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Male Lower Urinary Tract Symptoms and Benign Prostatic Hyperplasia provides urologists of all levels with a practical, highly clinical guide to the variety of different symptoms and problems concerning the male lower urinary tract, including benign prostatic hyperplasia, one of the conditions that urologists most regularly encounter.
Evidence-based throughout and written by the world's leading experts in the topic, it comprehensively reviews the very latest in diagnostics and imaging, patient phenotyping, genetic studies, medical and surgical therapies, and lifestyle management in order to help clinicians best manage their patients.
Highlights include chapters on:
Containing pitfall boxes and key points throughout to aid quick and easy understanding of the key information, this excellent book is an essential read for the modern-day urologist.
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Veröffentlichungsjahr: 2014
Cover
Title page
Copyright page
Contributors
Chapter 1: Etiology and Pathogenesis
Introduction
What is BPH/LUTS? The biology
Regulation of the normal prostate
Androgen regulation of the prostate
Estrogens, progesterone, prostatic regulation, and BPH
Growth factors and chemokines in BPH/LUTS
Inflammatory changes associated with BPH
Prostate-associated Gene 4 as a stress modulator within the prostate
The need for biomarkers of BPH
Conclusions
Bibliography
Chapter 2: Lower Urinary Tract Symptoms and Benign Prostatic Hyperplasia
Introduction
Descriptive epidemiology, risk factors, and correlates
Measurement and classification of LUTS symptoms in epidemiological research: new concepts and methods
Summary and conclusion
Bibliography
Chapter 3: Clinical Assessment and Diagnosis of Lower Urinary Tract Dysfunction
Introduction
Initial evaluation of men presenting with LUTS
Evaluation of the persistent or complicated LUTS in the male patient with LUTD
Bibliography
Chapter 4: Clinical Assessment and Diagnosis of Lower Urinary Tract Symptoms/Benign Prostatic Hyperplasia
Aim of the assessment
Investigational tests
What happens in real life in Europe?
Bibliography
Chapter 5: Clinical Assessment and Diagnosis of Lower Urinary Tract Symptoms/Benign Prostatic Hyperplasia
Why should primary care be concerned?
Definitions
What are LUTS?
History, physical, and laboratory evaluation
Other modalities in assessment
Reasons for referral
Assessing bother
Summary
Bibliography
Chapter 6: Watchful Waiting
Introduction
Symptom progression
Acute urinary retention
Prostate size and growth
Bladder function changes in men over time
Renal disease and benign prostatic hyperplasia
Associations in common between chronic kidney disease and benign prostatic hyperplasia
Inflammation
Diabetes
Hypertension
Metabolic syndrome
Autonomic nervous system
Monitoring renal function in men with benign prostatic hyperplasia
End-stage renal disease
Conclusion
Bibliography
Chapter 7: α-Adrenergic Antagonists for Lower Urinary Symptoms Secondary to Benign Prostatic Hyperplasia
Introduction
α-Adrenergic receptors in the prostate
Nonselective α-blockers
Selective α-blockers
α-Adrenergic antagonists and sexual dysfunction
α
1
-blockers and intraoperative floppy iris syndrome
Combination therapy
Adverse effects of combination therapy for benign prostatic hyperplasia
Summary
Bibliography
Chapter 8: 5α-Reductase Inhibitors
Introduction and history of 5α-reductase inhibitors
Hypothetical rationale, preclinical, and early clinical (phase I–II) evidence for the use of 5α-reductase inhibitors in benign prostatic hyperplasia
Clinical evidence (phase III or higher) for the use of 5α-reductase inhibitors in benign prostatic hyperplasia
Side effects of 5α-reductase inhibitor treatment
5α-Reductase inhibitors and prostate cancer
Bibliography
Chapter 9: Antimuscarinics
Introduction
Mechanism of action
Clinical studies
