www.kjurology.org http://dx.doi.org/10.4111/kju.2011.52.8.507 Review Article Metabolic Syndrome and Benign Prostatic Hyperplasia: Evidence of a Potential Relationship, Hypothesized Etiology, and Prevention Firas Abdollah, Alberto Briganti, Nazareno Suardi, Fabio Castiglione, Andrea Gallina, Umberto Capitanio, Francesco Montorsi Department of Urology, San Raffaele Hospital, Università Vita-Salte, Urological Research Institute (URI), Milan, Italy Benign prostatic hyperplasia (BPH) is highly prevalent in older men and causes sub- stantial adverse effects on health. The pathogenesis of this disease is not totally clear. Recent reports have suggested a possible relationship between metabolic syndrome (MetS) and BPH. Single components of MetS (obesity, dyslipidemia, hypertension, and insulin resistance) as well as the syndrome itself may predispose patients to a higher risk of BPH and lower urinary tract symptoms (LUTS). This may stem from changes in insulin resistance, increased autonomic activity, impaired nitrergic innervation, in- creased Rho kinase activity, pro-inflammatory status, and changes in sex hormones that occur in association with MetS. However, the exact underlying mechanisms that regulate the potential relationship between MetS and BPH/LUTS still need to be clarified. Increased physical activity and dietary strategies may help in decreasing the incidence of MetS and its impact on BPH/LUTS. However, differences in the definitions used to address the examined predictors and endpoints preclude the possibility of arriv- ing at definitive conclusions. Key Words: Insulin resistance; Metabolic syndrome X complications; Obesity com- plications; Prostatic hyperplasia etiology; Prostatic hyperplasia pathology This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Article History: received 4 April, 2011 accepted 13 May, 2011 Corresponding Author: Firas Abdollah Department of Urology, San Raffaele Hospital, University Vita-Salute, Via Olgettina 60, 20132 Milan, Italy TEL: +39-02-2643-7286 FAX: +39-02-2643-7298 E-mail: firas.abdollah@gmail.com INTRODUCTION Benign prostatic hyperplasia (BPH) is highly prevalent in older men [1]. Histologically, BPH is characterized by the presence of nonmalignant, unregulated overgrowth of the prostate gland. Clinically, BPH may be associated with lower urinary tract symptoms (LUTS) secondary to the en- suing prostate enlargement. About 60% of men aged ＞50 years have histologic evidence of BPH. This prevalence in- creases to 80% in patients aged ≥70 years [1]. Currently, BPH is the fourth most prevalent disease in men aged ＞50 years [2]. 　Despite the high prevalence of BPH and the socio- economic burden related to its treatment [3], the patho- genesis of BPH is not well understood. In the past two deca- des, an increasing number of reports (Table 1) have sug- gested a possible relationship between BPH/LUTS and several metabolic disturbances, known collectively as the Korean Journal of Urology Ⓒ The Korean Urological Association, 2011 metabolic syndrome (MetS). MetS is a disease process asso- ciated with defective insulin-mediated glucose uptake, which is becoming an increasingly prevalent problem worldwide [4,5]. MetS involves a constellation of abnor- malities including obesity, dyslipidemia, hypertension, and insulin resistance, with subsequent development of hyperinsulinemia and impaired glucose metabolism. Several definitions of MetS have been proposed by various organizations [6]. The Adult Treatment Panel III defi- nition is the one used most today because it incorporates the key concepts of MetS and relies on routinely available clinical parameters (Table 2) [7]. 　The aim of the current report was to summarize and crit- ically review the available literature that addresses the po- tential relationship between BPH/LUTS and MetS. More- over, we aimed to clarify the underlying mechanisms that may link these two pathologic conditions and the changes in lifestyle that may decrease their prevalence. 507 Korean J Urol 2011;52:507-516