i
DETERMINATION OF INCIDENCE AND
CORRELATIONS OF ERECTILE DYSFUNCTION AND LOWER URINARY TRACT SYMPTOMS IN ADULT
NIGERIAN PATIENTS.
BY
DR ABIAHU, JOSEPH AMAUZO MBBS (IBADAN)
DEPARTMENT OF SURGERY
NNAMDI AZIKIWE UNIVERSITY TEACHING HOSPITAL NNEWI
BEING A DISSERTATION SUBMITTED TO
THE NATIONAL POSTGRADUATE MEDICAL COLLEGE OF NIGERIA IN PART FULFILMENT OF THE REQUIREMENT FOR THE AWARD OF THE FELLOWSHIP OF THE MEDICAL
COLLEGE IN SURGERY (FMCS)
MAY 2013
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DECLARATION
I hereby declare that the research project leading to this dissertation was actually carried out by me under the guidance of my supervisors. This work has neither been presented in part or in full to any other college for a fellowship nor has it been submitted elsewhere for publication.
Signature/date ………..
Dr. Abiahu Joseph Amauzo
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ATTESTATION
This is to certify that I have supervised Dr Abiahu Joseph Amauzo in carrying out the research project leading to this dissertation titled “Determination of incidence and correlation of erectile dysfunction and lower urinary tract symptoms (LUTS) in adult Nigerian patients”
Signed………
Prof Mbonu O.O. MB (Lond), FRCS (Ed), FWACS, FMCS, FRCS (C) Consultant Urologist
Department of Surgery
Nnamdi Azikiwe University Teaching Hospital, Nnewi
Signed………
Prof Orakwe J.C. MB.BS (Ibadan), FMCS, FWACS, FICS, FISS.
Consultant Urologist
Head, Department of Surgery
Nnamdi Azikiwe University Teaching Hospital, Nnewi.
Signed………...
Prof Nwofor A.M.E. MB.BCH (Nig), FMCS, FWACS, FICS, FISS.
Consultant Urologist Dean, Faculty of Medicine
Nnamdi Azikiwe University, Nnewi.
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DEDICATION
This work is dedicated to God Almighty. He made all things possible.
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ACKNOWLEGEMENT
I wish to express my heart felt gratitude to my dear wife Dimma and our babies Maya and Jaachi for their patience despite the burden of my limited attention in the course of my Residency programme.
It was a big honour and privilege to have Prof. O.O. Mbonu supervise my work despite his busy schedule. It was a fatherly disposition. His critical corrections and encouragement kept me going.
I wish to specially thank Prof. J.C. Orakwe and Prof. A.M.E. Nwofor.
They “treated” my clinically induced nightmares of topic selection and sorting of materials. They were also quick to review my work. Their principles and attitude to work have remained a source of inspiration to me for bigger dreams in the profession. I also thank Prof. P.I.S Okafor for nursing the “Little Surgeon” in me.
He was patient with me and made me feel I can do it.
Let me use this opportunity to also thank Dr. C.K. Oranusi and Dr. T.U.
Mbaeri. They were also there to guide and advice me. This study would have been more hectic without them.
I also wish to thank my other colleagues and fellow Residents who directly or indirectly contributed to the success of this work. Thank you Mr. Dimkpa for your assistance in Statistical analysis of this work.
Last but not the least; I thank God for giving me the zeal, good health and wisdom to make this project a reality.
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TABLE OF CONTENTS
Title page --- --- --- --- --- --- --- --- --- --- i Declaration page --- --- --- --- --- --- --- --- --- ii Attestation page --- --- --- --- --- --- --- --- --- iii Dedication page --- --- --- --- --- --- --- --- --- iv Acknowledgment page --- --- --- --- --- --- --- --- v Table of Contents --- --- --- --- --- --- --- --- --- vi List of Abbreviations --- --- --- --- --- --- --- --- --- vii List of Tables --- --- --- --- --- --- --- --- --- --- viii List of Figures --- --- --- --- --- --- --- --- --- --- ix Summary--- --- --- --- --- --- --- --- --- --- --- x CHAPTERS
1. Introduction --- --- --- --- --- --- --- --- --- --- 1 2. Literature Review --- --- --- --- --- --- --- --- --- 5 3. Patients and Method --- --- --- --- --- --- --- --- 21 4. Results --- --- --- --- --- --- --- --- --- --- 26 5. Discussion --- --- --- --- --- --- --- --- --- --- 37 6. Conclusion and Recommendation --- --- --- --- --- --- 42 References --- --- --- --- --- --- --- --- --- --- 43 Appendices
Appendix I - Approval form of the Ethical Committee --- --- i
Appendix II - Consent form --- --- --- --- --- --- --- ii
Appendix III - Study proforma --- --- --- --- --- --- iv
Appendix IV - IPSS index form --- --- --- --- --- --- viii
Appendix V - IIEF-5 form --- --- --- --- --- --- --- ix
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LIST OF ABBREVIATIONS / KEYWORDS.