Antimuscarinic safety in men with lower urinary tract symptoms/benign prostatic hyperplasia
Other important treatment issues
Practical aspects of antimuscarinic use
Conclusion
Conflict of interest
Bibliography
Chapter 10: The Use of Phosphodiesterase Type 5 Inhibitors in the Treatment of Lower Urinary Tract Symptoms Due to Benign Prostatic Hyperplasia
Introduction
Epidemiology
Lower urinary tract symptoms treatment
Pathophysiology of lower urinary tract symptoms and the phosphodiesterase-5 signal pathway
Nitric oxide synthase/cyclic guanosine monophosphate pathway
Ras homolog gene family, member A/Ras homolog-kinase signaling
Mechanism of action of phosphodiesterase-5 inhibitors in benign prostatic hyperplasia/lower urinary tract symptoms
Summary of randomized controlled trials of phosphodiesterase-5 inhibitors versus placebo
Summary of randomized controlled trials of phosphodiesterase-5 inhibitors and urodynamics
Safety
Evidence-based outcomes of alpha blocker/phosphodiesterase-5 inhibitor combination on lower urinary tract symptoms
Indications and contraindications
Limitations
Bibliography
Chapter 11: Combination Medical Therapy for Male Lower Urinary Tract Symptoms
Combination medical therapy: alpha receptor blocker + 5α-reductase inhibitor
Alpha adrenergic receptor blocker + antimuscarinics
Alpha adrenergic receptor blocker + phosphodiesterase type 5 inhibitor
Bibliography
Chapter 12: Complementary Therapy
Phytotherapy
Common compounds in phytochemicals
Selected phytotherapeutic agents
Nutrients
Exercise
Bibliography
Chapter 13: Open Simple Prostatectomy
Introduction
Open simple prostatectomy
Surgical techniques
Perioperative antibiotic prophylaxis
Minimally invasive alternatives of simple prostatectomy
Single-port transvesical enucleation of the prostate
Bibliography
Chapter 14: Minimally Invasive Therapies
Overview
Transurethral needle ablation of the prostate
Transurethral microwave thermotherapy
Transurethral ethanol ablation of the prostate
Botulinum toxin A
Bibliography
Chapter 15: Holmium Laser Prostatectomy
Introduction
Laser physics
History
Holmium laser enucleation of the prostate technique
Equipment
Procedure
Patient selection
Outcomes
Learning curve
Conclusion
Bibliography
Chapter 16: Benign Prostatic Hyperplasia
532 nm wavelength laser
60 W data
80 W data
120 W
180 W 532 nm laser
Complications
Conclusion
Bibliography
Chapter 17: Principles of Electrocautery-Based Techniques
Overview
Monopolar transurethral resection of the prostate
Early experience with monopolar electrovaporization technology
Bipolar transurethral resection of the prostate
Bibliography
Index
End User License Agreement
Chapter 02
Table 2.1 Relevant epidemiologic studies of the relationship between LUTS and ED [61]
Chapter 03
Table 3.1 Example of frequency/volume chart and voiding diary
Chapter 04
Table 4.1 Investigational tests used in the clinical assessment of lower urinary tract symptoms in Europe (mean values and range) based on surveys
Chapter 05
Table 5.1 International Prostate Symptom Score Questionnaire
Table 5.2 Male lower urinary tract symptoms
Table 5.3 Lower urinary tract symptoms: differential diagnosis and other causes
Chapter 06
Table 6.1 Various modes of presentation and possible outcomes reflecting benign prostatic hyperplasia progression
Table 6.2 Watchful waiting outcomes at 4 years
Table 6.3 Acute urinary risk factors
Table 6.4 Prostate measurement options
Table 6.5 End-stage renal disease in the US
Chapter 07
Table 7.1 Risk of benign prostatic hypertension progression as measured by American Urological Association-International Prostate Symptom Scores, rates of acute urinary retention, and requirement for surgical Intervention: tamsulosin versus dutasteride versus combination therapy
Table 7.2 Drug-related adverse events occurring in ≥1% of subjects in any treatment group in the Medical Treatment of Prostatic Symptoms trial (McConnell et al.
N Engl J Med
2003; 349:2387–2398.)
