Of All Drugs Available Most Effective Agains Penile Dysfunction
Am Fam Physician. 2010 Feb 1;81(3):305-312.
Patient information: See related handout on erectile dysfunction, written by the writer of this article.
Commodity Sections
- Abstract
- Prevalence
- Pathophysiology
- Diagnosis and Evaluation
- Treatment
- Link to Cardiovascular Illness
- References
Erectile dysfunction (ED) is the most common sexual problem in men. The incidence increases with age and affects up to one third of men throughout their lives. It causes a substantial negative impact on intimate relationships, quality of life, and cocky-esteem. History and physical examination are sufficient to make a diagnosis of ED in almost cases, considering there is no preferred, first-line diagnostic exam. Initial diagnostic workup should usually exist limited to a fasting serum glucose level and lipid panel, thyroid-stimulating hormone test, and morning time total testosterone level. Kickoff-line therapy for ED consists of lifestyle changes, modifying drug therapy that may crusade ED, and pharmacotherapy with phosphodiesterase blazon 5 inhibitors. Obesity, sedentary lifestyle, and smoking greatly increase the risk of ED. Phosphodiesterase type v inhibitors are the nigh constructive oral drugs for treatment of ED, including ED associated with diabetes mellitus, spinal string injury, and antidepressants. Intraurethral and intracavernosal alprostadil, vacuum pump devices, and surgically implanted penile prostheses are culling therapeutic options when phosphodiesterase type 5 inhibitors neglect. Testosterone supplementation in men with hypogonadism improves ED and libido, only requires interval monitoring of hemoglobin, serum transaminase, and prostate-specific antigen levels because of an increased chance of prostate adenocarcinoma. Cerebral behavior therapy and therapy aimed at improving relationships may help to improve ED. Screening for cardiovascular risk factors should be considered in men with ED, considering symptoms of ED present on average three years before than symptoms of coronary artery illness. Men with ED are at increased risk of coronary, cerebrovascular, and peripheral vascular diseases.
Erectile dysfunction (ED) is defined past the National Institutes of Health every bit the inability to achieve or maintain an erection sufficient for satisfactory sexual performance.1 ED is the most common sexual problem in men; it ofttimes causes serious distress, prompting men to seek medical attention they may non otherwise seek. It often has a profound outcome on intimate relationships, quality of life, and overall self-esteem. ED may also be the presenting symptom or harbinger of undetected cardiovascular disease.ii The economic bear upon of ED is multifactorial, with direct costs that include medico evaluation, pharmacotherapy, and diagnostic testing, and indirect costs that include lost fourth dimension at work, lost productivity, and effects on the human being's partner, family, and coworkers.
SORT: Fundamental RECOMMENDATIONS FOR Exercise
| Clinical recommendation | Evidence rating | References |
|---|---|---|
| Diagnostic testing for erectile dysfunction should usually be limited to obtaining a fasting serum glucose level and lipid console, thyroid-stimulating hormone test, and morning full testosterone level. | C | 8 |
| Get-go-line therapy for erectile dysfunction should consist of oral phosphodiesterase type 5 inhibitors. | A | 8, 14, 17 |
| Phosphodiesterase type 5 inhibitors are most effective in the handling of erectile dysfunction associated with diabetes mellitus and spinal cord injury, and of sexual dysfunction associated with antidepressants. | A | ix, 12, 17, 19–21 |
| Additional therapy for erectile dysfunction may consist of psychosocial therapy and testosterone supplementation in men with hypogonadism. | B | eight, xiii, 36 |
| Testosterone supplementation in men with hypogonadism improves erectile dysfunction and libido. | B | 13, 29 |
| Screening for cardiovascular risk factors should be considered in men with erectile dysfunction. | C | 39 |
Prevalence
- Abstruse
- Prevalence
- Pathophysiology
- Diagnosis and Evaluation
- Treatment
- Link to Cardiovascular Disease
- References
Many men associate advancing age with declining sexual function and an overall decreased quality of life. ED affects up to one third of men throughout their lives, and the incidence increases with historic period. A population-based study of U.South. health professionals establish the prevalence of sexual dysfunction in men to exist 12 percent in those younger than 59 years, 22 percent in those 60 to 69 years of age, and 30 percent in those older than 69 years.3 Persons with type 2 diabetes mellitus have a threefold greater risk of ED compared with the general population.iv Depression increases the risk of ED, but it is not clear if this relationship is causal.5
Pathophysiology
- Abstract
- Prevalence
- Pathophysiology
- Diagnosis and Evaluation
- Handling
- Link to Cardiovascular Disease
- References
ED may result from organic causes (e.thousand., vascular, neurogenic, hormonal, anatomic, drug-induced), psychological causes, or a combination of both. A normal sexual erectile response results from the interaction between neurotransmitter, biochemical, and vascular smooth muscle responses initiated by parasympathetic and sympathetic neuronal triggers that integrate physiologic stimuli of the penis with sexual perception and want. Nitric oxide produced from endothelial cells after parasympathetic stimuli triggers a molecular cascade that results in smooth muscle relaxation and arterial influx of blood into the corpus cavernosum. This is followed past pinch of venous return, which produces an erection.6
Table 1.
