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It was March 1998 when sildenafil was approved by FDA, making possible an effective pharmacological approach to erectile dysfunction (ED). This discovery in this past 16 years has made possible to increase enormously our understanding on the molecular mechanisms involved in penile erection. These advancements have made possible to design new therapeutic algorithm, to develop new molecules, to find new application for this molecules in urology as well as in other human diseases. It is well established that ED is an extremely actual problem, with implications far beyond sexual activity. ED could be both a herald marker and a complication of several chronic disease states. Precisely, ED is now recognized as a marker of increased cardiovascular risk independent of conventional risk factors. Pre-clinical and clinical studies have strongly linked metabolic syndrome with lower urinary tract symptoms (LUTS) and ED. The metabolic syndrome is an endocrinopathy that starts with insulin resistance and continues with the addition of abdominal obesity, glucose intolerance or diabetes mellitus, dyslipidemia, hypertension and coronary artery disease. It has been shown to be associated with many disorders including cardiovascular disease. There are several hypothesis suggesting that metabolic syndrome promotes benign prostate hyperplasia (BPH) and LUTS. For example, components associated to metabolic syndrome such as endothelial dysfunction, chronic inflammation, pelvic atherosclerosis or the insulin growth factor pathway may lead to the development of nodules, prostate cell growth, ischemia of the bladder and prostate. Besides, there is a strong correlation between the severity of LUTS and the degree of ED in all age groups, which suggests a causal relationship or, more possibly, the presence of common pathogenetic pathways. Indeed, a common pathogenesis has been proposed for LUTS and ED i) the decreased nitric oxide synthesis with aging ii) the increased sympathetic activity following hypertension, obesity and hyperinsulinemia in metabolic syndrome iii) the decreased smooth muscle relaxation following the activation of the alpha adrenergic or rho-kinase iv) decreased blood flow to bladder, prostate and penis following pelvic atherosclerosys. However elucidation of the exact nature of this relationship between metabolic syndrome, LUTS and ED and the underlying mechanisms are not well defined. The aim of the meeting is to put together experts in the field of urology, cardiology and endocrinology in order to discuss on the novel findings that have been achieved recently. Additionally, the current therapies will be consolidated and/or discussed as well as novel targets identified. 

Co-Chairs of the Meeting Giuseppe Cirino and Vincenzo Mirone

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