Table 7.3 Drug-related adverse events occurring in ≥1% of subjects in any treatment group in the Combination of Avodart and Tamsulosin trial
Chapter 09
Table 9.1 Pivotal 12-week randomized placebo controlled studies investigating antimuscarinics for male lower urinary tract symptoms
Chapter 10
Table 10.1 Comparison of urodynamic parameters measured in placebo versus phosphodiesterase type 5 inhibitor randomized controlled trials [37]
Chapter 11
Table 11.1 α
1
-Adrenoceptor antagonists and 5α-reductase inhibitor combination trial characteristics and subjective outcome measures
Table 11.2 α
1
-Adrenoceptor antagonists and 5α-reductase inhibitor combination objective outcome measures
Table 11.3 α
1
-Adrenoceptor antagonists and 5α-reductase inhibitor combination selected side effects
Table 11.4 α
1
-Adrenoceptor antagonist and antimuscarinic combination: International Prostate Symptom Score outcome and trial characteristics
Table 11.5 α
1
-Adrenoceptor antagonist and antimuscarinic combination side effects, postvoid residual volume increase, and acute urinary retention
Table 11.6 Studies of alpha adrenergic receptor blockers and phosphodiesterase type 5 inhibitors in the treatment of male lower urinary tract symptoms
Chapter 12
Table 12.1 Common phytochemicals used for benign prostatic hyperplasia
Table 12.2 Common compounds within phytochemical extracts
Table 12.3 Mechanisms of action of isoflavones
Table 12.4 Summary of alternative treatment options for benign prostatic hyperplasia
Chapter 13
Table 13.1 Advantages of the various open approaches of prostatectomies
Table 13.2 Surgical outcome after open simple prostatectomy [2]
Table 13.3 Morbidity and mortality rates of open simple prostatectomy [2]
Chapter 14
Table 14.1 Characteristics, efficacy, safety, and costs of minimally invasive procedures analysed
Chapter 17
Table 17.1 Studies comparing monopolar TURP (mTURP) with bipolar TURP (bTURP)
Chapter 03
Figure 3.1 Algorithms for diagnosis and management of lower urinary tract dysfunction (LUTD). AUA-SI, American Urological Association-Symptom Index; DRE, digital rectal examination; LUTS, lower urinary tract symptoms. Professor Paul Abrams International Consultation on Urological Diseases (ICUD). Reproduced with permission of Paul Abrams.
Figure 3.2 American Urological Association (AUA) Symptom Index [15]. This is the breakdown of the AUA Symptom Index. The index comprises seven questions that address voiding symptoms, storage symptoms, and nocturia. Patients are classified as having mild (0–7), moderate (8–16), or severe (17–35) urinary-tract symptoms. The International Prostate Symptom Score also includes a question assessing the degree of bother related to urinary symptoms. BPH, benign prostatic hyperplasia. (Permission granted by Elsevier Publishing).
Figure 3.3 Examples of uroflowmetry curves. This schematic shows three theoretical examples of uroflowmetry curves. The
y
-axis represents flow rate (in milliliters per second), and the
x
-axis is time (in seconds). The area under the curve represents the volume voided. A “normal” uroflow curve tends to resemble a “loaf of bread” with a rapid rise in flow rate, followed by constant flow for a time period, until a rapid drop-off in flow at the completion of the void. Patients with obstruction or detrusor underactivity tend to exhibit flattened or interrupted uroflow curves with prolonged voiding times.
Chapter 04
Figure 4.1 Algorithm of male lower urinary tract symptoms (LUTS) assessment. FVC, frequency–volume charts; PCa, prostate cancer; PVR, postvoid residual urine volume; PSA, prostate-specific antigen.
Chapter 07
Figure 7.1 Prevalence of moderate-to-severe lower urinary tract symptoms and lower urinary tract symptoms with a
Q
max
of <15 mL/s, by age. AUA, American Urological Association. Fawzy A, Pool JL. Benign Prostatic Hypertrophy and the Role of Alpha-Adrenergic Blockade. MEDSCAPE 2002. Reproduced with permission of Ahmed Fawzy, MD.
Figure 7.2 Localization of α
1
receptors. Images © Copyright Visible Health, Inc. Images © Copyright Visible Health, Inc. Created using drawMD Urology (www.drawmd.com) and reproduced with permission by Visible Health, Inc.
Figure 7.3 American Urological Association Symptom Index score improvements for medical therapies by duration of follow-up. Missing bars indicate that data were not available.
