Primary and secondary prevention of erectile dysfunction

Erectile dysfunction has an incidence of up to 75% in men aged 80, thus making primary prevention really important. Aetiologically multiple reasons are responsible for erectile dysfunction; therefore, recommendations for primary prevention contain different parts. The first one is to maintain a healthy arterial system and prevent atherosclerosis. Besides that diabetes, neurogenic disturbances or mental distress should be avoided. Physical activity, balanced nutrition, nonsmoking, unsaturated fatty acids and moderate alcohol consumption are preventive. Regular erections cause oxygenation of the cavernous body and prevent fibrosis which could lead to an insufficient occlusion of the cavernous veins. If the patient already suffers from coronary heart disease or diabetes, blood pressure, pulse, blood lipids and blood sugar should be as normal as possible. Erectile dysfunction might be the primary symptom of coronary heart disease; therefore, consideration should be given to a cardiac examination in the diagnostic setting.     

Neurogenic erectile dysfunction

Neurogenic erectile dysfunction is a consequence of alterations in neural pathways, autonomic, somatic, the combination of both or brain components that induce erection. This review aims to explain the physiopathological mechanisms of the most frequent neurological alterations causing erectile dysfunction and sexual disorders.     

Neurologic erectile dysfunction

Neurologic erectile dysfunction presents a diagnostic and treatment challenge to the internist and urologist. Multiple chronic disease modalities and traumatic etiologies exist. Education regarding these conditions and a detailed and thorough history and office work-up are the best resources for the clinician. Treatment can follow the model of proceeding from the least to most invasive procedure (process of care), taking into account patient and partner satisfaction. Because the psychology of grief and loss may enter into treatment of some neurologic conditions (e.g., erectile dysfunction after radical retropubic prostatectomy, spinal cord injury, or chronic diseases), a whole-patient approach encompassing psychotherapy is warranted.     

Vascular erectile dysfunction

Vascular etiology is present in up to 60% of the patients with erectile dysfunction (ED). Both small vessel disease, such as that in diabetes mellitus, and arteriosclerosis of bigger size arteries, as in hypertension, cause arterial insufficiency and erectile dysfunction. Tobacco smoking alters the arterial hemodynamics in the penis, causing erectile dysfunction in a high percentage of advanced age smokers: pelvic arteries fibrosis and stenosis accelerates the existing arteriosclerosis. Venous occlusive dysfunction may be due to the decrease of corpora cavernosa compliance or tunica albuginea inherent anomalies. Vascular endothelial growth factor may play a role in the modulation of vascularization of the normal penile architecture. Various events, all of them important, may cause erectile dysfunction. Moreover, no cause can participate independently. A cascade of situations (including psychological factors as well as organic) may lead to erectile dysfunction. A continuous understanding of organic causes of erectile dysfunction will allow physicians to discover treatments for their correction, as well as to give confidence to the patient.     

Endothelial dysfunction in diabetic erectile dysfunction

Erectile dysfunction (ED) is highly prevalent in diabetes mellitus. Pathophysiological mechanisms underlying diabetes-associated ED are in large part due to endothelial dysfunction, which functionally refers to the inability of the endothelium to produce vasorelaxing messengers and to maintain vasodilation and vascular homeostasis. The precise mechanisms leading to endothelial dysfunction in the diabetic vasculature, including the penis, are not yet fully understood. Hyperglycemia affects endothelial nitric oxide synthase activity and nitric oxide production/bioavailability, nitric oxide-independent relaxing factors, oxidative stress, production and/or action of hormones, growth factors and/or cytokines, and generation and activity of opposing vasoconstrictors. Considering recent advances in the field of vascular biology and diabetes, the emphasis in this review is placed on the mechanisms of hyperglycemia-induced endothelial dysfunction in the pathophysiology of diabetes-associated ED.     

Imaging for erectile dysfunction

Radiological imaging in the field of erectile dysfunction has diminished in importance over the past 5 years with the advent of new therapies. However, in selected cases, Doppler scanning continues to have a role, and current research is aimed at optimizing the results of the tests. In addition, the new techniques of functional magnetic resonance imaging and positron emission tomography scanning are beginning to offer new insights into the central mechanisms which control erections.     

Hyperlipidemia and erectile dysfunction

We have done consecutive studies to investigate the effects of impaired lipid metabolism on the contractile and relaxation response of cavernous smooth muscles and to elucidate its pathogenesis: 1 ) incidence of hyperlipidemia in impotent patients; 2) erection response to intmcavemous injection of papaverine in impotent patients with hyperlipidemia; 3) relaxation responses of isolated cavemosal smooth muscles to endothelium-independent and endothelium-dependent vasodilators in impotent patients with hypercholesterolemia or hypertriglyceridemia; 4) involvement of superoxide radical in the impaired endothelium-dependent relaxation of cavernous smooth muscle in hypercholesterolemic rabbits; 5) effects of isolated lipoproteins and triglyceride, combined oxidized LDL plus triglyceride, and combined oxidized LDL plus HDL on contractile and relaxation response of rabbit cavernous smooth muscles; 6) involvement of e-NOS in the impaired endothelium-dependent relaxation of cavernous smooth muscle in hypercholesterolemic rabbit. Hypercholesterolemia may cause impairment of endothelium-dependent relaxation. Oxidized LDL is the major causative cholesterol of the impaired relaxation response. A chain reaction, the production of superoxide radicals and functional impairment of eNOS may be a major cause of the functional impairment in the early stages of hypercholesterolemia.     

