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Benign Prostate Hypertrophy (BPH)

NICE Clinical guideline [CG97] Lower urinary tract symptoms in men: management. Last updated: Jun 2015.

NICE CKS LUTS in men. Last revised: Jun 2025.

Background Information

Definition

BPH is defined as a benign enlargement of the prostate gland, caused by hyperplasia of the stromal and epithelial cells, predominantly in the transitional zone of the prostate.

 

Benign prostate hypertrophy (BPH) and benign prostatic enlargement (BPE) are slightly different terms:

  • BPH is a histological diagnosis of prostate hyperplasia of stromal and epithelial cells (abnormalities at the cellular level)
    • Only 25–50% of men with BPH have LUTS
  • BPE is an anatomical finding referring to the actual increase in prostate size.
    • Not all men with BPH develops BPE
    • Only ~50% of men with histological BPH develop anatomical BPE

In summary: BPH ≠ BPE, BPH can exist without causing BPE, and BPE occurs because of BPH (but not everyone with BPH gets BPE).

Terminology note:
This article uses the term benign prostatic hyperplasia (BPH) throughout for simplicity, as it is the term most commonly used in clinical teaching and practice.

Not all men with BPH develop prostate enlargement, but BPH is the underlying process that leads to LUTS in many patients. For practical purposes, the assessment and management principles discussed here apply to men with BPH-associated LUTS, including those who have developed BPE.

Anatomy

Clinical points:

  • BPH affects mainly the transition zone
  • Prostate cancer affects mainly the peripheral zone

Anatomy of prostate zones:

Prostate Zone Location % of prostate volume
Peripheral Posterior & lateral aspects (the part that is palpable on DRE) ~70%
Transition Surrounds the proximal prostatic urethra ~5–10%
Central Surrounds the ejaculatory ducts ~20–25%
Anterior fibromuscular stroma Anterior aspect (non-glandular) Minimal glandular tissue

Pathophysiology

The process driving BPH development is age-related hormonal changes: [Ref]

  1. ↑ Dihydrotestosterone (DHT) (5α-reductase converts testosterone into dihydrotestosterone) (DHT is more potent than testosterone)
  2. DHT stimulates hyperplasia of both stromal and epithelial cells in the prostate (transitional zone)
  3. Prostatic enlargement leads to compression of the prostatic urethra and increase alpha-1 receptor mediated smooth muscle tone
  4. Results in lower urinary tract symptoms

Aetiology

Risk factors: [Ref]

  • Age – most important (prevalence exceeds 80% in >70 y/o men)
    • Although serum testosterone falls with age, intraprostatic DHT activity remains high due to preserved 5-α-reductase activity and increased tissue sensitivity
  • Obesity
  • Diabetes and metabolic syndrome
  • Physical inactivity

Complications

Key complications: [Ref]

  • Urinary retention (acute / chronic)
  • Recurrent UTIs (due to urine stasis and incomplete emptying)

BPH is NOT considered a direct precursor or pre-malignant lesion for prostate cancer. [Ref]

Diagnosis

Clinical Features

BPH causes LUTS: [Ref]

  • Obstructive symptoms predominate in BPH (as a result from bladder outlet obstruction due to prostatic enlargement)
  • Storage symptoms may also co-exist (esp. when chronic bladder obstruction induces secondary changes in bladder function)
Obstructive (voiding) symptoms
  • Straining to void
  • Hesitancy
  • Weak / intermittent stream

Some sources classify the following as post-micturition symptoms:

  • Post-void dribbling
  • Sensation of incomplete emptying
Storage (irritative) symptoms
  • Urinary frequency
  • Urgency
  • Nocturia
  • Urge incontinence

Investigation and Diagnosis

BPH is primarily a clinical diagnosis. Typical DRE findings + compatible LUTS are usually sufficient to make a work diagnosis, provided that:

  • Prostate cancer red flags are excluded, and
  • Initial investigations do NOT suggest an alternative diagnosis

The following information overlaps with the Lower Urinary Tract Symptoms (LUTS) in Men article, but is adapted specifically for BPH. Remember, BPH is the most common cause of LUTS, but the terms are not interchangeable.

