Diabetes-associated Erectile Dysfunction

Abstract

Erectile dysfunction (ED) is a common complication of diabetes, with a prevalence ranging from 15 to 55%. The basis underlying diabetesassociated ED is multifactorial, involving changes in peripheral nerve activity and alterations in endothelial cell function. Due to the complexity of this pathology, the development of experimental models has been crucial in evaluating and translating fundamental results into clinical diabetes-associated ED. The concept of hard-to-treat patients, such as men with diabetes, is now fully accepted due to the complex mechanisms involved. In these men, the response to common oral treatments with phosphodiesterase type 5 inhibitors (PDE5Is) is far from desired, and maximal doses of the drugs are often needed. In addition, diabetes is commonly associated with other co-morbidities, such as hypertension, hypercholesterolaemia and obesity, clusters of the metabolic syndrome (MetS). ED is considered an early warning sentinel for coronary artery disease, just as endothelial dysfunction is seen as a major risk factor for ED. Testosterone deficiency syndrome, a very common syndrome in diabetes and MetS, has been shown to be an independent determinant of endothelial dysfunction, thus contributing to vascular pathology, including ED. This syndrome should be identified among patients, and therapeutic intervention may be required. PDE5Is may improve erectile function with or without the help of other second- or third-line treatments. Other strategies to maximise the response to PDE5Is include risk factor modification and daily dosing of the drugs, instead of on-demand treatment. However, better understanding of the fundamental molecular mechanisms underlying diabetes-associated ED is essential to improving and developing more effective therapies.