Introduction

The urologist/andrologist is the specialist responsible for diagnosis and treatment of health problems related to the genitourinary tract, and his or her participation in comprehensive care of erectile dysfunction (ED) is fundamental and often indispensable for the following reasons:

• The urologist/andrologist is responsible for the care of older patients with urological diseases in whom ED is highly prevalent and/or strongly associated with comorbid conditions, such as benign prostatic hyperplasia (BPH).
• He or she is familiar with specific urological diseases and treatments that lead to ED (eg prostate cancer, radical pelvic surgery, Peyronie's disease, and so on).
• He or she has sufficient medical and surgical qualifications to cover the whole spectrum of treatments for ED.

The role of the urology/andrology specialist is to apply the necessary methods to make a differential diagnosis between an organic or psychogenic etiology, and to diagnose, when indicated, the underlying organic disorder in the patient with ED.¹ Once a diagnosis has been established, treatment should be applied according to the method proposed in the core document, with the urology/andrology specialist responsible for management of second- and third-line treatments.

The possible sequelae of retropubic radical prostatectomy (RRP) include ED caused by damage to the neurovascular bundles of the penis during surgery. Virtually all patients undergoing this operation will report some ED.² The prevalence of ED has been reduced to 40–70% by the use of surgical techniques that attempt to preserve the neurovascular bundles uni- or bilaterally.

On the other hand, ED may also occur when radiotherapy is used for the treatment of prostate cancer. The incidence of ED is >45% following external radiotherapy³ and 50% (complete ED) to 72% (some ED) when radioactive implants (brachytherapy) are used.⁴ The cause of ED with external radiotherapy appears to be vasculogenic.

ED affects more than half of patients with renal failure, and of these patients only about 50% recover erectile function after transplantation.⁵

BPH is a very common disorder among middle-aged men. Recent publications suggest that BPH may be a risk factor for sexual dysfunction, as ED has been detected in up to 44% of patients with severe BPH and in 13% of milder cases.⁶ According to the EDEM (Epidemiologia de la Disfuncion Erectil Masulina) study, subjects with prostatic disease have a 2.9 and 2.7 times higher probability (OR) of developing ED than male subjects from the general population as measured by a Single Assessment Question and the Erectile Function Domain of the International Index of Erectile Function (IIEF), respectively.⁷ Furthermore, the EDEM study detected and quantified a strong association between lower urinary tract symptoms, measured with the International Prostate Symptom Score (IPSS), and the likelihood of developing ED, measured with the Erectile Function Domain of the IIEF.⁸ Taking subjects aged between 25 and 39 years with mild symptoms on the IPSS as a reference category, the risk of developing ED increases more than two-fold if urinary symptoms are moderate and more than three-fold if symptoms are severe in any of the age groups (Table 1).⁸

Table 1 - Risk of having ED by age and IPSS score (OR/95% CI).

Full table

ED may also be a consequence of some therapies used for BPH. ED has been reported in 4% of patients following transurethral incision of the prostate and transurethral resection of the prostate (TURP).⁵ Post-TURP ED appears to be secondary to damage to small nerve fibers innervating the penis.⁵ The incidence of ED reported with laser prostatectomy ranged from 3 to 17%.^{9, 10} When BPH is treated with finasteride, a 5-reductase inhibitor that blocks conversion of testosterone into dihydrotestosterone, erection may also be affected in 3.7% of patients;¹¹ erectile function is not affected by -blockers.

Diagnostic management of ED

The First International Consultation on Erectile Dysfunction held in Paris in 1999 under the patronage of the World Health Organization (WHO) was attended by a large number of experts from 29 countries. The objective was to develop recommendations for the diagnosis and treatment of ED.¹² This consultation established a classification of diagnostic tests for ED into highly recommended, recommended, optional, and specialized tests:

• Highly recommended tests should be performed in all patients and include a complete medical history and physical examination.
• Recommended tests should be performed in most patients. They are referred to in the section on basic laboratory tests of the core document.
• Optional tests are laboratory tests recommended in specific patient groups. Optional tests are considered to be those laboratory tests that should be requested based on an individualized assessment as well as a psychosocial and psychiatric assessment; these are described in the core document.
• Specialized tests are useful in certain patients and should be applied only by specialists. They are described in the following sections.

