Dr. med. Dirk Manski

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Benign Prostatic Hyperplasia (BPH): Definition, Epidemiology and Etiology

Definitions of Benign Prostatic Hyperplasia (BPH)

Benign prostatic hyperplasia is a common disease with proliferation of the periurethral zone (transitional zone) of the prostate, leading to lower urinary tract symptoms (LUTS). Review literature: (Burnett und Wein, 2006) (DGU guideline) (EAU guideline: Non-neurogenic male LUTS)

Pathological Definition of Benign Prostatic Hyperplasia (BPH)

BPH is a benign prostatic hyperplasia of the prostate's epithelial and stromal components, leading to a nodular enlargement of the organ. Symptoms are not obligatory for the pathological definition of BPH.

Lower Urinary Tract Symptoms (LUTS)

Lower urinary tract symptoms are obstructive symptoms and irritative symptoms, which are not specific for benign prostatic hyperplasia.

Benign prostatic obstruction (BPO):

BPO is the clinical definition of the coincidence of bladder outlet obstruction due to BPH, and LUTS, hematuria, or recurrent UTI.

Epidemiology of Benign Prostatic Hyperplasia (BPH)

The epidemiological data for BPH are highly dependent on the focus of the trials: pathological prostate volume, urine flow, LUTS, or a combination of mentioned parameters.

Prevalence of BPH:

Using the pathological definition, the prevalence of BPH is age-dependent: starting with age 35, the prevalence increases each decade by 15%. Nearly 100% of 90-year-old men have benign prostate hyperplasia (pathologic definition). The pathologic prevalence does not correlate with the clinical significance.

Prostatic Enlargement:

The prostate volume of the male population increases with age: 25 ml (30–35 years old) to 45 ml (70 years old). Transition zone volume increases from 15 ml to 25 ml (same age groups).

Maximum Flow Rate:

The maximum flow rate in the male population is age-dependent and decreases from 20 ml/s (40–44 years old) to 11 ml/s (75–79 years). At the same time, the micturition volume decreases from 355 ml to 223 ml.

Prevalence of BPH Using Several Parameters:

Clinically significant BPH may be defined using symptoms (IPSS > 7) and maximum flow rate (< 15 ml/s). The prevalence of benign prostate hyperplasia (clinical definition) is age-dependent: 14–17% (age 50–59 years), 25–27% (age 60–69 years) and 35–38% (age 70–79 years).

Mortality of Benign Prostatic Hyperplasia (BPH):

In western countries, a dramatic decrease in mortality has been noted (Duncan et al., 2011). Causes of death are postrenal kidney failure and urosepsis.

Incidence of Urinary retention:

The incidence of urinary retention is 50–200/100000. Symptoms (LUTS), prostate size, and a low maximum flow rate are risk factors for urinary retention.

Frequency of surgical treatment:

The incidence of surgical treatment (e.g., TURP or prostatectomy) is decreasing: In 2007, 60000 surgical therapies for BPH were performed in Germany (75/100000). Age, residual urine, low maximum urinary flow, and prostate size are risk factors for impending surgical treatment.

Epidemiologic Risk Factors for Benign Prostatic Hyperplasia (BPH):

The epidemiology of BPH is relatively constant; some genetic factors or environmental influences may modestly increase the risk for BPH.

Obesity, metabolic syndrome and physical activity:

Obesity increases circulating estrogen in men, leading to prostate epithelial hyperplasia. Obesity is a risk factor for LUTS and increases the risk for surgical therapy (RR 2.38). Physical activity decreases the risk for metabolic syndrome and reduces the prevalence of clinically significant BPH (RR 0.7) (Parsons et al., 2011).

Sexual activity:

Sexual activity is not a risk factor for BPH. On the other hand, BPH and the treatment of BPH may cause erectile dysfunction.


Smoking reduces the risk of clinically significant BPH moderately. The relationship is weak and of limited clinical significance since the cardiovascular and oncological effects of smoking are well known.

Medication and BPH

Medication like antidepressants, antihistamines, or bronchodilators may exacerbate LUTS.

Prostate cancer and benign prostatic hyperplasia:

Pathologically defined benign prostatic hyperplasia is not considered a risk factor for prostate cancer. However, the risk of prostate cancer is significantly increased in patients with urinary retention or surgical BPH therapy (RR 2,2–3,3 for incidence, RR 2–7,4 mortality) (Ørsted et al., 2011). The study is controversial (Kopp et al., 2011).

