Correlation of prostate MR Elastography with Surgical Specimen Amongst Men with Symptomatic BPH/LUTS

Benign prostatic hyperplasia (BPH) is among the most common age-related medical conditions, impacting more than half of men in their 60s and >80% of men in their 70s, with most affected individuals developing lower urinary tract symptoms (LUTS). Initial management—alpha blockers to facilitate urethral dilation and/or 5-alpha reductase inhibitors to reduce prostate volume—fails one in three men on maximal therapy, while one in six progress to acute retention or surgery, which itself is often ineffective if pursued too late in the disease course. This is compounded by the fact that treatment decisions rely almost exclusively on self-reported symptoms, which develop insidiously and correlate poorly with objective metrics like prostate volume and uroflowmetry, leaving clinicians without reliable tools to guide therapy.

Surgical pathology demonstrates that BPH results from variable hyperplasia of glandular and stromal cells, with fibrosis—stromal expansion and collagen deposition—emerging as a likely determinant of disease severity and treatment resistance; however, fibrosis has only been characterized in post-operative tissue and thus cannot presently inform treatment decisions. Magnetic resonance elastography (MRE), a quantitative imaging technique that non-invasively maps tissue stiffness via propagating shear waves, has already transformed liver disease management by enabling non-invasive fibrosis staging that largely supplants biopsy for treatment thresholds and monitoring. Our preliminary findings show that MRE-based prostate stiffness measurements correlate with patient symptom scores, suggesting analogous diagnostic and monitoring potential for BPH/LUTS—though the relationship between MRE-derived stiffness, disease severity, and tissue-level histology remains unclear. By pairing MRE with spatially-directed surgical pathology and ex vivo analysis of prostatic epithelial and stromal cells, we aim to bridge this gap, hypothesizing that MRE-derived stiffness metrics correspond with medically refractory disease, prostatic fibrosis, and cellular signatures of ECM deposition and myofibroblastic transition.