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Advances in pharmacologic therapy for ED have resulted in greater numbers of patients seeking primary and specialty care for sexual concerns. Oral PDE-5Is have emerged as the preferred first-line treatment of ED worldwide due to their efficacy, ease of use, and patient safety. Prior to their release, efficacious oral therapies for ED were unavailable and patient options were limited to nonspecific modalities including lifestyle modification, medication changes, vacuum devices, intraurethral agents, intracavernosal injection therapy, or penile prosthesis insertion. Over the last decade, nonsurgical approaches have replaced prosthetic surgery as the preferred choice of management. In most cases, nonspecific therapies appear to be more effective for ED; however, the patient should also be aware of specific therapies so that an informed treatment decision can be made.
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The beneficial effect of lifestyle change (total body weight loss of 10% or more by reducing caloric intake and increasing physical activity) was demonstrated in a randomized, single-blinded trial of 110 obese men (body mass index ≥30) aged 35–55 years, without diabetes, hypertension, or hyperlipidemia, but with ED (a score of 21 or less on the IIEF). The mean IIEF score improved in the intervention group (from 13.9 ± 4.0 to 17 ± 5; p< .001), but remained stable in the control group who were given general information about healthy food choices and exercise (Esposito et al, 2004). The beneficial effect was reproduced in a larger study of 209 nonobese men randomly assigned to interventional versus control group (Esposito et al, 2009).
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It is well known that ED is intimately related to the atherosclerotic coronary and peripheral vascular diseases, as well as the metabolic syndrome, characterized by central obesity, abnormal lipids, insulin dysregulation, and borderline hypertension. Regular exercise, a healthy diet, smoking cessation, and limiting use of alcohol can reduce the risk of ED or improve underlying dysfunction. A Mediterranean-style diet (fruits, vegetables, nuts, whole grain, olive oil, and decreased saturated lipids) has recently been shown to improve endothelial function scores and inflammatory markers (C-reactive protein) when compared with men on a control diet (Esposito et al, 2010). Obesity and smoking have been prospectively identified as risk factors for ED, while physical activity is inversely associated with the development of ED.
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Perineal compression on penile arteries from long-distance cycling may also represent a modifiable risk factor for ED. Changing the bicycle seat or riding practices will often improve erectile function if penile vascular compromise is identified; specific strategies include replacing a protruding nose with a noseless seat, changing posture to a more upright/reclining position, using a gel saddle, and tilting the seat downward (Huang et al, 2005).
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When a patient complains of sexual dysfunction after taking a particular medication, it is important to determine whether the problem is related to loss of sexual drive, impaired erection, or rapid/delayed ejaculation. In many situations, changing the medication to a different class of agents is a feasible first step. Antihypertensive agents therapeutically lower blood pressure; this primary effect has long been thought the mechanism of their adverse actions on erection. Switching patients to agents including alpha-adrenoceptor antagonists, calcium channel blockers, and angiotensin-converting enzyme (ACE) inhibitors may reverse ED in some patients. Patients complaining of sexual dysfunction while taking antidepressants may benefit from substitution (bupropion, nefazodone, buspirone, mirtazapine), drug holidays, selective serotonin reuptake inhibitor (SSRI) dosage reduction, and/or PDE-5 inhibitors.
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Therapies such as PDE-5Is or ICIs may provide more rapid relief for patients with ED compared with a prolonged course of psychosexual therapy. However, in patients with evidence of psychological problems, referral to a psychologist or sex therapist is highly recommended because the elimination of a specific underlying cause may result in a cure. Recent approaches to sex therapy have included cognitive-behavioral interventions focused on challenging or correcting maladaptive cognitions, behavioral techniques (desensitization and assertiveness exercises), exploration of past developmental experiences on present behavior, and couples' therapy. Moreover, in some patients with mixed psychogenic and organic ED, psychosexual therapy may help relieve the anxiety and remove unrealistic expectations associated with medical or surgical therapy.
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Referral to an endocrinologist is recommended for patients with thyroid, adrenal, pituitary, or hypothalamic dysfunction. Aging men with ED may show a variety of symptoms when hypogonadism coexists: low libido, depression, decreased intellectual abilities, lean body mass, bone mineral density, or skin turgor, changes in body hair distribution, changes in sleep patterns, and increased visceral fat. In the patient with documented hypogonadism and ED, it is reasonable to initiate androgen therapy; for hypogonadal patients unresponsive to PDE-5 inhibitor therapy alone, the addition of testosterone may enhance the treatment effect and improve erectile function (Morales, 2005). This discussion is limited to treatment of hypogonadism and hyperprolactinemia as they relate to ED.
