Male Sexual Dysfunction E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 1038

Veröffentlichungsjahr: 2016

Beschreibung

Sexual dysfunction affects men of all ages and incidence rates are expected to double by 2025 resulting in a major health burden. Though normal sexual function is an important aspect of health and well-being, sadly, this common condition still carries an associated stigma. As a result, affected men are often reluctant to approach their doctor and, instead, may live for many years with sexual dysfunction, often to the detriment of their personal lives.

Male Sexual Dysfunction: A Clinical Guide covers all the common problems encountered by the clinician in this rapidly expanding and developing field. With full color throughout, this easy to read guide provides a comprehensive and systematic approach to patient management. Packed with key features, every chapter will contain flow diagrams and algorithms, key points, clinical pearls, �what to avoid� boxes, and numerous tables, graphs and photographs . This book provides:

• Comprehensive focus on the core clinical areas of physiology/pharmacology, investigation, diagnosis, management and surgical options
• Coverage of all treatment pathways, including psychological, pharmacologic and surgical
• A straightforward, logical approach to clinical management
• An experienced and international editor and contributor team

Expertly-written, this book is the perfect resource for urologists and general practitioners with an interest in this highly topical area, as well as those about to undergo their urology trainee examinations.

Leseprobe

Table of Contents

Cover

Title Page

List of contributors

Foreword

CHAPTER 1: Epidemiology of male sexual dysfunction

Erectile dysfunction

Premature ejaculation

Peyronie’s disease

Hypogonadism

References

CHAPTER 2: Physiology of ejaculation

Introduction

The spinal cord and the brain of male rats

Peripheral nerves and ejaculation

Emission and the autonomic nervous system

Expulsion and the somatic nervous system

The central nervous system and ejaculation

Orgasm

References

CHAPTER 3: Physiology of penile erection

Functional anatomy

Hemodynamics of penile erection and detumescence

Neurophysiology of erections

Smooth muscle physiology

Summary

Further reading

CHAPTER 4: Anatomy of penile erection

Introduction

Penile anatomy

Neuroanatomy of penile erection

Hemodynamics and physiology of male erection

Molecular mechanisms of penile erection

Conclusions

References

CHAPTER 5: Endocrinology of male sexual dysfunction

Introduction

Central organization of sexual function

The kisspeptin‐GPR54‐neurokinin B pathway and regulation of GnRH release

Effect of gonadotropins at testicular level

Testosterone action in male sexual function

Endocrine disorders

Late‐onset hypogonadism

Treatment of sexual dysfunction associated with endocrinopathy

References

CHAPTER 6: Pharmacology of drugs used for the treatment of erectile dysfunction

Introduction

Oral agents

Intracavernosal agents

Other agents

Summary

References

CHAPTER 7: Pharmacology of drugs used in premature ejaculation

“Selective” neurotransmitter reuptake inhibitors

Use of locally active agents

Other potential “broad spectrum” approaches

Coming next?

Summary

References

CHAPTER 8: Cardiovascular risk and erectile dysfunction

Erectile dysfunction and cardiovascular disease: examining the link

The temporal relationship

Prediction of CVD events and mortality

Methods of evaluating the risk

Conclusion

A final thought…

References

CHAPTER 9: The evaluation of the patient with erectile dysfunction

Introduction

Sexual history

The physical examination

Questionnaires

Current guidelines

Laboratory investigations in the man presenting with ED: the key role of the GP

Specialist investigations

Penile abnormalities

Patient/partner education – consultation and referrals

Indications for secondary referral

Problems associated with prescribed drugs

The role of lifestyle modification

Current prescribing issues in ED

The role of testosterone replacement in ED

Conclusion

References

CHAPTER 10: Endocrinological investigation of men with erectile dysfunction

Introduction

Hypogonadism

Prolactin

Thyroid hormones

Other hormones

Obesity

Type 2 diabetes mellitus

Conclusion

References

CHAPTER 11: Duplex ultrasonography and its role in the assessment of male sexual dysfunction

Introduction

Uses of penile Doppler

Penile ultrasonographic anatomy

Standard operating technique

How to scan

Findings

References

CHAPTER 12: MRI in men with sexual dysfunction

Introduction

Scanning protocol and radiological anatomy

Penile fracture

Priapism

Fibrosis and Peyronie’s disease

Penile implants

Other conditions

References

CHAPTER 13: The metabolic syndrome and ED

Introduction

The metabolic syndrome: a cluster of findings increasing the risk of type 2 DM and CVD: its relationship to ED

Novel biomarkers (metabolic and imaging) to clarify CVS risk in the ED patient

Conclusion

References

CHAPTER 14: Psychological assessment of patients with ED

Introduction

Psychosocial impact of ED

Psychological assessment of patients with ED

Making referrals

Questionnaires

References

CHAPTER 15: Nocturnal penile tumescence study

Introduction

Investigation

Conclusion

References

CHAPTER 16: Psychosexual therapy for male sexual dysfunction

Introduction

Psychosexual therapy

Treatments

Erectile dysfunction: case examples using sex therapy techniques

Ejaculatory dysfunction

PLISSIT: a sexuality assessment and intervention tool

Conclusion

References

CHAPTER 17: Treatment of premature ejaculation and ejaculatory disorders

Introduction

Definition of premature ejaculation

Epidemiology and etiology of premature ejaculation

Treatment of premature ejaculation

Anejaculation

Delayed ejaculation

Retrograde ejaculation

Painful ejaculation

References

CHAPTER 18: Erectile dysfunction and infertility

Differences and common links between male infertility and erectile dysfunction

The impact of infertility on erectile dysfunction

Overview of the evaluation of erectile dysfunction

Treatment considerations for erectile dysfunction

Erectile dysfunction treatment for infertile men

Conclusion

References

CHAPTER 19: Drug therapy for erectile dysfunction

General approach to drug therapy

Pharmacological therapies

Intracavernosal injection therapy

Intraurethral therapy

Topical therapies

Future therapies for erectile dysfunction

Conclusion

References

CHAPTER 20: Priapism

Epidemiology and pathophysiology of priapism

Clinical assessment of the patient with priapism

Management of priapism

Conclusions

References

CHAPTER 21: Management of erectile dysfunction after pelvic surgery

Introduction

Mechanisms of erectile dysfunction

Treatment of erectile dysfunction

Conclusion

References

CHAPTER 22: Management of erectile dysfunction in men with diabetes

Introduction

Pathophysiology

Assessment and investigation

Treatment

Conclusion

References

CHAPTER 23: Management of erectile dysfunction in neurological patients

Neurological disorders and sexual dysfunction

Management of ED in the neurological patient

Conclusion

Acknowlegdements

References

CHAPTER 24: Non‐surgical therapy for Peyronie’s disease

Oral therapies in Peyronie’s disease

Topical agents

Injectable agents

Mechanical devices

Conclusion

References

CHAPTER 25: Micropenis and penile dysmorphobia: diagnosis, management, outcomes, and future developments in the field

