How is Peyronie's disease treated?

Most physicians recommend an initial conservative approach during the acute, inflammatory phase of Peyronie's disease, which can last from 6 to 18 months and is characterized by penile pain, curvature, and a palpable plaque. During this period, medical treatment options include oral therapy (Vitamin E, POTABA, Tamoxifen, Colchicine) and intralesional therapies (Verapamil, Interferon). None of these therapies are FDA approved for the treatment of Peyronie's disease, and there are limited well-designed studies evaluating their efficacy.

• Vitamin E—100 mg of Vitamin E three times a day for a minimum of 4 months. Vitamin E is an antioxidant, and it is thought that it decreases further plaque formation, although some studies suggest it is no more effective than placebo.

• Injectable verapamil—Although it has been used, it has not been shown to be better than placebo.

• POTABA (potassium para aminobenzoate)—POTABA is a member of the vitamin B complex and is believed to prevent fibrosis (scarring) from occurring through its effects on increased oxygen uptake by the tissues. It is rapidly excreted in the urine and as a result it needs to be taken frequently throughout the day, every 3 to 4 hours. The standard regimen is 12 grams/ day, divided into 6 doses of four 500 mg tabs, for a total of 24 tabs per day. It is recommended that POTABA be used for 6 to 12 months.

• Cortisone injection—There are two agents that have been used, dexamethasone (decadron) in a dose of 0.2 to 0.4 mg injected directly into the plaque weekly for a course of 10 weeks, and triamcinolone hexacetonide (Aristospan) 2 mg injected into the lesion once every 6 weeks for a total of 6 injections.

Surgical intervention is reserved for those individuals whose Peyronie's disease fails to resolve/improve with conservative therapy. Criteria for surgical intervention include: severe penile curvature which prevents intercourse, stable and unchanged disease for at least 3 months, and severe penile shortening.

There are three main approaches to the surgical management of Peyronie's disease:

1. Shortening of the tunica albuginea (plication procedure or corporoplasty) on the contralateral corpora

2. Lengthening of the affected corpora by incision or excision of the plaque and placement of a graft

3. Placement of a penile prosthesis to straighten the penis and restore erectile function

What are the current treatment options available for ED?

There are a variety of options available for the treatment of ED, ranging from oral therapy (PDE-5 inhibitors), intraurethral suppository, injection therapy, and the vacuum device to surgical intervention, placement of a penile prosthesis. Table 18 lists the currently available treatment options and they are discussed individually in greater detail in the following questions.

What if my testosterone level is low? What are the risks and benefits of testosterone therapy?

Hypogonadism is a condition in which low levels of testosterone are found in association with specific signs and symptoms, including decreased desire (libido) and sense of vitality, erectile dysfunction, decreased muscle mass and bone density, depression, and anemia. When hypogonadism occurs in an older male, it is referred to as andropause, or androgen deficiency of the aging male. Hypogonadism is estimated to affect 2 to 4 million men in the United States, and its incidence increases with age. Only about 5% of affected males are being treated.

Table 18. Treatment Options for Erectile Dysfunction

Despite the reported benefits of testosterone replacement therapy, including improvement in libido, bone density, muscle mass, body composition, mood, red blood cell count, and cognition, its use remains controversial.

Despite the reported benefits of testosterone replacement therapy, including improvement in libido, bone density, muscle mass, body composition, mood, red blood cell count, and cognition, its use remains controversial. There remain concerns regarding the risks of hormone therapy, particularly with respect to the risk of effects on the prostate, both benign and cancerous disease, as well as cardiovascular risks.

There is no definitive data to support that testosterone-replacement therapy increases cardiovascular risk. In fact, studies of testosterone replacement therapy have not demonstrated an increased incidence of cardiovascular disease or events such as myocardial infarction, stroke, or angina. Large scale placebo controlled long-term studies are needed to assess the long-term cardiovascular risks of testosterone therapy.

The data on the effects of testosterone replacement therapy on lipid profiles are inconsistent. Supraphysiologic (higher than normal) doses of androgens have been shown to decrease high-density lipoprotein (HDL) levels. However, when physiologic (normal) replacement doses of testosterone (both in the intramuscular and transdermal formulations) have been used, there appears to be no change or only a small decrease in HDL levels.

Higher levels of testosterone appear to stimulate erythropoiesis. It appears that injections are associated with a greater risk of erythrocytosis than topical preparations. In males receiving testosterone replacement therapy, the hematocrit or hemoglobin level should be monitored so that appropriate interventions, such as dose reduction, withholding of testosterone, therapeutic phlebotomy, or blood donation, may be performed if erythrocytosis occurs.

Testosterone replacement therapy has been associated with increases in prostate volume, primarily during the first 6 months of treatment. Despite the increase in size of the prostate there do not appear to be significant changes in voiding symptoms, urine flow rates, and postvoid residual volumes.

Controversy exists regarding the impact of testosterone replacement therapy on prostate cancer risk. Androgen ablation therapy remains one of the primary forms of therapy for metastatic prostate cancer. Despite the hormone responsiveness of prostate cancer there is no compelling data to associate the risk of developing prostate cancer with testosterone replacement therapy. There is also no compelling data to suggest that men with higher testosterone levels are at greater risk of prostate cancer or that treating men who have hypogonadism with supplemental testosterone therapy increases this risk. However, proper monitoring with measurement of PSA and digital rectal examination should promote the early diagnosis, thus potentially the cure, of most unmasked prostate cancers identified during testosterone treatment. The role of testosterone replacement therapy in hypogonadal men who have undergone curative treatment for prostate cancer is also controversial. Historically, it was felt that testosterone replacement therapy was contraindicated in men with a history of prostate cancer, but this is being challenged in the hypogonadal male who has been treated and cured of prostate cancer.

The currently used formulations of testosterone (intramuscular, gel, transbuccal, and patch) do not appear to have significant effects on liver function and routine monitoring of liver function is not necessary. Oral testosterone therapy, which is not FDA-approved in the United States, is associated with potential liver toxicity.

Testosterone replacement therapy has been associated with worsening of sleep apnea or with development of sleep apnea. This appears to be more common in men treated with intramuscular testosterone and who have other risk factors for sleep apnea.

Other reported adverse effects of testosterone therapy include: breast tenderness and swelling, decreased testicular size, adverse effects on fertility (particularly with the intramuscular formulation related to its high peaks), skin reactions (primarily erythema and pruritus) with transdermal formulations, pain and swelling at the site of injection for intramuscular testosterone, fluid retention which is usually mild in nature, but may be clinically significant in men with congestive heart failure, acne, oily skin, increased body hair, and flushing.