Data Daftar Pustaka BPH
Data Daftar Pustaka BPH
Data Daftar Pustaka BPH
In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan.
2022 Aug 8.
Affiliations expand
PMID: 32644346
Excerpt
Benign prostatic hyperplasia (BPH) refers to the nonmalignant growth or hyperplasia of prostate tissue
and is a common cause of lower urinary tract symptoms in men. Disease prevalence has been shown to
increase with advancing age. Indeed the histological prevalence of BPH at autopsy is as high as 50% to
60% for males in their 60's, increasing to 80% to 90% of those over 70 years of age.
Several definitions exist in the literature when describing BPH. These include bladder outlet obstruction
(BOO), lower urinary tract symptoms (LUTS), and benign prostatic enlargement (BPE). BPH describes the
histological changes, benign prostatic enlargement (BPE) describes the increased size of the gland
(usually secondary to BPH) and bladder outlet obstruction (BOO) describes the obstruction to flow.
Those with BPE who present with BOO are termed benign prostatic obstruction. Lower urinary tract
symptoms (LUTS) simply describe urinary symptoms shared by disorders affecting the bladder and
prostate (when in reference to men). LUTS can be subdivided into storage and voiding symptoms. These
terms have largely replaced those historically termed "prostatism."
The development of benign prostatic hyperplasia is characterized by stromal and epithelial cell
proliferation in the prostate transition zone (surrounding the urethra), this leads to compression of the
urethra and development of bladder outflow obstruction (BOO) which can result in clinical
manifestations of lower urinary tract symptoms (LUTS), urinary retention or infections due to incomplete
bladder emptying. Long-term, untreated disease can lead to the development of chronic high-pressure
retention (a potentially life-threatening emergency) and long-term changes to the bladder detrusor
(both overactivity and reduced contractility).
Treatment options for BPH range from watchful waiting, to medical and surgical intervention. Risk factors
may be divided into non-modifiable and modifiable, with factors such as age, genetics, geographical
location, and obesity, all shown to influence the development of BPH. It is, therefore, important to be
able to identify those at risk of disease progression and those who can be managed more conservatively
to reduce associated morbidity and health care burden.
This review provides an overview of the etiology, pathophysiology, recognition, and management of
benign prostatic hyperplasia as well as interprofessional aspects that may enhance patient care.
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Disclosure: Krishna Baradhi declares no relevant financial relationships with ineligible companies.
Sections
Introduction
Etiology
Epidemiology
Pathophysiology
Histopathology
Evaluation
Treatment / Management
Differential Diagnosis
Prognosis
Complications
Review Questions
References
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References
1.
1. Roehrborn CG. Benign prostatic hyperplasia: an overview. Rev Urol. 2005;7 Suppl
9(Suppl 9):S3-S14. - PMC - PubMed
2.
1. Abrams P. LUTS, BPH, BPE, BPO: A Plea for the Logical Use of Correct Terms. Rev Urol.
1999 Spring;1(2):65. - PMC - PubMed
3.
1. Silverman WM. "Alphabet soup" and the prostate: LUTS, BPH, BPE, and BOO. J Am
Osteopath Assoc. 2004 Feb;104(2 Suppl 2):S1-4. - PubMed
4.
1. Abrams P. New words for old: lower urinary tract symptoms for "prostatism". BMJ. 1994
Apr 09;308(6934):929-30. - PMC - PubMed
5.
1. Roehrborn CG. Pathology of benign prostatic hyperplasia. Int J Impot Res. 2008 Dec;20
Suppl 3:S11-8. - PubMed
6.
1. Parsons JK. Benign Prostatic Hyperplasia and Male Lower Urinary Tract Symptoms:
Epidemiology and Risk Factors. Curr Bladder Dysfunct Rep. 2010 Dec;5(4):212-218.
- PMC - PubMed
7.
1. Chughtai B, Forde JC, Thomas DD, Laor L, Hossack T, Woo HH, Te AE, Kaplan SA. Benign
prostatic hyperplasia. Nat Rev Dis Primers. 2016 May 05;2:16031. - PubMed
8.
9.
10.
11.
12.
13.
1. Kristal AR, Arnold KB, Schenk JM, Neuhouser ML, Weiss N, Goodman P, Antvelink CM,
Penson DF, Thompson IM. Race/ethnicity, obesity, health related behaviors and the risk
of symptomatic benign prostatic hyperplasia: results from the prostate cancer
prevention trial. J Urol. 2007 Apr;177(4):1395-400; quiz 1591. - PubMed
14.
1. Parsons JK, Carter HB, Partin AW, Windham BG, Metter EJ, Ferrucci L, Landis P, Platz EA.
Metabolic factors associated with benign prostatic hyperplasia. J Clin Endocrinol Metab.
2006 Jul;91(7):2562-8. - PMC - PubMed
15.
1. Furukawa S, Fujita T, Shimabukuro M, Iwaki M, Yamada Y, Nakajima Y, Nakayama O,
Makishima M, Matsuda M, Shimomura I. Increased oxidative stress in obesity and its
impact on metabolic syndrome. J Clin Invest. 2004 Dec;114(12):1752-61.
- PMC - PubMed
16.
17.
1. Sanda MG, Beaty TH, Stutzman RE, Childs B, Walsh PC. Genetic susceptibility of benign
prostatic hyperplasia. J Urol. 1994 Jul;152(1):115-9. - PubMed
18.
1. Meikle AW, Bansal A, Murray DK, Stephenson RA, Middleton RG. Heritability of the
symptoms of benign prostatic hyperplasia and the roles of age and zonal prostate
volumes in twins. Urology. 1999 Apr;53(4):701-6. - PubMed
19.
1. Rohrmann S, Fallin MD, Page WF, Reed T, Partin AW, Walsh PC, Platz EA. Concordance
rates and modifiable risk factors for lower urinary tract symptoms in twins.