Introduction

Causes of micropenis

Congenital micropenis

Assessment

Acquired micropenis

Treating micropenis

Techniques for the future

Penile dysmorphobia

References

CHAPTER 26: Surgical treatment of Peyronie’s disease

Introduction

Etiology and pathogenesis

Course of the disease

Diagnosis and evaluation

Medical treatment

Surgical treatment

Conclusion

References

CHAPTER 27: Penile implant surgery

Introduction

Indications

Types of prostheses

Preoperative counseling and surgical planning

Surgical technique

Complications

Outcomes

Conclusion

References

CHAPTER 28: Vascular surgery for erectile dysfunction

Introduction

Penile vascular anatomy

Arterial revascularization

Surgery for corporal veno‐occlusive dysfunction (CVOD)

Endovascular techniques

Conclusion

References

CHAPTER 29: Penile cancer

Introduction

Penile preserving surgery (PPS)

Carcinoma in situ (Tis) and non‐invasive verrucous carcinoma (Ta)

Tumor invading the subepithelium (T1) or corpus spongiosum (T2)

Tumor invading the corpus cavernosum (T2) or the urethra (T3)

Tumor invading adjacent structures (T4)

Summary

References

CHAPTER 30: Penile reconstruction and trauma

Introduction

Surgical principles

Skin grafting

Glans resurfacing of the penis

Male genital lichen sclerosus (LS)/balanitis xerotica obliterans (BXO)

Technique of glans resurfacing and SSG

Buried penis

Male genital lymphedema

Peyronie’s disease

Reconstruction following trauma

Summary

References

CHAPTER 31: Disorders of sex development

Introduction

Gonadal dysgenesis

Failure of androgen synthesis or receptors

Anti‐müllerian syndrome

Other anatomical disorders

Testicular regression syndromes

Other chromosomal anomalies

References

CHAPTER 32: Sexual dysfunction and prostate cancer therapy

Introduction

Sexual dysfunction

Preoperative sexual function and treatment – can outcome be predicted?

Radical prostatectomy

Penile rehabilitation after radical prostatectomy

Radiotherapy and brachytherapy

Androgen deprivation therapy (ADT)

Active surveillance

Ablative therapy

Conclusion

References

CHAPTER 33: Assessment and management of the male to female transgender patient

Background

Legislation and guidelines

The UK pathway

Male‐to‐female genital reconstructive surgery

Surgical complications

Non‐genital surgery

Follow‐up and patient satisfaction

References

Index

End User License Agreement

List of Tables

Chapter 05

Table 5.1 Classification of disorders that may be associated with endocrine and sexual dysfunction.

Table 5.2 Conditions associated with alterations in sex hormone‐binding globulin (SHBG) concentrations.

Chapter 06

Table 6.1 Affinity and selectivity of the phosphodiesterase type 5 (PDE5) inhibitors.

Table 6.2 Tissue distribution of the phosphodiesterase enzymes.

Table 6.3 Pharmacokinetics of the PDE5 inhibitors.

Chapter 08

Table 8.1 Erectile dysfunction (ED) predicts coronary events.

2

The younger the age group, the greater the cardiovascular risk from ED. In men in their 40s who have ED at baseline, cardiovascular risk over a 10‐year follow‐up is 50‐fold greater than men who have normal erections.

Table 8.2 Artery size and atherothrombosis. A significant restriction to flow in the penile arteries may be subclinical in larger vessels.

Table 8.3 Relative risk of increased events and mortality: erectile dysfunction (ED vs no ED).

Chapter 09

Table 9.1 Relative risks for men with erectile dysfunction.

Table 9.2 Further investigations to evaluate the man with erectile dysfunction (ED).

Chapter 10

Table 10.1 More and less specific clinical, biochemical, and instrumental parameters associated with hypogonadism.

Chapter 12

Table 12.1 Common MR sequences used in imaging the penis.

Chapter 14

Table 14.1 Scales that measure anxiety and distress.

Chapter 16

Table 16.1 Checklist for assessment of premature ejaculation (PE).

Table 16.2 Checklist for assessment of delayed ejaculation (DE).

Chapter 17

Table 17.1 Summary of the symptoms of the four premature ejaculation (PE) syndromes used in the classification of men with complaints of PE.

15

Table 17.2 Treatment options for the management of premature ejaculation (PE).

Table 17.3 Causes of retarded ejaculation.

63

Table 17.4 Adjunctive pharmacotherapy for SSRI‐induced retarded ejaculation.

64

Chapter 18

Table 18.1 Causes and distribution of male infertility.

Table 18.2 Classification of causes of erectile dysfunction.

Table 18.3 Etiologies common to male infertility and erectile dysfunction (ED).

Chapter 19

Table 19.1 Selection of drugs reported to cause erectile dysfunction as a side effect.

Table 19.2 Characteristics of three major phosphodiesterase inhibitors.

Table 19.3 Management of phosphodiesterase‐5 (PDE5) inhibitor non‐responders.

Table 19.4 Adverse events and efficacy reporting.

Table 19.5 Common drug therapies for erectile dysfunction.

Table 19.6 Contraindications to erectile dysfunction medications.

Chapter 20

Table 20.1 Etiology of ischemic priapism.

Table 20.2 Blood gas values.

Chapter 21

Table 21.1 Pharmacokinetics of phosphodiesterase type 5 inhibitors (PDE5i).

Table 21.2 Characteristics of erectile aids.

Chapter 22

Table 22.1 Pharmacokinetic data for sildenafil, tadalafil, and vardenafil.

Chapter 23

Table 23.1 The multidimensional nature of sexual dysfunction following neurological disease. Adapted from (6)

Table 23.2 Medications used in the management of neurological symptoms may contribute to sexual dysfunction. Adapted from (17)

Chapter 24

Table 24.1 Vascular risk factors in Peyronie’s disease.

Chapter 25

Table 25.1 Etiology of micropenis.

Table 25.2 Penile dimensions for normal adults.

Table 25.3 Mean stretched penile length (cm) in normal children.

Chapter 27

Table 27.1 Available penile prostheses.

Chapter 29

Table 29.1 Factors involved in deciding on the most appropriate method of treating the primary penile lesion tailored to the individual.

Table 29.2 Treatment options by stage: oncological outcome and effect on sexual function.

Chapter 30

Table 30.1 Techniques used to bridge soft tissue defects during reconstruction.

Table 30.2 Outcomes for glans resurfacing for lichen sclerosus (LS).

Table 30.3 The etiology and techniques of increasing relative penile length as a treatment for buried penis.

Chapter 31

Table 31.1 Classification of disorders of sex development (DSD).

Table 31.2 Sexual Function with a small penis.

List of Illustrations

Chapter 03

Figure 3.1 Pathways regulating smooth muscle contraction, which leads to detumescence.

Figure 3.2 Cellular pathways regulating smooth muscle relaxation necessary for tumescence.

Chapter 04

Figure 4.1 Ventral view of penile anatomy. The corpus spongiosum contains the urethra and lies within the groove between the two corpora cavernosa. The bulbar and urethral arteries are the first branches of the penile artery. The dorsal artery and nerve course lateral to the dorsal vein of the penis.

Figure 4.2 Cross‐sectional view of penile anatomy. The three erectile bodies (two corpora cavernosa and midline corpus spongiosum) are surrounded by the tunica albuginea, which is composed of an inner circular layer and an outer longitudinal layer. The subsequent layers of the penis from deep to superficial are penile fascia, deep (Buck’s) fascia, superficial (dartos fascia), and skin. The superficial dorsal vein courses through dartos fascia, and the deep dorsal vein runs through Buck’s fascia.