Penile structural erectile dysfunction

The delicate harmony by which the various elements in the penis work may be altered by different pathologies that damage its structure. Structural anomalies in the penis cause a failure of the hemodynamic event and erectile dysfunction, which is usually severe, resistant to medical treatment and generally non reversible. The most frequent physiopathologic mechanisms of these dysfunctions are loss of compliance in the erectile tissue, abnormal drainage, or severe alterations of penile geometry. Among possible etiologies are La Peyronie disease, priapism, diabetes, penile trauma, infiltration of corpora cavernosa by an inflammatory or neoplasic processes, and others.     

Pharmacotherapy of erectile dysfunction

Summary 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 developped at the moment, future pharmacological treatments will allow a more refined approach towards an individually adapted regimen.      

Epidemiology of erectile dysfunction

This review of the current epidemiological literature on erectile dysfunction (ED) suggests that approximately 5-20% of men have moderate-to-severe ED. Different definitions of ED, age distributions and concomitant medical conditions, as well as methodological differences, may explain much of the variance in reported prevalence rates. Various chronic disorders are associated with elevated rates of ED including depression, diabetes, and cardiovascular and neurological diseases. Such disorders are more common in the elderly, which may partially explain the elevated prevalence of ED in men over 60 y of age. Currently, up to 70% of men with ED are not treated. However, so many men experience considerable distress from their condition, that the increasing awareness of ED as well as the availability of noninvasive treatments may result in a greater proportion of patients seeking treatment, and eventually regaining satisfaction with their sex life.     

勃起功能障碍的药物治疗

勃起功能障碍的定义勃起功能障碍(erectile dysfunction,ED)是指持续或反复不能达到或维持足够阴茎勃起以完成满意性生活。ED是根据患者主诉来诊断的一种疾患,病程至少3个月以上。ED的病因很多,通过病史、体检、实验室检查和一些特殊检查,以期明确ED的病因是心因性还是器质性还是混合性ED,以及ED的程度(轻度、中度还是重度)。勃起功能障碍治疗的选择对ED治疗方法的选择,主要根据ED的病因、程度、医师的经验、患者的愿望以及技术条件等,此外尚需考虑到传统、伦理、社会经济状况及患者和配偶的喜好、期望和心理状况,还要考虑到宗教信仰…     

Testosterone and erectile dysfunction

Aging is associated with a decline in several important health factors in men, including libido. Serum testosterone concentrations also decrease with age, and many age-related clinical features are closely associated with androgen deficiency, including erectile function (ED). Approximately 70% of ED is of organic origin, with the major risk factors being diabetes mellitus, hypercholesterolemia, smoking and chronic medical illnesses. These are also established risk factors for atherosclerosis, which is the predominant predisposing factor of vasculogenic ED. The introduction of phosphodiasterase-5 (PDE-5) inhibitors for the treatment of ED made a significant impact both in terms of clinical efficacy, and increasing the awareness of the condition. In spite of this, some patients fail to respond to PDE-5 inhibitors alone. Both animal and clinical studies indicate that testosterone therapy improves both erectile function and the response to PDE-5 inhibitors in patients with ED and hypogonadism. Indeed, interventional studies demonstrate that testosterone replacement therapy improves erectile function in hypogonadal men who have previously failed to respond to PDE-5 inhibitors alone. Furthermore, it has been demonstrated that the full therapeutic potential of PDE5 inhibitors will only become manifest in a eugonadal state. Recent studies have demonstrated a close relationship between testosterone and ED and suggest that testosterone therapy may be a valuable option for an increasing number of affected men. European guidelines recommend that all men presenting with ED should have their testosterone concentrations measured.     

Diagnosis of erectile dysfunction

Erectile dysfunction (ED) is a problem that may affect up to 52% of men aged between 40 and 70. In the era of type-5 phosphodiesterase (PDE5) inhibitors, the treatment of ED can be simple and effective after the correct diagnosis which is made in the majority of cases with history, examination and some basic laboratory tests.     

Guidelines on erectile dysfunction

The introduction of new oral therapies has completely changed the diagnostic and therapeutic approach to erectile dysfunction. A panel of experts in this field have developed guidelines for clinical evaluation and treatment based on the review of available scientific information.