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  Disfunción eréctil masculina

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Los impulsos adrenérgicos mantienen el tono de la contracción del músculoi liso de los cuerpos cavernosos en el estado flácido. Las erecciones del pene son el resutlado del aumento del flujo sanguíneo provocado por la vasodilatación y relajación cavernosa atribuible a la estimulación nerviosa.

Diferentes son los estímulos capaces de estimular al cerebro. Los impulsos provienen de la médula espinal hasta el ganglio toracolumbar. El principal neurotransmisor producido es el óxido nítrico, derivado del factor endotelial de relajación, que causa aumenta el flujo sanguíneo Este agente produce relajación de las arteriolas y del músculo cavernoso del pene que permite aumentar el flujo sanguíneo y aumenta la presión intracorporal cavernosa hasta casi los niveles de la presión sistólica. Los cuerpos dilatados comprime el sistema venoso contra los tejidos elásticos de la túnica albuginea, que evita la salida de sangre venosa y aumenta, aún más, la presión intracavernosa por encima de la presión sistólica.

Justo antes de la ejaculación, se contraen los músculos isquicavernoso y pubocavernosos produciendose más presión y la eyaculación. Las fibras parasimpáticas también se estimulan por el tacto del pene, que se transmite por el nervio pudendo al arco espinal reflejo S-2-4. De esta forma se relaja el músculo cavernoso permitiendo la llegada de sangre al pene y subsecuentemente aumentando la presión del pene.

En condiciones normales, la erección depende de los dos mecanismos indicados, pero con la edad se produce menos estímulo nervioso central y depende más de la estimulación táctil del pene. Con el envejecimiento el varón precisa alargar la estimulación local, posiblemente por una disminución de la producción de óxido nítrico.

Aging-Related Erectile Changes Before the causes of erectile dysfunction are discussed, the normal aging-related changes in erectile function should be reviewed. Some men seeking help need only reassurance that their symptoms are age-related physiologic changes in function. In young men, the higher centers of the brain are easily stimulated by fantasizing or thinking about sex, which seems to cause an erection nearly at will. With aging, this ability decreases. Ability to reach arousal with suggestive photographs also becomes less effective, although arousal by viewing a suggestive video may remain longer. Increased interaction of the couple, especially with foreplay, is needed to achieve a satisfactory erection. Another aging-related change is an increase in the refractory period-that is, the time from ejaculation to the next erection. This interval may range from 30 minutes in a young man to several days in an octogenarian, according to the work of Masters and Johnson. Erections, once achieved through fantasy and foreplay, are more fragile as men age. Older men must maintain their focus; if they allow themselves to be distracted by thinking of work or other activities, detumescence may occur. The telephone ringing may be enough to cause detumescence. In addition, men may occasionally experience detumescence without ejaculation for no apparent reason.

Causes of Erectile Dysfunction

The two main categories of dysfunction are psychologic and organic. Often the category is "mixed," inasmuch as both factors are important. Every man who has some problem with erectile function has an element of performance anxiety, and determining whether psychologic factors are the main problem or merely a minor accompaniment may be difficult.

Organic causes are vascular, neurologic, hormonal, medical, or drug-related, and some men have multiple etiologic factors. Most of these causes affect the intrapenile vasculogenic mechanisms, whether arterial or venous. Another common finding is a decrease in local nitric oxide, which is thought to be the main neurotransmitter in initiating the erectile process. Intracorporeal fibrosis may also be present, which would limit the expandability of the corpora cavernosa, prevent the venules from compressing against the tunica albuginea, and thereby allow venous leakage from the penis.

Vascular Causes.-Among the vascular factors that can affect erectile function is a decreased blood flow to the penis. Decreased intrapenile circulation occurs if the corpora cavernosa cannot expand and fill with blood. Although atherosclerotic plaques, or damage by trauma or irradiation, decrease blood flow to the penis, vascular causes of erectile dysfunction are more often due to a failure of neural, muscular, or chemical factors. The vascular problem of venous origin, venous leakage, occurs when incomplete filling of the corpora, or intracavernosal fibrosis, causes failure of the veins to be pressed shut against the tunica albuginea.