Figure 4.3 Molecular mechanisms of penile smooth muscle relaxation. Nitric oxide is released from endothelial cells (eNOS) and neurons (nNOS). NO diffuses to the cytoplasm of smooth muscle cells leading to activation of its intracellular receptor, guanylyl cyclase. This binding activates guanylyl cyclase leading to the conversion of guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP). Through cGMP‐specific protein kinases cytosolic calcium levels decrease, leading to cavernosal smooth muscle relaxation. PDE5, phosphodiesterase type 5.

Chapter 05

Figure 5.1 Schematic diagram of the hypothalamic‐pituitary‐gonadal axis showing neural systems that regulate gonadotropin‐releasing hormone (GnRH) secretion and feedback of gonadal steroid hormones at the level of the hypothalamus and pituitary. CNS, central nervous system; CRH, corticotropin‐releasing hormone; FSH, follicle‐stimulating hormone; GABA, gamma‐aminobutyric acid; GALP, galanin‐like peptide; LH, luteinizing hormone; NE, norepinephrine; NPY, neuropeptide Y.

Figure 5.2 Schematic diagram showing the neuroanatomy of the kisspeptin‐GnRH pathway and the relationship between KNDy neurons and GnRH neurons in humans. Kisspeptin signals directly to the gonadotropin‐releasing hormone (GnRH) neurons, which express kisspeptin receptor. The location of kisspeptin neuron populations within the hypothalamus is species specific, residing within the preoptic area (POA) and the infundibular nucleus in humans. Kisspeptin neurons in the infundibular nucleus co‐express neurokinin B and dynorphin (KNDy neurons), which via neurokinin B receptor and kappa opioid peptide receptor autosynaptically regulate pulsatile kisspeptin secretion, with neurokinin B being stimulatory and dynorphin inhibitory. In humans, KNDy neurons in the infundibular nucleus relay both negative (red) and positive (green) sex steroid feedback. The role of the POA kisspeptin population in mediating sex steroid feedback in humans is incompletely explored. ME, median eminence; –, stimulatory; 2, inhibitory; ERα, estrogen receptor alpha; PR, progesterone receptor; Kiss1/KiSS1, kisspeptin; NKB, neurokinin B; Dyn, dynorphin. LH, luteinizing hormone; FSH, follicle‐stimulating hormone.

Figure 5.3 Production, transport, and metabolism of biologically active androgens. Testosterone is predominantly derived from the testis and is mainly bound to transport proteins in the circulation. In peripheral tissues it is metabolized or converted to other active steroids such as dihydrotestosterone or estradiol.

Figure 5.4 Schematic representation of the biochemical events leading to

a)

penile flaccidity or

b)

erection.

a)

Penile flaccidity: Noradrenaline (NA) binding generates inositol 1,4,5‐trisphosphate (InsP

3

), which, by increasing intracellular calcium (Ca

2+

) levels, activates Ca

2+

‐sensitive chloride channels (CLCAs), resulting in membrane depolarization with the diffusion of the stimulus to the neighboring cells and the opening of voltage‐operated channels (VOC). The increased Ca

2+

flow promotes, through calmodulin, activation of myosin light chain (MLC) kinase (MLCK) and cell contraction. Cell contraction is also obtained by altering the Ca

2+

sensitivity through a NA‐induced activation of a second pathway, RhoA/ROCK, which increases, through a series of kinase activations, the sensitivity of MLC to Ca

2+

. Testosterone is considered to negatively regulate the latter event.

b)

Penile erection: Nitric oxide (NO) diffuses into smooth muscle cells (SMC) and activates a soluble guanylate cyclase (sGC), which in turn transforms guanosine triphosphate (GTP) into cyclic guanosine monophosphate (cGMP). Cyclic GMP activates protein kinase G (PKG), which through the indicated pathways, finally decreases intracellular Ca

2

+ levels, leading to relaxation. Phosphodiesterase type 5 (PDE5) metabolizes cGMP into GMP, thereby limiting its effects. Testosterone enhances PDE5 activity. Other abbreviations: CPI‐17, protein phosphatase 1 regulatory, subunit 14A; eNOS, endothelial nitric oxide synthase; GAP, GTPase activating protein; GEF, guanine nucleotide exchange factor; MLCP, myosin light chain phosphatase; nNOS, neuronal nitric oxide synthase; PLC, phospholipase C; RhoA, Ras homolog gene family member A; ROCK, Rho‐associated coiled‐coil containing protein kinase; SR, sarcoplasmic reticulum.

Figure 5.5 Hypogonadism due to alterations in the hypothalamic‐pituitary‐testicular axis.

a)

Primary hypogonadism due to testicular disease. Classically, this results in both androgen deficiency and impairment of sperm production and elevated luteinizing hormone (LH) and follicle‐stimulating hormone (FSH) levels (hypergonadotrophic hypogonadism) due to loss of negative feedback regulation of gonadotropins. GnRH, gonadotropin‐releasing hormone; T, testosterone.

b)

Secondary hypogonadism due to hypothalamic and/or pituitary disease. This manifests as both androgen deficiency and impairment of sperm production and inappropriately normal or low LH and FSH levels (hypogonadotrophic hypogonadism).

Figure 5.6 Macroadenoma of the pituitary, with large suprasellar extension, causing secondary hypogonadism, and other features of hypopituitarism.

Figure 5.7 Clinical features of hypogonadism. A 32‐year‐old man with severe androgen deficiency caused by Kallmann’s syndrome (hypogonadotrophic hypogonadism and anosmia) who presented with poor sexual function, sparsity of body hair, and poorly developed secondary sexual characteristics and 3 cc testes. Luteinizing hormone <1.0; follicle‐stimulating hormone 0.4; testosterone level 1.2 U/L.

Figure 5.8 Right‐sided macroprolactinoma with extension into the right cavernous sinus causing a right sixth nerve palsy, and galactorrhea. Prolactin 33,400 mU/L (nomolar range <360).

Figure 5.9 Hypothalamo‐pituitary‐testicular axis and potential sites of therapeutic disruption. AR, androgen receptor; DHT, dihydrotestosterone; LH, luteinizing hormone; LHRH, luteinizing hormone releasing hormone.

Figure 5.10 Investigation and management of suspected hypogonadism. FSH, follicle‐stimulating hormone; GnRH, gonadotropin‐releasing hormone; hCG, human chorionic gonadotropin; LH, luteinizing hormone; MRI, magnetic resonance imaging; T, testosterone.

Chapter 07

Figure 7.1 The neurophysiology of ejaculation in the human male. ACh, acetylcholine; Bulbospongiosus muscle; D2, dopamine D2 receptors; 5‐HT, 5‐hydroxytryptamine (serotonin) receptors; NA; NO, nitric oxide; OT, oxytocin receptors.

Chapter 08

Figure 8.1 Angiogram identifies critical right coronary artery stenosis.

Figure 8.2 Successful stent insertion into right coronary artery as shown in Figure 8.1.

Figure 8.3 Algorithm for assessing cardiovascular disease (CVD) following a diagnosis of erectile dysfunction. Cardiac Computed Tomography Angiograph (CCTA).

