Sexuality and disease.

Disease is commonly associated with sexual dysfunction in both men and women. In many cases, effective treatments are available that can improve libido, erectile dysfunction, and vaginal dryness. Sexual problems in older persons with disease often lead to anxiety, marital discord, and withdrawal. It is the responsibility of all health care professionals to inquire about sexuality in all patients, no matter what the patient's age, and to be aware that frailty [79-81] is not, in itself, a barrier to sexuality. Health professionals need to give education, support, and counseling on sexuality for patients with disease.

Potential role of type 5 phosphodiesterase inhibition in the treatment of congestive heart failure.

Endothelial dysfunction is associated with impairment of aerobic capacity in patients with heart failure and may play a role in the progression of disease. Impaired endothelium-dependent vasodilation in patients with heart failure can be attributed to decreased bioavailability of nitric oxide and attenuated responses to nitric oxide in vascular smooth muscle. Impaired vasodilation in response to nitric oxide derived from vascular endothelium or organic nitrates in vascular smooth muscle may be related in part to increased degradation of the second messenger cyclic guanosine monophosphate by type 5 phosphodiesterase. Sildenafil, a specific type 5 phosphodiesterase inhibitor currently approved for the treatment of erectile dysfunction, has been shown to acutely enhance endothelium-dependent vasodilation in patients with heart failure. Further studies are warranted to characterize the safety and efficacy of type 5 phosphodiesterase inhibition in the treatment of chronic heart failure.

Advances in radical prostatectomy

In the western world, adenocarcinoma of the prostate is the most common malignant neoplasm of human males. In recent years, the incidence of the disease has increased dramatically in China. Surgery is an important treatment for prostate cancer. This article reviews the progress in radical retropubic and perineal prostatectomy, standard laparoscopic and robot-assisted laparoscopic radical prostatectomy. It covers the necessity, techniques and experience of surgery, nerve preserving techniques and erectile dysfunction, complications and outcomes, advantages and disadvantages of and comparison between various surgical approaches.

Sildenafil: emerging cardiovascular indications.

The discovery in 1989 of sildenafil, a highly selective inhibitor of phosphodiesterase-5 (PDE-5), was the result of extensive research on chemical agents targeting PDE-5 that might potentially be useful in the treatment of coronary heart disease. Initial clinical studies on Sildenafil Citrate ( Viagra ) in the early 1990s were not promising with respect to its antianginal potential. However, the incidental discovery of its antiimpotence effect led to its approval of for the treatment of erectile dysfunction. Thereafter, several reports of adverse cardiac events in patients on Sildenafil Citrate ( Viagra ) raised concerns about its safety in cardiovascular disorders. Novel therapeutic indications are emerging for Sildenafil Citrate ( Viagra ) with the recent discovery that PDE-5 is expressed in various other tissues such as the arterial vasculature, including pulmonary and coronary arteries, venous vasculature, skeletal muscles, platelets, and visceral and tracheobronchial muscles. In this review we briefly summarize the pharmacology of Sildenafil Citrate ( Viagra ) and the current available evidence on its potential therapeutic applications in cardiovascular disorders. erectile dysfunction Endothelial function and dysfunction. Part II: Association with cardiovascular risk factors and diseases. A statement by the Working Group on Endothelins and Endothelial Factors of the European Society of Hypertension.

Dysfunction of the vascular endothelium is a hallmark of most conditions that are associated with atherosclerosis and is therefore held to be an early feature in atherogenesis. However, the mechanisms by which endothelial dysfunction occurs in smoking, dyslipidaemia, hyperhomocysteinaemia, diabetes mellitus, arterial hypertension, cerebrovascular diseases, coronary artery disease and heart failure are complex and heterogeneous. Recent data indicate that endothelial dysfunction is often associated with erectile dysfunction, which can precede and predict cardiovascular disease in men. This paper will provide a concise overview of the mechanisms causing endothelial dysfunction in the different cardiovascular risk factors and disease conditions, and of the impact of the intervention measures and treatments.