It is very important to conduct a basic health assessment of a patient with ED. This assessment includes a complete medical history, physical examination, and laboratory tests. We should then establish the patient's motivations and expectations through discussions with the patient, and explain the advantages and disadvantages of different treatment options available.

Medical history

Important aspects that should be included in the medical history of a patient with ED are discussed in the core document. Here, we will highlight those aspects that are directly related to urological or andrological diseases.

In the medical history, the urologist/andrologist should pay special attention to searching for urological diseases, health problems, medications, or prior surgery that may cause ED:¹³

• Penile diseases: Peyronie's disease, penile trauma.
• Testicular diseases: anorchia, testicular atrophy.
• Pelvic or perineal traumatic conditions that compromise the penile nerve supply or injure the pudendal arteries.
• Chemotherapy and radiotherapy that cause vascular and gonadal disorders responsible for ED.
• Prior urologic surgery:
  • Bilateral orchiectomy.
  • Corporoplasties, tunica albuginea grafts, treatment of priapism causing a fistula.
  • Radical prostatectomy and cystoprostatectomy.
• Abdominal surgery:
  • Radical colorectal surgery.
  • Aortobifemoral bypass surgery.

As stated previously and in keeping with the results of the EDEM study, subjects with prostatic disease are at a higher risk of developing ED than general male subjects;⁷ therefore, the opportunity to detect ED in these subjects is a highly cost-effective task in the urological setting.

Similarly, the search for signs and symptoms that are related to hormonal disorders (testosterone, melatonin, and/or dehydro epiandrosterone (DHEA) disorders) in the aging man, such as fatigue, depression, decreased sexual desire, ED, changes in body mass, or psychiatric disorders, are other areas that the urologist/andrologist should investigate in patients older than 50 years of age.¹⁴

The first visit, which includes taking the detailed medical history, should be conducted in a relaxed atmosphere with enough time to understand the patient's demands. The medical history should be approached with patience because, together with the physical examination, it is the most important diagnostic method for determining the causes of ED.¹ The medical history should be complemented by a sexual history and psychosocial history of the patient, following the guidelines indicated in the core document.

Physical examination

The First International Consultation on Erectile Dysfunction by the WHO defined the physical examination as a highly recommended test, which should include the assessment of the following aspects from a urological and andrological perspective:

• Penis: morphology, elongability, presence of fibrous plaques.
• Testicles: consistency, location and volume.
• Prostate: digital rectal examination.
• Sexual characteristics and sequelae of endocrinopathies.
• Basic neurological examination: penile and perineal sensitivity, bulbocavernous reflex, anal sphincter tone.

Laboratory tests

Laboratory tests will assist physicians in diagnosing associated diseases that may be the cause of ED, such as diabetes, dyslipidemia, or hypogonadism. The results of blood tests may necessitate subsequent investigations by other specialists or specific treatments such as the correction of hormonal deficiencies in patients with hypogonadism.¹⁴ The laboratory tests referred to in the core document for management of ED should be performed.

The prostate-specific antigen (PSA) test may be requested for patients over 50 years of age with an anticipated lifespan of greater than 10 years or men aged 40–50 years with a family history of prostate cancer or of African-American ethnicity.¹⁵ Owing to the biological variability of prostate cancer and the lack of a randomized controlled trial proving the benefit of screening, the use of the PSA is controversial.¹⁶ It should be kept in mind that routine requesting of this test in asymptomatic patients or in patients without a family history of prostate cancer is controversial, because screening (unlike early diagnosis) for prostate cancer has not shown any benefit to date.

Specialized diagnostic tests

The WHO established that specialized tests are useful in certain patients and should be conducted only by specialists.¹² These tests distinguish whether ED is psychogenic or organic in origin, primarily in patients with a presumably psychogenic cause who may benefit from etiologic treatment (psychotherapy). Specialized tests are suggested for young patients with a history of pelvic trauma that may be treated with microsurgical revascularization. There may also be medicolegal reasons for performing these specialized diagnostic tests. Finally, in certain cases, the patient himself wishes to know the origin of his ED.