LUTS - Lower Urinary Tract Symptoms ED - Erectile Dysfunction
MSAM-7- Multinational Survey of the Ageing Male-7 NAUTH- Nnamdi Azikiwe University Teaching Hospital BPH - Benign Prostatic Hyperplasia
IIEF - International Index of Erectile Function IPSS - International Prostate Symptom Score QoL - Quality of Life
NO - Nitric Oxide
NOS - Nitric Oxide synthase nNOS - Neuronal NOS
iNOS - Induced NOS eNOS- Endothelial NOS
VIP- Vasoactive intestinal polypeptide PGE-1 Prostaglandin E1
c-GMP- cyclic Guanosine Monophosphate GTP- Guanosine triphosphate
c-AMP- cyclic adenosine monophosphate ATP- Adenosine triphosphate
ICP - Intracavernosal pressure BOO- Bladder Outlet Obstruction
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LIST OF TABLES
Table 1: Baseline characteristics of patients with range and mean --- 26 Table 2: Frequency distribution of other characteristics and
Life-style of patients --- --- --- --- --- --- --- 28 Table 3: LUTS, ED and QoL scores of patients --- --- --- --- 29 Table 4: Pearson’s bivariate correlation test associating ED
scores and LUTS scores --- --- --- --- --- --- 30 Table 5: Chi-square analysis relating severity of ED and
graded LUTS scores. --- --- --- --- --- --- --- 34 Table 6: Assessment of QoL of patients --- --- --- --- --- 35 Table 7: Chi-square analysis relating severity of LUTS
and ED with QoL --- --- --- --- --- --- --- 35 Table 8: Prevalence of co-morbidities in patients --- --- --- --- 36
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LIST OF FIGURES
Figure 1: Anatomy of the penis--- --- --- --- --- --- --- 6 Figure 2: The mechanism of penile erection--- --- --- --- --- 11 Figure 3: Bar chart showing age distribution of LUTS patients--- --- 26 Figure 4: Bar chart showing distribution of level of adiposity --- --- 27 Figure 5: Bar chart showing distribution of ED among LUTS
Patients that had sexual intercourse --- --- --- --- --- 30 Figure 6: Scatter plot of voiding phase LUTS and ED --- --- --- 31 Figure 7: Scatter plot of filling-storage phase LUTS and ED --- --- 32 Figure 8: Scatter plot of total LUTS and ED --- --- --- --- --- 33
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SUMMARY
Objective: This study aimed to determine the incidence of erectile dysfunction and its correlation with LUTS in adult Nigerian male patients presenting with LUTS to the Urologist.
Background: LUTS either singly or in combination with ED, represents a considerable problem for the ageing men. This is due to the negative impact they have on the patients’ QoL. Determination of the incidence of ED and its relationship with LUTS is therefore important in proper care of these patients.
Patients and Methods: One hundred and ten patients with LUTS were recruited from urological outpatient clinic of NAUTH. The sociodemographic data were collected while ED and LUTS were assessed with IPSS and IIEF questionnaires respectively. Findings were subjected to statistical analysis.
Results: The mean age of patients was 65 ± 7.97years. LUTS were most prevalent within age group 71-75years. In 54.5%, the highest level of education was primary. The total incidence of ED was 63.6% ranging from mild to moderate ED with no severe ED recorded. The severity of ED showed strong positive correlation (P=0.0001) with severity of total LUTS score, while QoL showed a significant relationship (p<0.05 and p<0.01) between severity of voiding phase LUTS and severity of ED.
Conclusion: The results from this study have shown that ED is prevalent in patients with LUTS. Its severity worsens with increasing severity of LUTS, with significant negative impact on QoL of patients especially the voiding phase LUTS.
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CHAPTER ONE
INTRODUCTION
Lower urinary tract symptoms (LUTS) may be defined as a constellation of filling-storage phase symptoms and voiding phase symptoms often as a result of increased bladder outlet resistance to outflow of urine or less frequently due to neuromyopathic bladder. The causes are variable and common among older men, increasing in incidence with age1-4.