Etiology (Causes) of Benign Prostatic Hyperplasia (BPH)

Prostatic Hyperplasia:

Prostate hyperplasia means an increase in the number of stromal and epithelial cells. For BPH, molecular data argue for a reduction of apoptosis rather than for actual cell proliferation. Furthermore, there is evidence for a lack of differentiation of the epithelial cells since, despite the increased cell number, the secretion volume of the prostate is decreased.

Androgens and BPH:

The presence of androgens is necessary for developing BPH; castrates do not develop BPH. For the intraprostatic effect, the circulating testosterone is converted to dihydrotestosterone (DHT) through the 5-alpha reductase. Type 1 of the 5-alpha reductase is found mainly in extraprostatic tissues (e.g., skin or liver); type 2 of the 5-alpha reductase is mostly found in the prostate. An increased activity of type 2 5-alpha reductase may cause BPH (Steers, 2001).

Extracellular matrix (ECM) and BPH:

The influence of an altered extracellular matrix on epithelial cells can lead to proliferation, similar to embryogenesis. Mechanisms of the ECM-induced proliferation may be the binding of growth factors to the ECM or altered proportions of extracellular matrix proteins.

Growth Factors and BPH:

The increased expression of growth factors (FGF, KGF, EGF, IGF, TGF-alpha) or their receptors leads to the proliferation and inhibition of apoptosis of prostate gland cells.

Genetic Factors of BPH:

If surgical treatment of BPH is necessary before the age of 60, genetic or familial factors are responsible in 50%. In patients over 60, only 9% are considered to have a familial risk. Responsible genes for familial BPH are not known yet.

Pathology and Pathophysiology of Benign Prostatic Hyperplasia

Gross Pathology:

The enlargement of the periurethral prostate [fig. prostate zones in BPH] can affect the so-called middle lobe, the lateral lobes, or a combination of both. The first BPH changes occur in the periurethral glands around the verumontanum. Because of the rigid prostatic capsule, the lumen of the prostatic urethra is compressed due to the prostatic hyperplasia. Since the size of the prostate does not correlate entirely with the degree of subvesical obstruction and symptoms, further anatomical and functional variations must be present (Figure autopsy findings of BPH).


Benign prostatic hyperplasia is a true hyperplasia with an increase in cell number. The first hyperplastic changes involve the stroma, followed by a small nodular hyperplasia of the glandular tissue. Some hypertrophy is also present at the cellular level (cell enlargement). The nuclei of the glands show no signs of malignancy. In the further course of the disease, large nodular hyperplasia develops.

The significant increase in the number of smooth muscle cells in the prostate stroma results in a dynamic component of subvesical obstruction by smooth muscle contraction. The muscle contraction is mediated via alpha-1A-adrenoceptors. In addition, smooth muscle cells of the prostate and bladder express type 4 and type 5 phosphodiesterase isoenzymes. Treatment of erectile dysfunction with inhibitors of phosphodiesterases has a beneficial effect on symptomatic BPH.

Impact of Subvesical Obstruction on the Bladder

The initial response of the bladder for subvesical obstruction is hypertrophy of the detrusor muscle; this allows the bladder to empty with higher voiding pressures. The response of the bladder to subvesical obstruction may cause detrusor instability, resulting in frequency and urgency. In addition, chronic subvesical obstruction leads to increased collagen deposition and decreased bladder compliance, resulting in trabeculation and residual urine. High voiding pressures lead to the formation of pseudodiverticula that increase the functional residual urine. The increasing dilatation of the bladder weakens the detrusor muscle and may lead to urinary retention. Later on, BPH leads to the decompensation of the bladder, resulting in progressive bladder dilatation, urinary retention, and urinary (overflow) incontinence.

Impact of Subvesical Obstruction on the Upper Urinary Tract

BPH may lead to the decompensation of the upper urinary tract with hydronephrosis, caused by micturition under high pressures, chronic urinary retention, and vesicoureteral reflux. Postrenal kidney failure is a late symptom of BPH and is usually associated with chronic urinary retention with incontinence. The consequences of untreated postrenal kidney failure are uremia and death.

The relief of the urinary tract often leads to massive polyuria. Polyuria is caused by the excretion of accumulated osmotically active substances. Secondly, the continuous perfusion of the renal medulla without urine flow wiped out the corticomedullary osmotic gradient, which is important for urine concentrating.

Aggravating Factors of BPH:

Symptoms of BPH may be aggravated by conditions that lead to polyuria (heart failure, COPD, diabetes ...) or affect the detrusor muscle (drugs, neurological disorders).

Index: 1–9 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z


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