It is important to perform objective tests of spontaneous erection to allow for a differential diagnosis between the psychogenic and organic nature of ED. Specific tests performed on selected patients are essential to let the etiopathogenesis of ED be known, mainly vascular and neurological studies.¹⁷

Spontaneous erection objective tests

The following tests are required for patients who want to determine whether ED is psychogenic or organic in origin.

Recording of nocturnal penile tumescence and rigidity (Rigiscan^®-NPTR)

This test records erections that occur during sleep and appear to fulfill the function of oxygenating penile smooth muscle. These erections have a pattern in terms of number, duration, and rigidity that are considered normal and is not achieved when alterations of erectile function exist. This test should be conducted on three successive nights.

The best-designed instrument for this purpose is Rigiscan, which consists of an ambulatory data storage unit and a computer for data processing and printing. It attaches comfortably to the leg and has two transducer loops that are placed around the base and the tip of the penis. These loops distend with changes in the size and rigidity of the penis.¹⁸ Rigiscan measures changes in penile circumference in centimeters and rigidity expressed in percentages and also records the number and duration of events per night. The presence of an erection of at least 60% rigidity recorded on the tip of the penis for 10 min or longer can be considered normal. The age of the subject should be taken into account.

The existence of nocturnal erections can be determined in a less sophisticated but more economical way with other instruments, some of which are quite rudimentary, such as a strip of stamps placed around the penis at bedtime. The breaking of the strip will indicate only changes in the volume and rigidity of the penis. Other instruments such as erection meters (Erectiómetros^®) consist of strips of textile material with a clip that gives them different resistance to traction. The sliding of the cloth, properly calibrated through the clip, measures the increase in penis circumference and, depending on the clip, the force exerted by the penis when it expands.¹⁸

Visual stimulation test

The visual stimulation test is based on the viewing of erotic films that cause erections in most men. This test can be completed from a strategically located booth or by using instruments that record the erection.¹⁹ Rigiscan is usually connected to the patient, and erotic films are shown while recording the presence or absence of tumescence and rigidity. If erections are present, an organic cause is ruled out. A negative response, however, does not rule out either a psychogenic or organic origin. The previously described instruments may also be used for this same purpose and with the same limitations. The Digital Inflection Rigidometer^®, another instrument that may be used, measures the axial rigidity of the penis, unlike the previous instruments that quantify the radial rigidity of the penis.²⁰

Tests to assess the vascular integrity of the penis

These tests are suggested for patients when etiologic therapy can be offered, such as penile revascularization in young patients who have suffered vascular trauma, when it is desired to know of the origin of ED in subjects whose history does not allow a likely pathophysiologic cause to be established, or when it is necessary for legal requirements.²¹

Intracavernous injection (ICI) of vasoactive substances: This ICI of prostaglandin E₁ (PGE₁) (Alprostadil^®) at doses of 10 or 20 g assesses response at 10, 20, and 30 min after administration. The 20-g dose of PGE₁ is the standard dose, except in young patients or in patients in whom a neurological or psychological health problem is suspected. When this is the case, an injection of 10 g is preferred.¹³

A positive test is defined as an erectile response with good rigidity, occurring within 10 min of ICI and lasting over 30 min. A positive response indicates only adequate relaxation of the corpora cavernosa smooth muscle and suggests a neurologic, hormonal, psychiatric, or mild arterial cause. Patients with mild arterial insufficiency may have a positive response to ICI if the veno-occlusive mechanism is intact. On the other hand, fear of injection into the penis may cause a sympathetic response that inhibits smooth muscle relaxation and causes no erection (false-negative result).

The main advantage of the ICI test is objectivity in results assessment. In addition to its diagnostic cost-effectiveness, the vasoactive drug allows for an evaluation of a possible drug therapy. In very severe cases, a combination of vasoactive drugs, such as papaverine, phentolamine, and PGE₁, can be injected, causing more complete relaxation of smooth muscle.

