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Cellek, S., Cameron, N.E., Cotter, M.A. and Muneer, A. (2013) Pathophysiology of Diabetic Erectile Dysfunction: Potential Contribution of Vasa Nervorum and Advanced Glycation Endproducts. International Journal of Impotence Research, 25, 1-6.
http://dx.doi.org/10.1038/ijir.2012.30

has been cited by the following article:

  • TITLE: Neurovascular Evaluation in Eugonadal Men with Type 2 Diabetes Mellitus and Erectile Disfunction: A Comparative Study between Responders and Not Responders to Phosphodiesterase 5 Inhibitors

    AUTHORS: Marcelo Rodriguez Peña, Elizabeth Ovando

    KEYWORDS: Erectile Dysfunction, Type 2 Diabetes Mellitus, Corpus Cavernosum Damage

    JOURNAL NAME: Advances in Sexual Medicine, Vol.5 No.4, October 8, 2015

    ABSTRACT: The aim of our study was to evaluate functional alterations of the corpus cavernusum and its correlation with the lack of response to treatment with PDE5i in eugonadal patients with Type 2 Diabetes Mellitus and Erectile Dysfunction. In this prospective randomized study we included 157 patients. All were treated with 5 mg tadalafil daily and 100 mg sildenafil on demand and the response to treatment was assessed in 6 month by dividing them into 2 groups: G1: Good response. Significative improvement of erectile function according to IIEF-5, and G2: There was not an improvement with the treatment. At the end of the treatment we performed neurological and vascular studies to both groups. Also we performed CC-EMG in order to evaluate penile autonomic neuropathy. 82 patients were included in G1 and 75 in G2. The time evolution of the ED was 1.5 years for G1 and 5 years for G2. Average fasting glucose and glycosilated hemoglobin values were significantly higher in G2 than in G1. Also we observed significant differences in penile vascular parameters between both groups. Peripheral neuropathy parameters did not show differences between both groups. Cavernous smooth muscle electromyography showed asynchronous and asymetric potentials in G1 (minimal autonomic neuropathy) and denervation potentials in G2 characteristic of severe CC damage. It is concluded that vascular and autonomic alterations are causes of severe CC damage and lack of response to treatment with PDE5i in this population. Peripheral neuropathy is not part of this process.