Neurologic Causes.-A cerebrovascular accident (CVA or stroke), demyelinating diseases, or even seizure disorders can cause erectile dysfunction. Tumors or trauma to the spinal cord could also be causative factors. Peripheral nerves may be damaged by trauma or transurethral resection of the prostate. A common cause of impaired erectile and ejaculatory function is peripheral nerve damage due to diabetic autonomic neuropathy. This prevalence increases with time in both type 1 and type 2 diabetes, and the frequency of occurrence increases when the plasma glucose is poorly controlled.

Hormonal Abnormalities.-Hormonal causes are related to sexual dysfunction, especially erectile dysfunction. Most problems revolve around dysfunction of the hypothalamic-pituitary-gonadal axis and are associated with either excess prolactin or decreased testosterone levels. Other endocrine disorders that may cause libido or erectile difficulties include hypothyroidism, hyperthyroidism, adrenal insufficiency, or excessive levels of adrenal corticosteroids. In such cases, the effect is a generalized fatigue or weakness from the effects of the illness. Tumors of the hypothalamic-pituitary area may cause hypogonadism by mass effect, destruction of pituitary tissue, or oversecretion of prolactin, which may suppress gonadotropins and cause secondary hypogonadism. Postreceptor action of increased prolactin levels may also cause erectile problems, even in the presence of a normal testosterone level. Prolactin overproduction due to medications, hypothyroidism with increased thyrotropin, chest wall injuries, or compression of the pituitary stalk can result in sexual problems. Rarely, if the patient has an excess of a variant large prolactin molecule, macroprolactin, the cause of the sexual difficulties will not be the prolactin because these molecules are biologically inert. Any major medical illness or surgical procedure can suppress the central axis and cause secondary hypogonadism. Primary hypogonadism occurs in some men as they age. A common cause of primary testicular failure is autoimmune destruction of the testicles. Another factor is unilateral mumps orchitis during the early adult years, with later failure of the "good testis." Hypogonadism is defined as a free testosterone level that is below the lower limit of normal for young adult control subjects. Previously, age-related decreases in free testosterone were once accepted as "normal." Currently, they are not considered normal. Several clinical conditions were once accepted as normal age-related disorders but now are thought to be unhealthy-for example, hypertension, osteoporosis, and menopause. No agreement exists on the exact normal level of testosterone as men age or the serum testosterone level at which a man loses his sexual function. The definition of relative hypogonadism is also uncertain. Many men have perfectly normal sexual function even if their testosterone levels decline into the age-adjusted lower normal range. Patients with low-normal to subnormal range testosterone levels warrant a clinical trial of testosterone. The threshold of response to testosterone, and thus the necessary dosage, varies-especially in the younger decades of life. If LH is increased and the testosterone level is low, the patient will have decompensated primary testicular failure. Testosterone replacement therapy is then essential. Men with testicular failure may suffer from sexual dysfunction, as well as osteoporosis, anemia, muscle weakness, depression, and lassitude, which is the clinical spectrum of hypogonadism. The sexual dysfunction, especially decreased libido and decreased erectile capacity, often reverses with testosterone replacement therapy. The variability of response in some patients may be related to comorbid medical illnesses, vascular dysfunction at the penile level, or psychologic factors. Medical Conditions.-Any medical condition that can cause general debility has the potential to decrease sexual desire and performance. Pain, shortness of breath, angina, muscle weakness, or a CVA may be responsible for the dysfunction. The most common medical conditions associated with sexual difficulties are diabetes mellitus and hypertension, possibly because of the microvascular and neurovascular changes that are inherent in these conditions. In patients with diabetes, these factors may lead to a decrease in nerve stimulation and in nitric oxide generation. Some investigators have found hypogonadism to be commonly associated with diabetes mellitus. Poorly controlled plasma glucose levels add a separate risk factor, as does the presence of diabetic neuropathy. Not only is hypertension a separate risk factor for sexual problems but hypertension and diabetes often coexist in the patient. Generalized atherosclerosis and peripheral vascular disease may impede blood flow to the penis, as may a damaged vessel from pelvic injury or radiation therapy to the groin. Tobacco (cigarette smoking) can cause vascular insufficiency as well as a decrease in intrapenile nitric oxide levels. Excessive consumption of alcohol or use of other recreational drugs may cause sexual dysfunction, either by a direct effect on the penile neurovascular system or by causing increased prolactin or decreased testosterone production (or both). Peyronie's disease is a condition in which collagen tissue is converted to fibrous tissue, for unknown reasons; a palpable fibrous plaque created in the tunica albuginea causes bending of the penile shaft. The usual manifestation is a bend to one side during erection, which can occasionally be painful.