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Parenteral depo-preparations of testosterone (T), such as testosterone cypionate and enanthate, are the least expensive form of androgen supplementation and are effective in restoring serum levels to normal. A normal circadian rhythm is not replicated by these agents. Rather, they are administered through deep intramuscular injection (200–250 mg every 2 weeks) and result in supraphysiologic levels of T for 72 hours with steady exponential decline to subphysiologic levels in 10–12 days; the initial supraphysiologic “rush” may be disconcerting to some patients, but others enjoy an improved sense of well-being, aggression, and libido.
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Transdermal delivery more closely simulates normal circadian levels of testosterone if patients apply a patch in the morning, as the higher initial absorption mimics normal diurnal variations. Several U.S. Food and Drug Administration (FDA)-approved preparations are available in the United States. Testoderm TTS, which has largely replaced the Testoderm scrotal patch, is convenient to use, as it is applied daily to the arm, back, or upper buttocks as a 5-mg patch. Another product, Androderm, comes as a patch that delivers 2.5 or 5 mg T per day. The most common adverse reactions to both are itching, chronic skin irritation, and allergic contact dermatitis. Patients should alternate application sites and avoid sun-exposed areas. Local application of cortisone cream may relieve irritated skin. AndroGel is a 1% gel pack (containing 50 mg, 75 mg, or 100 mg of T), which is also applied daily in the morning to clean, dry skin over the shoulders, upper arms, or abdomen. Hands should be washed thoroughly after application, as skin contact can transmit testosterone. Testim topical gel also contains 1% T, providing continuous transdermal delivery for 24 hours after a single application to intact, clean, dry skin of the shoulders and upper arms. One 5-g tube of Testim contains 50 mg of testosterone.
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When taken orally, methyl testosterone preparations are largely rendered metabolically inactive during “first pass” circulation through the liver. The large dosages (exceeding 200 mg/d) required to achieve therapeutic levels can be hepatotoxic, leading to hepatitis, cholestatic jaundice, hepatomas, hemorrhagic liver cysts, and hepatocarcinoma. Although unavailable in the United States, the only orally active and safe form of T is Andriol (testosterone undecanoate [TU] in oleic acid), which, owing to its lipophilic side chain, is partly taken up by the lymph and partially escapes hepatic inactivation. The maximal plasma concentration is generally observed within 2–3 hours, but after 6–8 hours, levels have returned to pretreatment values. A dosage of 40 mg three times a day generally provides adequate androgen replacement, yielding T levels within the (low) normal range, whereas dihydrotestosterone (DHT) levels are moderately increased (2–4 nmol/L). Absorption varies with food consumption and the dose required should be based upon plasma levels and clinical effects. Other FDA-approved delivery systems include Testopel subcutaneous pellets (dosage of 2–6 pellets [150–450 mg T]), which lasts for 4–6 months, and Striant, a tablet-like mucoadhesive buccal system used to deliver 30 mg of T twice daily.
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In patients with hyperprolactinemia with or without hypogonadism, androgen therapy does not improve sexual function. Treatment should first be aimed at eliminating the offending drugs, such as estrogens, sedatives, neuroleptics, or morphine. Bromocriptine, a dopamine agonist that lowers prolactin levels and restores T to normal, is used to reduce the size of prolactin-secreting adenomas. Surgical ablation may occasionally be required if the bromocriptine response is unsatisfactory or if visual field changes secondary to optic nerve compression occur.
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Potential Adverse Effects of Testosterone Replacement
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Testosterone replacement is clearly the treatment of choice for young hypogonadal men without contraindications. However, the potential risks of androgen therapy may outweigh the benefits for some patients. Supraphysiologic levels of T suppress LH and FSH production and can lead to infertility, breast tenderness, and gynecomastia. Erythrocytosis is the most common laboratory alteration noted with long-term therapy; increases in red cell mass, thromboxane A2, and platelet aggregation may increase cardiovascular risk. Androgens may also induce or worsen sleep apnea. Long-term therapy requires a commitment from the patient and the specialist for continued follow-up, as outlined in the following.