Epidemiology. 2006 Jul;17(4):419-27. - PubMed
20.
1. Berry SJ, Coffey DS, Walsh PC, Ewing LL. The development of human benign prostatic
hyperplasia with age. J Urol. 1984 Sep;132(3):474-9. - PubMed
21.
1. Platz EA, Joshu CE, Mondul AM, Peskoe SB, Willett WC, Giovannucci E. Incidence and
progression of lower urinary tract symptoms in a large prospective cohort of United
States men. J Urol. 2012 Aug;188(2):496-501. - PMC - PubMed
22.
1. Loeb S, Kettermann A, Carter HB, Ferrucci L, Metter EJ, Walsh PC. Prostate volume
changes over time: results from the Baltimore Longitudinal Study of Aging. J Urol. 2009
Oct;182(4):1458-62. - PMC - PubMed
23.
1. Wei JT, Calhoun E, Jacobsen SJ. Urologic diseases in America project: benign prostatic
hyperplasia. J Urol. 2005 Apr;173(4):1256-61. - PubMed
24.
1. Kupelian V, Wei JT, O'Leary MP, Kusek JW, Litman HJ, Link CL, McKinlay JB, BACH Survery
Investigators Prevalence of lower urinary tract symptoms and effect on quality of life in a
racially and ethnically diverse random sample: the Boston Area Community Health
(BACH) Survey. Arch Intern Med. 2006 Nov 27;166(21):2381-7. - PubMed
25.
26.
1. Stroup SP, Palazzi-Churas K, Kopp RP, Parsons JK. Trends in adverse events of benign
prostatic hyperplasia (BPH) in the USA, 1998 to 2008. BJU Int. 2012 Jan;109(1):84-7.
- PubMed
27.
1. Centers for Disease Control and Prevention (CDC) Trends in aging--United States and
worldwide. MMWR Morb Mortal Wkly Rep. 2003 Feb 14;52(6):101-4, 106. - PubMed
28.
1. Jin B, Turner L, Zhou Z, Zhou EL, Handelsman DJ. Ethnicity and migration as determinants
of human prostate size. J Clin Endocrinol Metab. 1999 Oct;84(10):3613-9. - PubMed
29.
1. Ganpule AP, Desai MR, Desai MM, Wani KD, Bapat SD. Natural history of lower urinary
tract symptoms: preliminary report from a community-based Indian study. BJU Int. 2004
Aug;94(3):332-4. - PubMed
30.
31.
1. Foo KT. Pathophysiology of clinical benign prostatic hyperplasia. Asian J Urol. 2017
Jul;4(3):152-157. - PMC - PubMed
32.
33.
1. Babinski MA, Manaia JH, Cardoso GP, Costa WS, Sampaio FJ. Significant decrease of
extracellular matrix in prostatic urethra of patients with benign prostatic hyperplasia.
Histol Histopathol. 2014 Jan;29(1):57-63. - PubMed
34.
1. McNeal J. Pathology of benign prostatic hyperplasia. Insight into etiology. Urol Clin North
Am. 1990 Aug;17(3):477-86. - PubMed
35.
1. Barry MJ, Fowler FJ, O'leary MP, Bruskewitz RC, Holtgrewe HL, Mebust WK, Cockett AT,
Measurement Committee of the American Urological Association The American
Urological Association Symptom Index for Benign Prostatic Hyperplasia. J Urol. 2017
Feb;197(2S):S189-S197. - PubMed
36.
1. Bohnen AM, Groeneveld FP, Bosch JL. Serum prostate-specific antigen as a predictor of
prostate volume in the community: the Krimpen study. Eur Urol. 2007 Jun;51(6):1645-
52; discussion 1652-3. - PubMed
37.
38.
1. Gormley GJ, Stoner E, Bruskewitz RC, Imperato-McGinley J, Walsh PC, McConnell JD,
Andriole GL, Geller J, Bracken BR, Tenover JS. The effect of finasteride in men with
benign prostatic hyperplasia. The Finasteride Study Group. N Engl J Med. 1992 Oct
22;327(17):1185-91. - PubMed
39.
1. Emberton M, Cornel EB, Bassi PF, Fourcade RO, Gómez JM, Castro R. Benign prostatic
hyperplasia as a progressive disease: a guide to the risk factors and options for medical
management. Int J Clin Pract. 2008 Jul;62(7):1076-86. - PMC - PubMed
40.
1. Roehrborn CG, Siami P, Barkin J, Damião R, Major-Walker K, Nandy I, Morrill BB, Gagnier
RP, Montorsi F, CombAT Study Group The effects of combination therapy with
dutasteride and tamsulosin on clinical outcomes in men with symptomatic benign
prostatic hyperplasia: 4-year results from the CombAT study. Eur Urol. 2010
Jan;57(1):123-31. - PubMed
41.
1. Regadas RP, Reges R, Cerqueira JB, Sucupira DG, Josino IR, Nogueira EA, Jamacaru FV, de
Moraes MO, Silva LF. Urodynamic effects of the combination of tamsulosin and daily
tadalafil in men with lower urinary tract symptoms secondary to benign prostatic
hyperplasia: a randomized, placebo-controlled clinical trial. Int Urol Nephrol. 2013
Feb;45(1):39-43. - PubMed
42.
43.
1. Yin L, Teng J, Huang CJ, Zhang X, Xu D. Holmium laser enucleation of the prostate versus
transurethral resection of the prostate: a systematic review and meta-analysis of
randomized controlled trials. J Endourol. 2013 May;27(5):604-11. - PubMed
44.
1. Garcia C, Chin P, Rashid P, Woo HH. Prostatic urethral lift: A minimally invasive treatment
for benign prostatic hyperplasia. Prostate Int. 2015 Mar;3(1):1-5. - PMC - PubMed
45.