ICI is a simple test that gives an initial differentiation between the psychogenic or organic origin of ED. If the response is negative, a vascular cause in the form of arterial or corporo-veno-occlusive insufficiency may exist. Similarly, a positive response suggests vascular integrity, although this does not exclude the existence of a penile arterial abnormality. However, a positive ICI test with PGE₁ does not guarantee arterial normality. For this reason, in young patients with a history of trauma, it may be advisable to perform a complete vascular study.²²

Dynamic Doppler duplex ultrasonography: This test provides an objective, minimally invasive, hemodynamic assessment of penile blood flow through a combination of real-time ultrasonography and a pulsed Doppler. It assesses cavernous artery diameter, flow rate, peripheral resistance, and venous flow. It should be performed after ICI of PGE₁.

The principal parameters assessed are peak systolic velocity, which should exceed 30 cm/s and is correlated to arterial flow, and end-diastolic velocity (EDV), which is <4 cm/s and is related to the veno-occlusive component.²¹ In doubtful cases, redosing of PGE₁ may be advisable to decrease the incidence of false veno-occlusive failures.

Dynamic Doppler duplex ultrasonography provides a magnificent study of the arterial component. However, we can never be sure of complete relaxation of smooth muscle during performance of the test and, therefore, assessment of the veno-occlusive mechanism may not be reliable.

Dynamic cavernosometry: This is the best procedure for evaluating the veno-occlusive component of the corpora cavernosa. It is an invasive procedure, consisting of a combination of vasoactive drugs using ICI, until complete relaxation of cavernous smooth muscle is achieved. According to Goldstein, a normal corporo-veno-occlusive mechanism exists when the flow required to maintain intracavernous pressures of 60, 90, 120, and 150 mmHg is <5 ml/min and when the fall in intracavernous pressure from 150 mmHg in 30 s is <45 mmHg.²² Dynamic cavernosometry also provides an examination of the arterial component by determining the occlusion pressure of the cavernous arteries. After cavernosometry, a cavernosography may be performed to determine the points of venous leakage in the corpora cavernosa. Dynamic cavernosometry is an invasive test that requires a special apparatus and should be reserved for very specific cases.²³

Internal pudendal arteriography: A selective arteriography of the internal pudendal artery should be reserved for candidates of vascular reconstructive surgery when nonarteriosclerotic traumatic artery disease is suspected. If vascular injury, previously confirmed by Doppler ultrasonography, is suspected, an arteriography is performed by injecting a contrast agent into both catheterized hypogastric arteries until the pudendal arteries—with intracavernous and dorsal penile branches—are selectively visualized.

Tests to assess the neurological component of ED

Penile biothesiometry: This test measures vibratory sensory perception along the penis compared with that to the fingertip at different frequencies and diagnoses sensory deficits in polyneuropathies.²⁴

Somatosensory-evoked potentials: This test records the conduction time of a peripherally applied stimulus to the penis until its perception by the cortex. It is used to assess sensory deficits.

Sacral-evoked potentials: This test records the latency time of the bulbocavernous reflex. It is used to assess the integrity of the sacral S2–S4 reflex arc.

Dorsal nerve conduction velocity: This test measures the conduction velocity in a peripheral nerve (dorsal penile nerve) in polyneuropathies.

Cavernous electromyography (CC-EMG): This test assesses the efferent pathway or autonomic neurological component with a device using single-potential analysis of electrical activity. However, it yields unreliable results that vary widely even in the same patient.

Therapeutic proposal

The main points for treatment of a patient presenting with ED are outlined in the core document. As mentioned in this document, patients with ED should avoid modifiable risk factors, treat causative health problems, and change their lifestyle or drug intake that may have been a cause. It is also important to provide patients with sexual counseling. In certain cases, therapeutic intervention with a curative intention (etiologic treatment) may be undertaken.¹ On the other hand, most patients with ED, regardless of the underlying cause, will benefit from symptomatic treatment, which can be first-, second- or third-line treatment.

The indication, dosage, safety, and suitability of combining two or more treatment options for ED has not been established, with the exception of known drug combinations for ICI.

Etiologic treatments

Etiologic treatments are described in the core document and may include psychotherapy, hormone therapy, and a procedure that is discussed below called penile revascularization.

