Erectile Dysfunction Overview and Treatment Considerations in Special Populations

Jenna L. Snoga, PharmD; Briana Williams, PharmD, BCPS; Lindsay A. Courtney, PharmD, BCACP, BCPS


US Pharmacist. 2022;47(6):18-23. 

In This Article

Abstract and Introduction


Erectile dysfunction (ED) is a common urologic condition that causes distress in men. Risk factors and predictors for ED include age, cardiovascular disease (CVD), hypertension, diabetes, smoking, and certain medications. CVD and ED share several risk factors, and ED may be a predictor of future cardiovascular events. Lifestyle modifications and phosphodiesterase type 5 inhibitors (PDE5Is) are considered first-line therapies for ED. PDE5Is can be less effective in patients with diabetes and should be used cautiously in certain patients with CVD. This review explores treatment options for ED with a focus on those with a history of diabetes or CVD.


Erectile dysfunction (ED), formerly termed impotence, is defined as the persistent inability to develop or maintain a penile erection allowing for satisfactory sexual performance.[1] ED is an important public health problem and can cause serious distress to men, particularly affecting their masculinity and self-esteem.[2,3] The Massachusetts Male Aging Study reported an overall prevalence of 52% for any degree of ED and demonstrated that prevalence clearly increases with age.[3] For instance, the annual incidence rate reported was 12.4 cases per 1,000 man-years, 29.8 and 46.4 for men aged 40 to 49, 50 to 59, and 60 to 69 years, respectively.[3]

Penile erection is a complex process that involves the vascular, hormonal, neurologic, and psychological systems.[4] In the presence of sexual stimulation, which is mediated by the central nervous system, nitric oxide (NO) is released from nonadrenergic, noncholinergic nerve fibers, resulting in the activation of guanylyl cyclase and an increase in cyclic guanosine monophosphate (cGMP). Additionally, parasympathetic cholinergic nerves release acetylcholine, leading to the activation of adenylyl cyclase, which results in an increase in cyclic adenosine monophosphate levels. These signaling pathways decrease intracellular calcium levels, which leads to smooth-muscle relaxation and increases blood flow into sinusoids of the corpora cavernosa. Subsequently, the subtunical veins become compressed, blocking venous outflow from the corpora, thus maintaining the erection.[4]

ED can result from an abnormality or combination of abnormalities in one of these four systems.[4,5] ED is categorized as organic (i.e., neurogenic, vasculogenic, hormonal), psychogenic, or mixed. Common causes of psychogenic ED include stress, performance anxiety, and depression. Vasculogenic ED is the most common cause of organic ED. Hypertension, atherosclerosis, diabetes, and lifestyle factors (e.g., smoking) can lead to alterations in the vascular flow of the corpora cavernosa and are common risk factors for ED. ED is now considered an underlying manifestation of cardiovascular disease (CVD), and its development often precedes clinical cardiovascular (CV) events. Neurogenic causes of ED include spinal cord injuries, stroke, and multiple sclerosis. Hypogonadism and thyroid disease are considered hormonal causes of ED.[4,5]

A detailed medical history, sexual history, and physical exam are warranted to identify causative or reversible factors involved in ED.[4] Select laboratory tests (e.g., serum testosterone, serum blood glucose, fasting lipid panel, thyroid-stimulating hormone) may be obtained to identify causative factors of ED. Additionally, a detailed medication history is necessary to identify medications that may be contributing to ED (see Table 1).[4,5]