Hyperprolactinemia in men: clinical and biochemical features and response to treatment.

Hyperprolactinemia induces hypogonadism by inhibiting gonadotropin-releasing hormone pulsatile secretion and, consequently, follicle-stimulating hormone, luteinizing hormone, and testosterone pulsatility. This leads to spermatogenic arrest, impaired motility, and sperm quality and results in morphologic alterations of the testes similar to those observed in prepubertal testes. Men with hyperprolactinemia present more frequently with a macroadenoma than a microadenoma. Symptoms directly related to hypogonadism are prevalent. In men hypogonadism leads to impaired libido, erectile dysfunction, diminished ejaculate volume, and oligospermia. It is present in 16% of patients with erectile dysfunction and in approx 11% of men with oligospermia. Treatment with bromocriptine or cabergoline (CAB) is effective in men with prolactinomas, with a response that is in general comparable to treatment in women. Seminal fluid abnormalities rapidly improve with CAB treatment, while other dopaminergic compounds require longer periods of treatment. Moreover, to improve gonadal function in men, the integrity of the hypothalamic-pituitary-gonadal axis is necessary. New promising data indicate that a substantial proportion of patients with either micro- or macroprolactinoma do not present hyperprolactinemia after long-term withdrawal from CAB. Whether this corresponds to a definitive cure is still unknown, but treatment withdrawal should be attempted in patients achieving normalization of prolactin levels and disappearance of tumor mass to investigate this issue.

Therapeutic strategies for optimizing PDE-5 inhibitor therapy in patients with erectile dysfunction considered difficult or challenging to treat.

Phosphodiesterase 5 (PDE5) inhibitors prevent the normal hydrolysis of cGMP. As the resulting cGMP accumulation facilitates penile smooth muscle relaxation, PDE5 inhibitors can partially reverse deficiencies in the nitric oxide (NO)/cGMP pathway to treat erectile dysfunction (ED). However, approximately 30-40% of men with ED do not respond to drug therapy. Patients with severe neurologic damage, diabetes mellitus, or severe vascular disease may be resistant to PDE5 inhibitors. Decreased expression or activity of neuronal or endothelial NO synthase (NOS), impaired NO release, or NO destruction will preclude sufficient cGMP formation to permit PDE5 inhibitor efficacy. This article discusses the possible reasons for unresponsiveness and strategies to overcome it. Therapeutic approaches proposed to increase available NO in penile tissue include facilitating NO release by using alpha-2 antagonists, enhancing NO synthesis by providing more substrate for the reaction, and using antioxidants to inhibit NO breakdown by reactive oxygen species.

Phosphodiesterase 5 inhibitors in rapid ejaculation: potential use and possible mechanisms of action.

Rapid (premature) ejaculation (RE) is a very common sexual disorder. This condition may be primary or secondary to underlying disease. Control of RE has been primarily focused on behavioural therapy, topical anaesthetics, tricyclic antidepressants and selective serotonin reuptake inhibitors; however, an approved treatment does not exist. Recently, a number of clinical trials have studied the potential effectiveness of the phosphodiesterase (PDE)-5 inhibitor Sildenafil Citrate ( Viagra ) in the treatment of RE. Results of most of these studies have been encouraging. Available data indicate that there is clinical, anatomical, physiological, pharmacological and genetic evidence to explain the efficacy of PDE5 inhibitors in RE. The rationale for the use of PDE5 inhibitors in the treatment of RE could be due to possible peripheral and central mechanisms. Possible peripheral ejaculation retarding capabilities may include modulation of the contractile response of the vas deferens (VD), seminal vesicles (SV), prostate and urethra, induction of a state of peripheral analgesia, and prolongation of the total duration of erection. Possible central mechanisms may involve lessening of the central sympathetic output. Furthermore, there is evidence from knockout mice to explain the efficacy of PDE5 inhibitors in RE. Mice lacking the gene for endothelial nitric oxide synthase develop a condition similar to RE. On the other hand, mice lacking the gene for heme oxygenase-2 develop a condition similar to delayed ejaculation. This review also discusses the findings against the use of these agents in RE. In conclusion, a review of the literature suggests the potential usefulness of PDE5 inhibitors as a promising line of therapy in RE but further studies are needed. erectile dysfunction Cavernosal nerve mapping: current data and applications.