1. Jacobsen SJ, Jacobson DJ, Girman CJ, Roberts RO, Rhodes T, Guess HA, Lieber MM.
Natural history of prostatism: risk factors for acute urinary retention. J Urol. 1997
Aug;158(2):481-7. - PubMed
46.
1. Pickard R, Emberton M, Neal DE. The management of men with acute urinary retention.
National Prostatectomy Audit Steering Group. Br J Urol. 1998 May;81(5):712-20.
- PubMed
47.
1. Nickel JC. Benign prostatic hyperplasia: does prostate size matter? Rev Urol. 2003;5
Suppl 4(Suppl 4):S12-7. - PMC - PubMed
48.
49.
50.
1. Kashif KM, Foley SJ, Basketter V, Holmes SA. Haematuria associated with BPH-Natural
history and a new treatment option. Prostate Cancer Prostatic Dis. 1998 Mar;1(3):154-
156. - PubMed
51.
1. Boettcher S, Brandt AS, Roth S, Mathers MJ, Lazica DA. Urinary retention: benefit of
gradual bladder decompression - myth or truth? A randomized controlled trial. Urol Int.
2013;91(2):140-4. - PubMed
52.
1. Thomas S. Good practice in continence services. Nurs Stand. 2000 Aug 9-15;14(47):43-5.
- PubMed
53.
Publication types
Study Guide
Related information
Books
MedGen
o NCBI Bookshelf
Benign Prostatic Hyperplasia
Go to:
Benign prostatic hyperplasia (BPH) is a common condition encountered in aging men and a common
cause of lower urinary tract symptoms. Histological prevalence of BPH is common, and disease
progression is associated with bladder outflow obstruction, this may present clinically in both the
emergency surgical and outpatient clinical settings. This activity reviews the natural history and
highlights the role of the interprofessional healthcare team in evaluating and managing these patients.
Objectives:
Go to:
Introduction
Benign prostatic hyperplasia (BPH) refers to the nonmalignant growth or hyperplasia of prostate tissue
and is a common cause of lower urinary tract symptoms in men. Disease prevalence has been shown to
increase with advancing age. Indeed the histological prevalence of BPH at autopsy is as high as 50% to
60% for males in their 60's, increasing to 80% to 90% of those over 70 years of age.[1]
Several definitions exist in the literature when describing BPH. These include bladder outlet obstruction
(BOO), lower urinary tract symptoms (LUTS), and benign prostatic enlargement (BPE). BPH describes the
histological changes, benign prostatic enlargement (BPE) describes the increased size of the gland
(usually secondary to BPH) and bladder outlet obstruction (BOO) describes the obstruction to flow.[2]
[3] Those with BPE who present with BOO are termed benign prostatic obstruction.[4] Lower urinary
tract symptoms (LUTS) simply describe urinary symptoms shared by disorders affecting the bladder and
prostate (when in reference to men). LUTS can be subdivided into storage and voiding symptoms. These
terms have largely replaced those historically termed "prostatism."
The development of benign prostatic hyperplasia is characterized by stromal and epithelial cell
proliferation in the prostate transition zone (surrounding the urethra), this leads to compression of the
urethra and development of bladder outflow obstruction (BOO) which can result in clinical
manifestations of lower urinary tract symptoms (LUTS), urinary retention or infections due to incomplete
bladder emptying.[5] Long-term, untreated disease can lead to the development of chronic high-
pressure retention (a potentially life-threatening emergency) and long-term changes to the bladder
detrusor (both overactivity and reduced contractility).
Treatment options for BPH range from watchful waiting, to medical and surgical intervention. Risk factors
may be divided into non-modifiable and modifiable, with factors such as age, genetics, geographical
location, and obesity, all shown to influence the development of BPH.[6][7] It is, therefore, important to
be able to identify those at risk of disease progression and those who can be managed more
conservatively to reduce associated morbidity and health care burden.
This review provides an overview of the etiology, pathophysiology, recognition, and management of
benign prostatic hyperplasia as well as interprofessional aspects that may enhance patient care.
Go to:
Etiology
The etiology of BPH is influenced by a wide variety of risk factors in addition to direct hormonal effects of
testosterone on prostate tissue.
Although they do not cause BPH directly, testicular androgens are required in the development of BPH
with dihydrotestosterone (DHT) interacting directly with prostatic epithelium and stroma.[5]
[8] Testosterone produced in the testes is converted to dihydrotestosterone (DHT) by 5-alpha-reductase
2 in prostate stromal cells and accounts for 90% of total prostatic androgens.[7] DHT has direct effects on
stromal cells in the prostate, paracrine effects in adjacent prostatic cells, and endocrine effects in the
bloodstream, which influences both cellular proliferation and apoptosis (cell death).[9]
BPH arises as a result of the loss of homeostasis between cellular proliferation and cell death, resulting in
an imbalance favoring cellular proliferation. This results in increased numbers of epithelial and stromal
cells in the periurethral area of the prostate and can be seen histopathologically[5].
Risk Factors
Non-modifiable and modifiable risk factors also contribute to the development of BPH. These have been
shown to include metabolic syndrome, obesity, hypertension, and genetic factors.[7]
Obesity has been shown to be associated with increased risk of BPH in observational studies.
[13][14] The exact cause is unclear but is likely multifactorial in nature as obesity makes up one
aspect of the metabolic syndrome. Proposed mechanisms include increased levels of systemic
inflammation and increased levels of estrogens.[15][16]
Genetic predisposition to BPH has been demonstrated in cohort studies, first-degree relatives in
one study demonstrated a four-fold increase in the risk of BPH compared to control.[17] These
findings have demonstrated consistency in twin studies looking at the disease severity of BPH,
with higher rates of LUTS seen in monozygotic twins.[18][19]
Go to:
Epidemiology
Differences in case definitions make interpretation of population-based studies regarding BPH difficult.