In the late 1990s, an association was suggested between LUTS and sexual dysfunction especially erectile dysfunction (ED). Both conditions are strongly associated with age1,4-9. Erectile dysfunction (ED) is defined as the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual intercourse1,10-15.This gained tremendous attention following the discovery of Nitric Oxide (NO) in the human body11,13,16. In the Multinational Survey of the Ageing Male-7 (MSAM-7), a survey of over 14,000 men aged 50 years to 80 years from the USA, UK, France, Germany, the Netherlands, Italy and Spain, the number of sexual activities per month decreased by about half in men with LUTS compared to those without LUTS8.
1.1 STATEMENT OF PROBLEM
LUTS, either singly or in combination with ED, represents a considerable problem for the ageing men due to negative impact they have on their quality of life1-3,13-15,17-22. Erectile dysfunction affects over 152 million men worldwide23. National Health and Social Life Survey of United States adult population aged 18 years to 59½ yearsrecorded 11% of men aged 40-49 and 18% of men aged 50-59 having trouble ‘maintaining or achieving an erection21. In community-based survey of men between the ages of 40 years and 70 years, 52% of respondents reported some degree of erectile difficulty. Based on these data, it was estimated
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that ED affects 20 – 30 million men in the USA11,21. In Africa, the prevalence of ED, currently estimated to exceed 12 million men, is projected to increase at a rate surpassing that of any other continent as a result of escalating risk factors and improved diagnosis15,23. Studies in some African, Arabic or Islamic countries with different sociocultural and religious characteristics found a higher prevalence of 54.9% in Egypt, 50.7% in Nigeria, 64.3% in Turkey, and 53.6% in Morocco22,24.
With the current ageing trends in the global population, the prevalence of ED is likely to increase significantly during the next 20 years25. With the estimated and projected male population distribution from the United Nations and prevalence rate of ED from the Massachusetts Male Ageing Study, projections for 2025 indicated an expected 111% rise in worldwide prevalence12. The largest increase is expected in the developing countries that have expanding populations and increasing life expectancies12,15,26. This can have both physical and psycho-social effects, and economic impact. Indeed, a spillover effect can occur in the partner with consequences like infidelity for sexual satisfaction, increased risk of sexually transmitted diseases like HIV, and marital discord.
In the last few years, several studies done in Caucasians, have explored the association between LUTS and ED while controlling for co-morbidities like Diabetes, Hypertension and Heart disease1,8,14,22,27-29. Other risk factors like sedentary lifestyle and obesity have also been associated with increased risk of ED30-33. These co-morbidities increase with age and could also directly or indirectly worsen the erectile function in this ageing study group.
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1.2 STUDY JUSTIFICATION AND RATIONALE FOR STUDY APPROACH
Most previous studies showed wide variation in prevalence of ED and LUTS in different population groups1. For example, a systemic review showed estimates of ED ranging from 2% in men <40 years to 86% in men >80 years34. This has been attributed partly to methodology and cultural background1,7,14,35,36. The use of patients with LUTS as the study population in this study emphasizes the need for hospital based study. This enables easy recruitment of subjects. This study will give an insight into the incidence of ED in a Nigerian hospital population among patients suffering from LUTS. However, the superiority of population-based study to hospital-based study is not questionable.
Sexual issues are sensitive and intimately interwoven with culture and self- esteem. This makes an average adult male in Africa feel reluctant to freely discuss this issue. This may have brought about under reporting of prevalence of ED in population-based studies13,22,36. Patients’ presentation to urology clinic because of LUTS offers an opportunity for further evaluation of ED and other associated co-morbidities. This will ensure proper diagnosis and management plan for the patients. However, the study group is selective compared to the general population. This study may be a sensitizer and indeed a saviour for the urologist from litigation for ED after prostatectomy in patients who presented with LUTS due to BPH. The need for increased awareness on this condition, increased demand for clinical services, and more aggressive pursuit for its treatment may be established by this study.
Although the usefulness of laboratory-based diagnostic procedures cannot be ruled out, it has been proposed that sexual function is best assessed in a naturalistic setting with patient self-reported techniques10,42. The abridged 5-item version of International Index of Erectile Function (IIEF-5) and International Prostate Symptom Score (IPSS) in this study were found useful in assessing ED
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and LUTS respectively39-42. Both are validated diagnostic tools for ED and LUTS respectively. All except one study had no control for prostatitis and painful bladder syndrome which manifest as LUTS1. In this study, questions were asked to control for these.
1.3 AIM AND OBJECTIVES.
The aim of this study was to determine the incidence of ED and its correlation with LUTS in adult Nigerian male patients who presented with LUTS in a hospital setting.