Chapter 09

Figure 9.1 Management of erectile dysfunction (ED) in all men with ED, especially those with known cardiovascular disease.

a

Sexual activity is equivalent to walking 1 mile on the flat in 20 minutes or briskly climbing two flights of stairs in 10 seconds.

b

Sexual activity is equivalent to 4 minutes of the Bruce treadmill protocol.

Figure 9.2 Algorithm for androgen therapy in a man presenting with erectile dysfunction (ED). PDE5I, phosphodiesterase type 5 inhibitor; T, testosterone.

Chapter 10

Figure 10.1 Prevalence of endocrinological problems as derived from a consecutive series of 4388 subjects seeking medical care for sexual dysfunction at our unit between 2000 and 2013. Hyperprolactinemia (circulating prolactin levels >420 mU/L or 20 ng/mL) was considered mild (prolactin levels 420–735 mU/L, or 20–35 ng/mL) or severe (prolactin levels >735 mU/L, or 35 ng/mL) as previously reported.

18,19

Gonadal status was identified according to the European Male Aging Study criteria: normal or eugonadal (testosterone ≥10.5 nmol/L and luteinizing hormone ≤9.4 U/L); secondary hypogonadism (testosterone <10.5 nmol/L and luteinizing hormone ≤9.4 U/L); primary hypogonadism (testosterone <10.5 nmol/L and luteinizing hormone >9.4 U/L); and compensated hypogonadism (testosterone ≥10.5 nmol/L and luteinizing hormone >9.4 U/L).

9

Subclinical hypo‐ and hyperthyroidism were defined when TSH values were outside the reference ranges (0.4–4.5 mU/L) with normal free thyroid hormones. Overt hypo‐ and hyperthyroidism were defined when both TSH and free thyroid hormone values were outside the reference ranges.

Figure 10.2 Algorithm for the diagnosis of testosterone deficiency. PRL, prolactin; cFT, calculated free testosterone; TT, total testosterone; LH, luteinizing hormone; SHBG, sex hormone‐binding globulin.

Chapter 11

Figure 11.1 Longitudinal image of the penis at the level of the penoscrotal junction (evident by the slight dorsal curvature of the penis) showing an accessory cavernosal artery that, in this patient, forms the dominant supply to the penis (red arrow). This was discovered after abnormally low values for peak systolic velocity (PSV) were seen at the level of the crura in the setting of a normal erection, illustrating the importance of looking for accessory vessels. Also visible (white arrow) is the dorsal artery, which lies outside of the tunica.

Figure 11.2

a)

Axial image of the flaccid penis at the midshaft level immediately following intracorporal injection of alprostadil showing increased echogenic material within the corporal tissue close to the ventral tunica. This should not be confused with calcified plaque, and reinforces the importance of scanning preinjection.

b)

Axial image of the same patient at the same level 15 minutes later demonstrating almost complete dispersal of the drug (scattered echogenic foci in the left corpus are all that remain).

Figure 11.3

a‐f Clockwise from top left.

a)

Longitudinal and

b)

axial: B‐mode ultrasound of the distal penis showing a classical appearing non‐calcified plaque on the dorsal tunical surface that appears as a focus of thickening (defined by the calipers).

c)

Longitudinal view of the midshaft showing a dorsal curvature cause by a non‐calcified plaque (defined by arrows).

d)

Axial view of the midshaft demonstrating fibrosis of the right corpus cavernosum as shown by the reduced caliber compared to the left and the focus of increased echogenicity.

e)

Longitudinal view of the midshaft showing marked wasting of the corpus caused by a combination of tunica plaque and intracorporal fibrosis.

f)

Axial ultrasound of the midshaft showing two adjacent calcified plaques with post‐acoustic shadowing involving the ventral tunica and septum (defined by calipers 1 and 2).

Figure 11.4 Waveforms. ED, end diastole; EDV, end‐diastolic velocity; PS, peak systole; PSV, peak systolic velocity.

Figure 11.5

a)

Longitudinal view of the cavernosal artery 30 minutes post‐injection of alprostadil showing a normal peak systolic velocity (97 cm/s) but with sustained, high end‐diastolic velocity of 30 cm/s (low resistance) suggestive of veno‐occlusive dysfunction. The patient had 70% tumescence.

b)

Cavernosography in the same patient revealed early filling of the periprostatic plexus and pelvic veins consistent with a venous leak.

Figure 11.6

a)

Longitudinal view of the penis at the penoscrotal junction showing a large fistula between the main cavernosal artery and the venous sinusoids as demonstrated by a focal area of turbulent flow in the corporal substance. Spectral trace shows both high peak systolic and high end‐diastolic velocities consistent with a low resistance pattern seen in non‐ischemic priapism.

b)

Longitudinal view at the level of the penoscrotal junction demonstrating the classically described ischemic waveform, which is low flow and high resistance. The calipers are positioned over the main cavernosal artery. The expanded corpora indicate tumescence, and the heterogeneity suggests early fibrosis.

c)

Longitudinal view of the penis in a second patient with ischemic priapism. This demonstrates very high peak systolic velocity (1.5 m/s) but crucially there is reversed flow in diastole, which clearly distinguishes it from both the high‐flow, low‐resistance waveform in image

a

(non‐ischemic priapism) and image

b

(classical ischemic priapism).

Chapter 12

Figure 12.1

a)

T2 sagittal and

b)

T1 post‐contrast images in a man with low‐flow priapism. Note in

a)

the normal corrugations (short white arrow) and the normal urethra (black arrow). Also, Buck’s fascia (long white arrow) is seen as a slightly higher signal layer than the adjacent (deeper) tunica albuginea. The T2 image shows low signal in the corpus cavernosum proximally, and high signal distally, but this does not correlate with the degree of infarction. For this, the post‐contrast image

b)

obtained at 8 min is necessary: it shows generally no enhancement in the corpora cavernosa (long arrows), except around the proximal cavernosal arteries (short white arrows). The patient went on to have a penile implant the same week, with a good functional outcome.

Figure 12.2

a)

T2 axial and

b)

sagittal images of a penile implant.

a)

This shows the two cavernosal components (long white arrows) lying in the left corpus cavernosum (true crossover). Note the periarterial post‐priapism fibrosis in the right corpus cavernosum (black arrow) and the normal urethra (short white arrow). The sagittal image in

b)

shows a “kink” at the point where the right cavernosal component crosses over to the left (long white arrow).

Chapter 15

Figure 15.1 A normal NPT trace.

Figure 15.2 An abnormal NPT trace.

Chapter 16

Figure 16.1 Annon’s PLISSIT model.

Chapter 18

Figure 18.1 Algorithm for the diagnostic evaluation of erectile dysfunction (ED).

Figure 18.2 Princeton III Consensus Panel recommendations for management of erectile dysfunction (ED) in cardiovascular disease (CVD).

a

Sexual activity is equivalent to walking one mile on flat surface in 20 minutes or briskly climbing two flights of stairs in 10 seconds.

b

Sexual activity is equivalent to four minutes of the Bruce treadmill protocol. Low‐risk patients are those able to perform exercise of moderate intensity without symptoms. This group also includes patients with a history of successful revascularization, asymptomatic controlled hypertension, mild valvular dysfunction, and left ventricular dysfunction (New York Heart Association (NYHA) class I and II). High‐risk patients are those with moderate to severe cardiac symptoms, including unstable angina pectoris, uncontrolled hypertension, congestive heart failure (NYHA class IV), recent myocardial infarction (MI; <2 weeks), high‐risk arrhythmia, severe cardiomyopathy, and moderate to severe valve disease.

