EPIDEMIOLOGY 

Typically seen in men > 50 years of age. The prevalence of histological BPH is over 80% of patients older than 80 years of age. 

RISK FACTORS 

• Race: Some evidence suggests black men are at increased risk of having severe BPH symptoms compared to white men, and this may be due in part to the fact that the average size of the prostate is bigger in black men compared to white men. 
• Genetics: Having a first-degree relative with BPH increases the odds of having severe BPH-related symptoms. 
• Obesity: The incidence of BPH symptoms is higher in patients with Obesity, dyslipdaemia, hypertension, and glucose intolerance, or so-called metabolic syndrome. 
• Coffee/Caffeine intake: The odds of severe BPH symptoms are higher with increased intake of coffee and caffeine. 
• Sedentary lifestyle: Lack of physical activity is associated with a greater risk of developing BPH symptoms. 

PATHOPHYSIOLOGY 

The growth of the prostate occurs under the influence of testosterone, and its more potent active metabolite, 5-Dihydrotestosterone (DHT). Evidence for the role of testosterone and DHT in prostatic growth is shown by the fact that BPH is not seen in men castrated before puberty or in men with congenital 5-alpha reductase deficiency. The conversion of testosterone to DHT is mediated by 5-Alpha Reductase II in the prostate or 5-alpha reductase 1 in the liver or skin. Testosterone and DHT bind to the androgen receptors within the prostatic epithelial cells, resulting in proliferation and hyperplasia of both the glandular and stromal elements. The stromal elements contain smooth muscle cells, which are rich in Alpha 1-adrenergic receptors. Activation of these receptors is responsible for the construction of the prostatic urethra (dynamic component of bladder outlet obstruction). The continuous growth of the prostate within the peri-urethral zone results in progressive obstruction of the prostatic urethra (static component) and its subsequent manifestations. Sometimes this aspect of the prostate grows unrestricted into the bladder as the median lobe creates a valve-like effect on the bladder outlet.

There’s also evidence that prostatic infection and resultant inflammatory response provide additional sources of growth factors for prostatic growth in humans. Inflammatory cytokines like IL-6 and 8 have been implicated in prostatic stromal growth and smooth muscle contraction. 

CLINICAL PRESENTATION 

A. HISTORY 

The history should include the assessment of the type of LUTS, their duration and severity, and, more importantly, their impact on the patient’s quality of life or degree of how it bothers the patient. This can be done using validated symptom questionnaires like the International Prostate Symptoms Score (IPSS). The International Prostate Symptom Score assesses 7 symptoms with severity grades 0 to 5: 

• Feeling of incomplete emptying 
• Frequent urination 
• Intermittency 
• Urgency, with or without incontinence 
• Weak or slow stream 
• Straining 
• Nocturia 

The Bother score is an eighth question that is included to assess patient opinion of symptom severity and 

effect on quality of life. “If you were to spend the rest of your life with your urinary condition just the way it is now, how would you feel about that?” 

Responses: Delighted, Pleased, most satisfied, Mixed, most dissatisfied, Unhappy, Terrible. Score of 7 or lower: mild quality of life bother, Score of 8 to 19: moderate quality of life bother, Score of 20 or higher: severe quality of life bother. 

History of possible etiology of LUTS – purulent urethritis, perineal trauma, or instrumentation. 

History should also ascertain complications like acute or chronic retention, recurrent groin or scrotal swelling, haematuria, or evidence of renal insufficiency, among others. It is important to assess a patient’s general medical history and drug history to identify other causes of 

LUTS like medications (e.g. frusemide) and associated comorbidities (e.g. Diabetes and cardiac failure). 

Sexual history/Erectile dysfunction: It is important to assess a patient's baseline sexual function because this may be adversely affected with certain interventions, and to guide the choice of medical therapy. 

B. EXAMINATION 

Physical examinations should focus on the abdomen, including digital rectal examination (DRE) and external genitalia. 

Abdomen: The bladder may be palpable if there’s urinary retention 

DRE confirms an enlarged prostate and excludes prostate cancer, although this is not mandatory for a diagnosis of BPH. The enlarged prostate, usually smooth surfaced, firm in consistency, with preserved median groove. A hard nodular prostate may indicate prostate cancer.

External Genitalia: Examine the penis, testis, epididymis and cord structures. Palpable induration along the urethra may suggest urethral stricture. 

Spine and Extremity: Neurological examination, including sphincter tone, sacral sensation, and bulbocavernosus reflex integrity, is important to rule out neurological disease as the aetiology of LUTS. Lower limb paraparesis or paraplegia may be seen in patients with metastatic prostate cancer. 