Penile revascularization

In young men with ED and a history of repeated trauma or microtrauma through riding a bicycle, a full diagnostic workup is advisable to determine whether there was an arterial injury that can be corrected surgically. If isolated arterial insufficiency is demonstrated, and the corporo-veno-occlusive mechanism is unaffected, penile revascularization microsurgery may be proposed. This treatment produced good results between 60 and 70% of patients.²⁵ In these patients, a detailed diagnostic study is required including Doppler ultrasonography, dynamic cavernosometry with a vasoactive drug, or selective arteriography of the internal pudendal artery. If a localized arterial lesion is involved, a technique of penile arterial revascularization in a specialized center may be proposed. Penile revascularization techniques that are based on arterialization of the dorsal penile vein should be considered experimental and require more prolonged follow-up to assess their efficacy and side effects.

Symptomatic treatments

The use of symptomatic treatment is necessary in most men with ED and helps to achieve adequate penile rigidity for sexual intercourse. It is advisable to discuss the available treatment options for ED with the patient and his partner, as well as success rates, invasiveness, cost, and potential complications. Symptomatic treatment is usually given in a stepwise manner, that is, from a less aggressive to a more aggressive treatment.

First-line symptomatic treatments

The most important aspects of first-line treatments are described in the core document. Only aspects related to their use in the treatment of ED caused by urological or andrological disease are discussed here.

Oral drug therapy

The overall response rate to sildenafil following RRP is 43% compared with 15% for placebo, although the result varies depending on various factors, among which the greater or lesser degree preservation of neurovascular bundles during surgery is particularly notable.²⁶ One study²⁷ shows that the efficacy of sildenafil varies from 72% in patients with ED secondary to RRP with bilateral preservation, to 50% when preservation is unilateral, and 15.4% in surgery with no preservation of neurovascular bundles.

Other factors that influence treatment success are patient age and the amount of time that has elapsed since surgery. Patient satisfaction rates after sildenafil treatment varied from 26% at 0 to 6 months after surgery to 60% at 18 months to 2 years in 198 patients who underwent RRP.²⁸

In a prospective study conducted on 50 patients after receiving external radiotherapy for the treatment of prostate cancer, 74% of patients reported an improvement in the firmness of erections after sildenafil treatment.²⁹ In patients receiving brachytherapy, a response rate to sildenafil of approximately 62% has been reported.³⁰

In chronic renal failure, 60% of patients with ED have a positive response to 50 or 100 mg of sildenafil.³¹ This response rate is observed in both hemodialysis and ambulatory peritoneal dialysis patients. In all, 60% of renal transplant patients with ED who were treated with sildenafil reported an improvement in achieving and maintaining erections. The response to sildenafil is greater in patients who have been under dialysis for a shorter period before renal transplantation. Sildenafil does not alter the safety and efficacy profile or plasma levels of cyclosporine/FK506.^{32, 33}

The most important aspects of apomorphine hydrochloride are presented in the core document. Owing to recent marketing efforts, efficacy data are not available in patients who underwent radical prostatectomy or pelvic surgery. One study analyzed the results for a subset of patients with other concomitant diseases and found that 50% of patients with ED and BPH who took 3 mg of apomorphine achieved an erection with sufficient firmness to engage in sexual intercourse vs 33% of those who took placebo.³⁴

Vacuum devices and constriction rings

The application of a vacuum to the penis causes venous blood to be aspirated into and fill the corpora cavernosa. The blood is then trapped inside the corpora cavernosa by placing a constriction ring around the base of the penis. This device can be used in patients with stable relationships who do not have difficulty understanding its mechanism. This treatment is more readily accepted by elderly men. It should be removed within 30 min, and side effects include penile pain, ecchymosis, hypoesthesia, and delayed ejaculation.³⁵

Second-line symptomatic treatments

Intracavernous drugs

The gold standard among intracavernous drugs for the treatment of ED is PGE_l.³⁶ When the erection is inadequate, it can be combined with other drugs such as papaverine, phentolamine, and chlorpromazine. These combinations (PGE_l+phentolamine, PGE_l+papaverine, PGE_l+papaverine+phentolamine, PGE_l+chlorpromazine) are used to treat patients who do not respond to a single drug or to reduce the side effects of the drug (pain in the case of PGE₁, and fibrosis and prolonged erection in the case of papaverine).³⁷