Figure 18.3 Treatment algorithm for management of erectile dysfunction (ED). BPH, benign prostatic hyperplasia; LUTS, lower urinary tract symptoms; PDE5i,phosphodiesterase type 5 inhibitor; VED, vacuum erection device.

Chapter 21

Figure 21.1 Pathophysiology of erectile dysfunction (ED) after pelvic surgery.

Chapter 22

Figure 22.1 The International Index of Erectile Function 5 (IIEF‐5) assessment tool.

Figure 22.2 Investigation of the diabetic patient with erectile dysfunction (ED).

Figure 22.3 Photo of vacuum device with different sized cylinders and constriction rings.

Figure 22.4 Treatment algorithm for erectile dysfunction (ED).

Chapter 24

Figure 24.1 The pathophysiological theories for Peyronie’s disease.

Chapter 26

Figure 26.1 A surgical algorithm for the treatment of Peyronie’s disease.

Chapter 27

Figure 27.1 Typical setup for an inflatable penile prosthesis (IPP) placement with the AMS 700 LGX device.

Figure 27.2 Cylinder erosion.

Figure 27.3 SST (“supersonic transporter”)deformity.

Figure 27.4 Reservoir placement in a patient with a previous robotic assisted laparoscopic prostatectomy (RALP) led to deep venous thrombosis after obstructing the right external iliac vein.

Chapter 28

Figure 28.1 Penile vascular anatomy. CIA, common iliac artery; EIA, external iliac artery; IIA, internal iliac artery; IPA, internal pudendal artery.

Chapter 29

Figure 29.1 Post operative appearance after total glans resurfacing.

Chapter 30

Figure 30.1 The technique of glans resurfacing for (a) balanitis xerotica obliterans (BXO) and (b) carcinoma in situ. (c) After excision of the glans epithelium. (d) Following skin grafting, the long‐term outcome.

Figure 30.2 Release of the buried penis in an obese patient with phimosis due to lichen sclerosus (LS) affecting the penile shaft skin.

a)

Preoperatively, despite losing approximately 20 kg, the patient still had a significant pre‐pubic fat pad.

b)

A wide incision is used to excise the pre‐pubic fat pad;

c)

excision of the LS‐affected skin resulted in exposure of the penile shaft, which was amenable to a thick SSG

(d)

.

Figure 30.3 Treatment of a fractured penis

(a)

with a bilateral corporal and urethral injury

(b)

. Repair of the corporal defect and urethra

(c)

, through the midline peno‐scrotal incision

(d)

obviates the need for a circumcision and degloving of the penis.

Guide

Cover

Table of Contents

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Male Sexual Dysfunction

A Clinical Guide

EDITED BY

Suks Minhas MD, FRCS(Urol)

Consultant Urologist

University College Hospital

London, UK

John Mulhall MD, MSc, FECSM, FACS

Memorial Sloan‐Kettering Cancer Center

New York, USA

This edition first published 2017 © 2017 by John Wiley & Sons Ltd

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The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by health science practitioners for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising herefrom.

Library of Congress Cataloging‐in‐Publication Data

Names: Minhas, Suks, 1966– editor. | Mulhall, John, editor.Title: Male sexual dysfunction : a clinical guide / edited by Suks Minhas, John Mulhall.Other titles: Male sexual dysfunction (Minhas)Description: Oxford ; Ames, Iowa : John Wiley & Sons, Inc., 2017. | Includes bibliographical references and index.Identifiers: LCCN 2016022487 (print) | LCCN 2016022873 (ebook) | ISBN 9781118746554 (cloth) | ISBN 9781118746448 (pdf) | ISBN 9781118746547 (epub)Subjects: | MESH: Erectile Dysfunction | Penile Diseases | Sexual Dysfunction, Physiological–diagnosis | Sexual Dysfunction, Physiological–therapyClassification: LCC RC889 (print) | LCC RC889 (ebook) | NLM WJ 709 | DDC 616.6/921–dc23LC record available at https://lccn.loc.gov/2016022487

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: © Don Farrall/Gettyimages

List of contributors

James BellringerParkside HospitalLondon, UK

Catherine BenedictMemorial Sloan Kettering Cancer CenterNew York, USA

Pierre‐Marc G. BoulouxThe Royal Free HospitalLondon, UK

Gerald BrockSt Joseph’s Health Sciences Centre; and Lawson Health Research InstituteLondon, ON, Canada

Culley CarsonUniversity of North CarolinaChapel Hill, NC, USA

Lizzie ChandraSt James Hospital, Leeds Teaching Hospitals NHS TrustLeeds, UK

Kelly A. ChilesGeorge Washington UniversityWashington, DC, USA

Eric ChungPrincess Alexandra HospitalBrisbane, Queensland, Australia

Giovanni CoronaMaggiore‐Bellaria Hospital Bologna, Italy

Victoria DawsonUniversity Hospital SouthamptonSouthampton, UK

Ian EardleyLeeds Teaching Hospital TrustLeeds, UK

Mark EmbertonUniversity College HospitalLondon, UK

Francisco J. GarciaUniversity of Western Ontario;St Joseph’s Health Sciences Centre;Lawson Health Research InstituteLondon, ON, Canada

Angela GregoryNottingham University HospitalNottingham, UK

Geoffrey HackettUniversity of Bedfordshire, Luton, UKGood Hope Hospital,Sutton Coldfield, UK

Paul K. HegartyMater Private HospitalMahon, Cork, Ireland

Wayne J.G. HellstromTulane UniversityNew Orleans, LA, USA

Graham JacksonGuy’s and St Thomas’ Hospitals NHS TrustLondon, UK

Salim JanmohamedUniversity College LondonLondon, UK

Ates KadiogluIstanbul Faculty of Medicine, Istanbul UniversityIstanbul, Turkey

Jas KalsiFrimley Health NHS Foundation Trust and Imperial CollegeHealthcare, London, UK

Oliver KayesSt James Hospital, Leeds Teaching Hospitals NHS TrustLeeds, UK

Mohit KheraBaylor College of MedicineHouston, TX, USA

Michael KirbyThe Prostate CentreLondon, UK

Alex KirkhamUniversity College Hospital LondonLondon, UK

Stephen LarsenUniversity College Hospital LondonLondon, UK

Chi‐Ying LiUniversity College Hospital LondonLondon, UK

Marc LuckyAintree University HospitalLiverpool, UK

Tom F. LueUniversity of CaliforniaSan Francisco, CA, USA

Mario MaggiUniversity of FlorenceFlorence, Italy

Martin MinerBrown UniversityProvidence, RI, USA

Suks MinhasUniversity College HospitalLondon, UK

Caroline MooreUniversity College HospitalLondon, UK

John MulhallMemorial Sloan Kettering Cancer CenterNew York, NY, USA

Asif MuneerUniversity College Hospital LondonLondon, UK

Christian J. NelsonMemorial Sloan Kettering Cancer CenterNew York, USA

Jalesh N. PanickerThe National Hospital for Neurology and Neurosurgery and UCL Institute of NeurologyLondon, UK

