Published online Nov 24, 2014. doi: 10.5410/wjcu.v3.i3.330
Revised: June 21, 2014
Accepted: July 25, 2014
Published online: November 24, 2014
Processing time: 175 Days and 22.8 Hours
Recently, clinical and epidemiologic data indicating the involvement of metabolic syndrome (MetS) in the pathogenesis and progression of lower urinary tract symptom (LUTS)/benign prostatic hyperplasia (BPH) are reported. This review evaluates the reports on the influence of MetS in the development and progression of LUTS/BPH, and discusses possible clinical implications for the management and treatment of this disease. Recent studies on the epidemiological relationship between MetS and LUTS hypothesize that MetS may be associated with an overactivity of the autonomic nervous system for which hyperinsulinemia, a key element of the MetS, might be responsible. An alternative explanation is that LUTS are associated with chronic ischemia of pelvis resulting from atherosclerotic changes in blood vessels, which leads the production of reactive oxygen species, which can damage the bladder detrusor. Control of autonomic nervous system overactivity and control of chronic bladder ischemia have potential as new targets for LUTS treatment. Studies suggest an association of MetS with LUTS/BPH, although further research is needed to understand how MetS influences LUTS/BPH. MetS should be considered a new domain in basic and clinical research in patients with LUTS/BPH and as a target for treatment.
Core tip: Associations between metabolic syndrome (MetS) and lower urinary tract symptom (LUTS) are noteworthy. MetS treatment may have the potential to prevent LUTS from worsening as well as to prevent the occurrence of new LUTS. Medication for LUTS patients with MetS should not only target the lower urinary tract, but should also be recognized as systemic treatment. Medications which are essentially thought to be unrelated to LUTS treatment may have potential for development as a specific medical treatment for LUTS with MetS.