Whereas BPH can refer to histology, benign prostate enlargement, and physician-diagnosis of BPH, LUTS
refers to the urinary symptoms shared by disorders affecting the prostate and bladder.
Age is a significant predictor of both development of BPH and subsequent LUTS, with 50% of men over
the age of 50 shown to have evidence of BPH and the association with the development of LUTS shown
to increase with age in a linear fashion.[20][21] This is supported by studies that have demonstrated
increases in prostate volume with age (2% to 2.5% increase in size per year).[22] In the US, studies have
shown BPH prevalence to be as high as 70% in those between 60 and 69 years of age and more than 80%
in those over 70 years.[23] The prevalence of male LUTS alone demonstrated a significant increase with
age from 8% (30 to 39yrs) to 35% (60 to 69yrs) in the Boston area community health survey, other US
population-based studies have shown 56% of men between 50-79yrs reported symptoms.[24][25]
At a population-level, the prevalence of BPH increased dramatically between 1998 and 2007 in the US,
nearly doubling in the number of cases.[26] These increases are suggested to be attributable to an aging
population, with those over 80 years of age projected to be around 19.5 million in 2030 (from 9.3 million
in 2003).[27] As populations age, the number of cases can, therefore, be expected to rise.
International studies have suggested that Western populations have significantly higher prostate
volumes compared to those from southeast Asia.[28] Further studies looking at the correlation of
prostate volume with LUTS, however, found that lower prostate volumes did not necessarily correlate
with symptoms, with higher mean IPSS (international prostate symptom scores) observed in a cohort of
Indian men compared to western populations.[29]
Go to:
Pathophysiology
Both the development of lower urinary tract symptoms and bladder outlet obstruction in men with BPH
can be attributable to static and dynamic components.[30] Static obstruction is a direct consequence of
prostate enlargement resulting in periurethral compression and bladder outlet obstruction. Here,
periurethral compression requires increasing voiding pressures to overcome resistance to flow; in
addition, prostate enlargement distorts the bladder outlet causing obstruction to flow.[31]
Dynamic components include the tension of prostate smooth muscle (hence the use of 5-alpha
reductase inhibitors to reduce prostate volume and alpha-blockers to relax smooth muscle).[32] This is
explained by decreases in elasticity and collagen in the prostatic urethra in men with BPH, which may
further exacerbate bladder outlet obstruction due to loss of compliance and increased resistance to flow
and may explain why prostate size alone is not always a predictor of disease.[33]
Go to:
Histopathology
Histological examination demonstrates that BPH is a hyperplastic process with an increase in cell number
on histology (hyperplasia); these occur both in the periurethral and transition zones. Histological studies
have demonstrated both glandular and stromal proliferation. Specifically, periurethral zones
demonstrate stromal nodules, whereas glandular nodular proliferation is seen within the transition zone.
[34]
Go to:
History
In the elective setting, a focused medical history should include all aspects of symptomatology, and this
includes onset, timing, exacerbating, and relieving factors.
Lower urinary tract symptoms can be divided into storage (frequency, nocturia, urgency) and voiding
symptoms (stream, straining, hesitancy, prolonged micturition) and can help establish other causes of
urinary symptoms such as urinary tract infections/overactive bladder, in addition to determining the site
affected (bladder vs. prostate). Men with BPH are likely to report predominant symptoms of nocturia,
poor stream, hesitancy, or prolonged micturition.
Red flags help point to more sinister causes of urinary symptoms such as bladder/prostate cancer,
neurology such as cauda equina, or chronic high-pressure retention (which can lead to silent renal
failure). The presence of these can be established by asking about visible haematuria/bone pain/weight
loss, neurology, and nocturnal enuresis/incontinence, respectively.
Complete medication history should be taken, including any medications they have tried and use of
anticoagulants or antiplatelets, which may increase the risk of intra-operative bleeding or need to be
held before surgery.
The overall fitness of the patient should also be established to determine suitability for any future
interventions (fitness for anesthesia, independence, exercise tolerance, ability to complete activities of
daily living), and the symptom burden on quality of life should also be established.
Physical Examination
In the elective setting, the examination should include abdominal examination (looking for a palpable
bladder/loin pain) and examination of external genitalia (meatal stenosis or phimosis). The examination
should then conclude with a digital rectal examination making a note in particular of the size, shape
(how many lobes), and consistency (smooth/hard/nodular) of the prostate (BPH is characterized by a
smooth enlarged prostate).
Frequency-volume chart
Questionnaires
Both the American urological association symptom index and IPSS can be used to assess the impact of
LUTS on quality of life.[35] They are useful when quantifying the disease burden on the patient and can
be used to stratify patients into disease categories for treatment.[7] The IPSS stratifies patients into three
groups on the basis of symptoms. They are mild (0-7), moderate (8-19), and severe (20-35). Those with
more severe symptoms are less likely to benefit from conservative or medical measures.
Go to:
Evaluation
Standard investigation of BPH may include bedside urine dipstick, post-void residual, IPSS, and urine flow
studies to establish if there is evidence of obstructive voiding. Further tests may be indicated depending
on the patient/history.
Blood Tests
Blood tests, including renal function tests, are useful to establish baseline renal function and can help
support the diagnosis of renal failure/acute kidney injury in someone with chronic high-pressure
retention or acute retention, for example.
Urinalysis
Urine specimen testing can help detect infection, non-visible haematuria, or metabolic disorders
(glycosuria). Leucocytes and nitrites are common findings with infection; the presence of proteinuria
may point towards nephrological conditions. The American urological association recommend urinalysis
using a dipstick test, further tests may be requested based on abnormal dipstick findings (culture, etc.).