Risk Factors for Erectile Dysfunction
| Advancing age |
| Cardiovascular disease |
| Cigarette smoking |
| Diabetes mellitus |
| History of pelvic irradiation or surgery, including radical prostatectomy |
| Hormonal disorders (e.g., hypogonadism, hypothyroidism, hyperprolactinemia) |
| Hypercholesterolemia |
| Hypertension |
| Illicit drug use (due east.g., cocaine, methamphetamine) |
| Medications (e.g., antihistamines, benzodiazepines, selective serotonin reuptake inhibitors) |
| Neurologic weather condition (east.k., Alzheimer affliction, multiple sclerosis, Parkinson disease, paraplegia, quadriplegia, stroke) |
| Obesity |
| Peyronie disease |
| Psychological conditions (e.g., anxiety, depression, guilt, history of sexual abuse, marital or relationship problems, stress) |
| Sedentary lifestyle |
| Venous leakage |
Diagnosis and Evaluation
- Abstract
- Prevalence
- Pathophysiology
- Diagnosis and Evaluation
- Treatment
- Link to Cardiovascular Disease
- References
In that location is no preferred, first-line diagnostic test for ED, and routine screening is not recommended. History and physical examination are sufficient in making an accurate diagnosis of ED in most cases. Penile duplex ultrasonography is not a useful diagnostic exam for ED.7 The American Urological Association (AUA) recommends that the initial evaluation of ED include a complete medical, sexual, and psychosocial history.8 The medical history may reveal comorbid conditions, risk factors related to ED (Table 1),9 or medications that contribute to ED (Tabular array 2).half dozen Sexual history should focus on erection adequacy, altered libido, quality and timing of orgasm, volume and advent of ejaculate, presence of sexually-induced genital pain or penile curvature (Peyronie disease), and partner sexual role. The v-item version of the International Index of Erectile Function Questionnaire is a validated survey musical instrument that can exist used to assess the severity of ED symptoms (Tabular array 3).10
Table ii.
Medications and Substances That May Cause or Contribute to Erectile Dysfunction
| Medication class or substance | Examples |
|---|---|
| Analgesics | Opiates |
| Anticholinergics | Tricyclic antidepressants |
| Anticonvulsants | Phenytoin (Dilantin), phenobarbital |
| Antidepressants | Lithium, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, tricyclic antidepressants |
| Antihistamines | Dimenhydrinate, diphenhydramine (Benadryl), hydroxyzine (Vistaril), meclizine (Antivert), promethazine (Phenergan) |
| Antihypertensives | Alpha blockers, beta blockers, calcium channel blockers, clonidine (Catapres), methyldopa, reserpine |
| Anti-Parkinson agents | Bromocriptine (Parlodel), levodopa, trihexyphenidyl |
| Cardiovascular agents | Digoxin, disopyramide (Norpace), gemfibrozil (Lopid) |
| Cytotoxic agents | Methotrexate |
| Diuretics | Spironolactone (Aldactone), thiazides |
| Hormones | 5-alpha reductase inhibitors, corticosteroids, estrogens, luteinizing hormone-releasing hormone agonists, progesterone |
| Illicit drugs, alcohol, and nicotine | Amphetamines, barbiturates, cocaine, heroin, marijuana |
| Immunomodulators | Interferon-alfa |
| Tranquilizers | Benzodiazepines, butyrophenones, phenothiazines |
Table 3.
