The Correlation between Metabolic Syndrome and Prostatic Growth in Patients with Benign Prostatic Hyperplasia

141

137

BACKGROUND: Epidemiological data indicate that lower urinary tract symptoms (LUTS)/BPH can be associated with metabolic syndrome (MetS). Chronic inflammation has been proposed as a candidate mechanism at the crossroad between these two clinical entities. Aim of study is to examine the correlation among pre-operatory LUTS/BPH severity, MetS features and inflammatory infiltrates in prostatectomy specimens. METHODS: A total of 271 consecutive men treated with simple prostatectomy were retrospectively selected for this study in two tertiary referral centers for LUTS/BPH. Prostate diameters and volume were measured by transrectal ultrasound, LUTS scored by International Prostate Symptom Score (IPSS) and obstruction by uroflowmetry. The International Diabetes Federation and American Heart Association and the National Heart, Lung and Blood Institute was used to define MetS. The inflammatory infiltrate was investigated combining anatomic location, grade and extent of flogosis into the overall inflammatory score (IS); the glandular disruption (GD) was used as a further marker. RESULTS: Eighty-six (31.7%) men were affected by MetS. Prostatic volume and anterior-posterior (AP) diameter were positively associated to the number of MetS components. Among MetS determinants, only dyslipidaemia (increased serum triglycerides and reduced serum high-density lipoprotein) was associated with an increased risk of having a prostatic volume 460 cm 3 (hazard ratio (HR) ¼ 3.268, Po0.001). A significant positive correlation between the presence of MetS and the IS was observed. MetS patients presented lower uroflowmetric parameters as compared with those without MetS (Maximum flow rate (Q max ): 8.6 vs 10.1, P ¼ 0.008 and average flow rate (Q ave ): 4.6 vs 5.3, P ¼ 0.033, respectively), and higher obstructive urinary symptoms score (P ¼ 0.064). A positive correlation among both IS-GD and IPSS Score was also observed (adjusted r ¼ 0.172, P ¼ 0.008 and adjusted r ¼ 0.128, P ¼ 0.050). CONCLUSIONS: MetS is associated with prostate volume, prostatic AP diameter and intraprostatic IS. The significantly positive association between MetS and prostatic AP diameter could support the observation that MetS patients presented lower uroflowmetric parameters. In conclusion, MetS can be regarded as a new determinant of prostate inflammation and BPH progression.

Section: Introductionmentioning

confidence: 79%

Metabolic syndrome and lower urinary tract symptoms: the role of inflammation

Gacci

Vignozzi

Sebastianelli

et al. 2012

141

137

“…In an epidemiological study, Dahle et al 16 reported that a higher waist-to-hip ratio and higher serum insulin increased the risk for BPH. Ozden et al 17 studied 78 patients with BPH and found that those with the metabolic syndrome vs those without the syndrome had a significantly greater growth rate for both the whole prostate and especially the transitional zone. These data collectively suggest that hyperinsulinemia is an important factor in the development of BPH.…”

Section: Discussionmentioning

confidence: 99%

Effect of diet and exercise intervention on the growth of prostate epithelial cells

Barnard

Kobayashi

Aronson

2008

Epidemiological studies suggest a positive association between nutrient intake, hyperinsulinemia and risk of Benign prostatic hyperplasis (BPH). This study tests the hypothesis that a low-fat, highfiber diet and daily exercise would lower serum insulin and reduce the growth of serum-stimulated primary prostate epithelial cells in culture. Serum samples were obtained from eight overweight men before and after the Pritikin residential, 2-week diet and exercise intervention and from seven men who were long-term followers of the low-fat, high-fiber diet and regular exercise lifestyle. The serum was used to stimulate primary prostate epithelial cells in culture. Growth was measured after 48 and 96 h and apoptosis after 96 h. At 48 h there was no significant difference in growth within the Pre, 2-week or Long-Term groups. At 96 h growth was significantly reduced in the 2-week (13%) and in the Long-Term (14%) groups compared to the Pre data. At 96 h, apoptosis was not significantly different among the three groups. Fasting insulin was reduced by 30% in the 2-week group and by 52% in the Long-Term group compared to the Pre data. Testosterone was unchanged in the 2-week group. The results of this study indicate that a low-fat, high-fiber diet and daily exercise lowers insulin and reduces growth of prostate primary epithelial cells and suggests that lifestyle may be an important factor in the development or progression of BPH. Future prospective trials should address the effects of this lifestyle modification on BPH symptomatology and progression.

“…[6][7][8][9][10][11][12] Our group started its research prompted by the clinical observation that diabetic and/or obese men seem to have a larger prostate gland than men without these disorders. In our reports, 11 out of 11 components of the metabolic syndrome were linked to fast-growing BPH.…”

Section: Introductionmentioning

confidence: 99%

Insulin and free oestradiol are independent risk factors for benign prostatic hyperplasia

Hammarsten

Damber

Karlsson

et al. 2008

The aetiology of benign prostatic hyperplasia (BPH) remains unclear. The objective of the present study was to test the insulin, oestradiol and metabolic syndrome hypotheses as promoters of BPH. The design was a risk factor analysis of BPH in which the total prostate gland volume was related to endocrine and anthropometric factors. The participants studied were 184 representative men, aged 72-76 years, residing in Gö teborg, Sweden. Using a multivariate analysis, BPH as measured by the total prostate gland volume correlated statistically significantly with fasting serum insulin (b ¼ 0.200, P ¼ 0.028), free oestradiol (b ¼ 0.233, P ¼ 0.008) and lean body mass (b ¼ 0.257, P ¼ 0.034). Insulin and free oestradiol appear to be independent risk factors for BPH, confirming both the insulin and the oestradiol hypotheses. Our findings also seem to confirm the metabolic syndrome hypothesis. The metabolic syndrome and its major endocrine aberration, hyperinsulinaemia, are possible primary events in BPH.