Drug-Related Causes.-Both prescription and over-the-counter medications have been shown to be the cause of erectile problems in as many as 25% of cases (Table 1). Although single medications can induce erectile dysfunction, the adverse medication effects are often additive. This situation is particularly frequent in older men who are taking multiple medications and in whom partial or complete erectile dysfunction often results. A psychologic component can make partial erectile dysfunction progress to complete erectile dysfunction. Some medications can affect libido, whereas others affect erectile function or ejaculation. Nonprescription medications, such as antihistamines or decongestants, may affect erectile function. Most psychotropic drugs can affect libido or erectile function, through either a direct action or an increased prolactin or a decreased testosterone level. Although antidepressants may cause dysfunction in susceptible patients, they may also be beneficial in improving libido in depressed men. Antihypertensive medications may cause erectile dysfunction either by drug-specific effects or by decreasing the systolic pressure and thereby decreasing the intracavernosal penile pressure. This result is especially prevalent in patients with diabetes or hypertension who have an underlying microvascular disease. Ketoconazole, aminoglutethimide, and similar drugs actually decrease the production of testosterone. Most of the earlier antihypertensive agents-such as reserpine, guanethidine, and hydralazine-caused sexual dysfunction. Some b-adrenergic blocking agents may cause sexual problems, but dysfunction with angiotensin-converting enzyme inhibitors or calcium channel blockers is less common. Some drugs (spironolactone, cimetidine, flutamide, or cyproterone acetate) may block the peripheral androgen receptors. Cimetidine may assume a greater importance because it can now be purchased without a prescription. Drugs such as a-methyldopa, spironolactone, digoxin, metoclopramide, and many psychotropic agents may raise prolactin levels. Thiazide diuretics, finasteride, anticholinergics, and pain medications cause dysfunction in a certain percentage of patients.

