Original evaluation of endothelial dysfunction in men with erectile dysfunction and metabolic syndrome

Abstract

We have recently demonstrated the diagnostic value of a new immunophenotype of blood endothelial progenitor cells (EPCs ¼ CD45neg/CD34pos/CD144pos) and endothelial microparticles (EMPs ¼ CD45neg/CD144pos/AnnexinVpos) in patients with arterial erectile dysfunction (ED) according to severity of cavernous arterial insufficiency evaluated through penile Doppler. The aim of this study was to evaluate both EPCs and EMPs in patients with arterial ED and metabolic syndrome (MetS), comparing these patients with another group of patients without MetS and ED and a third group with MetS but without ED. For this study 50 patients with arterial ED and MetS were selected (age: 55.0±3.0 years; range: 47--60). A group of age-matched (age: 54.0 ± 2.0 years; range: 44--60) patients without arterial ED and MetS INTRODUCTIONWe have recently demonstrated the diagnostic value of a new immunophenotype of blood endothelial progenitor cells (EPCs ¼ CD45neg/CD34pos/CD144pos) and endothelial microparticles (EMPs ¼ CD45neg/CD144pos/AnnexinVpos) in patients with arterial erectile dysfunction (ED) according to severity of cavernous arterial insufficiency evaluated through penile Doppler, showing that serum concentrations of these immunophenotypes are significantly higher compared with patients with psychogenic ED and among patients with arterial ED, those with severe arterial insufficiency showed significantly higher serum concentrations of EPCs and EMPs. 1 On this basis, the present study was undertaken to evaluate the number of EPCs and EMPs in patients with metabolic syndrome (MetS) and ED of arterial origin, which is a very common category among patients with sexual dysfunction in clinical practice. This clinical model seemed to us suitable to gain more insight into the balance between bone marrow endothelial repair mechanism and endothelial dysfunction in the manifestation of the clinical symptoms. To accomplish this, 50 patients with arterial dysfunctional-based ED and MetS, established by the Adult Treatment Panel (ATP) III criteria (NCEP ATPIII, 2002), were selected and the number of circulating EPCs and EMPs was determined. Two different groups of patients were enrolled as control: (a) patients without arterial ED and MetS; and (b) patients with MetS but without ED.

Arterial erectile dysfunction: Different severities of endothelial apoptosis between diabetic patients “responders” and “non responders” to sildenafil

“…In our opinion the importance of these results is associated with two aspects: the confirmation of the potential diagnostic use of the following immunophenotypes of EPCs (CD45neg/CD34pos/CD144pos) and EMPs (CD45neg/CD144pos/Annexin Vpos) [10][11][12] and the possible clinical significance of this finding, in fact, it may be a useful first level test to evaluate the presence of endothelial dysfunction in diabetic patients with aED.…”

“…Regarding this problem, the physician should recognize it as a possible sign of early endothelial damage and undertake the appropriate diagnostic work-up. In fact, the effectiveness of the iPDE5 is conditioned by normal bioavailability of nitric oxide and its deficiency in the presence of reduction of arterial penile flow, causes an increase in serum concentrations of EMPs, which determines a compensatory increase of the EPCs [10][11][12]15,26].…”

“…We have recently proposed and published data about an original immunophenotype of endothelial microparticles (EMPs = CD45neg/ CD144pos/Annexin V pos) and of circulating endothelial progenitor cells (EPCs = CD45neg/CD34pos/CD144pos), being evaluated for diagnostic reliability in the field of endothelial dysfunction in patients with ED [10][11][12].…”

Mean platelet volume and platelet distribution as a diagnostic marker for penile vascular disease in patients with erectile dysfunction

“…4 Aging, a sedentary life style, diabetes mellitus (DM), cardiovascular diseases (CVD), smoking, invasive surgical procedures performed due to prostate cancer, and chronic neurological diseases are the main risk factors in ED. 5,6 Those risk factors cause increased oxidative stress and endothelial damage, and as a result, nitric oxide production decreases. 7 Endothelial dysfunction forms the basis of common pathophysiological mechanisms of ED, atherosclerosis, stroke, and coronary artery disease.…”