Alexander W. PastuszakBaylor College of MedicineHouston, TX, USA

Mark PaulosBrown UniversityProvidence, RI, USA

David RalphUniversity College Hospital LondonLondon, UK

Tina G. RashidCharing Cross HospitalLondon, UK

Rowland ReesUniversity Hospital SouthamptonSouthampton, UK

Ashley RidoutUniversity College HospitalLondon, UK

Emre SalabasIstanbul Faculty of Medicine, Istanbul UniversityIstanbul, Turkey

Varun SahdevUniversity College Hospital LondonLondon, UK

Patrick SelphUniversity of Alabama at BirminghamBirmingham, AL, USA

Majid ShabbirGuy’s HospitalLondon, UK

Alan ShindelUC DavisSacramento, CA, USA

C.J. ShuklaWestern General Hospital, NHS LothianEdinburgh, UK

Vikram SoniBaylor College of MedicineHouston, TX, USA

Conrad von StempelUniversity College HospitalLondon, UK

Raanan TalRambam Healthcare CampusHaifa, Israel

Ronny B.W. TanTan Tock Seng Hospital, Singapore

Phillip ThomasBrighton and Sussex University Hospitals NHS Trust, Brighton, UKParkside Hospital, London, UK

Katarina Ivana TudorDepartment of Neurology, University Hospital Center ZagrebZagreb, Croatia

Linda VignozziUniversity of Florence, Florence, Italy

Marcel D. WaldingerDrexel University College of MedicinePhiladelphia, PA, USA

Miles WalkdenUniversity College HospitalLondon, UK

Dan WoodUniversity College HospitalLondon, UK

Michael Grant WyllieGlobal Pharma ConsultingBanbury, UK

Tet YapSt George’s HospitalLondon, UK

Andrew YatesLeeds & York Partnership NHS Foundation TrustLeeds General InfirmaryLeeds, UK

Lindsay YuhUC DavisSacramento, CA, USA

Uwais B. ZaidUniversity of CaliforniaSan Francisco, USA

Xiaoyu ZhangUniversity of CaliforniaSan Francisco, USA

Foreword

This is a very important book. Its importance lies in the fact that male sexual health is these days central to very many men’s quality‐of‐life. Male sexual dysfunction, resulting from aging or some disease process, such as diabetes, can therefore have serious, and often underestimated, repercussions. Men, particularly as they age, are extremely dependent on a lasting relationship with their partner for their well‐being. In general, single or divorced men have a lower quality‐of‐life and higher risk of mortality than those who sustain their relationships in the longer term. Marital breakdown, which may be the consequence of male sexual dysfunction, can also have an impact on the next generation. The financial and emotional strains resulting from a fractured relationship may take a significant toll on the children, as well as on the two conflicted adults themselves.

As populations around the world age and increase, the incidence of male sexual dysfunction is set to rise and rise. Fortunately, as so well described in this book, its management has been transformed over the last 20 years by the advent of safe and effective pharmacotherapy, and, in selected cases, specialized andrological surgery. Viagra is still the world’s most instantly recognizable pharmaceutical brand, and is now much more affordable in its generic form: sildenafil. However, counterfeit products, often containing hazardous ingredients, are unfortunately increasingly available, often over the internet, and have recently been associated with several deaths in the Far East. Intracavernosal injection therapy, pioneered originally by the impressive Professor Giles Brindley, has an increasingly important role to play in the more difficult‐to‐treat men, who are usually either post‐pelvic surgery or longstanding diabetics. The third‐line treatment for refractory cases of erectile dysfunction by implantation of inflatable or semi‐rigid penile implants, which, provided that it is skillfully performed, can yield excellent results, is also well described in this excellent volume, along with other specialized surgical procedures for Peyronie’s disease and other andrological conditions that can impact negatively on sexual function.

After many years in the wilderness “men’s health” is at last beginning to take center stage. Sexual health is central to a man’s self‐esteem and well‐being. I have high hopes that this book, edited by two of the world’s leading experts in the specialty, which I whole‐heartedly commend to you, will be widely read, not only by those with a special interest in male sexual health, but also by generalists and family practitioners, as well as nurse specialists. Only by improving the lamentably deficient knowledge about the safe and effective treatment options now available for the very many men who are affected by male sexual dysfunction, will their lives be improved and their relationships preserved. This is undoubtedly a most laudable ambition.

Roger KirbyThe Prostate CentreLondonW1G8GT

CHAPTER 1Epidemiology of male sexual dysfunction

Raanan Tal

Rambam Healthcare Campus, Haifa, Israel

The broad term of sexual dysfunction includes erectile dysfunction, ejaculatory dysfunction, hypogonadism and low sexual desire, Peyronie’s disease and other penile morphological alterations, and urinary incontinence associated with sexual function. Knowledge of the epidemiology of various sexual dysfunctions is important in designing sexual health programs and allocation of budget and healthcare resources, in patients’ and partners’ education, and in clinical assessment of individual subjects. There are numerous epidemiologic studies in the contemporary medical literature, comprehensively detailing the prevalence of sexual dysfunctions; however, reported epidemiologic data vary greatly. Several factors account for these inconsistent data. The main one is probably the definition used to define a particular sexual dysfunction. For example, in selected high‐quality studies reporting on erectile function outcome in the post radical prostatectomy male population, more than 20 different definitions of favorable erectile function were used. Hence, the reported incidence of adequate erectile function varies, ranging from 25 to 78%.1 Since the definition of sexual dysfunction is not unified, it is not unreasonable to expect variation in sexual dysfunction epidemiologic data: the higher the threshold for normal sexual function, the greater is the incidence of sexual dysfunction. Moreover, sexual dysfunction is commonly assessed using questionnaires. More objective modalities, such as hemodynamic assessment of the penis by Doppler ultrasound of the erect penis to establish a diagnosis of vasculogenic erectile dysfunction, or stopwatch‐measured intravaginal ejaculatory latency time for establishing a diagnosis of premature ejaculation, are not commonly employed to define a sexual dysfunction. Not surprisingly, the type of questionnaire used in a certain study may also have an impact on epidemiologic findings.2 Another issue in sexual function epidemiologic research is the study population, as the prevalence of sexual dysfunction varies greatly according to age, risk factors, demographic population characteristics, and other population‐related factors.3–8 An important consideration in the epidemiology of sexual dysfunction is the existence of specific risk factors in specific populations. There are many well‐studied risk factors for sexual dysfunction.9 Common risk factors include cardiovascular diseases, obesity, hypertension, hyperlipidemia, smoking, lower urinary tract symptoms, radical pelvic surgery and, of course, diabetes.10–12 Radical pelvic surgery has a multi‐faceted impact on sexual function. For example, radical prostatectomy affects erectile function mainly by disruption of neural pathways, causing un‐ejaculation resulting from removal of anatomic structures – the prostate and seminal vesicles – and increasing the risk of urinary incontinence during sexual activity owing to urinary sphincter weakness and even increasing the risk of penile morphologic changes, penile length loss, and Peyronie’s disease.13,14 There are also other, less commonly discussed but nonetheless important, factors that may be associated with the epidemiology of sexual dysfunction. It has been suggested that the prevalence of sexual dysfunction may be related to the availability of therapies and interventions for sexual dysfunction.4 New therapies may increase patients’ and partners’ awareness and hence increase reporting of sexual dysfunction. In the light of these difficulties in measuring and reporting sexual dysfunction, epidemiologic data should be interpreted cautiously.