Table 1 Sexual Side Effects of Common Prescription Medications ------------------------ Generic name Brand name Sexual side effects ---------------------------- Antihypertensive medications Diuretics Spironolactone Aldactone Decreased libido, breast swelling, impotence Thiazides Diuril, HydroDIURIL, Naturetin, Naqua, many others Impotence Furosemide Lasix None Centrally acting agents Methyldopa Aldomet Decreased libido, impotence Clonidine Catapres Impotence Reserpine Serpasil, Raudixin, Ser-Ap-Es Decreased libido, impotence, depression a-Adrenergic blockers Prazosin Minipress "Dry" (retrograde) ejaculation Terazosin Hytrin "Dry" (retrograde) ejaculation b-Adrenergic blockers Propranolol Inderal Impotence, decreased libido Metoprolol Lopressor Impotence, decreased libido Combined a- and b-adrenergic blockers Labetalol Normodyne, Trandate Inhibited ejaculation Nonadrenergic vasodilators Hydralazine Apresoline None Sympathetic nerve blockers Guanethidine Ismelin Impotence, "Dry" (retrograde) ejaculation Angiotensin-converting enzyme inhibitors Captopril Capoten None Enalapril Vasotec None Lisinopril Zestril Impotence in a small percentage (1%) of cases Psychiatric medications Antidepressants Tricyclics: Amitriptyline Elavil Inhibited ejaculation, impotence Amoxapine Asendin Decreased libido, impotence Desipramine Norpramin Inhibited ejaculation Doxepin Sinequan Inhibited ejaculation, impotence Imipramine Tofranil Inhibited ejaculation, impotence Maprotiline Ludiomil Inhibited ejaculation Nortriptyline Aventyl, Pamelor Inhibited ejaculation Protriptyline Vivactil Inhibited ejaculation, impotence Atypical agent: Trazodone Desyrel Priapism Monoamine oxidase inhibitors: Isocarboxazid Marplan Inhibited ejaculation Phenelzine Nardil Inhibited ejaculation, decreased libido Tranylcypromine Parnate Inhibited ejaculation Antipsychotic medications Phenothiazine group: Thioridazine Mellaril Inhibited ejaculation, priapism, decreased libido Chlorpromazine Thorazine Inhibited ejaculation Mesoridazine Serentil Inhibited ejaculation, decreased libido Fluphenazine Prolixin Inhibited ejaculation, decreased libido Serotonin reuptake inhibitors: Fluoxetine Prozac Anorgasmy (8%) Perphenazine Trilafon Inhibited ejaculation Trifluoperazine Stelazine Inhibited ejaculation Thioxanthene group: Chlorprothixene Taractan Inhibited ejaculation Thiothixene Navane Inhibited ejaculation, impotence Butyrophenone: Haloperidol Haldol Inhibited ejaculation Antimania medication Lithium carbonate Eskalith, Lithobid Possible impotence Antiulcer medications Cimetidine Tagamet Decreased libido, impotence, gynecomastia Ranitidine Zantac None Famotidine Pepcid None From Spark RF. Male Sexual Health: A Couple's Guide. Yonkers: Consumer Reports Books, 1991. 117-118.


An algorithm for evaluation of erectile dysfunction is shown in Figure 3.

Evaluation of the Couple The initial assessment of a male patient with sexual dysfunction and his partner is best performed by a physician who has the training, experience, and interest in evaluating the relevant medical, psychologic, and hormonal factors. In many ways, the clinical endocrinologist is the physician best suited to direct the evaluation and treatment by the multidisciplinary team. Ideally, the couple should undergo assessment together at the first visit or soon thereafter. A discussion about the partner is important. Is the patient married, single, divorced, or widowed? Newer relationships may have adjustment problems. The duration of the relationship is important, as is the age disparity between the partners. The health of the partner is very important because 15% of men report a decreased sexual frequency or ability because of health problems that their partners are experiencing, and the men are infrequently aware of this connection. The question of whether a couple is still sexually active in other ways is more revealing: do they practice alternative sexual techniques even if intravaginal penetration is not possible? This adjustment highlights their relationship in general and how comfortable they are with each other. The interviewer has to determine whether any relationship problems exist between the partners or whether external stresses may be a predominant factor. The dynamics between the partners should be carefully observed. Relationship problems may be due to intrinsic philosophic differences between the two, and expectations about sexual fulfillment may also vary. Occasionally, the level of commitment to each other differs. Stresses may be present strictly because of performance anxiety or work problems, financial worries, or perhaps problems with children or other relatives. Oftentimes, inadequate communication between the couple, which is due to embarrassment, may be mistaken for lack of caring. The couple may begin to avoid contact and drift apart because of isolation or frustration. Even before sex therapy is considered, one or both parties may require stress management, or the couple might consider marital counseling before sexual counseling.

Sexual History The examiner must evaluate the symptoms carefully because the sexual history is of considerable importance. Many men have only aging-related sexual changes, and reassurance is all that is necessary. With erectile dysfunction, the most common complaint is attainment of only partial erections that may not achieve vaginal penetration, or if the initial erections penetrate, early detumescence occurs without ejaculation. These problems may coexist in many patients. When organic factors cause the erectile dysfunction, the patient can also develop a fear of failure, which may then lead to a decrease in sexual interest and even avoidance of the partner. Total loss of all penile rigidity is uncommon. The duration of the problem is useful to know because patients who have had sexual difficulties for years tend to have more psychologic adjustments to make, even with successful therapy. If nocturnal or morning erections are present and strong, it will direct the evaluation toward psychologic causes, or it may simply mean that a certain medication might have decreased its concentration (and its adverse effect) during the night. The absence of nocturnal erections can mean that the patient is no longer awakening out of rapid eye movement (REM) sleep, during which time most erections occur, and it does not necessarily mean that the patient has organic erectile dysfunction.