Five-Item Version of the International Index of Erectile Office Questionnaire
| Questions | Scores | ||||
|---|---|---|---|---|---|
| one | 2 | 3 | four | five | |
| Over the past six months: | |||||
| 1. How do you rate your confidence that y'all could get and keep an erection? | Very low | Low | Moderate | High | Very high |
| 2. When y'all had erections with sexual stimulation, how ofttimes were your erections hard enough for penetration? | Nigh never or never | A few times* | Sometimes† | Well-nigh times‡ | Well-nigh e'er or always |
| iii. During sexual intercourse, how frequently were you able to maintain your erection after you had penetrated (entered) your partner? | Almost never or never | A few times* | Sometimes† | Near times‡ | Nearly always or e'er |
| 4. During sexual intercourse, how difficult was it to maintain your erection to completion of intercourse? | Extremely difficult | Very difficult | Difficult | Slightly difficult | Not hard |
| 5. When you attempted sexual intercourse, how often was it satisfactory for yous? | Almost never or never | A few times* | Sometimes† | Most times‡ | Virtually always or always |
The concrete examination should appraise blood force per unit area and heart charge per unit; trunk habitus, for central obesity; and cardiovascular, neurologic, and genitourinary systems, including penile, testicular, and digital rectal examinations ( Figure 1 ).8,9,11–xiv The AUA and World Health Organization recommend limited diagnostic testing in men with ED. This may include a fasting serum glucose level and lipid panel, thyroid-stimulating hormone examination, and morning total testosterone level.viii,11 Additional diagnostic testing and urologic evaluation may be warranted in cases of ED refractory to standard therapies (Table 4).11 Clues to the diagnosis of ED are listed in Table five.
Diagnosis and Treatment of Erectile Dysfunction
Figure one.
Algorithm for the diagnosis and treatment of erectile dysfunction.
Adapted from references viii,nine, and 11 through xiv.
Table iv.
Additional Testing in the Workup of Erectile Dysfunction
| Optional diagnostic tests |
| Laboratory investigations (complete blood count; free testosterone, luteinizing hormone, and prolactin levels; sexual practice hormone-bounden globulin test; urinalysis) |
| Psychological or psychiatric consultation |
| Specialized evaluation and diagnostic tests |
| In-depth psychosexual and relationship evaluation |
| Neurophysiologic testing (vibrometry; bulbocavernosus reflex latency; cavernosal electromyography; somatosensory evoked potential test; pudendal and sphincter electromyography) |
| Nocturnal penile tumescence and rigidity assessment |
| Psychiatric evaluation |
| Specialized endocrinologic testing (hypothalamic-pituitary-gonadal role studies; magnetic resonance imaging of the sella turcica) |
| Vascular diagnostics (duplex ultrasonography; penile pharmacocavernosometry and pharmacocavernosography; penile arteriography; computed tomography or magnetic resonance imaging; nuclear imaging) |
Treatment
- Abstract
- Prevalence
- Pathophysiology
- Diagnosis and Evaluation
- Handling
- Link to Cardiovascular Disease
- References
LIFESTYLE MODIFICATIONS
Outset-line therapy for ED is aimed at lifestyle changes and modifying pharmacotherapy that may contribute to ED8 (Table 26). Sedentary lifestyle, a significant risk factor for cardiovascular disease, may too be a modifiable adventure factor for ED.15 Obesity most doubles the risk of ED3; ane written report determined that one third of men who were obese improved their ED with moderate weight loss and an increase in the amount and duration of regular practice.14 The risk of moderate or full ED is almost double in men who fume compared with nonsmokers.16 Patient teaching should be aimed at increasing exercise, losing weight to achieve a torso mass index (BMI) less than thirty kg per ktwo, and stopping smoking.
Tabular array five.
