Erectile dysfunction in diabetes

Abstract

Several exciting new therapies for erectile dysfunction (ED) have been released or will shortly appear for the management of erectile failure in diabetes and other conditions. These are the result of significant advances in knowledge about the pathophysiology of ED, which have allowed a targeted approach to each of the elements involved in producing an erection. Diabetes results in ED in 50-75% of men. In men with diabetes, the incidence of ED is 9% from age 20 to 29 years and increases to 95% by age 70. It may be the presenting symptom of diabetes. More than 50% of men develop ED within 10 years of the diagnosis, and it may precede the other complications of diabetes. Neuropathy, vascular dispase, glycation of cavernosal elastin, nutrition, endocrine disorders, and psychogenic factors, as well as drugs used in the treatment of diabetes and its complications, are among the multiple etiologies of ED in diabetes. Gradual onset and progression are the hallmarks of organic ED. Decreased rigidity and incomplete tumescence occur before total failure; morning or dream-related erections are lost along with spontaneous, tactile, visual, or fantasy induced erections. Organic ED is present with all partners and with masturbation, and there is no loss of libido. Sudden loss of erections with a particular partner while maintaining morning erections and nocturnal penile tumescence suggests a psychogenic cause. The neurological manifestations are those of dysfunction of the autonomic nervous system (ANS) or peripheral sensory nerves, both of the Aδ and C fiber types. Buttock claudication is the usual manifestation of vascular disease, but this may be absent when the stenotic vessel is the internal pudendal artery. A penile/brachial index of < 0.7 indicates diminished blood supply. Unresponsiveness to vasodilators is the harbinger of a venous leak; this requires evaluation by penile Doppler sonography. A logical stepwise progression is used for making a diagnosis of the cause of ED (see algorithm). In all instances, a careful history for the rapidity of onset of ED, presence or absence of morning erections, uniformity of sexual dysfunction with all partners and in all situations, evidence of autonomic or sensory nerve dysfunction, vascular insufficiency, hormonal inadequacy, and drugs used in the treatment of satellite disorders must be appraised. Oral therapies can be used in any form of ED; failure should lead to intracavernous injection of a vasodilator as part of the evaluation, both for diagnostic purposes and as an aid in choosing among the therapeutic options. Only problematic cases need be tested for nocturnal penile tumescence (NPT). Normal NPT defines psychogenic ED, and a negative response to vasodilators implies vascular insufficiency. Antihypertensive and cardiovascular drugs should be changed to those with no or a lower potential for ED, and glycemic control should be optimized. For psychogenic dysfunction, the patient should be referred to a therapist with expertise in treating sexual dysfunction. Oral regimens will be most acceptable as initial therapy and can include the α2 antagonist yohimbine, trazadone, or the apparently more frequently successful type V phosphodiesterase inhibitor seldinafil. Vacuum erection devices are satisfactory for many patients. Men responsive to intracavernous injections have this as a therapeutic option, but those who are unresponsive usually have vascular disease or venous leaks and require prostheses or vascular surgery. No attempt should ever be made to treat ED without first consulting the significant other.