Medical History In determining the possible medical risk factors that might be related to erectile dysfunction and other aspects of sexual dysfunction, both prescription and over-the-counter medications should be listed. (A list should be prepared in advance by the patient in order to save time.) The patient should be asked about tobacco and alcohol abuse as well as use of other recreational drugs. High-risk disorders must be reviewed. Is diabetes mellitus, hypertension, coronary artery disease, or peripheral vascular disease present? Loud snoring should prompt a workup for sleep disorders. Conditions such as sleep apnea, nocturnal myoclonus, or restless legs may directly affect the higher sexual centers or cause secondary hypogonadism. CVA or seizure disorders (and seizure medications) occasionally are associated with sexual dysfunction from central nervous system mechanisms. Any severe debilitating disease can be a potential cause of sexual dysfunction. A history of emotional illness or surgical procedures, especially of the colon and prostate, should be elicited. Transurethral resection of the prostate is associated with a substantial risk of nerve damage to the penile nerves. As the patient ages, the possibility of multiple factors causing erectile dysfunction increases. If one adds concurrent performance anxiety and stresses of daily living, the situation often is difficult to assess. Teaching the patient and his mate the interrelationships of the multiple factors, however, helps to eliminate the barriers to successful treatment.

Physical Examination A comprehensive physical examination is necessary for assessment of blood pressure, secondary sex characteristics, gynecomastia, thyroid abnormalities, femoral pulses, scrotal formation, urethral position, and the penile shaft for fibrous plaques. The testicles should be evaluated for size and consistency and to exclude nodules. Linear measurements (length and width) may be used, but a more accurate determination can be obtained with the Prader orchidometer-a series of elliptical spheres of various volumes to assess testicular size (in different reports, the lower limit of normal volume has varied from 15 to 18 cc). Sensory adequacy of the penile shaft and perineum can be evaluated roughly by touch and pinprick. A more sophisticated bioesthesiometry apparatus may be used, but the investigator must be aware that nerve conduction and penile sensation normally decrease with age. The bulbocavernosus reflex and rectal sphincter tone must be assessed because both are mediated by the S2-4 spinal reflex arc. The bulbocavernosus reflex is tested with the finger in the rectum directed laterally to where the muscle is inserted. A moderate squeeze on the glans penis will cause the bulbocavernosus muscle to contract if the reflex arc is intact. A screening neurologic examination is necessary.

Diagnostic Tests Diagnostic testing may be categorized as follows:

Blood chemistry Vascular assessment Sensory studies Blood Tests.-Blood testing should assess anemia, increased plasma glucose levels, or impaired renal function. Thyroid testing should be done if clinically indicated. Other hormone screening should include serum testosterone level and a prolactin level. The "normal" range for testosterone is also controversial. The Massachusetts Male Aging Study confirmed that free testosterone decreases 1.2% per year and bioavailable testosterone decreases 1.0% per year, while the sex hormone binding globulin increases 1.0% per year, between the ages of 40 and 70 years. For this reason, free or bioavailable testosterone assays are preferred over the total testosterone level. The free fraction of testosterone may be assessed by equilibrium dialysis or by ultrafiltration. It may also be calculated after total testosterone and sex hormone binding globulin levels are determined. Because of the diurnal variation of testosterone secretion, obtaining several morning samples or pooling of multiple samples would be advisable. These and other recommendations have been elucidated fully in the AACE clinical practice guidelines for evaluation of hypogonadism in adult male patients. If the testosterone level is low, or even borderline, a serum LH level should be obtained to distinguish primary from secondary hypogonadism. Compensated primary hypogonadism is present when the testosterone level is normal but the LH level is increased. Some testosterone deficiency is present, but the testicle is still compensating. Further testicular failure can be anticipated. Whether to follow the patient or to initiate treatment is an individual clinical decision.