Before treatment, the response to the drug or drugs and the optimum dose should be determined. It is mandatory to perform a response test to the intracavernous drug or drugs in the physician's office, educating and instructing the patient so that he can perform self-injection properly at home. This training is crucial for treatment maintenance and minimizes the side effects resulting from poor injection technique (ecchymosis, fibrosis, urethrorrhagy from accidental injection into the urethra, and so on).³⁷ Fear of the needle or of injection into the penis may require the use of pen-type injectors, which automatically inject the drug. This therapy is effective in 60–90% of patients, with an erection occurring within 5–15 min of injection.³⁷ The most common side effects include prolonged erections or priapism, penile pain, and fibrosis.^{36, 37} In the case of priapism, the patient should contact his physician if the erection is maintained for more than 4 h after injection so that measures can be taken to reverse it. Aspiration of blood and irrigation of the corpora cavernosa with saline, in addition to injection of adrenergic drugs, restore detumescence to the penis in virtually all cases, if the measures are not delayed for more than 6 h. ICI of phenylephrine at a dose of 0.2 mg every 5 min (maximum of three doses) may also be given. If detumescence is not achieved, surgical techniques (cavernosa–spongiosum shunt) may be used to prevent irreversible damage to the corpora cavernosa. The risk of new prolonged erections cannot be predicted, and the dose of PGE₁ should be reduced with the next injection.

Penile pain commonly occurs with PGE_l. Management requires switching to another drug or looking for combinations in which the dose of PGE₁ can be reduced without losing efficacy.

It is accepted that fibrosis may be due to poor injection technique, but the drug itself cannot be ruled out as the cause. More often associated with the use of papaverine, discontinuation of treatment is mandatory, which normally results in the disappearance of the fibrosis. In persistent cases, it should be managed as if Peyronie's disease were involved. Complications such as superficial ecchymoses or accidental subdermal or intraurethral injections are not serious and can be resolved with adequate training.

Third-line symptomatic treatment

Penile prosthesis

Implantation of a penile prosthesis is an effective treatment option in patients who do not respond to oral drugs or ICI because of structural lesions in the corpora cavernosa.³⁸ It entails crushing and pushing aside trabecular tissues and cavernous sinusoids, with the consequent rupture of the intracavernous artery, thus precluding the future use of noninvasive treatments.

There are basically three types of prostheses: flexible, malleable, and hydraulic. The latter are the ones that best adapt to the corpora cavernosa, imitating a more 'physiological' erection. The postoperative appearance and functioning of the penis is better with the inflatable vs the semirigid prostheses, although the amount of mechanical failures and complications is higher. The only advantage of malleable or semirigid prostheses is that their price is considerably lower.

The most common complications of penile prostheses are infection and decubitus ulcer with the consequent exteriorization of the device, requiring its removal. Diabetic patients are most often affected by these problems. Exact measurement of the corpora cavernosa during the surgical implantation procedure is mandatory; if the size of the prosthesis is larger than the corpus cavernosum, decubitus ulcer and erosion occur, and the prosthesis is exteriorized. Conversely, if the prosthesis is shorter than the length of the corpus cavernosum, deformation, concorde (drooping glans), and lateral perforation may occur.

A penile prosthesis provides the same benefit for the patient's sexuality as drug-induced erections, that is, adequate rigidity for penetration and performance of sexual intercourse. Sexual desire, ejaculation, and orgasm are unaffected, except for the ability to have erections after drug administration.

Penile prosthesis implantation entails surgery and is subject to complications (infection, erosion, mechanical failure, prosthesis malfunctioning), which should be clearly explained to the patient.

Referral criteria

ED is a health problem that affects the penis and, therefore, it is the task of the urologist/andrologist to coordinate management of patients in collaboration with a primary care physician and other specialists involved. The aim of this document is to provide integrated or integral care to the patient with ED. This means that the urologist/andrologist should not only treat ED but also ensure that his or her collaboration with other specialists is not limited to failures or contraindications of first-line treatments. In this regard, collaboration with the cardiologist is mandatory when impaired cardiac functional capacity is suspected; with the endocrinologist when endocrine disease is complex, with the psychiatrist, psychologist, or sexologist when the underlying disease requires their intervention; and, in general, with any specialist whose participation in the treatment process results in improved care for the patient.