Figure 7.4 Peak urinary flow rate improvements for medical therapies by duration of follow-up. Missing bars indicate that data were not available.
Chapter 09
Figure 9.1 Overlap between voiding, storage and post-voiding lower urinary tract symptoms (LUTS) in men: most men have both voiding and storage LUTS. Adapted from Coyne KS, Sexton CC, Kopp ZS, Ebel-Bitoun C, Milsom I, Chapple C. The impact of overactive bladder on mental health, work productivity and health-related quality of life in the UK and Sweden: results from EpiLUTS. BJU international. 2011;108(9):1459–71.
Figure 9.2 Relationship between benign prostatic hyperplasia (BPH), bladder outlet obstruction (BOO) and Storage lower urinary tract symptoms (LUTS)/overactive bladder (OAB). Storage LUTS/OAB may occur due etiologies affecting bladder function not related to BPH. OAB is commonly associated with detrusor overactivity (DO) in men.
Figure 9.3 Traditional explanation for mechanism of action of antimuscarinics in patients with storage lower urinary tract symptoms (LUTS)/overactive bladder presumed secondary to detrusor overactivity. Antimuscarinics act on both the M
2
and M
3
receptors that are present in the detrusor. M
3
receptors are thought to be most important for detrusor contraction. Acetylcholine (Ach) is released from parasympathetic nerve endings then act on M
2
and M
3
receptors. Activation of M
2
receptors inhibits adenylyl cyclase which causes a reduction in intracellular cyclic AMP which is a mediator of bladder relaxation. M
3
receptor stimulation leads to activation of phospholipase C (PLC) and inositol triphosphate (IP
3
) generation which leads to intracellular Ca
2+
release and activation of the cell contractile apparatus. Reproduced from Karl-Eric Anderesson. Antimuscarinics for the treatment of overactive bladder. The Lancet Neurology. Jan 2004 with permission from Elsevier.
Figure 9.4 At usual doses antimuscarinics have a low plasma concentration allowing anatgonism of the effects of acetylcholine (ACh) in the urothelial and myocyte signaling pathways during bladder filling (“therapeutic window”) whilst not affecting detrsuor voiding contraction. When doses are increased voiding contraction may become impaired resulting in urinary retention. LUTS, lower urinary tract symptoms; OAB, overactive bladder. Adapted from Karl-Erik Andersson. Antimuscarinic Mechanisms and the Overactive Detrusor: An Update.
European Urology
, Volume 59, Issue 3, 2011, 377–386.
Figure 9.5 Simplified male lower urinary tract symptoms (LUTS) pharmacotherapy treatment algorithm.
Chapter 10
Figure 10.1 Graph showing how sexual function declines as the severity of lower urinary tract symptoms (LUTS) increases and with age. Severity of LUTS assessed by International Prognostic Scoring System: none, 0; mild, 1–7; moderate, 8–19; severe, 20–35. Rosen 2003 [3]. Reproduced with permission of Elsevier.
Figure 10.2 Decreased enjoyment of sexual activity due to lower urinary tract symptoms (LUTS): Epidemiology of Lower Urinary Tract Symptoms Study. Wein 2009 [5]. Reproduced with permission of John Wiley & Sons Ltd.
Figure 10.3 Nitric oxide synthase/nitric oxide (NOS/NO) theory of erectile dysfunction and lower urinary tract symptoms (LUTS). SMC, smooth muscle cell. McVary 2005 [27]. Reprinted with permission of MedReviews®, LLC.
Figure 10.4 Masson’s trichrome stain of urothelium in bladder tissues from control, hypercholesterolemia, moderate bladder ischemia, and severe bladder ischemia groups. Chronic moderate bladder ischemia produces marked structural damage in urothelium, causing thickening, disruption of mucosa, vacuolization, and dense fibrosis of the suburothelial layer. Severe bladder ischemia produced more extensive changes causing thickening of urothelium, distortion of mucosa, and more extensive fibrosis in the suburothelial layer. Hypercholesterolemia produced only mild regional thickening of the urothelium but did not produce any destructive changes or fibrosis of the suburothelial layer. Azadozoi 1999 [22]. Reproduced with permission of Elsevier.