Vascular Assessment.-Vascular flow to the corpora cavernosa may be quantified with the use of a penile Doppler examination. With use of penile blood pressure and brachial blood pressure, a ratio called the penile brachial index (PBI) is determined. Unfortunately, it has been suggested that a low PBI, which is supposed to correlate with a decreased penile blood flow, correlates better with coronary artery disease than it does with erectile dysfunction. Routine measurement is not recommended. The one instance in which the PBI may be of value is in the pelvic steal syndrome. A minor blockage of a small artery may not cause symptoms in the relatively inactive state of foreplay; thus, an erection may be normal. After penetration and pelvic thrusting, however, shunting of the blood to the pelvic musculature may cause detumescence prematurely. This condition is diagnosed by obtaining a PBI before and after exercise, either on a treadmill or with multiple deep knee bends; a decrease in the PBI of 0.15 or more is presumptive evidence of the pelvic steal syndrome. A screening office examination may be done to assess the effect of a penile injection with 10 mg of prostaglandin E1 or 10 mg of papaverine, with or without visual sexual stimulation. If an erection capable of penetration is obtained, a serious vascular deficiency is ruled out. If needed, the erection can be reversed by a penile injection of 0.2 to 0.4 mg of phenylephrine. A more sophisticated evaluation can be achieved by using color duplex ultrasonography, which measures cavernous artery diameter and inflow pressure, along with the end-diastolic pressure, which assesses venous leakage. This procedure is performed after a similar penile injection of prostaglandin or papaverine. It has also been suggested that endogenous epinephrine, generated by a patient's embarrassment, fear, or anxiety, affects the validity of the test results. Venous leakage is tested by the intracavernous infusion of saline and radiopaque dye at various rates of flow and pressure. Sensory Testing.-Bioesthesiometry testing was mentioned previously for penile sensory testing. A more sophisticated testing method might involve the use of electromyography, especially in diabetic neuropathy. Various other tests will screen for autonomic neuropathy. Recently, investigators have attempted to use pelvic evoked potentials, but experience with this technique is limited. No currently available test can assess the penile stimulating nerves clinically. Nocturnal Penile Tumescence and Rigidity Testing.-Occasionally, the measurement of nocturnal penile tumescence and rigidity is useful. This technique was developed in sleep laboratories several decades ago when normal men were found to have appreciable erectile activity during REM sleep. Tumescence is monitored by the placement of mercury strain gauges to the base and tip of the penile shaft. When a substantial tumescence episode is noted on the monitor, the sleep laboratory technician presses down on the head of the penis with a pressure plate to determine at what force the glans will buckle-hence the term "buckling pressure." This finding correlates roughly with an erection that is rigid enough for vaginal penetration. This type of testing is expensive, and some results are questionable because of the unfamiliar surroundings, the startle response, and the embarrassment when the patient is awakened for measurement of the buckling pressure. A Velcro strap, called the "snap gauge," has also been developed for use by the patient at home. It has three plastic bands that break at different tensile strengths-80, 120, and 160 mm Hg. It responds to the enlarging penis (that is, the tumescence) but gives limited or little information about penile rigidity. Penile rigidity was originally thought to correlate with tumescence, but it is now believed that up to 20% of men with organic erectile dysfunction have normal penile tumescence but abnormal rigidity when tested at night and would be incorrectly diagnosed as having normal nocturnal penile activity. The snap gauge also responds to one nocturnal event but does not reveal the number and duration of nocturnal events, factors that are considered important in evaluating nocturnal penile tumescence and rigidity activity. These deficiencies have been corrected with the development of the RigiScan portable home monitor. The recording unit is inserted into the Velcro thigh holster, and disposable strain gauge loops are placed on the base and tip of the penis. Tumescence and rigidity, at both the base and the tip, are recorded separately and stored on a computer chip inside the device. The measurement of rigidity is indirect-that is, circumferential rather than the more direct axial pressure measured in the sleep laboratory with use of buckling pressure. Good correlation has been shown, however, between the two techniques. The alternative to using the portable home monitor is to refer the patient to a sleep laboratory that evaluates nocturnal penile activity. The RigiScan monitor is useful in certain situations and can easily be set up in the physician's office. The machine is demonstrated to the patient by attaching the strain gauges and obtaining a 5-minute baseline measurement. The patient then uses the monitor at night while sleeping, in the privacy of his own home, for 2 nights. The monitor is then returned, the information is downloaded, and a graph is generated for analysis by the physician. The main purpose of the RigiScan test is to distinguish between normal and abnormal nocturnal erectile function. The main indications are as follows: (1) inability to determine clinically whether the problem is organic or psychologic, (2) ability to diagnose psychologic erectile dysfunction clinically but refusal by the patient to believe the physician, and (3) continued erectile dysfunction after correction of medical factors, and the differential diagnosis again is between organic and psychologic dysfunction. Situations in which the results of nocturnal penile testing could be misleading include (1) severe psychosis, from either anxiety or depression (the pattern may be abnormal, such as seen in organic disease) and (2) the presence of sleep disorders that can disrupt REM sleep, during which 90% of nocturnal erections occur. Simple questions about sleep apnea, nocturnal myoclonus, or severe snoring prove to be an adequate screen. If these conditions are present, the patient should be referred to a sleep laboratory for a comprehensive evaluation.


