Benign prostatic hyperplasia

Benign prostatic hyperplasia (BPH), also known as benign prostatic enlargement (BPE), is an extremely common condition in elderly males and a major cause of bladder outflow obstruction. 

Terminology

The term benign prostatic hypertrophy was formerly used for this condition, but since histology demonstrates an increase in the number of epithelial and stromal cells in the periurethral area of the prostate, not an enlargement of cells, the more accurate descriptor term is hyperplasia. The term prostate adenoma (plural: adenomas or adenomata) is also used, as histopathologically the nodular hyperplasia organises into nodules of adenoma ¹¹¹.

Although the term prostatomegaly is often used synonymously with benign prostatic hyperplasia, strictly speaking prostatomegaly may refer to any cause of prostatic enlargement. Moreover, a significant number of patients with symptomatic benign prostatic hyperplasia do not have enlarged prostates ¹¹¹. By the same token, benign prostatic enlargement is also a poor term for this condition.

Epidemiology

By the age of 60, 50% of men have benign prostatic hyperplasia, and by 90 years of age, the prevalence has increased to 90%. As such it is often thought of essentially as a "normal" part of ageing ¹².

Risk factors

• increasing age

• family history

• race: Black population > White population > Asian population

• cardiovascular disease

• use of beta-blockers

• metabolic syndrome: diabetes, hypertension, obesity ⁸

Clinical presentation

Although a degree of prostatomegaly may be completely asymptomatic, the most common presentation is with lower urinary tract symptoms (LUTS) including ^12-4: 

• poor stream despite straining

• hesitancy, frequency, and incomplete emptying of the bladder

• nocturia

An enlarged prostate may also be incidentally found on imaging of the pelvis or on digital rectal exam. 

The international prostate symptom score (IPSS) is an 8 question-question (7 symptom questions + 1 quality of life question) scoring system used in assessing clinical severity, tracking symptoms, and aiding the management of benign prostatic hyperplasia.

Pathology

Benign prostatic hyperplasia is due to a combination of stromal and glandular hyperplasia, predominantly of the transition zone** (as opposed to prostate cancer which typically originates in the peripheral zone).

Androgens (DHT and testosterone) are necessary for the development of benign prostatic hyperplasia but are not the direct cause forof the hyperplasia.

**BPH mainly arises within the para-urethral transition zone, although BPH adenomas can be seen occasionally in other zones.

Markers

• prostate-specific antigen (PSA): elevated but non-specific

Radiographic features

Fluoroscopy

On IVP, the bladder floor can be elevated and the distal ureters lifted medially (J-shaped ureters or fishhook ureters). Chronic bladder outlet obstruction can lead to detrusor hypertrophy, trabeculation, and the formation of bladder diverticula.

Ultrasound

Ultrasound has become the standard first-line investigation after the urologist's finger.

• there is an increase in the volume of the prostate with a calculated volume exceeding 30 mL (width x height x length x 0.52)

• the central gland is enlarged and is hypoechoic or of mixed echogenicity

• Medianmedian lobe hypertrophy with intravesical masse effect and protrusion

• calcification may be seen both within the enlarged gland as well as in the pseudocapsule (representing the compressed peripheral zone)

• post-micturition residual volume is typically elevated

• associated bladder wall hypertrophy and trabeculation due to chronically elevated filling pressures

CT

Not typically used to assess the prostate, benign prostatic hyperplasia is more frequently an incidental finding. Extension above the symphysis pubis was used as a marker on axial imaging, however now that volume acquisition and coronal reformats are standard, the same criteria as on ultrasound can be used (>30 mL).

MRI

• enlarged transition zone

• heterogeneous signal with an intact low signal pseudocapsule in the periphery

Treatment and prognosis

Medical management for early disease typically commences with an alpha-blocker such as tamsulosin given in combination with a 5-alpha reductase inhibitor such as dutasteride. 

Surgical management for symptomatic patients is typically achieved with transurethral resection of the prostate (TURP), and careful patient selection is important given the high prevalence of both benign prostatic hyperplasia and lower urinary tract symptoms (LUTS) in this population. A prostatic urethral lift may be used as intermediate therapy before medication or more invasive TURP ¹⁰. Intermittent self-catheterisation is an option for those unsuitable for surgery. 

Other laser procedures can also be used which includes a Holmium laser enucleation of the prostate​.

Prostatic arterial embolisation (PAE) is an emerging minimally invasive procedure which has been shown to have similar efficacy to traditional surgical techniques, with a lower risk of major adverse events such as haemorrhage, urinary tract infection, and sexual dysfunction ⁹. 

Urodynamic studies and prostate size estimation are often used to guide therapy, although prostate size in isolation is a poor predictor of symptom severity ⁴.

Complications

Complications of untreated benign prostatic hyperplasia include ⁴:

• urinary retention

• bladder calculi and bladder diverticula

• recurrent urinary tract infection

• recurrent gross haematuria

• hydronephrosis and hydroureter and eventually renal failure

Despite much debate, it remains unclear if benign prostatic hyperplasia is a risk factor for prostate adenocarcinoma, or if the co-occurrence of the two pathologies is simply an epiphenomenon ¹²¹¹.

Differential diagnosis

The main differential is prostate carcinoma.