Recent advances in the treatment of erectile dysfunction in patients with diabetes mellitus.
OBJECTIVE: To present current information on the pathogenesis of and available therapeutic options for erectile dysfunction (ED) in patients with diabetes. METHODS: We provide a detailed review of the following topics: (1) peripheral and central neurotransmitter pathways involved in the penile erectile process (for example, nitric oxide, acetylcholine, vasoactive intestinal polypeptide, and prostaglandin E(1)), (2) pathogenesis of ED in patients with diabetes (vascular insufficiency, endothelial dysfunction, and autonomic neuropathy), (3) currently available treatment options for ED and their advantages and disadvantages, (4) potential new avenues for future research, and (5) the possibility of preventive treatment. RESULTS: Clearly a need exists for effective treatment options for ED in patients with diabetes. Because the development of ED in patients with diabetes is often caused by several interrelated mechanisms, including vascular disease, endothelial dysfunction, autonomic neuropathy, hormone imbalance, and certain medications, a thorough understanding of the various pathways involved in penile erection and their modulation in diabetes is essential for physicians to design an effective treatment plan. Interventions that modulate the erectile pathway at different points include therapies that enhance the erectile mechanism (amplification of the nitric oxide pathway), inhibit the detumescence mechanism, or affect the final common pathway by augmenting smooth muscle relaxation. Oral therapy, intracavernosal injections, transurethral pellets, combination therapy, and surgical procedures are available treatment strategies. CONCLUSION: Despite the availability of many treatment options for ED, early intervention and prevention (by such measures as improved glycemic control and general reduction of associated risk factors) should be emphasized because many of the diabetes-related complications leading to ED are irreversible.