Prostate-specific antigen testing has been shown to predict prostate volume.[36] Prostate-specific
antigen (PSA) testing should be used with caution, however, and should not be done routinely in the
investigation of BPH. Levels may be raised in a large range of conditions (large prostate, infection,
catheterization, prostate cancer) and can cause undue anxiety or further unnecessary investigations for
the patient. It is the author's preference to conduct PSA testing in specific circumstances, i.e., where
cancer is suspected (malignant feeling prostate, metastatic disease suspected) or a previous baseline
established.
Ultrasound
Ultrasound scans are used to look for evidence of hydronephrosis and are indicated in patients with high
residual volumes or renal impairment. Other indications include suspicion of urinary tract stones or the
investigation of haematuria.
Flow Studies
Urine flow studies are used to determine the volume of urine passed over time. This can help establish
whether there is objective evidence for obstruction to flow. Urodynamic studies are used to see how the
bladder empties and fills. They can help further assess patients where the diagnosis is not certain or
where a neurogenic/overactive bladder is suspected (i.e., neurological conditions that may affect the
bladder, flow studies equivocal, diagnosis not clear).
Cystoscopy
Flexible cystoscopy should be used to investigate red flag symptoms such as visible
haematuria/suspected bladder cancer and can also be used to look for urethral strictures, which may
also result in poor flow/decreased urinary flow studies.
Go to:
Treatment / Management
Men with BPH may present acutely with urinary retention or may be seen in the clinic or primary care
setting. Management of male urinary retention is covered in a separate topic.
In those with LUTS, treatment options range from watchful waiting to medical and surgical intervention
and depend on the degree of "bother" or disease burden to the patient (as assessed by IPSS).
Observation
Watchful waiting is a process to manage patients by giving lifestyle advice. Examples include weight loss,
reducing caffeine intake or reducing fluid intake in the evening, and avoiding constipation to try and
reduce risk factors and improve LUTS. Patients should be involved in the discussion and informed of the
risks of disease progression. Clinical progression has shown to be around 31% in one observational study,
with 5% developing acute urinary retention.[37] These measures may be trialed in those with mild
symptoms (IPSS<7).[7]
Medical Therapy
Both static and dynamic components contribute to the pathophysiology of BPH. Medical therapy aims to
address both of these components.
Alpha-blockers:
Alpha 1-adrenoreceptors are present on prostate stromal smooth muscle and bladder neck. Alpha 1-
adrenoreceptor blockage results in stromal smooth muscle relaxation addressing the dynamic
component of BPH and thus improving flow. Examples include selective Alpha-blockers such as
Tamsulosin (400mcg once daily) and Alfuzosin (10mg once daily).
5 alpha-reductase inhibitors:
Alpha-reductase inhibitors such as finasteride (5mg once daily) and dutasteride block conversion of
testosterone to DHT.[38]. This addresses the static component of BPH by causing shrinkage of the
prostate and takes several weeks to show noticeable improvement, with six months needed for maximal
effectiveness.[7] As a result of treatment serum, PSA can be reduced by 50%, with prostate volume
decreasing by up to 25%. This has been shown to alter the disease process and subsequent disease
progression.[39]
Antimuscarinics:
Bladder detrusor instability can develop in patients with worsening bladder outlet obstruction. This can
result in increased urgency (overactive bladder) and frequency. Muscarinic receptor antagonists can help
with these symptoms by blocking muscarinic receptors on detrusor muscle. This reduces smooth muscle
tone and can improve symptoms in those with overactivity. Examples include solifenacin, tolterodine,
and oxybutynin. Those who fail antimuscarinic treatment may be considered for mirabegron use (a Beta-
3 adrenoreceptor agonist), which causes detrusor relaxation.
In practice, the combination of an alpha-blocker and alpha-reductase inhibitor is often used to achieve
improvements in voiding symptoms. This is backed by studies confirming the effectiveness of
combination therapy over monotherapy.[40][41]
Surgery
Guidelines for the indications for surgery in BPH as outlined by the European Association of Urology
(EAU) are as follows:[42]
Renal insufficiency
Bladder stones
Surgical management of BPH has broadened significantly over the years, with the development of
further minimally invasive techniques. Recommended procedures include transurethral incision of the
prostate, transurethral resection fo the prostate, in addition to newer techniques such as laser
vaporization and holmium laser enucleation, which have largely replaced open prostatectomy. Surgical
management options are outlined below.
TURP/TUIP
Transurethral resection surgery focuses on debulking the prostate to produce an adequate channel for
urine to flow. This is achieved using diathermy to produce a high-frequency current that allows the
cutting of tissue. By resecting all obstructing prostatic tissue, an adequate channel can be created to
allow urine to flow. Bipolar diathermy has largely replaced monopolar diathermy techniques for TURP,
with increased benefits such as resection in saline and reduced risk of "TUR syndrome."
HOLEP
Previously, open prostatectomy allowed adenoma to be removed or enucleated off its capsule. This can
now be achieved with laser enucleation, referred to as HoLEP (Holmium laser enucleation of the
prostate). Meta-analysis has shown improved Qmax (flow rate), reduction in post-void residual, and IPSS
compared to TURP.