Some men simply require reassurance that their concerns reflect aging changes and that their sexual function is indeed what is expected for their age. Some men refuse treatment. They only wish to be reassured that their sexual deficiency is not a symptom of a more serious illness. Most men, and indeed couples, prefer a diagnostic evaluation and therapeutic counseling. After discussion of the therapeutic options, some couples do not wish any treatment for erectile problems directed toward intravaginal penetration and would prefer just to engage in alternative sexual techniques such as mutual masturbation. Psychologic Treatment The couple should be compatible. Both partners should be willing to participate and cooperate with therapy. Major relationship problems should be addressed before therapy is introduced. Similarly, major stresses with work, finances, or family will need to be evaluated and treated first. Performance anxiety, specifically related to fear of sexual failure, is best evaluated and treated by a qualified sex therapist (psychologist or psychiatrist). At times, minor relationship problems manifest after organic causes of sexual dysfunction have been corrected. These minor problems may be caused by fear of failure, fear of frustration, or embarrassment. Decreased libido may be psychologic in origin and may necessitate sexual therapy and possibly pharmacologic treatment. Ejaculation problems can be either organic or psychologic, and the sex therapist will help patients with premature ejaculation as well as with problems involving anejaculation or retarded ejaculation. At times, a female partner might not be knowledgeable about, and may be reluctant to participate in, the increased foreplay that men require to obtain erections as they age. The therapist can reaffirm the need and teach the techniques. Medical Treatment If organic problems seem to be dominant, the first step is to discover which are reversible. Alcohol intake should be decreased, or stopped, if excessive. Use of illicit drugs must be discontinued. Cessation of tobacco abuse is important, with or without the use of pharmacotherapy. Offending medications could be changed or stopped. Plasma glucose must be regulated in uncontrolled diabetes mellitus. Hypertensive medication must be optimized. Sexual dysfunction can be a motivational tool to increase patient compliance in chronic disease. Hormonal Treatment Benign prostatic hyperplasia, prostate cancer, sleep apnea, and polycythemia must be evaluated before and after initiation of testosterone therapy. A baseline prostate-specific antigen level should be determined before treatment; if this value is even slightly increased, the patient should be referred to a urologist for a prostate evaluation. Any patient treated with replacement androgens should be reassessed within a few months after initiation of therapy and then at 6- to 12-month intervals to ensure that clinical problems have not appeared or worsened during such treatment. The presence of prostate cancer is a contraindication to androgen therapy, whereas sleep apnea, peripheral edema, polycythemia, and benign prostatic hyperplasia are relative contraindications that may respond to adjustments in the medication or specific treatments (use of continuous positive-airway pressure or weight reduction). Testosterone replacement for the treatment of hypogonadism may also correct sexual dysfunction, unless the patient has other comorbid illnesses. For decades, the standard has been a depot intramuscular injection of testosterone enanthate or cypionate every 2 or 3 weeks (200 mg or 300 mg, respectively). Smaller dosages and more frequent injections, however, are better at maintaining circulating testosterone in the normal range (that is, 50 to 150 mg of testosterone enanthate or cypionate intramuscularly at 7- to 14-day intervals). An alternative approach is to administer 100 mg on days 1, 11, and 21 of each month, while allowing some flexibility of injection days. If testosterone levels are measured, they