Clues to the Diagnosis of Erectile Dysfunction
| Clinical inkling | Suggested diagnosis |
|---|---|
| History | |
| Altered or impaired partner sexual function | Psychological causes (eastward.one thousand., anxiety, depression, guilt, history of sexual abuse, marital or relationship problems, stress) |
| Decreased appearance and book of ejaculate | Chronic prostatitis, normal aging process, obstruction of ejaculatory duct(s), retrograde ejaculation |
| Decreased libido | Chronic fatigue syndrome, hypogonadism, hypothyroidism, psychological atmospheric condition |
| Impaired quality and timing of orgasm, including anorgasmia | Alcohol abuse, Cushing syndrome, hyper- or hypothyroidism, medications (east.k., antihistamines, antipsychotics, beta blockers, selective serotonin reuptake inhibitors, thiazides, tricyclic antidepressants), psychological causes, surgery of the pelvis or prostate |
| Presence of sexually-induced genital pain | History of sexual abuse, genital piercings, sexually transmitted infections (e.one thousand., genital herpes) |
| Concrete examination | |
| Cess of body habitus for key obesity | Cushing syndrome, diabetes mellitus, metabolic syndrome |
| Decreased perineal sensation | Cauda equina syndrome, spinal stenosis, surgery of the pelvis or prostate, trauma |
| Decreased peripheral pulses | Atherosclerotic and peripheral vascular disease |
| Elevated blood pressure | Atherosclerotic vascular illness, cerebrovascular disease |
| Enlarged prostate on digital rectal examination | Beneficial prostatic hyperplasia, prostate cancer |
| Penile curvature | Peyronie disease, ruptured corpora cavernosum, venous leakage |
| Tachycardia | Anxiety, hyperthyroidism, stimulant abuse, underlying cardiovascular disease |
| Testicular abnormalities | Epididymitis, hypogonadism, testicular cancer, varicocele |
| Thyroid goiter | Hyper- or hypothyroidism |
PHARMACOTHERAPY
Phosphodiesterase blazon 5 (PDE5) inhibitors are the most effective oral drugs in the treatment of ED,9,12 and should be considered kickoff-line therapy.8,xiv,17 Retail sales of sildenafil (Viagra), tadalafil (Cialis), and vardenafil (Levitra) approached $1.48 billion in 2007.18 Sildenafil has been found to be effective and condom in cases of ED associated with diabetes mellitus17,19 and spinal string injury,20 and in men with sexual dysfunction secondary to antidepressant therapy.21 Compared with placebo, sildenafil has been shown to amend erections (74 versus 21 per centum; number needed to treat [NNT] = 2)22 and results in more frequent intercourse attempts (57 versus 21 percent; NNT = 3).23 Approximately one third of men with ED do not respond to therapy with PDE5 inhibitors. These agents are not constructive for improving libido.24
The three PDE5 inhibitors are considered to be relatively like in effectiveness, but at that place are differences in dosing, onset of action, and duration of therapeutic effect (Table half dozen).25 At that place are no rigorous information to suggest that i PDE5 inhibitor is superior to some other. An open-label trial plant that patients preferred tadalafil and vardenafil over sildenafil,26 however most evidence supports equal effectiveness betwixt sildenafil and vardenafil.27 PDE5 inhibitors are more often than not well tolerated, with mild transient adverse furnishings of headache, flushing, dyspepsia, rhinitis, and abnormal vision. Headache is the almost ordinarily reported adverse issue, occurring in approximately 10 pct of patients. Rare just important adverse effects include dizziness, syncope, and nonarteritic anterior optic neuropathy (predominantly from crossover phosphodiesterase type half-dozen inhibition). PDE5 inhibitors should non be taken concomitantly with nitrates because this may lead to a synergistic effect, resulting in a potentially serious, even fatal, decrease in blood pressure. PDE5 inhibitors are metabolized by the cytochrome P450 3A4 and may bear upon metabolism of protease inhibitors and antifungal medications.
Table half dozen.
Phosphodiesterase Type v Inhibitors for Erectile Dysfunction
| Drug | Standard dose* | Recommended fourth dimension betwixt dosing and intercourse | Onset of action | Elapsing † |
|---|---|---|---|---|
| Sildenafil (Viagra) | l to 100 mg | I hour | 14 to 60 minutes | Upward to four hours |
| Tadalafil (Cialis) | 10 to 20 mg | I to 12 hours | 16 to 45 minutes | Up to 36 hours |
| Vardenafil (Levitra) | 10 to twenty mg | One hour | 25 minutes | Upwards to four hours |
Intracavernosal pressure and PDE5 activity are androgen-dependent. The prevalence of hypogonadism (defined equally a morn serum total testosterone level less than 300 ng per dL [10.41 nmol per L]) in men with ED is estimated to be five to ten percent.13,28 In men with hypogonadism, testosterone supplementation is superior to placebo in improving erections and sexual function. Response rates are higher in principal versus secondary testicular failure, and with transdermal versus oral or intramuscular testosterone.thirteen Supplementation is also associated with improved satisfaction with erectile function and sexual desire.29 Men with hypogonadism who failed a trial of sildenafil were found to have pregnant improvement in erectile office with the add-on of testosterone supplementation.xxx Testosterone supplementation may event in erythrocytosis, elevated serum trans-aminase levels, exacerbation of untreated slumber apnea, beneficial prostatic hyperplasia, and an increased risk of adenocarcinoma of the prostate. Men receiving testosterone supplementation crave more than frequent monitoring of hemoglobin, serum transaminase, and prostate-specific antigen levels, and prostate examinations.31
SURGICAL AND PROCEDURAL THERAPY
Alprostadil (Caverject) is a viable 2nd-line therapeutic pick for the treatment of ED. It should initially be administered in the physician's part at the lowest dose and sequentially titrated to an adequate erectile response while monitoring for syncope. The physicians should too provide education on self-assistants.8 Intra-cavernosal alprostadil is more than effective, amend tolerated, and preferred past men over the intraurethral form.32 Mutual adverse effects of intraurethral alprostadil include local penile pain, urethral haemorrhage, dizziness, and dysuria. Common adverse effects of intracavernosal alprostadil include penile hurting, edema and hematoma, palpable nodules or plaques, and priapism. Patients should be informed about the potential for occurrence of prolonged erections and should seek emergent medical evaluation for rigid erections lasting longer than four hours. Priapism is virtually commonly treated with aspiration of claret from the corpus cavernosum under local coldhearted. If this treatment is insufficient, then intra-cavernosal injections of phenylephrine should be performed with hemodynamic monitoring to watch for severe hypertension, tachycardia, or arrhythmia.
