Erectile Dysfunction Case Discussion

A 48-year-old man had experienced acute onset of erectile dysfunction 6 months earlier. He had no other medical problems. Pubertal development had been normal. He was the father of three children

On further questioning, the patient said that he had lost his job 4 months ago. He was having problems in his relationship with his wife, and had increased his alcohol consumption from two beers a week to four beers a day.
The physical examination was normal. The serum testosterone level was 450 ng/dL.
The patient was advised that his drinking was probably contributing to his erectile dysfunction and that he should reduce his intake. Referral for psychological counseling was offered, but he refused because of the cost. Instead, the physician discussed the patient's circumstances with him. A 6-week trial of yohimbine, 5.4 mg thrice a day, was prescribed.
The patient returned 8 weeks later and reported some improvement in erectile function.
He felt that yohimbine had been helpful; however, he had also found a job, was experiencing less psychological stress, and had reduced his alcohol consumption.
What was the major factor in this patient's erectile dysfunction?
How do you approach psychological erectile dysfunction?
What are the pharmacologic options for treatment?

Case Discussion
What was the major factor in this patient's erectile dysfunction?
Although the history in this case indicated that psychological stress was the major trigger for the erectile dysfunction, it was important to consider the possibility of other components. As noted, erectile dysfunction rarely results from an isolated cause. In this case, further questioning was needed to reveal that alcohol was almost certainly a major contributor.
Obtaining an accurate history of alcohol intake is notoriously difficult. Instead of asking the patient, “Do you drink?” ask, “When you drink, do you drink beer, whiskey, or wine?” After identifying the drink of choice, pick a large amount and let patients come down from there; with beer, for example, ask if they drink a six-pack at a time. Determining the true amount of alcohol intake often requires several discussions.
Also ask patients when they drink, because they may not understand that intermittent drinking can have persistent effects. Some patients who drank heavily on the weekend and nothing at all during the week may present with erectile dysfunction and painful right-sided gynecomastia (which was worse on Mondays). Their liver enzymes were not severely elevated, but the drinking had nevertheless caused a symptomatic imbalance of testosterone and estradiol.
In patients with a history of chronic alcohol abuse, liver function tests should be ordered. Their erectile function may not return even if they reduce their alcohol intake. Because this patient's increase in alcohol intake was fairly acute, his erectile function improved as soon as he began to drink less.
How do you approach psychological erectile dysfunction?
Despite the ubiquity of the psychological component in erectile dysfunction, there have been no controlled studies to show whether psychotherapy or counseling actually helps. Even assuming that such intervention would be helpful, there are no
data on the best approach. Should patients receive behavioral therapy? Counseling? Is simply talking with the primary care physician sufficient?—considerations such as these can help in approaching psychological erectile dysfunction, but there are no clear answers.
The primary care physician should at least acknowledge psychological stress as a component of erectile dysfunction. Sometimes acknowledging the problem is enough; the patient just needs to talk about it. Sometimes further intervention is required. Whether this is provided by the primary care physician depends on his or her level of comfort with that aspect of treatment. Insurance coverage is often an important factor as well.
What are the pharmacologic options for treatment?
The options for treatment of erectile dysfunction have radically changed with the introduction of sildenafil (Viagra), the first truly effective oral medication for this condition, and more recently approved related medications, vardenafil (Levitra) and tadalafil (Cialis).
Advances in our knowledge of the physiology of erection have facilitated understanding of the pharmacodynamics of sildenafil. Erection is initiated by dilation of the arterial bed, which increases blood flow and pressure; it is maintained by restriction of venous outflow. Previously it was believed that the parasympathetic system was critical in maintaining erection. Now, we know that the major player is the nonadrenergic, noncholinergic (NA-NC) system, which was identified 50 years ago but never studied in detail until relatively recently. The NA-NC system uses nitric oxide as a neurotransmitter. Through its second messenger, cyclic guanine monophosphate (cGMP), nitric oxide triggers relaxation of penile endothelium and smooth muscle, allowing expansion of the lacunar spaces within the corpora and the trapping of blood by compression of peripheral draining venules.
Sildenafil, a type 5 phosphodiesterase inhibitor, prevents the breakdown of cGMP, thereby prolonging erection. It has no effect on libido and does not cause erection without stimulation, but it maintains an erection once it has been achieved. Although the NA-NC system is particularly prominent in the penis, it is also found in the heart, the brain, and other organs. Its presence in the eye explains the blue visual hue that some patients experience after taking sildenafil.
The most common side effects of sildenafil are headache, flushing, and dyspepsia. It can also decrease BP. Because the decrease in BP may be synergistic with the hypotensive action of nitrates, sildenafil is contraindicated in patients taking a medication that contains nitrates, such as nitroglycerin.
In addition, sildenafil alters the half-life of many other medications, and many medications change the half-life of sildenafil. The list of agents that can interact with sildenafil includes such common medications as nonselective β-blockers, erythromycin, itraconazole, potassium-sparing diuretics, and cimetidine. It is not known whether those interactions affect the side effects of sildenafil, particularly the incidence or severity of hypotension. In initial clinical trials, hypotension was reported in approximately 3% of patients, but those trials included a large percentage of young men with psychogenic impotence. Obviously, patients with vascular disease or diabetes have more problems with BP regulation and theoretically with orthostatic
hypotension. Deaths have been reported among patients taking sildenafil since it became available. The FDA is investigating those deaths.
The first study of data on different patient populations taking sildenafil was published several months after the drug became available for clinical use. Although the package insert indicated an overall efficacy of 82% (vs. 24% for placebo), analysis since has found more modest efficacy of 68% in patients with hypertension, 57% in diabetes, and 61% after transurethral prostatectomy. Moreover, published results are frequently obtained in a selected patient population, not from general clinical use.