Benefits include a lower transfusion rate with no increase in complications compared to TURP. However,
limitations include specialized equipment required making it less readily available.[43]
Urolift
Tissue-sparing approaches, such as Urolift, have also been developed. This can help minimize the risk of
bleeding in co-morbid patients and the associated risks of more invasive surgery (such as anesthesia risk,
prolonged surgery time, etc.). By compressing prostate lobes, the channel can be widened in the
prostatic urethra, improving LUTS. Studies have shown benefits, including the possibility of day-case
surgery, preserved sexual function, and improved symptom scores (IPSS), and flow rates (QMax).[44]
Go to:
Differential Diagnosis
Differential diagnoses for lower urinary tract infections are broad and include the following:
Bladder/prostate cancer
Other conditions:
Prostatitis
Urethral stricture
Go to:
Prognosis
Observational studies have demonstrated that when left without treatment, clinical progression of BPH
increased over a 48 month period, with 31% of the cohort requiring presentation at 48 months and 5%
developing acute retention in the 48 month period.[37]
The risk of acute urinary retention also increased with age, in the Olmsted County study, the incidence of
retention in men increased over ten-fold, from 3/1000 (40-49yrs) to 34.7/1000 (70-79yrs).[45] Left
untreated, BPH, therefore, has a significant risk of progression and presentation. Indeed, up to 42% of
men who presented with retention in 1 study, went on to have surgery.[46] Men with significantly
enlarged prostates (>30ml) have also been shown to be at an increased risk of disease progression.[47]
Go to:
Complications
Common Complications
Urinary retention
Chronic retention
Haematuria
Bladder calculi
Other complications may arise as a result of catheterization for management of LUTS in BPH and include:
Urinary Retention
International studies have demonstrated that BPH accounts for over two-thirds of cases of acute urinary
retention.[48] Further to this, 15% of those who experience acute urinary retention experience another
episode in the future, with 75% requiring surgery compared to those with precipitating causes (only
26%).[49]
Men with BPH can also develop chronic retention. This is usually chronic high-pressure retention due to
high voiding detrusor pressures in the bladder as a result of outflow obstruction.[48] Due to the inability
to empty the bladder completely, the pressure within the bladder can increase, resulting in
hydronephrosis and subsequent deterioration in renal function leading to renal failure. Management of
these subsets of patients is, therefore, urgent catheterization and urgent surgery to relieve the
obstruction (TURP) or long-term catheter (those with high-pressure retention should not undergo
TWOC).
This occurs due to incomplete bladder emptying resulting in incomplete bladder emptying and stagnant
urine. Recurrent infections may indicate a need for treatment or long-term antibiotics to prevent
associated co-morbidity (admissions with urosepsis).
Haematuria
This is a common complication in BPH and a common cause for referral for further investigation. Due to
the increased vascularity of larger prostate vessels may be disrupted, causing bleeding.[48] Finasteride
has been shown to decrease the density of vessels and can help manage problematic BPH related
haematuria.[50]
Management consists of catheterization to relieve the bladder pressure and definitive management to
prevent retention and further renal dysfunction. Management options include TURP or long-term
catheter/intermittent self-catheter. Following catheterization, the patient may undergo post-obstructive
diuresis. This is characterized by increased urine output in the following 24 to 72 hours and may require
IV fluid supplementation if exceeding >200 ml per hour. There is no evidence to suggest any benefit in
gradual vs. rapid decompression, and so patients should be left on free drainage following
catheterization for HPCR.[51]
Go to:
Lifestyle factors such as weight loss or improved diabetic control should be explained to the patient to
allow modifiable risk factors to be addressed. This may also translate to reducing the risk of the surgery
itself in the future, by reducing anesthetic and post-operative complication risks. Lifestyle measures such
as reducing caffeine and timing of fluid intake can also be used as a measure to address specific
problematic urinary symptoms.
Those managed with long-term catheters or intermittent self-catheterization should be taught the
importance of hygiene and catheter care to prevent urinary tract infections. This may be done with the
assistance of dedicated specialist nurses. The provision for managing the catheter in the community
should also be made.
Patients with BPH should understand the risks of disease progression before committing to treatment
options and should be counseled on alternative management options such as watchful waiting, medical
therapy along with any other surgeries available in order to make an informed decision.
Go to:
Healthcare outcomes can be optimized through the use of IPSS or AUA scoring systems. These can help
stratify patients according to disease severity and guide physician decision making. Adherence to lifestyle
factors affecting BPH may also be addressed through diet advice, weight loss, and glycaemic control. The
role of primary care/endocrine/diabetic nurse specialists can help address these areas, and early referral
to these areas can help ensure medical conditions are optimized. Optimizing these factors prior to
surgery can also be beneficial in reducing the risk of co-morbidity and the risk of post-operative
complications.
Pharmacists are of particular importance due to the increasing incidence of BPH with age and increasing
polypharmacy associated (multiple medications) with these patients. It is therefore important that any
drug interactions are identified, further to this, the use of concomitant anticoagulants should be
recognized to ensure that they may be held before surgery or other treatments offered to the patient
depending on co-morbidity.
Go to:
Review Questions
Figure
CT of pelvis showing multiple bladder stones in 65 year old male with benign prostatic hyperplasia.
Contributed by Patrick J. Shenot, MD
Go to:
References
1.
Roehrborn CG. Benign prostatic hyperplasia: an overview. Rev Urol. 2005;7 Suppl 9(Suppl 9):S3-
S14. [PMC free article] [PubMed]
2.
Abrams P. LUTS, BPH, BPE, BPO: A Plea for the Logical Use of Correct Terms. Rev Urol. 1999
Spring;1(2):65. [PMC free article] [PubMed]
3.
Silverman WM. "Alphabet soup" and the prostate: LUTS, BPH, BPE, and BOO. J Am Osteopath
Assoc. 2004 Feb;104(2 Suppl 2):S1-4. [PubMed]
4.
Abrams P. New words for old: lower urinary tract symptoms for "prostatism". BMJ. 1994 Apr
09;308(6934):929-30. [PMC free article] [PubMed]
5.
Roehrborn CG. Pathology of benign prostatic hyperplasia. Int J Impot Res. 2008 Dec;20 Suppl 3:S11-
8. [PubMed]
6.
Parsons JK. Benign Prostatic Hyperplasia and Male Lower Urinary Tract Symptoms: Epidemiology and
Risk Factors. Curr Bladder Dysfunct Rep. 2010 Dec;5(4):212-218. [PMC free article] [PubMed]
7.
