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Published on: August 14, 2019

Atherosclerosis as a risk factor for benign prostatic hyperplasia

Andreas P Berger1, Georg Bartsch, Martina Deibl

  • 1Department of Urology, Medical University of Innsbruck, Austria. andreas.p.berger@uibk.ac.at

BJU International
|August 2, 2006
PubMed

Insights

Vascular damage, including diabetes and peripheral arterial occlusive disease, is linked to reduced prostate blood flow and benign prostatic hyperplasia (BPH) symptoms. Impaired blood supply may drive BPH development.

Area of Science:

  • Urology
  • Vascular Medicine
  • Medical Imaging

Background:

  • Benign prostatic hyperplasia (BPH) is a common condition in aging men.
  • Atherosclerosis, a condition affecting blood vessels, is prevalent in aging populations.
  • The relationship between systemic vascular health and prostate health requires further investigation.

Purpose of the Study:

  • To investigate the association between clinical benign prostatic hyperplasia (BPH) and atherosclerosis.
  • To evaluate prostatic vascularity and symptoms in men with varying degrees of vascular disease.

Main Methods:

  • Colour Doppler ultrasonography (CDUS) assessed prostatic vascularity in four groups: healthy controls, coronary artery disease (CAD), diabetes mellitus, and peripheral arterial occlusive disease (PAOD).
  • Resistive index (RI) and colour pixel density (CPD) quantified prostatic perfusion.
  • International Prostate Symptom Score (IPSS) measured lower urinary tract symptoms.

Main Results:

  • Diabetic patients and those with PAOD exhibited significantly lower prostatic transition zone (TZ) perfusion (CPD) and higher RI compared to controls and CAD patients.
  • Mean prostate volume was larger in diabetic patients and those with PAOD.
  • Patients with vascular disease (diabetes, PAOD) reported significantly worse IPSS scores.

Conclusions:

  • Reduced prostatic blood flow (lower CPD, higher RI) in patients with vascular disease supports the role of impaired blood supply in BPH development.
  • Age-related vascular changes may significantly contribute to the pathogenesis of benign prostatic hyperplasia.
Abstract

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