Metabolic syndrome and male lower urinary tract symptoms.

Historically, urologists regarded prostate enlargement as the sole cause for male bladder problems. Nocturia, hesitancy, weak stream, and post void dribbling are classical symptoms that seemed to correlate solely to an enlarged prostate (benign prostate enlargement BPE resulting from benign prostatic hyperplasia BPH leading to bladder outlet obstruction BOO due to benign prostatic obstruction BPO). Over time, subdivision of symptoms into storage, voiding and post-voiding symptoms raised awareness of the urinary tract fine-tuning associated with urine storage and voiding, and led to the umbrella term "lower urinary tract symptoms (LUTS)", which respects bladder and prostate function. Storage symptoms consist of altered bladder sensation, increased daytime frequency, nocturia, urgency +/- incontinence; voiding symptoms of hesitancy, intermittency, weak or irregular stream, straining and terminal dribble. Post-void dribbling and sensation of incomplete voiding are considered post-voiding symptoms. In a similar manner in the past, urinary problems seemed to have either a functional or an organrelated origin. Symptoms would result from a malfunction of the nervous system or at least one of the following: bladder, prostate, urethra. While research goes on, it seems as if the more we know about urine storage and voiding, the more complicated it gets: different mechanism can mimic the same symptoms. Clinically, it remains ever the more challenging to understand the pathophysiological context of each patient. Metabolic syndrome, too, is an umbrella term. The term relates to interconnected biochemical, physiologic, metabolic and clinical factors, that increase the individual's risk of type 2 diabetes mellitus (T2DM), heart disease, and early mortality.1 According to the WHO, three of the following findings defines the Metabolic Syndrome (MetS): - waist/hip ratio >0.85 in women, >0.9 in men or BMI >30 kg/m2; - type 2 diabetes mellitus (T2DM), increased fasting glucose or impaired glucose; tolerance; - Triglyceridemia ≥150 mg/dl; - HDL concentration < 39 mg/dl in women/<35 mg/dl in men; - Blood pressure ≥140/90 mmHg; - Microalbuminuria. Metabolic changes caused by MetS pathophysiologically start with visceral adiposity. It leads to different changes in the signaling pathway including cytokines, elevated transmitters of inflammation, higher levels of free fatty acids (FFA), and adipokines, resulting in vasoconstriction, insulin resistance, impaired glucose uptake and high insulin secretion. Furthermore, MetS is thought to be associated with nephrolithiasis, BPH, LUTS, erectile dysfunction (ED), and infertility2. Associated testosterone deficiency, whether correlated to MetS or physiological ageing, may alter the structure of the lower urinary tract, such as urethral and bladder epithelial cells.3 This review aims at synthesizing interactions and consequences of LUTS with MetS. There are numerous connections between the two umbrella terms. Our review subdivides into bladder and prostate function, which lead to LUTS and how the metabolic syndrome interferes with these aspects. As asked for by the editor, it will focus on the male lower urinary tract, although women suffer from LUTS as well, even in the absence of a prostate.