should be in the normal range just before the next injection. Currently available tablets for oral administration have generally not been used because of potential liver toxicity. A newer oral tablet, testosterone undecanoate, has been used for more than a decade in Europe but has not yet been approved for use in the United States. Although the safety is not questioned, multiple daily doses are required and the absorption is erratic. Other orally and sublingually administered tablets are being evaluated. Implantable testosterone pellets, which are used in other countries, and other forms of intramuscular testosterone preparations are also being evaluated. Testosterone scrotal and nonscrotal patches have now been approved by the Food and Drug Administration (FDA). Testosterone absorption is greater through scrotal skin. The scrotal patch was the first to be introduced. These patches are placed on the scrotal skin and are changed daily, in the morning. For many patients, weekly shaving of the scrotum is necessary. The patch increases testosterone levels to the normal range, which remain stable. Because 5a-reductase in scrotal skin is high, the dihydrotestosterone (DHT) level in serum is quite high. The role of DHT is currently being investigated. It may have little biologic activity because it is largely bound to sex hormone binding globulin. The nonscrotal patch, applied daily in the evening, may be worn in various sites on the skin. The manufacturer recommends that it not be used over bony prominences. The levels of testosterone increase during the nighttime hours, a pattern mimicking the body's normal diurnal variation. The levels remain stable in the middle of the normal range, and the DHT levels remain normal. Contact dermatitis at the site of application is seen in approximately a third of the patients. Some patients may control this skin reaction with triamcinolone cream, but 10% of patients may have to discontinue the use of testosterone patches. With any form of testosterone treatment, the patient may have a slow and steady increase in libido and erectile capacity during a course of months. If no improvement is noted after 3 months, the hormone deficiency may not be the only cause of the sexual dysfunction. A comorbid medical illness might also be present, or perhaps performance anxiety is dominant. The hypothalamic-pituitary-gonadal axis has been shown to decrease functioning temporarily after acute medical events or surgical procedures; this action can cause low gonadotropin and testosterone levels. Such a temporary decrease in testosterone levels may also occur as a result of less serious circumstances, such as anxiety, alcohol excess, multiple medications, or uncontrolled diabetes. Patients with these causes are less likely to respond to testosterone replacement. Stimulation of gonadotropins with clomiphene citrate and the subsequent increase in testosterone levels emphasize the functional and reversible nature of this phenomenon; short-term use of clomiphene citrate may help some patients. Occasionally, low testosterone levels are due to suppressed gonadotropins attributable to an increased prolactin level. This situation can be reversed by treatment with bromocriptine or pergolide. If increased prolactin is due to a psychotropic drug, however, withdrawing or switching the medication may be all that is needed. Treatment of other endocrine disorders, such as hypothyroidism or hyperthyroidism, reverses the libido or erectile dysfunction that accompanies these and other hormonal disorders. Uncontrolled diabetes mellitus may respond to improved plasma glucose control, especially in patients with recently diagnosed diabetes. Even patients with diabetes who have been afflicted for more than 10 years may respond to better control if major neuropathy is absent. Hypogonadism also seems to be especially prevalent in patients with diabetes, and many respond to testosterone treatment.

Ultima revisión: 1 junio 2001

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