Erectile dysfunction

Erectile dysfunction is the most commonly researched and discussed sexual dysfunction, and the most prevalent sexual dysfunction in older men. The first landmark study that looked at the epidemiology of erectile dysfunction was the Massachusetts Male Aging Study, by Feldman et al. and published in 1994.15 This was a community‐based observational study, and looked at a random sample of non‐institutionalized men aged 40–70 years in the Boston area. Erectile function was assessed by a self‐administered questionnaire, and the study’s main findings were that the combined prevalence of minimal, moderate, and complete impotence was as high as 52%; subject age was the variable most strongly associated with impotence; and the prevalence of complete impotence tripled from 5 to 15% between subject ages 40 and 70 years.15 Another pivotal erectile dysfunction epidemiologic study was the Cologne Male Survey by Braun et al., published in 2000.10 This study looked at a European population, not a random sample but a representative sample of 8000 men, using a validated questionnaire. Results of this study were based on approximately 4500 evaluable questionnaires yielding a response rate of 56%. The prevalence of erectile dysfunction in this study was 19.2%, with a steep age‐related increase (2.3 to 53.4%) and a high rate of conditions comorbid with erectile dysfunction – hypertension, diabetes, pelvic surgery, and lower urinary tract symptoms – corroborating findings of earlier studies of different populations. The most extensively studied risk factors for erectile dysfunction are cardiovascular risk factors, primarily diabetes, and other risk factors, including the metabolic syndrome and its components (abdominal obesity, dyslipidemia, hypertension, and impaired fasting glucose), smoking, ischemic heart disease, and peripheral vascular disease and other cardiovascular risk factors.7,16,17 Recognition of these important risk factors, especially modifiable cardiovascular risk factors, may improve patient knowledge and awareness, and provide a window for cardiovascular disease diagnosis and early intervention in men with newly diagnosed erectile dysfunction, leading to not only better sexual health but also better overall health.18–20 The main pathophysiologic link between erectile dysfunction and cardiovascular morbidity is probably endothelial dysfunction.21 However, there are risk factors other than cardiovascular ones, both organic and psychological, that are associated with increased risk of erectile dysfunction. Among the significant organic non‐vascular risk factors is Peyronie’s disease, an underdiagnosed condition in men presenting with newly diagnosed erectile dysfunction.22 Peyronie’s disease may contribute to the development of erectile dysfunction probably by altering the elastic properties of the penile tunica albuginea.23 Another not uncommon risk factor for erectile dysfunction is testosterone deficiency (hypogonadism). It is well established that adequate testosterone levels are required not only for the penile vascular response during erection, but also to preserve penile structural integrity.24,25 Erectile dysfunction is more prevalent in men with certain non‐organic risk factors, such as emotional, couple related, and socioeconomic factors, creating a complex picture when the epidemiology of erectile dysfunction is discussed in certain specific populations.8,26 A good example of an emotional risk factor for erectile dysfunction is depression. In a study by Shiri et al. the incidence of erectile dysfunction was 59/1000 person‐years in men with depressive mood and 37/1000 person‐years in those without depression.27 Theses authors also found that the association of depression and erectile dysfunction is bidirectional: not only were men with depression at increased risk for erectile dysfunction, but also men with erectile dysfunction were at increased risk for depression.

In summary, the prevalence of erectile dysfunction is high and age‐dependent, with more than half of men at age of 50 years or older being affected. There are many risk factors for erectile dysfunction, hence epidemiologic data in specific populations should be viewed with careful consideration of the specific characteristics of the population reviewed.

Premature ejaculation

Premature ejaculation is likely the most common sexual dysfunction in men across all age groups and populations, with a worldwide prevalence of approximately 30%.28,29 For clinical research purposes the accepted definition of premature ejaculation is an intravaginal ejaculatory latency time (IELT) of 1–2 minutes; a prospectively stopwatch‐measured IELT is preferred over self‐ or partner‐reported IELT upon recall. While there is a definition of premature ejaculation for research purposes, in clinical practice there is no agreed definition. Waldinger et al. surveyed a population of 500 couples who were recruited from five countries, aged 18 years or older, had a stable heterosexual relationship for at least 6 months, with regular sexual intercourse. In their study, the median IELT was 5.4 minutes and the range was 0.55 to 41 minutes.30 In their study, the median IELT decreased significantly with age, from 6.5 minutes in the 18–30 years group, to 4.3 minutes in the group older than 51 years, while other studies did not show this age‐related increase in prevalence of premature ejaculation.31,32 Regardless of whether the prevalence of premature ejaculation is clearly age‐related or not, it is obvious that in younger men who are less likely to have other sexual dysfunctions such as organic erectile dysfunction, premature ejaculation is the most prevalent sexual dysfunction. In the real‐world clinical setting, the use of stopwatch IELT to define premature ejaculation is definitely not a practical approach. Other ways to categorize men as having premature ejaculation are based on men self‐reporting low or absent control over ejaculation irrespective of the duration of the ejaculation time, on the resulted distress for them or their sexual partner or both, or on patients’ report that they “climax too soon.” Indeed, in a Canadian web‐based study of more than 3800 men, the prevalence of premature ejaculation (PE) ranged from 16% to 24% depending on the definition of PE utilized.31 The etiology underpinning this high prevalence remains to be clarified, but current evidence reflects a shift from psychogenic theories to more neurobiological bases. While elucidation of the etiology of premature ejaculation is undoubtedly important for development of more effective therapies, it is clear that, whatever the cause of the condition, it is associated with a significant burden on psychological and overall health.29 Generally, men with premature ejaculation are more likely to self‐report other sexual dysfunctions (e.g., anorgasmia, low libido, erectile dysfunction) and psychological disturbances (e.g., depression, anxiety, excessive stress) than men without PE.33 Similarly, as for other sexual dysfunctions, the epidemiology of PE may vary in special groups. Tang and Khoo showed that PE prevalence varied according to ethnicity.32 It is worth mentioning that in their study, which included men in a primary care setting not a general population sample, the prevalence of PE was about 40%, significantly higher than in the general population. Shindel et al. looked at the prevalence of PE in another population of great interest, infertile couples, and found that about 50% of men reported that they ejaculated more rapidly than they wished. When men reported PE, their partners agreed with the diagnosis in 47% of cases. Female partners of men who did not report PE, reported PE in 11% of cases. Partner frustration related to PE was reported by 30% of men. Partners agreed that they were frustrated in 43% of these cases. Among the 70% of men who did not report partner frustration from PE, 93% of the partners agreed that they were not frustrated.

In summary, PE is hard to define exactly, yet it is the most prevalent sexual dysfunction and the most significant sexual dysfunction in young men.