Chapter 11
Figure 11.1 International Prostate Symptom Score over time for three treatment groups in the Combination of Avodart and Tamsulosin trial stratified by baseline prostate volume (PV) by tertiles (unpublished data on file at GSK). COMBO, combination; DUT, dutasteride; TAM, tamsulosin.
Figure 11.2 Incidence of acute urinary retention or benign prostatic hyperplasia-related surgery for three treatment groups in the Combination of Avodart and Tamsulosin study stratified by baseline prostate volume (PV) by tertiles. *
P
< 0.001 versus combination therapy (unpublished data on file at GSK).
Figure 11.3 Incidence rates of overall, symptomatic progression, acute urinary retention and invasive therapy in the Medical Therapy of Prostatic Symptoms study by baseline median prostate volume and serum prostate-specific antigen (PSA). AUA-SI, American Urological Association Symptom Index; AUR, acute urinary retention; BPH, benign prostatic hyperplasia; TPV, total prostate volume. Crawford [30]. Reproduced with permission of Elsevier.
Figure 11.4 International Prostate Symptom Score (IPSS) and maximum flow rate changes in studies combining alpha adrenergic receptor blockers and phosphodiesterase type 5 (PDE5) inhibitors [51]. IIEF, International Index of Erectile Function. Gacci M,
et al
. A systematic review and meta-analysis on the use of phosphodiesterase 5 inhibitors alone or in combination with alpha-blockers for lower urinary tract symptoms due to benign prostatic hyperplasia.
Eur Urol
. 2012;61(5):994–1003. Epub 2012/03/13. Reproduced with permission of Elsevier.
Chapter 13
Figure 13.1 (A) Incision of the bladder neck mucosa only from the 5- to 7-o'clock position. (B) At the apex, the index finger sweeps ventrally to fracture the anterior prostatic commissure. (C) Both lobes of the adenoma are separated in this fashion up the area of the bladder neck. Modlin C. Open Benign Prostatectomy in Novick AC et al. (eds). Operative Urology at the Cleveland Clinic. 2006 Humana Press. Reproduced with permission of Humana Press Inc.
Figure 13.2 (A) Exposure of anterior surface of the prostate and bladder neck. (B) Horizontal incision through the prostatic capsule with a steel or electric knife. (C) Index finger is inserted through this incision and the adenoma enucleated with a sweeping motion. Modlin C. Open Benign Prostatectomy in Novick AC et al. (eds). Operative Urology at the Cleveland Clinic. 2006 Humana Press. Reproduced with permission of Humana Press Inc.
Chapter 17
Figure 17.1 Schematic diagram of traditional monopolar transurethral resection of the prostate (top) vs. bipolar transurethral resection of the prostate (bottom). Olympus. Reproduced with permission of Olympus America Inc.
Figure 17.2 Olympus PlasmaKinetic™ SuperPulse bipolar current generator with cut and coagulation foot pedal. Olympus. Reproduced with permission of Olympus America Inc.
Figure 17.3 Olympus OES Pro Resectoscope apparatus with continuous flow sheath. Olympus. Reproduced with permission of Olympus America Inc.
Figure 17.4 Olympus PlasmaButton™ vaporization electrode inside of continuous flow resectoscope sheath. Olympus. Reproduced with permission of Olympus America Inc.
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Edited by
Steven A. Kaplan, MD
E. Darracott Vaughan Jr. Professor of Urology
Weill Cornell Medical College
Director, Iris Cantor Men’s Health Center
New York Presbyterian Hospital
New York, NY, USA
Kevin T. McVary, MD, FACS
Professor and Chair
Division of Urology
Southern Illinois University School of Medicine
Springfield, IL, USA
This edition first published 2014 © 2014 by John Wiley & Sons, Ltd
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Library of Congress Cataloging-in-Publication Data
Male lower urinary tract symptoms and benign prostatic hyperplasia / edited by Steven A. Kaplan, Kevin T. McVary. p. ; cm. Includes bibliographical references and index.
ISBN 978-1-118-43799-5 (cloth) I. Kaplan, Steven A., editor. II. McVary, Kevin T., editor. [DNLM: 1. Lower Urinary Tract Symptoms. 2. Prostatic Hyperplasia. WJ 752] RC877 616.6′5–dc23
2014013140
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.