Although nerve-sparing prostatectomy is widely practised, the results with respect to preserving potency often do not meet expectations. The concept of intraoperative cavernosal nerve stimulation is reasonable. Data that link the response to Sildenafil Citrate ( Viagra ) after prostatectomy with bilateral nerve sparing has increased the importance of optimizing nerve sparing. The cavernosal nerves are often difficult to visualize and may have a variable course. A tumescent response to nerve stimulation can be shown consistently; the response may be subtle, and characterized by a minimal increase in penile circumference and blood flow. Immediately after prostatectomy, proximal nerve stimulation identifies whether neural continuity has been maintained, and is predictive of recovery of erectile function. The Cavermap system (Uromed Corporation, Boston, MA, USA) was developed to permit intraoperative nerve stimulation with tumescence monitoring. An initial phase 2 and subsequent phase 3 single-blinded, randomized, multicentre study that compared Cavermap-assisted prostatectomy with conventional nerve sparing showed a significant benefit in terms of the duration of nocturnal tumescence at 1 year. Other approaches are being explored, including incorporating the device into sural or genito-femoral nerve grafting, use of nerve stimulation during cystectomy or abdominal-perineal resection, and direct corpus cavernosal pressure monitoring during nerve stimulation. These approaches warrant further evaluation.

Erectile dysfunction and the cardiovascular patient: endothelial dysfunction is the common denominator.

Erectile dysfunction (ED) is a common condition and studies predict that it will become even more common in the future. There is increasing evidence to suggest that it is predominantly a vascular disease and may even be a marker for occult cardiovascular disease. The common pathological process is at the level of the endothelium, and cardiovascular risk factor control may be the key to preventing ED. Many men with established cardiovascular disease have ED. Specific guidelines for the management of ED in these patients have been produced by an expert panel. Cardiovascular risk stratification is an important initial step in managing such patients. In cardiac patients considered to have low cardiovascular risk, the management of ED can be safe and effective.

Causes of erectile dysfunction.

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.

Phosphodiesterase 5 inhibitors in rapid ejaculation: potential use and possible mechanisms of action.

Rapid (premature) ejaculation (RE) is a very common sexual disorder. This condition may be primary or secondary to underlying disease. Control of RE has been primarily focused on behavioural therapy, topical anaesthetics, tricyclic antidepressants and selective serotonin reuptake inhibitors; however, an approved treatment does not exist. Recently, a number of clinical trials have studied the potential effectiveness of the phosphodiesterase (PDE)-5 inhibitor Sildenafil Citrate ( Viagra ) in the treatment of RE. Results of most of these studies have been encouraging. Available data indicate that there is clinical, anatomical, physiological, pharmacological and genetic evidence to explain the efficacy of PDE5 inhibitors in RE. The rationale for the use of PDE5 inhibitors in the treatment of RE could be due to possible peripheral and central mechanisms. Possible peripheral ejaculation retarding capabilities may include modulation of the contractile response of the vas deferens (VD), seminal vesicles (SV), prostate and urethra, induction of a state of peripheral analgesia, and prolongation of the total duration of erection. Possible central mechanisms may involve lessening of the central sympathetic output. Furthermore, there is evidence from knockout mice to explain the efficacy of PDE5 inhibitors in RE. Mice lacking the gene for endothelial nitric oxide synthase develop a condition similar to RE. On the other hand, mice lacking the gene for heme oxygenase-2 develop a condition similar to delayed ejaculation. This review also discusses the findings against the use of these agents in RE. In conclusion, a review of the literature suggests the potential usefulness of PDE5 inhibitors as a promising line of therapy in RE but further studies are needed.