title: Vascular damage induced by type 2 diabetes mellitus as a risk factor for benign prostatic hyperplasia.
abstract: OBJECTIVE
  The aim of this study was to evaluate the relationship between benign prostatic hyperplasia (BPH) and arteriosclerosis shown in a model of type 2 diabetes in a trans-sectional population study using contrast-enhanced colour Doppler ultrasound for exact assessment of prostatic blood flow.
  
  
  METHODS
  Contrast-enhanced transrectal colour Doppler ultrasound was performed using a microbubble-based ultrasound enhancer SonoVue for evaluating prostate vascularity (transitional zone [TZ] and peripheral zone [PZ]) in diabetic BPH patients, non-diabetic BPH patients and healthy subjects. Computer-assisted quantification of colour pixel intensity (CPI) was used to objectively evaluate the prostate vascularity. Resistive index measurements were obtained in the TZ and the PZ. Findings were compared between these three groups.
  
  
  RESULTS
  TZ-CPI was significantly lower in diabetic patients than in non-diabetic BPH men (p=0.001), whereas the CPI of the PZ showed no difference between these two groups (p=0.978). TZ-CPI of patients with diabetic and non-diabetic BPH were significantly lower than in controls (p<0.001), but no difference was found between diabetic and healthy patients in the PZ (p=0.022) and borderline significance was seen when comparing patients of the BPH group with the control patients (p=0.019). Resistive index values of the TZ in diabetic patients showed significantly higher values (p<0.001) than the BPH and control groups.
  
  
  CONCLUSIONS
  The significantly lower CPI and higher resistive index values of the TZ in diabetic patients compared with patients with non-diabetic BPH and healthy subjects indicate considerable vascular damage in the TZ of these patients. Diabetic vascular damage may cause hypoxia and may contribute to the pathogenesis of BPH.
authors.affiliation: Department of Urology, University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria. andreas.p.berger@uibk.ac.at
authors.forename: A P
authors.initials: AP
authors.lastname: Berger
authors.forename: M
authors.initials: M
authors.lastname: Deibl
authors.forename: E J
authors.initials: EJ
authors.lastname: Halpern
authors.forename: M
authors.initials: M
authors.lastname: Lechleitner
authors.forename: J
authors.initials: J
authors.lastname: Bektic
authors.forename: W
authors.initials: W
authors.lastname: Horninger
authors.forename: G
authors.initials: G
authors.lastname: Fritsche
authors.forename: H
authors.initials: H
authors.lastname: Steiner
authors.forename: A
authors.initials: A
authors.lastname: Pelzer
authors.forename: G
authors.initials: G
authors.lastname: Bartsch
authors.forename: F
authors.initials: F
authors.lastname: Frauscher
mesh_terms: D000328:Adult; D000368:Aged; D001158:Arteries / Q000473:pathology; D001161:Arteriosclerosis / Q000150:complications / Q000473:pathology; D001794:Blood Pressure / Q000502:physiology; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D003925:Diabetic Angiopathies / Q000150:complications* / Q000209:etiology / Q000473:pathology; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008297:Male; D008875:Middle Aged; D011467:Prostate / Q000098:blood supply / Q000473:pathology; D011470:Prostatic Hyperplasia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D012039:Regional Blood Flow / Q000502:physiology; D012307:Risk Factors; D018615:Ultrasonography, Doppler, Color