Cover image: ©iStockphoto/ArtopatCover design by Andy Meaden
Aaron M. Bernie, MD, MPHDepartment of UrologyWeill Cornell Medical CollegeNew York-Presbyterian HospitalNew York, NY, USA
Benjamin N. Breyer, MD, MASUniversity of California San FranciscoDepartment of UrologySan Francisco, CA, USA
Reginald Bruskewitz, MDUniversity of WisconsinMadison, WI, USA
Christopher R. Chapple, BSc, MD, FRCS(Urol)Department of UrologyRoyal Hallamshire HospitalSheffield, UK
Bilal Chughtai, MDDepartment of UrologyWeill Cornell Medical CollegeNew York-Presbyterian HospitalNew York, NY, USA
Anne Darves-Bornoz, MDGarden CityNew York, NY, USA
Jean J. M. C. H. de la Rosette, MD, PhDDepartment of UrologyAcademic Medical CenterUniversity of AmsterdamAmsterdam, The Netherlands
Christopher P. Filson, MD, MSUniversity of MichiganDepartment of UrologyDivision of Health Services ResearchAnn Arbor, MI, USA
Nathaly François, MDDivision of UrologySouthern Illinois University School of MedicineSpringfield, IL, USA
Claudius Füllhase, MDDepartment of UrologyGroßhadern HospitalLudwig-Maximilians-UniversityMunich, Germany
Mauro Gacci, MDDepartment of UrologyUniversity of FlorenceCareggi HospitalFlorence, Italy
Robert H. Getzenberg, PhDGTx Inc.Memphis, TN, USA
Peter J. Gilling, MBChB, MD, FRACSUniversity of AucklandUrology BOP LimitedTauranga, New Zealand
Christian Gratzke, MDDepartment of UrologyLMU MunichMunich, Germany
Stavros Gravas, MDDepartment of UrologyUniversity of ThessaliaLarissa, Greece
Annika Herlemann, MDDepartment of UrologyLMU MunichMunich, Germany
Aaron E. Katz, MDGarden CityNew York, NY, USA
Prakash Kulkarni, PhDJames Buchanan Brady Urological InstituteJohns Hopkins University School of MedicineBaltimore, MD, USA
Richard Lee, MD MBADepartments of UrologyWeill Cornell Medical CollegeNew York-Presbyterian HospitalNew York, NY, USA
Casey Lythgoe, MDDivision of UrologySouthern Illinois University School of MedicineSpringfield, IL, USA
Marty M. Miner, MDWarren Alpert School of MedicineBrown University, Providence, RI, USA
Matthias Oelke, MD, FEBUDepartment of UrologyHannover Medical SchoolHannover, Germany
Nadir I. Osman, MBChB, MRCSDepartment of UrologyRoyal Hallamshire HospitalSheffield, UK
Raunak D. Patel, MSDivision of UrologySouthern Illinois University School of MedicineSpringfield, IL, USA
John B. RileyMid Michigan Health CentersJackson, MI, USA
Claus G. Roehrborn, MDDepartment of UrologyUT Southwestern Medical CenterDallas, TX, USA
Raymond C. Rosen, PhDNew England Research InstitutesWatertown, MA, USA
Matt T. Rosenberg, MDMid Michigan Health CentersJackson, MI, USA
Matteo Salvi, MDDepartment of UrologyUniversity of FlorenceCareggi HospitalFlorence, Italy
Arcangelo Sebastianelli, MDDepartment of UrologyUniversity of FlorenceCareggi HospitalFlorence, Italy
Roberto Soler, MD, PhDDivision of UrologyFederal University of São PauloSão Paulo, Brazil
Alexis E. Te, MDDepartment of UrologyWeill Cornell Medical CollegeNew York-Presbyterian HospitalNew York, NY, USA
Simon van Rij, MBChB, FRACSTauranga HospitalTauranga, New Zealand
John T. Wei, MD, MSUniversity of MichiganDepartment of UrologyDivision of Health Services ResearchAnn Arbor, MI, USA
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