Peyronie’s disease

Peyronie’s disease is commonly undiagnosed.34 The main clinical symptom is penile curvature; however, men may have significant Peyronie’s disease, manifested by penile plaques, erectile dysfunction, penile pain, and penile shortening, even without a curvature. Not uncommonly, the underlying cause of erectile dysfunction in poor responders to phosphodiesterase 5 inhibitors is Peyronie’s disease. The diagnosis of Peyronie’s disease in these men is established by physical examination and penile Doppler ultrasound in certain cases.35 Moreover, in men who are not sexually active or in men who are sexually active without achieving erection and performing penetration, the penile curvature may not be seen and Peyronie’s disease may exist but remain undiagnosed. Therefore, the reported prevalence of Peyronie’s disease depends on the manifestations of this condition, on a high index of suspicion, and on patients, partners, and sexual health care providers’ awareness. Epidemiological data on Peyronie’s disease are limited. Prevalence rates of 0.4–9% have been published, but the majority of the medical literature supports a prevalence rate of 3–8% or 5–8%.36,37 In the past, Peyronie’s disease was considered a condition that is limited to older men. However, newer data show that Peyronie’s disease does occur also in younger men and even in teenagers, but the prevalence in these very young men remains unknown.38 Men younger than 40 years are more likely to present at an earlier stage of Peyronie’s disease, to have diabetes, and to have more than one plaque at the time of presentation.39 In certain populations at risk, the prevalence of Peyronie’s disease is far greater. Diabetes, genetic predisposition, trauma of the penis, systemic vascular diseases, smoking, and alcohol consumption are all mentioned in the medical literature as risk factors for Peyronie’s disease.40,41 In diabetic men, not only is Peyronie’s disease more prevalent, but also it tends to manifest in older age, and present with longer duration and greater severity: There is greater penile curvature and more pronounced penile deformity, and a greater prevalence of coexisting erectile dysfunction, probably resulting both from penile structural alterations due to Peyronie’s disease itself and from diabetic vascular disease.42 Tal et al. looked at the incidence of Peyronie’s disease in a very distinct population consisting of men who had had radical prostatectomy as a monotherapy for prostate cancer, and calculated the 3‐year post‐prostatectomy incidence to be 16% and a mean time to presentation of 14 months after surgery.14 Rhoden et al. conducted a case‐control study to shed more light on Peyronie’s disease risk factors, and found that race is a strong risk factor for Peyronie’s disease, with an odds ratio of 8.5.43 Interestingly, in this study, higher low‐density lipoprotein (LDL)‐cholesterol level (>130 mg/dL) and increased waist circumference (>102 cm) actually had a protective effect in Peyronie’s disease, with an odds ratio of 0.5 for both. Moreno and Morgentaler investigated the association of testosterone deficiency and Peyronie’s disease. Their study is of special significance since testosterone is a principal anabolic hormone in men and definitely has a major role in maintaining the health of penile tissues. In their pilot study, the severity of penile curvature correlated significantly with free testosterone level but not with total testosterone level, and a possible important association between testosterone deficiency and Peyronie’s disease was suggested.44 Besides the epidemiology of Peyronie’s disease itself, sexual healthcare professionals should be aware of the epidemiology of emotional conditions in Peyronie’s disease, which are under‐represented in the medical literature and often under‐diagnosed and treated in daily clinical practice. Consistent data from two leading sexual medicine centers in the United States show that the psychological burden in men with Peyronie’s disease is great, possibly greater than in men with other sexual dysfunctions.45,46 Overall very high rates of emotional burden and relationship problems attributable to Peyronie’s disease were found: 81% and 54%, respectively, predictors of which were penile length‐loss and inability to have intercourse. Using validated instruments, it was demonstrated that 48% of men with Peyronie’s disease had clinically meaningful depression that would warrant medical evaluation. This high level of depression stayed consistent across time since diagnosis, suggesting that most men do not psychologically adjust to their diagnosis of Peyronie’s disease; all men with Peyronie’s disease should be considered for appropriate mental health screening. This high prevalence of psychological morbidity may be attributable to the fact that there is no fully effective treatment for Peyronie’s disease, and men with symptomatic Peyronie’s disease will never regain their pre‐morbid penile function, appearance, and length.

In summary, the epidemiology of Peyronie’s disease is intriguing: Its prevalence is higher and its age distribution is broader than previously thought; there are numerous suggested risk factors and a very high risk of associated psychological morbidity, inherent to changes in penile appearance and function, that should not be overlooked.

Hypogonadism

Hypogonadism (low testosterone) is under‐diagnosed and under‐treated. The significance of hypogonadism diagnosis and treatment cannot be over‐emphasized, as androgen receptors and testosterone activity exist in most body tissues, organs, and systems. Testosterone deficiency effects are not limited to sexual function: besides desire and erection, it may also affect bone health, muscle mass, hematopoiesis, cognitive function, spermatogenesis and seminal fluid production, vascular and cardiac performance, lipid and glucose metabolism, and many other metabolic, primarily anabolic, processes. The key to diagnosis is awareness of the high prevalence of testosterone deficiency, identification of populations at risk, and early symptoms and laboratory evaluation. Worth mentioning is that symptoms of hypogonadism are not specific and can be attributed to other medical conditions, such as hypothyroidism or depression. Therefore, questionnaires are neither sensitive nor specific for hypogonadism screening or diagnosis, and must be combined with measured plasma testosterone levels.47,48 Clinically, it was suggested that the findings that are best correlated with late onset hypogonadism are sexual symptoms (poor morning erection, low sexual desire, erectile dysfunction) and total testosterone level of less than 11 nmol/L (<320 ng/dL).49 Epidemiologic questionnaire‐based studies without testosterone measurement failed to correctly define the true prevalence of hypogonadism, yielding an overestimated prevalence of up to 80%.50 Combining hypogonadism symptoms and plasma testosterone levels, Araujo et al. found that the overall prevalence of symptomatic testosterone deficiency in a random sample of men from the Boston Area Community Health Survey was 5.6%. In this study, symptomatic testosterone deficiency prevalence increased with age, yielding a prevalence of 18.4% in men over 70 years old.51 Age‐related increased prevalence of hypogonadism was also demonstrated in the Baltimore Longitudinal Study of Aging: the prevalence of hypogonadal testosterone levels was about 20% in men over 60 years old, 30% in men over 70 years old, and 50% in those over 80 years of age, using total testosterone criteria; the prevalence was even greater when free testosterone criteria were employed.52 The prevalence of testosterone deficiency is increased in men with certain risk factors such as diabetes, cancer, lung disease, other systemic diseases, obesity, the metabolic syndrome, and erectile dysfunction, and in men with reduced mass and function of testicular tissue, for example, infertile men, men having varicocele, and men after unilateral orchiectomy.53–55 Diabetes is a well‐studied risk factor for testosterone deficiency: in a study by Corona et al. the prevalence of hypogonadism was 24.5% in diabetic men versus 12.6% in non‐diabetic subjects, which was statistically significant after adjustment for age and body mass index (BMI).56 Similar results were recently published by Al Hayek et al.: the prevalence of hypogonadism was 24.3% in diabetic and 8.3% in non‐diabetic patients.57 Hypogonadism also is common in men with erectile dysfunction, with a reported prevalence of approximately 30–40%.58,59 Not uncommonly, erectile dysfunction is the presenting symptom. This population of men presenting with erectile dysfunction deserves special attention: it is a unique opportunity to impact men’s health. Correct evaluation and management of testosterone deficiency and other cardiovascular risk factors may actually reduce future cardiovascular morbidity and mortality. Therefore, symptomatic treatment of erectile dysfunction in these men without in‐depth risk factor identification should be discouraged.