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Regarding prostate safety, a number of studies in the literature suggest that androgen replacement does not induce prostate cancer in men with normal prostates, and placebo-controlled studies show little difference in prostate volume, PSA, and obstructive symptoms. No increased risk of prostate cancer has been noted in (1) clinical trials of T supplementation, (2) longitudinal population-based studies, or (3) in a high-risk population of hypogonadal men receiving T treatment (Morgentaler, 2006). Although the fear of exacerbating an occult cancer of the prostate remains a concern, many older hypogonadal patients whose libido and erectile function can be restored by T therapy likely should not be denied this treatment option. When a patient desires T replacement, a digital rectal examination and a serum PSA level should be obtained. When in doubt, ultrasound-guided biopsy is performed before T therapy is given. The presence of prostate or breast cancer is an absolute contraindication to androgen supplementation. Patients are followed every 6 months with a rectal examination and serum PSA indefinitely while on therapy. Laboratory surveillance should also include hemoglobin/hematocrit levels, liver function tests, and cholesterol and lipid profile. The efficacy of supplementation is determined by clinical response rather than blood levels of testosterone.
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Oral Pharmacologic Therapy
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Phosphodiesterase Inhibitors
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Sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis), the three selective PDE-5Is currently approved for clinical use in the United States, have become the preferred first-line therapy for most men with ED due to their efficacy, safety, and ease of use. All are highly effective in enhancing erectile function across a wide range of outcome measures, causes of ED, patient subgroups, and regional populations. The three PDE-5Is appear to have equivalent efficacy in the treatment of ED, are generally well tolerated, and have similar contraindications and warnings (Carson and Lue, 2005).
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Sexual stimulation results in the release of NO from nerve endings and vascular endothelial cells in the penis, which then diffuses into vascular and cavernous smooth-muscle cells of the corpus cavernosum. Stimulation of guanylyl cyclase by NO elevates levels of cGMP, lowering cytoplasmic calcium and resulting in smooth-muscle relaxation and subsequent penile erection. PDE-5Is amplify the NO-cyclic cGMP pathway through competitive inhibition of cGMP degradation by type 5 phosphodiesterase. Without sexual stimulation and resultant NO release, however, these inhibitors are ineffective.
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The clinical efficacy and safety of sildenafil, vardenafil, and tadalafil has been evaluated in many placebo-controlled, double-blinded trials and open label studies (Brock et al, 2002; Carson and Lue, 2005; Goldstein et al, 1998; Porst et al, 2003). Treatment effect was principally assessed by items 3 and 4 of the IIEF-15 questionnaire (ability to attain and maintain erection, respectively). For sildenafil, improvements in erectile function were reported by 56–84% of subjects taking 25–100 mg of sildenafil versus 25% in the placebo group. Little ED benefit and considerably more side effects were noted above 100 mg. For specific etiologies, sildenafil was effective in 70% of hypertensive patients, 57% of diabetic patients, 43% of radical prostatectomy patients, and 80% of spinal cord injury patients. The efficacy of vardenafil was similarly evaluated with 10-mg and 20-mg dose. Mean IIEF scores increased from 12.8 at baseline to 21 at week 12 of treatment (compared with 13.6 to 15.0 for placebo). Similarly, integrated phase III studies of tadalafil involving 1112 patients demonstrated IIEF erectile domain scores of 24 in men receiving a 20-mg dose versus 15 for placebo. More than 70% of intercourse attempts were successfully completed from >30 minutes to 36 hours after dosing. For difficult to treat groups, including diabetics, severe ED, and postradical prostatectomy, the three PDE-5Is represent effective therapies for many men.
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The onset of activity, in reports with similar methods, is 14 minutes with sildenafil, 10 minutes with vardenafil, and 16 minutes with tadalafil. However, success rates after 20 minutes are much less than after 1 hour; therefore, if patients do not experience a rapid beneficial effect, they should be advised to delay sexual intercourse for one (sildenafil or vardenafil) or 2 hours (tadalafil)—when serum concentrations have peaked. High-fat meal intake has been shown to delay absorption of vardenafil and sildenafil; this effect is not seen with tadalafil (Carson and Lue, 2005).
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Tadalafil therapy has a broader window of clinical responsiveness than either sildenafil or vardenafil because of its longer half-life (17.5 vs 4–5 hours for sildenafil or vardenafil). Tadalafil enhances erectile function in men with ED for up to 36 hours and may mean less planning and pressure to have sexual intercourse according to a schedule.
