Erectile dysfunction may be the consistent or recurrent inability to attain and maintain penile erection sufficient for sexual satisfaction.
Although some cases, particularly in younger men, may primarily reflect psychological concerns, in many cases ED results from organic disease — notably, cardiovascular disease, diabetes mellitus, hyperlipidemia, and hypertension.
Thus, ED may serve as a marker for medical conditions in need of treatment. Regardless of the cause, however, ED can have negative effects on patients’ self-esteem, relationships, and overall quality of life.
Causes in Detail
ED is relatively common, affecting at least 12 million U.S. men. The five-question International Index of Erectile Function allows rapid clinical assessment of ED. The condition can be caused by vascular, neurologic, psychological, and hormonal factors.
Common conditions related to ED include diabetes mellitus, hypertension, hyperlipidemia, obesity, testosterone deficiency, and prostate cancer treatment. Performance anxiety and relationship issues are common psychological causes.
Medications and substance use can cause or exacerbate ED; antidepressants and tobacco use are the most common. ED is associated with an increased risk of cardiovascular disease, particularly in men with metabolic syndrome.
Tobacco cessation, regular exercise, weight loss, and improved control of diabetes, hypertension, and hyperlipidemia are recommended initial lifestyle interventions. Oral phosphodiesterase-5 inhibitors are the first-line treatments for ED.
Second-line treatments include alprostadil and vacuum devices. Surgically implanted penile prostheses are an option when other treatments have been ineffective. Counseling is recommended for men with psychogenic ED.
Current smoking is significantly associated with ED, and smoking cessation has a beneficial effect on the restoration of erectile function.
Medications and Substance Use
Many medications cause or exacerbate ED. Antidepressants are a common cause, especially the selective serotonin reuptake inhibitors citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft), and the serotonin-norepinephrine reuptake inhibitor venlafaxine.
Bupropion (Wellbutrin), mirtazapine (Remeron), and fluvoxamine are less likely to cause ED. Tobacco, alcohol, and illicit drugs can cause ED. Marijuana use may cause ED, although further study is needed.
Metabolic Syndrome
ED has been linked to each component of the metabolic syndrome, including increased fasting serum glucose levels, diabetes, hypertension, and abdominal obesity, as well as to an increased risk of cardiovascular disease (CVD).
History and Physical Examination
Medical and surgical history, sexual history, use of medications and other substances, and an assessment of psychological and relationship health are key components of the patient history.
Essential parts of the physical examination include measurement of blood pressure, body mass index, and waist circumference to assess abdominal obesity; a genital examination; and an assessment of male secondary sex characteristics.
Laboratory Evaluation
The A1C or fasting glucose level can be used to assess for diabetes. A lipid panel can assess for hyperlipidemia. A thyroid-stimulating hormone level is recommended for men with signs or symptoms of hypothyroidism.
Routine measurement of testosterone levels is controversial. A diagnosis of hypogonadism must be based on more than just an abnormal laboratory test result.
Measurement of morning total testosterone may be considered for men with small testes, lack of male secondary sex characteristics, significantly low libido, or a history of inadequate response to phosphodiesterase-5 (PDE-5) inhibitors; if the initial result is abnormal, the test should be repeated in a few months.
Free testosterone levels vary widely across laboratories and are not uniformly recommended for screening. However, when hypogonadism is clinically suspected but the morning total testosterone level is repeatedly normal, bioavailable testosterone or free testosterone may account for the effects of sex hormone-binding globulin levels on testosterone activity.
Levels of follicle-stimulating hormone, luteinizing hormone, sex hormone-binding globulin, estradiol, and prolactin can help differentiate between primary and secondary causes of testicular hypogonadism.
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