C. INVESTIGATIONS

• Transrectal USS - more accurate in assessing the prostate size and configuration, which is an important consideration in guiding therapeutic intervention. 
• Abdominal USS - may show trabeculations, diverticula, bladder wall thickness, bladder stone, elevated PVR, pelvicalyceal dilatation, hydroureter/hydronephrosis due to the outlet obstruction. PVR>150ml requires surgical intervention.
• Uroflowmetry: determines the urine flow rate. Qmax <10ml/sec suggests bladder outlet obstruction (BOO).
• PSA - useful as a surrogate marker for prostate size, or in assessing risk for prostate cancer. It should be done after thorough counselling. Patients with a PSA >1.4ng/ml are at increased risk of disease progression due to BPH. 
• Urea and Creatinine: Should be measured if renal insufficiency is suspected. 
• Cystoscopy: Not mandatory, recommended if the patient presents with recurrent UTI or haematuria. May reveal bladder pathology (sacculation, trabeculation, bladder tumor, etc.), obstructing kissing prostate lobes. 
• Urodynamic study: Not recommended for routine evaluation due to cost and invasiveness. Indicated in patients with suspected neurologic bladder dysfunction. It is useful to differentiate poor detrusor contraction from bladder outlet obstruction. BOO is diagnosed by high intravesical voiding pressure (>60cm water) and low urine flow rate (Qmax <15mL/s). 
• Urinalysis - may show proteinuria, glycosuria, haematuria, or nitrite. Infection should be treated when identified, as this may account for the patient’s LUTS. 
• Bladder diary - a 48-hour – 72-hour record of the patient’s fluid intake and voiding history, including frequency and volume of each void. This is useful in evaluating polyuria and nocturnal polyuria. 
• Prostate biopsy: where indicated. NB BPH is a histological diagnosis, while BPE is a clinical diagnosis.

 DIFFERENTIAL DIAGNOSIS 

1. Prostatic cancer 
2. Urethral stricture 
3. Bladder cancer 
4. Bladder stone 
5. Neurogenic bladder 
6. Prostatitis 
7. Cystitis 
8. Overactive bladder Syndrome 

 TREATMENT 

• Aims of Treatment:
• Alleviate symptoms
• Improve urinary flow, 
• Preventing complications

The treatment depends on the severity of the disease as determined by the IPSS score 

[Severity of symptoms (IPSS) mild (0-8), Moderate (9 – 19), Severe (20-35)] Coexisting medical conditions; patient’s personal preference. 

MILD SYMPTOMS WITH LITTLE OR NO BOTHER. 

1. Watchful waiting 
2. Education/Lifestyle changes/Behavioural modifications:

• Restrict fluid intake to 2 hours before bedtime 
• Empty bladder before bed 
• Avoid late-night or bedtime drinking water 
• Avoid caffeine 
• Maintain an ideal weight 

MILD TO MODERATE LUTS WITH BOTHERSOME SYMPTOMS 

1. Medical therapy 

• Small prostate, predominant obstructive symptoms, and/or low PSA (<1.5ng/mL), alpha-adrenergic blocker, e.g., Tamsulosin 
• Large prostate, predominant obstructive symptoms, and/or high PSA (>1.5ng/mL). Combine alpha-adrenergic and 5-alpha reductase inhibitor, e.g., Tamsulosin and Dutasteride. Predominant irritative symptoms/Overactive bladder without elevated PVR. Antimuscarinic anticholinergic agents e.g. tolterodine. LUTS symptoms with ED. Phosphodiesterase-5 inhibitors e.g. tadalafil 

SEVERE LUTS WITH COMPLICATIONS AND PERSISTENT BOTHERSOME SYMPTOMS AFTER MEDICAL THERAPY 

1. Surgical treatment – recommended in patients with any of the following: 

• Refractory AUR 
• Recurrent UTI 
• Renal Insufficiency due to BPH 
• Recurrent haematuria from bleeding BPH 
• Bladder stones symptoms refractory to medical therapy

1. Surgical options – includes: 

• Open Surgery/Endoscopic procedures 
• Open simple prostatectomy 
• Transurethral resection of the Prostate (TURP) 
• Holmium Laser Enucleation of the Prostate (HoLEP) 
• Thulium Laser Enucleation of the Prostate (ThuLEP) 
• Laparoscopic simple prostatectomy 
• Robotic simple prostatectomy      

In summary, the treatment landscape for BPH is continually evolving and no longer follows a uniform approach. Instead, the selection of treatment is influenced by the severity of the disease, the patient's personal preferences, the surgeon's expertise, and the available local resources.