic in 47%, and mixed in 19%. Mean age of the overall patients was 43.48. When the ages of the patients with organic erectile dysfunction and those with psychogenic erectile dysfunction were compared, it was clearly seen that those with organic erectile dysfunction were much older (52.73 versus 33.02).
To expand our crosscultural understanding of erectile dysfunction, we investigated erectile dysfunction among Ariaal men, pastoral nomads of northern Kenya. To measure erectile dysfunction, we administered the International Index of Erectile Function (IIEF-5) to 198 men aged 20 y and older during interviews. Marital status and anthropometric measures of body composition were also obtained. Men were classified into 10-y age groups. ANOVA revealed that erectile dysfunction increases with age (P<0.0005), with men 60 y and older showing significantly higher erectile dysfunction compared with men in their 20s, 40s and 50s. In a MANCOVA model, erectile dysfunction increased with age group (P<0.001), was negatively related to right-hand grip strength (P<0.01) and negatively related to number of wives (P<0.05). In addition, there was a significant interaction between age group and marital status (P<0.01). Erectile dysfunction showed no independent relationship to measures of body composition, including body mass index, fat free mass and percentage body fat. These findings provide further evidence of age-related increases in erectile dysfunction, even when factors commonly associated with erectile dysfunction (eg, metabolic complications of obesity, use of medicines causing erectile dysfunction) are absent. The finding that number of wives is negatively related to erectile dysfunction may represent the specific cultural conditions (political power and wealth) associated with polygyny among the Ariaal.
An assessment tool to identify erectile dysfunction is useful to diabetes educators in recognizing patients with sexual dysfunction requiring further counseling, education, and treatment. Use of an assessment tool serves as a first step in creating dialogue between diabetes educators and patients living with undiagnosed erectile dysfunction. The assessment tool helps identify underlying causes of erectile dysfunction, its impact on psychological well-being, and identification of treatment and referral needs. The purpose of this article is to discuss the value of assessing erectile dysfunction as a component of comprehensive diabetes care. An example of an erectile dysfunction assessment tool developed in 1991 is presented.
Cardiovascular disease and erectile dysfunction share many common risk factors. In fact, recent studies have demonstrated evidence of occult coronary artery disease, undiagnosed hyperlipidemia, and hypertension in men presenting with erectile dysfunction. It is therefore incumbent upon all physicians, especially cardiologists, to query their patients about their erectile function.
The cause of erectile dysfunction was evaluated by a multidisciplinary approach in 120 impotent patients. Out of these, the CCAT was proposed to 20 patients with vasculogenic erectile dysfunction, 19 of them accepted this therapy. The dosage of phentolamine mesylate-papaverin hydrochloride injection required was determined in each patient individually. Usually we injected initially 1 cc in one corpus cavernosum. Eighteen patients followed the regimen successfully at home. In 2 patients prolonged erections were observed, which were successfully relieved by simple corpus puncture, however, discontinuation of therapy was not necessary. CCAT failed in 1/19 patients with a severe venous leak. Follow up was carried out weekly.