Chronic Inflammation on top of Benign Prostatic Hyperplasia

Introduction

Benign prostatic hyperplasia (BPH) is one of the most frequent conditions affecting older men. It causes both voiding and storage urinary symptoms, which can severely reduce quality of life. Increasing evidence now shows that chronic prostatic inflammation contributes to BPH development and progression. Understanding this link is essential for medical students and junior doctors to improve patient care.

Important concepts

BPH: Non-cancerous enlargement of the prostate due to epithelial and stromal proliferation, often leading to bladder outlet obstruction.

Chronic prostatic inflammation: Long-standing immune response with lymphocyte infiltration and tissue remodeling in the prostate.

Lower urinary tract symptoms (LUTS): Divided into voiding (e.g., weak stream, hesitancy) and storage symptoms (e.g., frequency, urgency, nocturia).

Bladder outlet obstruction (BOO): Resistance to urine flow, caused by enlarged prostate tissue or smooth muscle contraction.

Cytokines: Chemical messengers such as interleukin-17 and interleukin-8 that mediate inflammation and promote prostate tissue changes.

HEV-like vessels: High endothelial venule-like vessels identified by immunostaining, representing sites of lymphocyte infiltration into prostatic tissue.

What we know

Chronic inflammation has a close relationship with prostate enlargement. Some large clinical studies have shown that men with inflamed prostates tend to have larger gland volumes. Inflammation promotes tissue proliferation by releasing cytokines like interleukin-17 and interleukin-8, which stimulate growth factors. However, not all studies agree, and the difference in prostate size is often small.

Inflammation also contributes to functional obstruction. Rather than just compressing the urethra mechanically, inflamed prostates may release cytokines that increase smooth muscle contraction. This can worsen bladder outlet obstruction and lead to acute urinary retention. Experimental data from other organs support this idea, and clinical studies have shown higher rates of retention in inflamed cases.

Storage symptoms are another key area. Inflammation in the prostate can trigger cross-sensitization between the prostate and bladder nerves. This makes the bladder more excitable and prone to overactivity, leading to frequency and urgency. Animal studies confirmed that prostatic inflammation shortens bladder contraction intervals and alters nerve signaling.

Important numbers

46.5 vs. 43.4 mL — Average prostate volume with vs. without chronic inflammation in REDUCE trial. Slight but statistically significant enlargement.

61.19 vs. 52.28 mL — Prostate volume in men with vs. without histological prostatitis. Demonstrates stronger link between inflammation and growth.

66.2% vs. 33.3% — Proportion of acute urinary retention in inflamed vs. non-inflamed patients. Inflammation doubles the risk.

Hazard ratio 1.6–1.8 — Increased risk of urinary retention with chronic inflammation. Confirms inflammation as a clinical risk factor.

23.94 vs. 21.86 — International Prostate Symptom Score (IPSS) in patients with vs. without histological prostatitis. Indicates worse LUTS severity.

Clinical clue (diagnostic work-up)

1. Symptom assessment — Start with history and IPSS scoring to grade severity of voiding and storage symptoms.

2. Prostate evaluation — Perform digital rectal examination and assess prostate volume by ultrasound.

3. Laboratory markers — PSA measurement may provide indirect evidence, as higher values are sometimes linked with inflammation.

4. Histological assessment — Consider biopsy or surgical tissue analysis if clinically indicated; presence of lymphocytic infiltration indicates chronic inflammation.

5. Functional testing — In refractory cases, urodynamics may be used to evaluate bladder outlet obstruction.

The point

Chronic inflammation is a central factor in worsening BPH symptoms and increasing risk of urinary retention. Recognizing this link opens the way for better therapeutic strategies.

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The Urologist

By:

Dr. Ahmed M. Bakr, MD, FEBU

Reference: Inamura S, Terada N. Chronic inflammation in benign prostatic hyperplasia: Pathophysiology and treatment options. Int J Urol. 2024;31:968–974.