Pathophysiology of clinical benign prostatic hyperplasia

Abstract

A disease can be defined as an abnormal anatomy (pathology) and/or function (physiology) that may cause harm to the body. In clinical benign prostatic hyperplasis (BPH), the abnormal anatomy is prostate adenoma/adenomata, resulting in a varying degree of benign prostatic obstruction (BPO) that may cause harm to the bladder or kidneys. Thus clinical BPH can be defined as such and be differentiated from other less common causes of male lower urinary tract symptoms. Diagnosis of the prostate adenoma/adenomata (PA) can be made by measuring the intravesical prostatic protrusion (IPP) and prostate volume (PV) with non-invasive transabdominal ultrasound (TAUS) in the clinic. The PA can then be graded (phenotyped) according to IPP and PV. Multiple studies have shown a good correlation between IPP/PV and BPO, and therefore progression of the disease. The severity of the disease clinical BPH can be classified into stages from stage I to IV for further management. The classification is based on the effect of BPO on bladder functions, namely that of emptying, normal if post-void residual urine (PVRU) < 100 mL; and bladder storage, normal if maximum voided volume (MVV) > 100 mL. The effect of BPO on quality of life (QoL) can be assessed by the QoL index, with a score ≥3 considered bothersome. Patients with no significant obstruction and no bothersome symptoms would be stage I; those with no significant obstruction but has bothersome symptoms (QoL ≥ 3) would be stage II; those with significant obstruction (PVRU > 100 mL; or MVV < 100 mL), irrespective of symptoms would be stage III; those with complications of the disease clinical BPH such as retention of urine, bladder stones, recurrent bleeding or infections would be stage IV. After assessment, further management can then be individualised. A low grade and stage disease can generally be watched (active surveillance) while a high grade and stage disease would need more invasive management with an option for surgery. The final decision making would take into account the patient's age, co-morbidity, social economic background and his preferences/values. Proper understanding of pathophysiology of clinical BPH would lead to better selection of patients for individualised and personalised care and more cost effective management.

Keywords: Clinical benign prostatic hyperplasia; Clinical relevance; Definition; Grading; Pathophysiology; Staging.

Figure 1

Bladder outlet obstruction depends on the site of the adenoma at the prostate.

Figure 2

Sagittal view of the prostate adenoma.

Figure 3

Transabdominal ultrasound (TAUS) measurements of prostate volume (PV) and intravesical prostatic protrusion (IPP). (A) Transverse view, (B) Sagittal view. PV is measured in grams by tracing the area of prostate in the transverse view to obtain the estimated size of the prostate using the ellipsoid formula and classified as follows: Grade a, ≤20 g; b, >20–40 g; c, >40 g. In the sagittal view, the IPP is measured in millimetres from the innermost protruding tip of the prostate adenoma to the base of the prostate at the circumference of the bladder and classified accordingly: Grade 1, ≤5 mm; 2, >5–10 mm; 3, >10 mm . This ultrasound image is from a 62-year-old patient who first presented with raised prostate specific antigen (PSA) of 7.7 μg/L with no lower urinary tract symptoms at age 53 years. He had three negative transrectal biopsies. In spite of medical treatment, he eventually had transurethral enucleating and resection of the prostate adenomata weighing 54 g (TUERP), for episodes of urinary infection and deteriorating symptoms. He recovered well, had benign prostatic hyperplasia on histology, and a postoperative PSA level of 1 μg/L.