CONTEXT: Metabolic syndrome (MetS), a cluster of several metabolic abnormalities with a high socioeconomic cost, is considered a worldwide epidemic. Recent epidemiologic and clinical data suggest that MetS is involved in the pathogenesis and progression of prostatic diseases such as benign prostatic hyperplasia (BPH) and prostate cancer (PCa). OBJECTIVE: This review evaluates the available evidence of the role of MetS in BPH and PCa development and progression and discusses possible clinical implications for the management, prevention, and treatment of these diseases. EVIDENCE ACQUISITION: A National Center for Biotechnology Information (NCBI) PubMed search for relevant articles published between 1995 and September 2011 was performed by combining the following Patient population, Intervention, Comparison, Outcome (PICO) terms: male, metabolic syndrome, prostate, benign prostatic hyperplasia, prostate cancer, prevention, diagnosis, treatment, and prognosis. Additional references were obtained from the reference list of full-text manuscripts. EVIDENCE SYNTHESIS: MetS is a complex, highly prevalent disorder and a worldwide epidemic. Central obesity, insulin resistance, dyslipidemia, and hypertension are the main components of MetS. Notwithstanding all the attempts made to correctly define MetS, a major problem related to most definitions remains the applicability to different populations and ethnic groups. Although there is growing evidence of the association of MetS with the initiation and clinical progression of BPH and PCa, molecular mechanisms and effects on treatment efficacy remain unclear. Further research is required to better understand the role of MetS in BPH and PCa. CONCLUSIONS: Data from the peer-reviewed literature suggest an association of MetS with BPH and PCa, although the evidence for a causal relationship remains missing. MetS should be considered a new domain in basic and clinical research in patients with prostatic disorders.
CONTEXT: Metabolic syndrome (MetS), a cluster of several metabolic abnormalities with a high socioeconomic cost, is considered a worldwide epidemic. Recent epidemiologic and clinical data suggest that MetS is involved in the pathogenesis and progression of prostatic diseases such as benign prostatic hyperplasia (BPH) and prostate cancer (PCa). OBJECTIVE: This review evaluates the available evidence of the role of MetS in BPH and PCa development and progression and discusses possible clinical implications for the management, prevention, and treatment of these diseases. EVIDENCE ACQUISITION: A National Center for Biotechnology Information (NCBI) PubMed search for relevant articles published between 1995 and September 2011 was performed by combining the following Patient population, Intervention, Comparison, Outcome (PICO) terms: male, metabolic syndrome, prostate, benign prostatic hyperplasia, prostate cancer, prevention, diagnosis, treatment, and prognosis. Additional references were obtained from the reference list of full-text manuscripts. EVIDENCE SYNTHESIS: MetS is a complex, highly prevalent disorder and a worldwide epidemic. Central obesity, insulin resistance, dyslipidemia, and hypertension are the main components of MetS. Notwithstanding all the attempts made to correctly define MetS, a major problem related to most definitions remains the applicability to different populations and ethnic groups. Although there is growing evidence of the association of MetS with the initiation and clinical progression of BPH and PCa, molecular mechanisms and effects on treatment efficacy remain unclear. Further research is required to better understand the role of MetS in BPH and PCa. CONCLUSIONS: Data from the peer-reviewed literature suggest an association of MetS with BPH and PCa, although the evidence for a causal relationship remains missing. MetS should be considered a new domain in basic and clinical research in patients with prostatic disorders.
Authors: M Gacci; M Carini; M Salvi; A Sebastianelli; L Vignozzi; G Corona; M Maggi; K T McVary; S A Kaplan; M Oelke; S Serni Journal: Drugs Aging Date: 2014-06 Impact factor: 3.923
Authors: Katharine N Sourbeer; Lauren E Howard; Gerald L Andriole; Daniel M Moreira; Ramiro Castro-Santamaria; Stephen J Freedland; Adriana C Vidal Journal: BJU Int Date: 2014-10-20 Impact factor: 5.588