Vacuum pump devices are a noninvasive second-line selection (Figure 2). They are contraindicated in men with sickle prison cell anemia or blood dyscrasias, and in those taking anticoagulants. If used properly, adverse furnishings and potential risks are negligible, withal there may be a substantial learning curve. When first- and second-line therapies take failed, surgical implantation of an inflatable penile prosthesis can be considered in consultation with a urologist (Effigy 3). Patients should exist counseled regarding risks, benefits, and expectations of this procedure. The AUA does not endorse penile venous reconstructive surgery or surgeries to limit venous outflow from the penis. Penile arterial reconstructive surgery is controversial and more rigorous trials are needed to testify short- and long-term effectiveness.xvi
Figure 2.
Erec-Tech vacuum therapy system.
Figure 3.
Coloplast Alpha-1 inflatable penile prosthesis.
ALTERNATIVE THERAPIES
Korean cherry-red ginseng (Panax ginseng) at 900 mg three times daily has been reported to improve erections only not overall sexual feel.33 Yohimbine has shown superiority over placebo for treatment of ED with express adverse effects,34 only is not recommended by the AUA because of questions about its condom and effectiveness.eight Some dietary supplements marketed for treatment of ED obtainable via the Internet (e.g., Super X, Stamina-Rx) contain PDE5 inhibitors (sildenafil 30 mg and tadalafil xx mg, respectively). Although these and other like products claim to be free of any adverse furnishings, they accept the same risks as PDE5 inhibitors.35
BEHAVIOR THERAPY
When at that place is no obvious medical etiology for ED, psychosocial factors should be explored. The potential clue that psychosocial factors may be a cause is that a man is able to achieve normal erections and orgasm through masturbation or sex with a partner other than the "index case" partner with whom he has erectile dysfunction (e.1000., a spouse with whom there is substantial disharmonize). Group or individual cognitive behavior therapy; psychosexual therapy, including sensate focus technique; and therapy aimed at improving relationship difficulties may assistance to improve sexual dysfunction in men. A 2007 Cochrane review found that men who received group therapy plus sildenafil had more successful intercourse and were less probable to driblet out of the report compared with those who received just sildenafil.36 When comparison psychosocial interventions versus alprostadil injections and vacuum pump devices, no differences in effectiveness were found.36 In some cases, education about medical and psychosocial etiologies of ED in conjunction with physician reassurance may prove adequate to restore normal male sexual function.
Link to Cardiovascular Affliction
- Abstract
- Prevalence
- Pathophysiology
- Diagnosis and Evaluation
- Treatment
- Link to Cardiovascular Disease
- References
Men with ED should be considered for cardiovascular risk screening.15 ED rates differ significantly in patients with established coronary artery disease (CAD). On average, ED symptoms present three years earlier than CAD symptoms.37 Men with ED have a 75 percent increased run a risk of peripheral vascular affliction.38 The Prostate Cancer Prevention Trial determined that men with ED have a significantly greater likelihood of having angina, myocardial infarction, stroke, transient ischemic assail, congestive eye failure, or cardiac arrhythmia compared with men without ED.39 Because nearly men are asymptomatic before an astute coronary syndrome, ED may serve equally a sentinel marker for prompting discussions centered on promotion of cardiovascular risk stratification and modification.
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REFERENCES
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33. Hong B, Ji YH, Hong JH, Nam KY, Ahn TY. A double-blind crossover study evaluating the efficacy of korean cerise ginseng in patients with erectile dysfunction: a preliminary written report. J Urol. 2002;168(5):2070–2073.
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35. Fleshner N, Harvey M, Adomat H, et al. Show for contamination of herbal erectile dysfunction products with phosphodiesterase type 5 inhibitors. J Urol. 2005;174(2):636–641.
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