DRE Findings in BPH

DRE finding BPH Prostate cancer
Prostate size Symmetrically enlarged Normal / asymmetrically enlarged
Consistency / texture Smooth, rubbery Hard, firm, stony
Surface Regular Irregular, nodular
Median sulcus Preserved May be obliterated

Prostate tenderness is suggestive of prostatitis; BPH and prostate cancer do not typically cause tenderness.

Note that a prostate gland that feels normal does NOT exclude prostate cancer.

Assessments

Initial assessment for ALL patients with suspected BPH (can be performed in primary care):

Assessment Purpose
IPSS (International Prostate Symptom Score) Assess symptom severity and impact on quality of life (guides treatment choice)
Bladder diary (urine frequency-volume chart) Characterise LUTS pattern (obstructive vs storage) (guides treatment choice)
Urinalysis Exclude differential diagnoses (e.g. UTI, urological malignancy, diabetes, renal disease)
PSA testing Exclude prostate cancer and guide management (as PSA level correlates with prostate volume)

Renal function test (serum creatinine and eGFR) is only necessary if renal impairment is suspected

Information About PSA Testing

Description PSA is a protein produced by the prostate gland:
  • It is secreted by prostate epithelial cells into prostatic fluid.
  • Function: liquefy semen and allow spermatozoa to move more freely.
  • Prostate cancer tends to increase PSA levels, due to the altered prostate architecture, causing more PSA to leak out into the blood

The aim of PSA testing is to detect early prostate cancer when treatment can be offered that may cure cancer or extend life.

Indications Any of the following:
  • LUTS are suggestive of bladder outlet obstruction secondary to BPH
  • Prostate feels abnormal on DRE
  • Patient is concerned about prostate cancer (or >50 y/o patient who requests it)

Before offering PSA testing, provide appropriate information and advice to enable the person to make an informed choice about testing

Interpretation Normal PSA level: 0-4 micrograms/L

However, the normal upper limit varies according to age (and race)

Limitations
  • ~15% false-negative tests (~15% people with a normal PSA level may have prostate cancer)
  • ~75% false-positive (~75% people with a raised PSA level have a -ve prostate biopsy) → unnecessary investigations

There is a particular risk of over-diagnosing and overtreating prostatic cancer in >79 y/o men, where the prevalence is highest but the proportion of cancers which are clinically significant is lowest

PSA levels may be increased by the following conditions:

  • Prostate cancer
  • BPH
  • Prostatitis and UTI
  • Age naturally increases PSA level
Precautions before PSA testing Before a PSA test, the patient should NOT have:
  • Ejaculated in the past 48 hours
  • Exercised vigorously (e.g. cycling) in the past 48 hours
  • An UTI (including prostatitis) in the past 6 weeks
  • An urological intervention (e.g. prostate biopsy) in the past 6 weeks

The above factors can raise the PSA and therefore give a false-positive result. Apart from those, BPH and advancing age also increase PSA levels.

Prostate Cancer Red Flags and Referral

NICE recommends to consider a DRE and PSA test in those with:

  • Any LUTS, or
  • Erectile dysfunction, or
  • Visible haematuria

 

When to refer:

  • Abnormal DRE (see below for suggestive features of malignancy), or
  • Prostate cancer is suspected (based on symptoms) and ↑ PSA levels (above the age-specific thresholds)
Age (years) PSA threshold (micrograms/litre)
Below 40 Use clinical judgement
40 to 49 >2.5
50 to 59 >3.5
60 to 69 >4.5
70 to 79 >6.5
Above 79 Use clinical judgement

Histology

Typical histological findings:

  • Glandular hyperplasia
  • Corpora amylacea within glands (laminated eosinophilic secretions)
  • Fibromuscular stromal hyperplasia

Histology is included here for educational completeness.