Chughtai B, Forde JC, Thomas DD, Laor L, Hossack T, Woo HH, Te AE, Kaplan SA. Benign prostatic
hyperplasia. Nat Rev Dis Primers. 2016 May 05;2:16031. [PubMed]
8.
Foster CS. Pathology of benign prostatic hyperplasia. Prostate Suppl. 2000;9:4-14. [PubMed]
9.
Isaacs JT. Antagonistic effect of androgen on prostatic cell death. Prostate. 1984;5(5):545-57. [PubMed]
10.
Gacci M, Corona G, Vignozzi L, Salvi M, Serni S, De Nunzio C, Tubaro A, Oelke M, Carini M, Maggi M.
Metabolic syndrome and benign prostatic enlargement: a systematic review and meta-analysis. BJU
Int. 2015 Jan;115(1):24-31. [PubMed]
11.
Rohrmann S, Smit E, Giovannucci E, Platz EA. Association between markers of the metabolic syndrome
and lower urinary tract symptoms in the Third National Health and Nutrition Examination Survey
(NHANES III). Int J Obes (Lond). 2005 Mar;29(3):310-6. [PubMed]
12.
Golbidi S, Laher I. Bladder dysfunction in diabetes mellitus. Front Pharmacol. 2010;1:136. [PMC free
article] [PubMed]
13.
Kristal AR, Arnold KB, Schenk JM, Neuhouser ML, Weiss N, Goodman P, Antvelink CM, Penson DF,
Thompson IM. Race/ethnicity, obesity, health related behaviors and the risk of symptomatic benign
prostatic hyperplasia: results from the prostate cancer prevention trial. J Urol. 2007 Apr;177(4):1395-
400; quiz 1591. [PubMed]
14.
Parsons JK, Carter HB, Partin AW, Windham BG, Metter EJ, Ferrucci L, Landis P, Platz EA. Metabolic factors
associated with benign prostatic hyperplasia. J Clin Endocrinol Metab. 2006 Jul;91(7):2562-8. [PMC free
article] [PubMed]
15.
16.
De Nunzio C, Aronson W, Freedland SJ, Giovannucci E, Parsons JK. The correlation between metabolic
syndrome and prostatic diseases. Eur Urol. 2012 Mar;61(3):560-70. [PubMed]
17.
Sanda MG, Beaty TH, Stutzman RE, Childs B, Walsh PC. Genetic susceptibility of benign prostatic
hyperplasia. J Urol. 1994 Jul;152(1):115-9. [PubMed]
18.
Meikle AW, Bansal A, Murray DK, Stephenson RA, Middleton RG. Heritability of the symptoms of benign
prostatic hyperplasia and the roles of age and zonal prostate volumes in twins. Urology. 1999
Apr;53(4):701-6. [PubMed]
19.
Rohrmann S, Fallin MD, Page WF, Reed T, Partin AW, Walsh PC, Platz EA. Concordance rates and
modifiable risk factors for lower urinary tract symptoms in twins. Epidemiology. 2006 Jul;17(4):419-
27. [PubMed]
20.
Berry SJ, Coffey DS, Walsh PC, Ewing LL. The development of human benign prostatic hyperplasia with
age. J Urol. 1984 Sep;132(3):474-9. [PubMed]
21.
Platz EA, Joshu CE, Mondul AM, Peskoe SB, Willett WC, Giovannucci E. Incidence and progression of
lower urinary tract symptoms in a large prospective cohort of United States men. J Urol. 2012
Aug;188(2):496-501. [PMC free article] [PubMed]
22.
Loeb S, Kettermann A, Carter HB, Ferrucci L, Metter EJ, Walsh PC. Prostate volume changes over time:
results from the Baltimore Longitudinal Study of Aging. J Urol. 2009 Oct;182(4):1458-62. [PMC free
article] [PubMed]
23.
Wei JT, Calhoun E, Jacobsen SJ. Urologic diseases in America project: benign prostatic hyperplasia. J
Urol. 2005 Apr;173(4):1256-61. [PubMed]
24.
Kupelian V, Wei JT, O'Leary MP, Kusek JW, Litman HJ, Link CL, McKinlay JB., BACH Survery Investigators.
Prevalence of lower urinary tract symptoms and effect on quality of life in a racially and ethnically
diverse random sample: the Boston Area Community Health (BACH) Survey. Arch Intern Med. 2006 Nov
27;166(21):2381-7. [PubMed]
25.
Parsons JK, Bergstrom J, Silberstein J, Barrett-Connor E. Prevalence and characteristics of lower urinary
tract symptoms in men aged > or = 80 years. Urology. 2008 Aug;72(2):318-21. [PMC free article]
[PubMed]
26.
Stroup SP, Palazzi-Churas K, Kopp RP, Parsons JK. Trends in adverse events of benign prostatic hyperplasia
(BPH) in the USA, 1998 to 2008. BJU Int. 2012 Jan;109(1):84-7. [PubMed]
27.
Centers for Disease Control and Prevention (CDC). Trends in aging--United States and worldwide. MMWR
Morb Mortal Wkly Rep. 2003 Feb 14;52(6):101-4, 106. [PubMed]
28.
Jin B, Turner L, Zhou Z, Zhou EL, Handelsman DJ. Ethnicity and migration as determinants of human
prostate size. J Clin Endocrinol Metab. 1999 Oct;84(10):3613-9. [PubMed]
29.
Ganpule AP, Desai MR, Desai MM, Wani KD, Bapat SD. Natural history of lower urinary tract symptoms:
preliminary report from a community-based Indian study. BJU Int. 2004 Aug;94(3):332-4. [PubMed]
30.
Caine M. The present role of alpha-adrenergic blockers in the treatment of benign prostatic
hypertrophy. J Urol. 1986 Jul;136(1):1-4. [PubMed]
31.
Foo KT. Pathophysiology of clinical benign prostatic hyperplasia. Asian J Urol. 2017 Jul;4(3):152-
157. [PMC free article] [PubMed]
32.