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Eleven distinct families (PDE-1–PDE-11) are known to have or are implicated in a broad range of cellular functions. PDE-5 is present in high concentrations in the smooth muscle of the penile corpora cavernosa. Sildenafil and vardenafil cross-react slightly with PDE-6, that is, the IC50s for PDE-5 are only four- to tenfold lower than those for PDE-6. This may explain why some patients using sildenafil complain of visual disturbances. Tadalafil minimally cross-reacts with PDE-11. Most side effects associated with PDE-5Is result from inhibition of PDE-5 in other tissue or organs. In randomized controlled trials, flushing (10%) and visual side effects were more common in patients receiving sildenafil or vardenafil, and back pain/myalgia (1–4%) was more common for tadalafil users. These events were mostly mild, abated with time (within 2–4 weeks), and prompted treatment discontinuation in only a small number of patients (Brock et al, 2002; Goldstein et al, 1998; Porst et al, 2003). Except for visual disturbances, the other reported side effects of PDE-5Is (headaches 15%, flushing, rhinitis 5–10% for vardenafil and sildenafil, slight lowering of blood pressure, dyspepsia, etc.) are likely caused by PDE-5 inhibition in vascular or gastrointestinal smooth muscle.
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ED is common among men who have atherosclerotic coronary artery disease. With regard to overall cardiac safety, controlled and postmarketing studies of the three FDA-approved PDE-5Is demonstrated no increase in MI or death rates in double-blinded, placebo-controlled, or open-label studies when compared with expected study population rates. Patients who develop angina during sexual activity with a PDE-5I should discontinue sexual activity, relax for 5–10 minutes and if pain persists, seek emergency care and inform emergency medical personnel that a PDE-5I was taken. Patients who have an acute MI after a PDE-5I may be given standard therapies (except for organic nitrates). Nitroglycerin should not be given with 24 hours of sildenafil or vardenafil use, or 48 hours for tadalafil. Patients who develop hypotension after organic nitrates and PDE-5Is should be placed in the Trendelenburg position and given IV fluids, with alpha-agonists (such as phenylephrine) added as needed. In patients with refractory hypotension, intra-aortic balloon counterpulsation should be administered, as suggested by the American College of Cardiology/American Heart Association (ACC/AHA) guidelines. At present, there is no pharmacologic antidote to the PDE-5 inhibitor/nitrate interaction (Kostis et al, 2005).
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Because of its effect on QTc interval, vardenafil is not recommended for patients who take type-1A antiarrhythmics (such as quinidine or procainamide), type-3 antiarrhythmics (such as sotalol or amiodarone), or with congenital prolonged QT syndrome.
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Finally, there have been reports of the development of nonarteritic anterior ischemic optic neuropathy (NAION) in men using PDE-5Is. Epidemiologically, NAION is the second most common acquired optic neuropathy in men aged 50 years and older. Risk factors for NAION, cardiovascular disease, and ED are shared and include age, dyslipidemia, diabetes, hypertension, and cigarette smoking. Given the large number of men safely using these agents and a limited number of events, it is not possible to determine whether NAION is directly linked to the use of PDE-5Is. Nevertheless, physicians should continue to advise patients to stop use of a PDE-5 inhibitor and seek immediate medical attention in the event of a sudden loss of vision as a safety measure (Laties, 2009).
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Warnings and Drug Interaction
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PDE-5Is are contraindicated for patients using nitrates, as a precipitous and potentially life-threatening hypotensive episode may occur with concurrent use. PDE-5Is are either not recommended or are to be used with caution in men with unstable angina, cardiac failure, recent MI, uncontrolled or life-threatening arrhythmia, or poorly controlled blood pressure (resting BP <90/50 mm Hg or >170/100–110 mm Hg). Caution is also advised when an alpha-blocker and a PDE-5 inhibitor are given together, as interaction can lead to excessive vasodilation and hypotension.
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The recommended starting doses are 50 mg for sildenafil and 10 mg for vardenafil and tadalafil. The dose may be increased to 100 mg (sildenafil) or 20 mg (vardenafil and tadalafil) or decreased to 25 mg or 5 mg, respectively, based on individual efficacy and tolerability. Several reports have shown that daily dose of 5 mg of tadalafil was able to reduce side effects while matching the effectiveness of 20 mg of tadalafil taken as needed (Seftel et al, 2009). Patients should also be counseled to trial a PDE-5I several times before declaring it “ineffective”; for instance, the cumulative probability of success with sildenafil increases with the first nine to ten attempts, after which it stabilizes (McCullough et al, 2002).
