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Diabetes and Erectile Dysfunction

Diabetes and ED

Men with Diabetes

Diabetes Mellitus is a common chronic disease with a prevalence of 0.5-20%, characterized by hyperglycaemia secondary to lack of insulin (Type I, insulin dependent DM), or over-production of glucose with insulin insensitivity (type II, non-insulin dependent DM) which leads to pathological changes in a number of cellular and organ systems.

Young man with diabetes JPEG Web.jpg

About 50% of all diabetic men suffer from ED

This usually develops during the course of the disease, but can sometimes be a presenting complaint. The likelihood of ED is related to the quality of Blood Glucose control.

The prevalence of ED is three times higher in diabetic men (28% versus 9.6%), occurs at an earlier age and increases with disease duration, being approximately 15% at age 30 rising to 55% at 60 years [11,12]. The Pathophysiology is multifatorial:

  1. Diabetic Neuropathy – Nonsexual nocturnal erections are seen during rapid eye movement sleep in normal men. In diabetics, alterations in potassium efflux across non- junctional ion channels of the corporal smooth muscle may lead to a state of hyper-contraction and lack of erectile response in men. [13] Healthy men experience nocturnal erections several times each night during REM sleep as nature's way of maintaining good penile health for reproductive purposes and intimate relations. When night-time erections do not occur the patient is considered to have organic or physical erectile dysfunction and the penis develops non-use atrophy.

  2. Diabetic Arterial Disease - Penile erection depends upon a greatly increased blood flow into the corpora cavernosa, which is in turn dependent upon perfusion pressure, relaxation of the supplying arterial tree and relaxation of cavernosal smooth muscle. Large vessel atheromatous disease is 40 times more prevalent amongst men with diabetes, occurring at a younger age, and within the penile arterial tree is more commonly associated with ED. [14]

  3. Hyperglycaemia - has both a direct action on smooth muscle cells by increasing the contractile response to noradrenaline and affecting the level of NO synthesis and release mediated by endothelial (reduced eNOS enzyme activity) - and neurogenic means, reducing the level of NO-induced relaxation in corporal tissue. [15-17] A body of evidence exists detailing the various mechanisms by which levels of oxygen free radicals may be elevated in diabetes which quench released NO thereby reducing the vasodilator response. Glucose reacts non-enzymatically with the amino acids of proteins to produce Advanced Glycosalation End Products (AGE's), known to generate Reactive Oxygen Species (ROS). [18] Electron micrographs in diabetic men have shown reduction in smooth muscle content, increased collagen deposition (Peyronie's disease is more common in diabetics) and thickening of the basal lamina compared with controls. [19]

 

Young man with diabetes JPEG Web.jpg

Diabetes and ED

Diabetes Mellitus is a common chronic disease with a prevalence of 0.5-20%, characterized by hyperglycaemia secondary to lack of insulin (Type I, insulin dependent DM), or over-production of glucose with insulin insensitivity (type II, non-insulin dependent DM) which leads to pathological changes in a number of cellular and organ systems.

References

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  • R Raina, A Agarwal, S Ausmundson, M Lakin, KC Nandipati, DK Montague, D Mansour and CD Zippe, Early use of vacuum constriction device following radical prostatectomy facilitates early sexual activity and potentially earlier return of erectile function. International Journal of Impotence Research (2006) 18, 77–81
  • Huber N, Wood C, Babauan R, Madsen L, Shem Y, Wen S, Wang R. Recovering penile length and erectile function following radical prostatectomy. J Sex Med 2006;3(Suppl 1):21 (Abstract 60).
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  • Hinh P, Wang R. Overview of contemporary penile rehabilitation therapies. Adv Urol 2008 in printing.
  • Moreland RB, Traish A, McMillin, Smith B, Goldstein I, Saenz deTejada I. PGE1 suppresses the induction of collagen synthesis by transforming growth factor B1 in human corpus cavernosum smooth muscle. J Urol, 153: 826,1995.
  • Nehra A, Gettman MT, Nugent M, Bostwick DG, Barrett DM, Goldstein I, Krane RJ, Moreland RB. Transforming growth factor-Beta 1 (TGF-Beta 1) is sufficient to induce fibrosis of rabit cavernosum in vivo. J Urol, 162: 910-915, 1999.
  • Saenz de Tejada I, Moroukian P, Tessier J, Kim JJ, Goldstein I, Frohrib D. The trabecular smooth muscle modulates the capacitor function of the penis. Studies on a rabbit model. Am J Physiol, 260 (Heart and Cir.Physiol 29): H1590, 1991.
  • Nehra A, Azadzoi KM, Moreland RB, Pabby A, Siroky MB, Krane RJ, Goldstein I, Udelson D. Cavernosal expandibility is an erectile tissue mechanical property which predicts trabecular histology in an animal model of vasculogenic erectile dysfunction.
  • J Urol, 159: 2229-2236, 1998. McCulloch DK, Campbell IW, Wu FC, Prescott RJ, Clarke BF. The prevalence of diabetic impotence. Diabetologia, 18:279-283, 1980. Mcculloch DK, Young RJ, Prescott RJ, Campbell IW, Clarke BF. The natural history of impotence in diabetic men. Diabelogia, 26: 437-440, 1984.
  • Melman A, Christ GJ, Integrative erectile biology: the effects of age and disease on gap junctions and ion cannels and their potential value to the treatment of ED Urol clin North Am. 2001; 28: 217-231 Herman A, Adar R, Rubeinstein Z. Vascular lesions associated with impotence in diabetic and non-diabetic arterial occlusive disease. Diabetes, 27: 975-981, 1978.
  • Saenz De Tejada I, Goldstein I, Azadzoi K, Krane RJ, Cohen RA. Impaired neurogenic and endothelium-mediated relaxation of penile smooth muscle from diabetic men with impotence. N Engl J Med, 320: 1025-1030, 1989.
  • Pickard RS, King P, Zar MA, Powell PH. Corpus cavernosal relaxation in impotent men. Br J Urol, 74: 485-491, 1994. Pickard RS, Powell PH, Zar MA. Nitric Oxide and cyclic GMP formation following relaxant nerve stimulaton in isolated human corporus cavernosum.
  • Br J Urol, 75: 516-522, 1995. Seftel AD, Vazin ND, Ni Z, Razmjouei K, Fogarty J, Hampel N, Polak J, Wang RZ. Advanced Glycation end products in human penis: elevation in diabetic tissue, site of deposition and possible effect through iNOS and eNOS. Urology, 50: 1016-1026, 1997.
  • Mersdorf A, Goldsmith PC, Diederischs W, Padula CA, Lue TF, Fishman IJ, Tanagho EA. Ultrastructural changes in impotent penile tissue: a comparison of 65 patients. J Urol, 145: 749-758, 1991
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  • Azadzoi KM, Krane RJ, Saenz de Tejada I, Goldstein I, Siroky MB. Relative roles of cyclo-oxygenase and Nitric Oxide Synthase pathways in ischaemia induced increased contraction of cavernosal smooth muscle. J Urol, 161: 1324-1328, 1999.
  • Azadzoi KM, Krane RJ, Saenz de Tejada I, Goldstein I, Traish AM, Siroky MB. Mechanisms of ischaemia-induced cavernosal smooth muscle relaxation impairment in a rabbit model of vasculogenic ED. J Urol, 160: 2216-2222, 1998.
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