Lepor H. Pathophysiology of benign prostatic hyperplasia in the aging male population. Rev Urol. 2005;7
Suppl 4(Suppl 4):S3-S12. [PMC free article] [PubMed]
33.
Babinski MA, Manaia JH, Cardoso GP, Costa WS, Sampaio FJ. Significant decrease of extracellular matrix
in prostatic urethra of patients with benign prostatic hyperplasia. Histol Histopathol. 2014 Jan;29(1):57-
63. [PubMed]
34.
McNeal J. Pathology of benign prostatic hyperplasia. Insight into etiology. Urol Clin North Am. 1990
Aug;17(3):477-86. [PubMed]
35.
Barry MJ, Fowler FJ, O'leary MP, Bruskewitz RC, Holtgrewe HL, Mebust WK, Cockett AT., Measurement
Committee of the American Urological Association. The American Urological Association Symptom Index
for Benign Prostatic Hyperplasia. J Urol. 2017 Feb;197(2S):S189-S197. [PubMed]
36.
Bohnen AM, Groeneveld FP, Bosch JL. Serum prostate-specific antigen as a predictor of prostate volume
in the community: the Krimpen study. Eur Urol. 2007 Jun;51(6):1645-52; discussion 1652-3. [PubMed]
37.
Djavan B, Fong YK, Harik M, Milani S, Reissigl A, Chaudry A, Anagnostou T, Bagheri F, Waldert M, Kreuzer
S, Fajkovic H, Marberger M. Longitudinal study of men with mild symptoms of bladder outlet obstruction
treated with watchful waiting for four years. Urology. 2004 Dec;64(6):1144-8. [PubMed]
38.
Gormley GJ, Stoner E, Bruskewitz RC, Imperato-McGinley J, Walsh PC, McConnell JD, Andriole GL, Geller
J, Bracken BR, Tenover JS. The effect of finasteride in men with benign prostatic hyperplasia. The
Finasteride Study Group. N Engl J Med. 1992 Oct 22;327(17):1185-91. [PubMed]
39.
Emberton M, Cornel EB, Bassi PF, Fourcade RO, Gómez JM, Castro R. Benign prostatic hyperplasia as a
progressive disease: a guide to the risk factors and options for medical management. Int J Clin
Pract. 2008 Jul;62(7):1076-86. [PMC free article] [PubMed]
40.
Roehrborn CG, Siami P, Barkin J, Damião R, Major-Walker K, Nandy I, Morrill BB, Gagnier RP, Montorsi F.,
CombAT Study Group. The effects of combination therapy with dutasteride and tamsulosin on clinical
outcomes in men with symptomatic benign prostatic hyperplasia: 4-year results from the CombAT
study. Eur Urol. 2010 Jan;57(1):123-31. [PubMed]
41.
Regadas RP, Reges R, Cerqueira JB, Sucupira DG, Josino IR, Nogueira EA, Jamacaru FV, de Moraes MO,
Silva LF. Urodynamic effects of the combination of tamsulosin and daily tadalafil in men with lower
urinary tract symptoms secondary to benign prostatic hyperplasia: a randomized, placebo-controlled
clinical trial. Int Urol Nephrol. 2013 Feb;45(1):39-43. [PubMed]
42.
43.
Yin L, Teng J, Huang CJ, Zhang X, Xu D. Holmium laser enucleation of the prostate versus transurethral
resection of the prostate: a systematic review and meta-analysis of randomized controlled trials. J
Endourol. 2013 May;27(5):604-11. [PubMed]
44.
Garcia C, Chin P, Rashid P, Woo HH. Prostatic urethral lift: A minimally invasive treatment for benign
prostatic hyperplasia. Prostate Int. 2015 Mar;3(1):1-5. [PMC free article] [PubMed]
45.
Jacobsen SJ, Jacobson DJ, Girman CJ, Roberts RO, Rhodes T, Guess HA, Lieber MM. Natural history of
prostatism: risk factors for acute urinary retention. J Urol. 1997 Aug;158(2):481-7. [PubMed]
46.
Pickard R, Emberton M, Neal DE. The management of men with acute urinary retention. National
Prostatectomy Audit Steering Group. Br J Urol. 1998 May;81(5):712-20. [PubMed]
47.
Nickel JC. Benign prostatic hyperplasia: does prostate size matter? Rev Urol. 2003;5 Suppl 4(Suppl 4):S12-
7. [PMC free article] [PubMed]
48.
Speakman MJ, Cheng X. Management of the complications of BPH/BOO. Indian J Urol. 2014
Apr;30(2):208-13. [PMC free article] [PubMed]
49.
Roehrborn CG, Bruskewitz R, Nickel GC, Glickman S, Cox C, Anderson R, Kandzari S, Herlihy R, Kornitzer G,
Brown BT, Holtgrewe HL, Taylor A, Wang D, Waldstreicher J. Urinary retention in patients with BPH
treated with finasteride or placebo over 4 years. Characterization of patients and ultimate outcomes. The
PLESS Study Group. Eur Urol. 2000 May;37(5):528-36. [PubMed]
50.
Kashif KM, Foley SJ, Basketter V, Holmes SA. Haematuria associated with BPH-Natural history and a new
treatment option. Prostate Cancer Prostatic Dis. 1998 Mar;1(3):154-156. [PubMed]
51.
Boettcher S, Brandt AS, Roth S, Mathers MJ, Lazica DA. Urinary retention: benefit of gradual bladder
decompression - myth or truth? A randomized controlled trial. Urol Int. 2013;91(2):140-4. [PubMed]
52.
Thomas S. Good practice in continence services. Nurs Stand. 2000 Aug 9-15;14(47):43-5. [PubMed]
53.
Disclosure: Krishna Baradhi declares no relevant financial relationships with ineligible companies.