Note that, prostate biopsy is NOT routinely performed when the clinical picture is consistent with BPH. Biopsy is reserved only when there is suspicion of prostate cancer.

Management

Management depends on the predominant LUTS category. Although voiding symptoms commonly predominate, many patients also experience storage symptoms, and treatment should be directed accordingly.

Voiding Symptoms (Most BPH-Relevant)

Approach (step up if ineffective):

  • All patients should be offered conservative management
  • Consider pharmacological management in all patients (as per indications below)
  • Last resort (if pharmacological management failed): invasive management

Conservative Management

Advise on the following:

  • Regulate fluid intake
  • Avoid bladder stimulants (e.g. caffeine)
  • Urethral milking – if there is post-micturition dribbling

Pharmacological Management

2 main drug classes are used to manage obstructive LUTS:

Drug class MoA Examples Indications
Alpha blocker Block α1-adrenergic receptors in prostatic and bladder-neck→ smooth muscle relaxation → improve urinary flow Doxazosin, tamsulosin
  • Moderate / severe voiding symptoms (based on IPSS)
5-alpha reductase inhibitor Reduce conversion of testosterone into dihydrotestosterone → reduction in prostate volume → improve obstruction Finasteride
  • Enlarged prostate (PSA level >1.4 ng/mL or prostate size >30 g), and
  • High-risk of progression (e.g. older men)

If the patient meets BOTH criteria above, offer combination therapy (an alpha-blocker AND a 5-alpha reductase inhibitor)

As mentioned above, an enlarged prostate (>30 g) is the indication to start an 5-alpha reductase inhibitor. There are 2 ways to estimate the prostate size:

  1. PSA level correlates with prostate volume (>1.4 ng/mL is approximately >30g)
  2. Imaging (often trans-rectal ultrasound) can be used to measure prostate volume – this is widely used in clinical practice but not explicitly mentioned in NICE guideline

Note that alpha blocker gives rapid symptomatic relief (within days to weeks), while 5-alpha reductase inhibitor has a slow onset of action, with clinically significant effects typically taking 3-6 months to manifest.

Invasive Management

1st line:

  • Transurethral resection of the prostate (TURP) – most widely used
  • Transurethral vaporisation of the prostate (TUVP)

 

Other options:

  • If prostate <30g → transurethral incision of the prostate (TUIP)
  • If prostate >80g → open prostatectomy is preferred

If surgery is not appropriate (e.g. patient does not wish to undergo surgery, surgery is contraindicated):

  • 1st line: intermittent bladder catheterisation
  • 2nd line: indwelling urethral / suprapubic catheterisation

Storage Symptoms

Approach (step up if ineffective):

  • Step 1: conservative management
  • Step 2: pharmacological management
  • Step 3: invasive management

Conservative Management

Advise on the following:

  • Regulate fluid intake
  • Avoid bladder stimulants (e.g. caffeine)
  • Specific trainings for incontinence:
    • Urge incontinence (overactive bladder) → bladder retraining
    • Stress incontinence → pelvic floor muscle training for at least 3 months

Offer temporary containment products (for example, pads or collecting devices) if there is urinary incontinence

Pharmacological Management

All patients:

  • 1st line: anti-cholinergic (e.g. oxybutynin, tolterodine, darifenacin)
  • 2nd line: beta-3 receptor agonist (e.g. mirabegron, vibegron)

 

If the patient also experience bothersome nocturia, consider:

  • Late afternoon loop diuretic (off-label)
  • Desmopressin

Common reasons to avoid anti-muscarinics are:

  • Glaucoma
  • Patient of old age / at risk of cognitive impairment / with cognitive impairment
  • Known myasthenia gravis

Invasive Management

Consider the following:

  • Botulinum toxin A injection (patient must be willing and able to self-catheterise)
  • Augmentation cystoplasty (patient must be willing and able to self-catheterise)
  • Implanted sacral nerve stimulation
  • Artificial sphincter implantation (for stress incontinence)
  • Last resort: urinary diversion

References

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