Benign Prostat Hyperplasia

8326207819059 >

ISBN 978-1-905832-62-0

Fast Facts:Benign ProstaticHyperplasiaRoger S Kirby and Peter J GillingSixth edition

Fast Facts: Benign Prostatic Hyperplasia

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enig

n Pro

static Hyp

erplasia

Sixth edition

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Fast Facts

9 Pathophysiology

22 Diagnosis

40 Medical management

64 Traditional surgical treatment options

73 Minimally invasive treatment options

81 Considerations in treatment decisions

92 Future trends

© 2010 Health Press Ltd. www.fastfacts.com

Fast Facts

Fast Facts: Benign ProstaticHyperplasiaSixth edition

Roger S Kirby MA MD FRCS

Professor of Urology

The Prostate Centre

London, UK

Peter J Gilling FRACS

Head of School

Bay of Plenty Clinical School, and

Associate Professor of Surgery (Honorary)

University of Auckland

New Zealand

Declaration of IndependenceThis book is as balanced and as practical as we can make it. Ideas for improvement are always welcome: [email protected]


Fast Facts: Benign Prostatic HyperplasiaFirst published 1995; second edition 1997; third edition 1999;fourth edition 2002; fifth edition 2005Sixth edition January 2010

Text © 2010 Roger S Kirby, Peter J Gilling© 2010 in this edition Health Press LimitedHealth Press Limited, Elizabeth House, Queen Street, Abingdon, Oxford OX14 3LN, UK Tel: +44 (0)1235 523233Fax: +44 (0)1235 523238

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ISBN 978-1-905832-62-0

Kirby, RS (Roger) Fast Facts: Benign Prostatic Hyperplasia/Roger S Kirby, Peter J Gilling

Illustrated by Dee McLean, London, UK.Typesetting and page layout by Zed, Oxford, UK.Printed by Latimer Trend & Company, Plymouth, UK.

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Pathophysiology 9

Introduction 7

Glossary 5

Diagnosis 22

Medical management 40

Minimally invasive treatment options 73

Considerations in treatment decisions 81

Traditional surgical treatment options 64

Future trends 92

Useful resources 96

Index 98


5

α1-blockers: drugs that blockα1-adrenoceptors in the prostate, thereby relieving outflow obstruction(e.g. alfuzosin, doxazosin, indoramin,tamsulosin, terazosin)

5α-reductase inhibitors: drugs thatinhibit the enzyme 5α-reductase, andthus lower prostatic dihydrotestosteronelevels and can result in some decrease inprostate size (e.g. dutasteride,finasteride)

AUR: acute urinary retention

BII: BPH impact index

Bladder outlet obstruction (outflowobstruction, BOO): an obstruction inthe bladder outlet, resulting fromanatomic (e.g. BPH) or neurogeniccauses

BPE: benign prostatic enlargement

BPH: benign prostatic hyperplasia

Chemoprevention: the concept ofpreventing cancer using a drug or othercompound

CombAT: Combination of Avodart andTamsulosin. A study comparingdutasteride and tamsulosinmonotherapies anddutasteride/tamsulosin combinationtherapy

Combination therapy: the combinationof an α-blocker with a 5α-reductaseinhibitor to reduce the risk of BPHprogression

Detrusor muscle: the smooth muscle inthe bladder wall

DHT: dihydrotestosterone, the activemetabolite of testosterone

Diverticulum (plural diverticula): apouch or sac in a hollow organ, usuallythe bladder

DRE: digital rectal examination

ED: erectile dysfunction

HoLEP: holmium laser enucleation ofthe prostate

Holmium laser: a laser that permitsbloodless removal of prostate tissue

Hyperplasia: an increase in the numberof normal cells in a tissue

IPSS: International Prostate SymptomScore

Irritative symptoms: symptoms arisingfrom detrusor instability, such asurgency, frequency, nocturia and urgeincontinence

IVU: intravenous urogram

LUTS: lower urinary tract symptomsassociated with, but not always theresult of, BPH

Microscopic BPH: BPH that isdetectable only histologically

MTOPS: Medical Treatment of ProstaticSymptoms study

Nocturia: necessity to rise from bed atnight to pass urine

Obstructive symptoms: symptomsarising from outflow obstruction, suchas hesitancy, weak flow, urinaryretention and overflow incontinence

Glossary


6


PLESS: Proscar Long-term Efficacy andSafety Study

PSA: prostate-specific antigen, aglycoprotein secreted by the prostatethat acts as a marker for prostate disease

PVR: post-void residual (urine)

SMART-1: Symptom Management AfterReducing Therapy study

Stents: mesh-like structures inserted intothe prostatic urethra to maintainpatency

TRUS: transrectal ultrasonography

TUIP: transurethral incision of theprostate

TUMT: transurethral microwavethermotherapy

TUNA: transurethral needle ablation

TURP: transurethral resection of theprostate


Introduction

Benign prostatic hyperplasia (BPH), sometimes referred to as benign

prostatic enlargement (BPE), is a frequent cause of bladder outflow

obstruction (BOO) and is one of the most common diseases to affect

men beyond middle age. Histological disease (microscopic BPH) is

present in more than 60% of men in their sixties, and over 40% of men

beyond this age have lower urinary tract symptoms (LUTS) (Figure 1);

about half of this group has an impaired quality of life. The prevalence

increases with age, and thus the absolute number of patients affected

is rising worldwide as a result of aging populations. At current

intervention rates, about one-fifth of patients with symptomatic disease

who present to a doctor will eventually be treated surgically. The

remainder will often be managed initially by active surveillance

(‘watchful waiting’). However, the majority of these individuals suffer

gradual progression of symptoms and the bother associated with them,

and increasingly require treatment either with medication or surgery.