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Centrally Acting Oral Agents
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Apomorphine is a proerectile D1/D2 dopamine receptor agonist, but it may also stimulate 5-HT(2C) receptor to enhance penile erection (Kimura et al, 2008). Uprima, a sublingual form designed for buccal absorption, has been approved for ED in Europe (but not in the United States) and reported to induce erection in 67% of men with psychogenic ED. Apomorphine has a rapid onset of action, with a window of sexual opportunity of approximately 2 hours from ingestion. Maximal plasma concentrations are reached in 50 minutes. In a double-blind placebo-controlled study of 2- and 4-mg dosages, erections firm enough for intercourse were reported by 45% and 55% of patients, respectively, with placebo responses of 35% and 36%. Adverse events included nausea 16.9%, dizziness 8.3%, sweating 5%, somnolence 5.8%, yawning 7.9%, and emesis 3.7%. There were no documented food/drug interactions in clinical trials (with the exception of ethanol) and, specifically, no documented pharmacologic interactions for subjects using nitrate drugs.
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Yohimbine is a centrally acting alpha-2-adrenergic antagonist that is not recommended for use in the treatment of ED by the 2005 American Urological Association (AUA) guidelines. Side effects include gastrointestinal intolerance, palpitations, headache, agitation, anxiety, and increased blood pressure (precautions are advised in men with cardiovascular disease). Trazodone is also not recommended; efficacy in pooled analyses was statistically equivalent to placebo. Side effects include drowsiness, nausea, emesis, blood pressure changes (both hypotension and hypertension are reported), urinary retention, and priapism (especially at therapeutic antidepressant levels) (Montague et al, 2005).
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Transurethral Therapy
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Alprostadil, a synthetic formulation of prostaglandin E-1, is the only FDA-approved pharmacologic agent approved for the management of ED via intracavernous and transurethral routes. After absorption from the urethra to the corpus spongiosum and then corpus cavernosum, alprostadil stimulates adenyl cyclase to increase intracellular levels of cAMP and lower levels of intracellular calcium, thereby relaxing arterial and trabecular smooth muscle. MUSE (medicated urethral system for erection) consists of a small semisolid pellet (3 × 1 mm) administered into the distal urethra (2–3 cm) by a proprietary applicator (MUSE; VIVUS Inc., Menlo Park, CA). Clinical studies showed that 66% of men responded to in-office trials; however, postmarketing studies have produced less successful results of about 50% (Mulhall et al, 2001). Penile rigidity can be enhanced by placing an elastic ring at the base of the penis (ACTIS, VIVUS Inc.) to mechanically assist veno-occlusion. Penile and/or scrotal pain or discomfort is a ubiquitous side effect of alprostadil-based therapies and is clearly dosage related and was reported in 33% of men in MUSE trials. Hypotension and syncope have been noted in 1–5.8% of patients, thus mandating initial trial dose administration in the office setting. Some female partners also report vaginal discomfort (about 10%) after ejaculation by a man using MUSE.
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Intracavernous Injection
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ICI of vasoactive drugs is considered the most effective nonsurgical therapy for ED. It remains the first-line therapy for select patients and a valuable treatment option for PDE-5I nonresponders or those that cannot tolerate side effects of oral agents. ICI treatment offers several potential advantages to the patient, including a rapid onset of action, essentially no systemic side effects and drug interactions, and dependable efficacy for all forms of ED. Men who have failed first-line oral pharmacotherapy constitute the largest group of ICI-treated patients, with a significant erectile response rate of >80% demonstrated among PDE-5I nonresponders indicating that progression to second-line injection therapy is appropriate. A list of drugs that have been used clinically is presented in Table 39–5, and the most commonly used agents and combinations are discussed later.
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Papaverine, an alkaloid isolated from the opium poppy, induces relaxation of cavernous smooth muscle and penile vessels via nonspecific inhibition of phosphodiesterase. It is metabolized by the liver, with a plasma half-life of 1–2 hours. Monotherapy doses range from 15 to 60 mg. Advantages include low cost and stability at room temperature, while adverse effects include priapism (up to 6%), corporal fibrosis (6–30%; thought to be associated with poor technique, minimal injection site compression time, >1 cc injection volume, pH 3–4), and occasional elevation of liver enzymes (Bella and Brock, 2004).