References

1. Lue TF. Erectile dysfunction. N Engl J Med 2000; 342: 1802–1813. | Article | PubMed | ISI | ChemPort |
2. Siegel T et al. The development of erectile dysfunction in men treated for prostate cancer. J Urol 2001; 165: 430–435. | Article | PubMed | ISI | ChemPort |
3. Potosky AL et al. Health outcomes after prostatectomy or radiotherapy for prostate cancer: results from the Prostate Cancer Outcomes Study. J Natl Cancer Inst 2000; 92: 1582–1592. | Article | PubMed | ChemPort |
4. Talcott JA, Clark JA, Stark PC, Mitchell SP. Long-term treatment related complications of brachytherapy for early prostate cancer: a survey of patients previously treated. J Urol 2001; 166: 494–499. | Article | PubMed |
5. Martin E, Bennett A. Iatrogenic causes of impotence. In: Bennett A (ed). Impotence: Diagnosis and Management of Erectile Dysfunction. WB Saunders: Philadelphia, 1994, p 135.
6. Baniel J et al. Sexual function in 131 patients with benign prostatic hyperplasia before prostatectomy. Eur Urol 2000; 38: 53–58. | Article | PubMed |
7. Martin-Morales A et al. Prevalence and independent risk factors for erectile dysfunction in Spain: results of the Epidemiologia de la Disfuncion Erectil Masculina Study. J Urol 2001; 166: 569–574, discussion 574–575. | Article | PubMed | ISI | ChemPort |
8. Martin-Morales A. Lower Urinary Tract Symptoms (LUTS) and erectile dysfunction in a population-based survey. Data from the EDEM study. Int J Impot Res 2001; 13: S39. | Article | PubMed |
9. Sengor F et al. Neodymium:YAG visual laser ablation of the prostate: 7 years of experience with 230 patients. J Urol 2002; 167: 184–187. | PubMed |
10. Chen J et al. Erectile dysfunction following Nd-YAG visual laser-assisted prostatectomy (VLAP). Int J Impot Res 1998; 10: 45–48, discussion 48–49. | Article |
11. Stoner E. Three-year safety and efficacy data on the use of finasteride in the treatment of benign prostatic hyperplasia. Urology 1994; 43: 284–292, discussion 292–294. | Article | PubMed |
12. Giuliano F. Recommendations of the First International Consultation for the Treatment of Erectile Dysfunction. Available at http://www.ahc-net.at/uprima/ed/del_5.htm. Accessed 2003.
13. Rodríguez-Vela L, Gonzalvo A. Historia clínica y manejo inicial de la disfunción eréctil. In: Saenz de Tejada I, Allona A (ed). Erección, eyaculación y sus trastornos. Fomento Salud: Madrid, 1997, p 65.
14. Morales A, Heaton JP. Hormonal erectile dysfunction. Evaluation and management. Urol Clin N Am 2001; 28: 279–288.
15. Prostate-specific antigen (PSA) best practice policy. American Urological Association (AUA). Oncology (Huntingt) 2000; 14: 267–272, 277–268, 280 passim.
16. Woolf SH. Screening for prostate cancer with prostate-specific antigen. An examination of the evidence. N Engl J Med 1995; 333: 1401–1405. | Article | PubMed | ISI | ChemPort |
17. Rodríguez-Vela L, Gonzalvo APG. Evaluación inicial del paciente impotente. Manejo diagnóstico y terapéutico. In: Rodríguez-Vela L, Rioja LA E (ed). Actualización en Andrología. Pulso: Barcelona, 2000, p 321.
18. Karacan I, Howell J. Use of nocturnal penile tumescence in diagnosis of male erection dysfunction. In: Tanagho E, Lue T, McClure R (ed). Contemporary Management of Impotence and Infertility. Williams and Wilkins: Baltimore, MD, 1988, p 95.
