Overactive bladder: Is there a link to the metabolic syndrome in men?

Kirby, Michael; Wagg, Adrian; Cardozo, Linda; Chapple, Christopher R.; Castro-Díaz, David; Ridder, Dirk De; Espuña‐Pons, Montserrat; Haab, F.; Kelleher, Con; Kölbl, H.; Milsom, Ian; Kerrebroeck, Philip Van; Vierhout, Mark E.; Salvatore, Stefano; Tubaro, Andrea

doi:10.1002/nau.20892

Cited by 61 publications

(64 citation statements)

References 40 publications

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“…In line with these clinical findings, bladder dysfunction has also been reported in rat models of metabolic syndrome (Chung et al 2013;Lee et al 2008). In line with others (Bunn et al 2015;Kirby et al 2010), we conclude that metabolic syndrome apparently exhibits a more robust association with LUTS than its individual components of dyslipidemia and diabetes.…”

Section: Clinical Associations Between Atherosclerosis Risk Factors Asupporting

confidence: 92%

Are blood vessels a target to treat lower urinary tract dysfunction?

Michel

Chess-Williams

Hegde

2015

Naunyn-Schmiedeberg's Arch Pharmacol

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Bladder dysfunction is common in the general population (Stewart et al. 2010) and even more so among patients seeing a physician for any reason (Goepel et al. 2002). It often manifests as lower urinary tract symptoms (LUTS), a term originally coined to describe voiding and storage symptoms in men with benign prostatic hyperplasia (BPH) but now more universally used to describe any type of voiding and storage symptoms in both sexes. Studies into possible causes of urinary bladder dysfunction have long focused on detrusor smooth muscle cells (Turner and Brading 1999). More recently, it became clear that several other types of cells and organs contribute to regulating detrusor smooth muscle function. These include the urothelium (Andersson and McCloskey 2014; Michel 2015), afferent nerves (Michel and Igawa 2015; Yoshimura et al. 2014b), and the central and autonomic nervous systems (Fowler and Griffiths 2010; Yoshimura et al. 2014a). Alterations in any of these may at least partly be responsible for detrusor dysfunction and, accordingly, be potential targets for the treatment of bladder dysfunction. As highlighted by an article in this issue of Naunyn-Schmiedeberg's Archives of Pharmacology (Bayrak et al. 2015), there is an additional suspect, the bladder vasculature. This article will discuss the currently available experimental and clinical evidence for a role of the vasculature in causing bladder dysfunction, and how existing and emerging treatments may modulate bladder function by acting on blood vessels. Due to a similarity in concept, data on prostate perfusion will also be discussed to some extent.

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Section: Clinical Associations Between Atherosclerosis Risk Factors Asupporting

confidence: 92%

Are blood vessels a target to treat lower urinary tract dysfunction?

Michel

Chess-Williams

Hegde

2015

Naunyn-Schmiedeberg's Arch Pharmacol

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“…And, MetS are known to cause autonomic sympathetic overactivity through complex mechanisms 2,3 . It is suggested that overactivity of the sympathetic nervous system takes part in the development of BPH and LUTS 4 .…”

Section: Introductionmentioning

confidence: 99%

The impact of abdominal aortic calcification and visceral fat obesity on lower urinary tract symptoms in patients with benign prostatic hyperplasia

Motoya

Matsumoto

Yamaguchi³

et al. 2014

Int Urol Nephrol

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“…The activation of the parasympathetic nervous system can cause detrusor muscle contraction and may therefore contribute to detrusor over-activity, which is characteristic of the prevalence of storage symptoms [51].…”

Section: Discussionmentioning

confidence: 99%

Connections between lower urinary tract symptoms related to benign prostatic enlargement and metabolic syndrome with its components: a systematic review and meta-analysis

Russo¹,

Castelli²,

Urzì³

et al. 2015

The Aging Male

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A significant amount of epidemiological evidences have underlined an emerging link between metabolic syndrome (MetS) and lower urinary tract symptoms (LUTS) secondary to benign prostatic enlargement a (BPE). We aimed to assess the connections between LUTS and MetS with its components. Meta-analysis were conducted to determine the mean differences (MD) and confidence intervals of IPSS total score, IPSS-voiding, IPSS-storage and prostate volume (PV) in patients with or without MetS. Ln(odds-ratio) were calculated to estimate the risk of having moderate-to-severe LUTS (IPSS ≥ 8). Nineteen studies were identified as eligible for this systematic review, with a total of 18,476 participants, including 5554 (30.06%) with and 12,922 (69.94%) without MetS. Pooled analysis did not demonstrate significant MD of IPSS, IPSS-voiding and IPSS-storage in men with or without MetS but PV was significantly different (MD = 2.18; p = 0.03). Presence of MetS was not significantly associated with moderate-to-severe LUTS (odds ratio = 1.13; p = 0.53) and only altered serum triglycerides and diabetes were associated with this risk. The association between MetS and LUTS/BPE remain unclear and further observational studies in a population with metabolic disorders should be conducted in order to address it's potential role in determining LUTS/BPE.

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Overactive bladder: Is there a link to the metabolic syndrome in men?

Cited by 61 publications

References 40 publications

Are blood vessels a target to treat lower urinary tract dysfunction?

Are blood vessels a target to treat lower urinary tract dysfunction?

The impact of abdominal aortic calcification and visceral fat obesity on lower urinary tract symptoms in patients with benign prostatic hyperplasia

Connections between lower urinary tract symptoms related to benign prostatic enlargement and metabolic syndrome with its components: a systematic review and meta-analysis

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