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Alprostadil (Prostaglandin E1)
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Alprostadil causes smooth-muscle relaxation, vasodilation, and inhibition of platelet aggregation through elevation of intracellular cAMP. It is metabolized by the enzyme prostaglandin 15-hydroxydehydrogenase, which has been shown to be active in human corpus cavernosum. After ICI, 96% of alprostadil is locally metabolized within 60 minutes and no change in peripheral blood levels is observed. Alprostadil have been approved by the FDA for intracavernous therapy as Caverject (Pfizer, NYC) and Edex (Schwarz Pharma, Milwaukee, WI). Cumulative data yield a success rate of 70–75% across ED etiologies, utilizing a median dose of 12–15 mg. Common adverse effects include pain at the injection site or during erection (11–15%), small hematoma or bruising, penile fibrosis (1–3%), and burning sensation at the time of injection. Rates of priapism are low (1–3%) and systemic side effects are rare (Bella and Brock, 2004).
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The most commonly used drug combinations for ICI in the United States are bimix (papaverine/phentolamine) and trimix (papaverine/phentolamine/alprostadil) in various concentrations (Montorsi et al, 2010). A combination of vasoactive intestinal polypeptide and phentolamine has also been used in other countries. Multiple series have demonstrated patient satisfaction rates of >75% and low rates of priapism or fibrosis. Side effects are reduced, as smaller amounts of each agent are required, and the targeting of multiple pathways increases therapeutic efficacy.
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Priapism and fibrosis are the two serious side effects associated with ICI therapy. Priapism occurred in 1.3% of 8090 patients in 48 studies with alprostadil, which is about five times lower than with papaverine or bimix (Linet and Ogrinc, 1996). Fibrosis can occur as a nodule, diffuse scarring, plaque or curvature. Scar tissue can be prevented by >5 minutes compression of the injection site to reduce bleeding and trauma. Priapism is best prevented by careful dosage titration.
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Dosage and Administration
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Patients must have the first injection performed by medical personnel and receive appropriate training and education before home injection. An initial dose of 2.5 μg for alprostadil is recommended. If the response is inadequate, increases in 2.5-μg increments can be given until a full erection is achieved or a maximum of 60 μg is reached. For drug combinations, treatment is initiated with a small dose (eg, 0.1 mL) and titrated according to erectile response. The goal is to achieve a full erection of <1-hour duration to avoid priapism.
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Treatment of Prolonged Erection or Priapism
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The best treatment is prevention; prolonged erections, a potentially devastating adverse effect of ICI, are often secondary to rapid dose escalation by the patient, missed initial injection with second attempt, or use among neurogenic and/or young patients. It is imperative that the clinician prescribing intracavernous therapies emphasizes to the patient that priapism represents a urologic emergency, and any erection lasting >4 hours necessitates urgent medical evaluation. The best regimen for averting priapism is ICI of diluted phenylephrine 250–500 μg every 3–5 minutes until detumescence. In patients with cardiovascular disease, monitoring of blood pressure and pulse is recommended (Montague et al, 2003). If the priapism lasts for more than 2–3 days, T-shunt with intracavernous tunneling may be required (Brant et al, 2009).
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ICI is contraindicated in patients with sickle cell anemia, schizophrenia, or a severe psychiatric disorder. Because monoamine oxidase (MAO) in involved in catecholamine (including phenylephrine) metabolism, if a man on an MAO inhibitor developed prolonged erection/priapism after ICI, a simple T-shunt might be a better treatment than ICI of phenylephrine. For patients using an anticoagulant or aspirin, compressing the injection site for 7–10 minutes after injection is recommended. In patients with poor manual dexterity, the sexual partner can be instructed to perform the injection.
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Vacuum Constriction Device
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The vacuum constriction device consists of a plastic cylinder connected directly or by tubing to a vacuum-generating source (manual or battery-operated pump). Only devices containing a vacuum limiter should be used, as injury to the penis may occur with extremely high negative pressures (Montague et al, 2005). After the penis is engorged, a constricting ring is applied to the base to maintain the erection. The ring may be uncomfortable or painful; to avoid injury, it should not be left in place for <30 minutes. The erection produced differs from a physiologic or ICI-induced erection as the portion of the penis proximal to the ring is not rigid, which may result in a pivoting effect. The penile skin may be cold and dusky, and ejaculation may be trapped by the constricting ring. Complications include penile pain and numbness, difficult ejaculation, ecchymosis, and petechiae. Patients taking aspirin or Coumadin should exercise caution when using these devices.
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In some patients, the device can produce an erection that is of sufficient rigidity for coitus or engorge the glans for men with glanular insufficiency. In patients with severe vascular insufficiency, the device may not produce adequate erection. Although it is a safe and less costly means of treating ED when used properly, low patient acceptability limits the application or use of this therapy.