19. Morales A, Harris C, Condra M, Heaton J. Validation of visual sexual stimulation in the etiological diagnosis of impotence. In J Impot Res 1990; 2: 109.
20. Roselló M. Rigidometría de Inflexión Digital, Rigiscan y Eco-doppler en el diagnóstico de la disfunción eréctil. In: Rosello M (ed). Ultimos avances en el diagnóstico de la disfunción eréctil. Cuasba: Palma de Mallorca, 1996, p 179.
21. Rao DS, Donatucci CF. Vasculogenic impotence. Arterial and venous surgery. Urol Clin N Am 2001; 28: 309–319.
22. Pescatori ES, Hatzichristou DG, Namburi S, Goldstein I. A positive intracavernous injection test implies normal veno-occlusive but not necessarily normal arterial function: a hemodynamic study. J Urol 1994; 151: 1209–1216. | PubMed |
23. Rodríguez-Vela L, Gonzalvo A, Pascual D, LA R. Disfunción Eréctil. Acta Urol Españ 2002; 26: 667–690.
24. Nehra A, Moreland RB. Neurologic erectile dysfunction. Urol Clin N Am 2001; 28: 289–308.
25. Sarramon JP, Bertrand N, Malavaud B, Rischmann P. Microrevascularisation of the penis in vascular impotence. Int J Impot Res 1997; 9: 127–133. | Article |
26. Padma-Nathan H, Giuliano F. Oral drug therapy for erectile dysfunction. Urol Clin N Am 2001; 28: 321–334. | ChemPort |
27. Zippe CD et al. Role of Viagra after radical prostatectomy. Urology 2000; 55: 241–245. | Article | PubMed | ISI | ChemPort |
28. Hong EK, Lepor H, McCullough AR. Time dependent patient satisfaction with sildenafil for erectile dysfunction (ED) after nerve-sparing radical retropubic prostatectomy (RRP). Int J Impot Res 1999; 11: S15–S22. | Article | PubMed |
29. Zelefsky MJ, McKee AB, Lee H, Leibel SA. Efficacy of oral sildenafil in patients with erectile dysfunction after radiotherapy for carcinoma of the prostate. Urology 1999; 53: 775–778. | Article | PubMed | ChemPort |
30. Potters L et al. Potency after permanent prostate brachytherapy for localized prostate cancer. Int J Radiat Oncol Biol Phys 2001; 50: 1235–1242. | Article | PubMed | ISI | ChemPort |
31. Turk S et al. Erectile dysfunction and the effects of sildenafil treatment in patients on haemodialysis and continuous ambulatory peritoneal dialysis. Nephrol Dial Transplant 2001; 16: 1818–1822. | Article | PubMed | ISI | ChemPort |
32. Barrou B et al. Early experience with sildenafil for the treatment of erectile dysfunction in renal transplant recipients. Nephrol Dial Transplant 2003; 18: 411–417. | Article | PubMed | ChemPort |
33. Prieto Castro RM et al. Treatment with sildenafil citrate in renal transplant patients with erectile dysfunction. BJU Int 2001; 88: 241–243. | Article | PubMed |
34. Dula E, Bukofzer S, Perdok R, George M. Double-blind, crossover comparison of 3 mg apomorphine SL with placebo and with 4 mg apomorphine SL in male erectile dysfunction. Eur Urol 2001; 39: 558–563, discussion 564. | Article | PubMed | ISI | ChemPort |
35. Levine LA, Dimitriou RJ. Vacuum constriction and external erection devices in erectile dysfunction. Urol Clin N Am 2001; 28: 335–341. | Article | ISI | ChemPort |
36. Porst H. The rationale for prostaglandin E1 in erectile failure: a survey of worldwide experience. J Urol 1996; 155: 802–815. | Article | PubMed | ISI | ChemPort |
37. Rodríguez-Vela L, Moncada Irribarren I, Gonzalvo A. Tratamiento de la disfuncion eréctil mediante farmacoterapia intracavernosa. Acta Urol Espan 1998; 22: 291–319.
38. Montague DK, Angermeier KW. Penile prosthesis implantation. Urol Clin N Am 2001; 28: 355–361.