Nowadays, BPH is rarely a life-threatening condition. Deterioration of

symptoms and urinary flow is usually slow, and serious outcomes, such

as renal insufficiency, are uncommon. The risk of acute urinary retention

7

Figure 1 The incidence of both histological benign prostatic hyperplasia (BPH)

and lower urinary tract symptoms (LUTS) increases progressively with age.

Histological BPH

LUTS

40 45 50 55 60 65 70 75 80

Age (years)

100

80

60

40

20

0

Prop

ortio

n of

men

(%)


(AUR), however, increases with prostate size and severity of symptoms,

and requires urgent hospitalization and often surgery. The relatively

less serious symptoms of frequency, nocturia and incomplete bladder

emptying can nevertheless be very bothersome, and may impact

substantially on the patient’s quality of life. In addition, men with LUTS

due to BPH are also prone to sexual dysfunction, including erectile

dysfunction (ED) and disorders of ejaculation.

Extensive research into BPH in recent years has resulted not only in a

clearer understanding of its pathogenesis, but also in the development of

new medical and minimally invasive surgical treatments. At the same

time, patients’ awareness of prostate disease has increased. Today,

therefore, the choice of treatment for BPH requires a balance between

several factors:

• clinical need and considerations concerning the prevention of disease

progression and deterioration in quality of life for the individual

• the preferences of the patient and of his immediate family

• cost–benefit ratio and long-term effectiveness of therapy.

Treatment that is proven to safely enhance the quality of life has to be

tailored to the affected individual with these factors in mind.

The sixth edition of Fast Facts: Benign Prostatic Hyperplasia

provides a concise overview of the pathophysiology, diagnosis and

treatment of BPH. The latest data on the safety and efficacy of various

treatment strategies are included, as well as new preventive

considerations. The emphasis is on providing up-to-date evidence-based

and practical information that will enable the patient and the primary

care physician – who is becoming increasingly involved in the care of the

broad spectrum of prostatic diseases – to decide together the nature of

the problem and the most appropriate treatment.

8


Key references

Girman CJ, Jacobsen SJ, Rhodes T et al. Association of health-relatedquality of life and benign prostaticenlargement. Eur Urol 1999;35:277–84.

Kirby RS. The natural history ofBPH: What have we learned in thelast decade? Urology 2000;56:3–6.


The prostate consists predominantly of three distinct zones (Figure 1.1):

• a central zone

• a peripheral zone

• a transition zone, adjacent to the urethra.

1 Pathophysiology

9

Prostaticurethra

Urethra

External urethralsphincter

Prostate

Anterior commissure

Bladder

Ejaculatoryductopenings

Ejaculatoryduct

Frontal view

Sagittal view

Peripheral zone

Transition zone

Central zone

Verumontanum

Verumontanum

Figure 1.1 The prostate consists of a central zone, a peripheral zone and a

transition zone, the last of which is the usual site of development of BPH.


BPH develops almost exclusively in the transition zone, whereas

prostate cancer usually develops in the peripheral zone.

Pathogenesis The growth and development of the prostate is influenced by the male

hormone testosterone and its more active metabolite dihydrotestosterone

(DHT). The enzyme 5α-reductase is responsible for the conversion

of testosterone to DHT. It has two isoforms: type 2 5α-reductase

predominates in the prostate, whereas both type 1 and type 2

5α-reductase are common in extraprostatic tissues. BPH requires

DHT stimulation of androgen receptors; this results in the transcription

and translation of growth factors, such as epidermal growth factor

(EGF). This in turn promotes the stromal and epithelial hyperplasia

characteristics of BPH. Other factors underlying the hyperplastic

process include a reduction in programmed cell death (apoptosis)

and inflammation, which may be involved by a variety of potential

mechanisms. Transforming growth factor β (TGFβ) is one of the factors

involved in this process. Imbalance between molecules stimulating

proliferation and those inducing apoptosis results in progressive

hyperplastic enlargement of the transition zone of the prostate

(Figure 1.2). There is also a genetic component to BPH; the gene has

yet to be properly identified, but it is probably autosomal dominant.

Patients with the familial form generally have larger prostates and

undergo surgery at an earlier age.

Although BPH is often thought to be the result of glandular

proliferation, in fact up to 60% of hyperplastic tissue is composed of

smooth muscle cells and connective tissue. Contraction of these smooth

muscle cells is under the control of the sympathetic nervous system.

When norepinephrine (noradrenaline) is released from dense core

vesicles contained within the sympathetic nerve terminal, it diffuses

across the synaptic gap to bind to numerous α1-adrenoceptors located

on the membrane of prostatic smooth muscle cells. The resultant

influx of calcium increases prostatic smooth muscle tone. Several

α1-adrenoceptor subtypes are known. The α1A-subtype is the predominant

receptor in the prostate, while the α1B-subtype seems to be mainly

involved in peripheral vasoconstriction, and the α1D-adrenoceptors10



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