Specific objectives include:
1. To determine the incidence of ED in men presenting with LUTS.
2. To determine the correlation between severity of LUTS and ED.
3. To evaluate the effect of ED and LUTS on QoL.
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CHAPTER TWO
2.0 LITHERATURE REVIEW 2.1 ANATOMY OF THE PENIS
Penis is a Latin word meaning “tail”43. It is the male organ of copulation and common outlet for urine and semen. The Penis is composed of three erectile bodies (corpora).The paired bodies are larger, dorsally located and extend the length of the penis to invaginate the glans distally. Proximally, they diverge at the level of the pubic symphysis to end as the crura (legs) of the penis. Here, they are attached to the inferior pubic rami by a fibrous extension of the Buck’s fascia termed the suspensory ligament. These two columnar bodies contain cavernosal vascular tissues hence termed corpora cavernosa. Within these lie interconnected cavernosal (sinusoidal) spaces separated by smooth muscle trabeculae surrounded by elastic fibers, collagen, and loose areolar tissue44. The third columnar body; the corpus spongiosum contains the urethra43-45. The distal end is bulbous forming the glans penis.The corpus spongiosum is attached proximally to the perineal membrane and at the most proximal portion; it is enlarged to form the bulb44. Each of the corporal bodies is encased in its own white fibrous bilaminar capsule called the tunica albuginea.This consists of inner circular and outer longitudinal layers composed of collagen and elastin. The tunica albuginea condenses between the corpora cavernosa to form the incomplete septum. The three corporal bodies are surrounded by deep fascia of the penis (Buck’s fascia).
Superficial to this lies the dartos tunic which is in turn covered by the skin. The penile skin is thin, loose and usually hairless.
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Figure 1: Anatomy of the Penis.
ABOVE: Midshaft cross-sectional anatomy of the penis. BELOW: A, Arterial supply to the penis. B, Venous drainage of the Penis.
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Arterial supply to the penis is classified into two groups: Superficial and Deep45. The superficial group originates from the external pudendal artery. They form the subdartos plexus and supply the penile skin. The deep group consists of branches from the common penile artery that originates from the internal pudendal artery. The dorsal arteries of penis run distally on the dorsum of the penis deep to Buck’s fascia and lateral to the deep dorsal vein. It also contributes to retrograde blood supply and engorgement of the glans penis during erection.
The deep arteries to the penis pierce the crura and run the length of the corpora cavernosa through the centre of the erectile bodies. They give off numerous branches that open directly into the cavernous (sinusoidal) spaces. These branches are coiled when the penis is flaccid thus termed helicine arteries. They become dilated and straight during erection. The artery to the bulb pierces the bulb of the penis to supply the corpus spongiosium and the urethra.
Blood from the cavernous spaces is drained by tiny venules coming from the peripheral cavernous spaces immediately beneath the tunica albugenea.
These venules travel in the trabeculae between the tunica and the peripheral cavernous spaces to form the subtunical venular plexus before exiting as the emissary veins. The emissary veins drain laterally into the circumflex veins and end in the deep dorsal vein. This passes beneath the pubic arch and joins the prostatic venous plexus. Blood from superficial coverings of penis drain into the superficial external pudendal vein via the superficial dorsal vein.
Nerve supply to the penis is by autonomic (sympathetic T10-L2 and parasympathetic S2-S4) and somatic (sensory and motor) nerves. The autonomic innervations arise from neurons in the spinal cord and peripheral ganglia. They merge to form the cavernous nerve. This supplies the corpora cavernosa and corpus spongiosum to effect the neurovascular events of erection and detumescence. The somatosensory pathway is responsible for penile sensation. It originates at the penile receptors. These form nerve fibers that converge to form
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the dorsal nerve of penis. This nerve joins other nerves to form the pudendal nerve. The later enters the spinal cord via S2-S4 roots to terminate on spinal interneurons from where signals ascend via the spinothalamic and spinoreticular pathways to the brainstem and sensory cortex. Central to somatomotor penile innervations is the Onuf’s nucleus located in S2-S4 spinal segments. This innervates the ischiocavernous and bulbocavernous muscles via the pudendal nerve. Stimulation of this nerve causes contraction of these muscles to produce rigid erection phase and ejaculation respectively45.
The lymph vessels from most of the penis drain into the superficial inguinal lymph node. Vessels from the glans penis drain into the deep inguinal lymph node43.
2.2 NORMAL PENILE ERECTION
Historically, physicians have always had a concern for the sexual issues of their patients. Hippocrates, the Father of Medicine, believed that “preoccupation with business and lack of attractiveness can cause impotence.” Later, Aristotle discussed engorgement and recognized some of the physiologic aspects of ejaculation46.
An erection is a complex interaction between psychogenic, neuroendocrine, and vascular mechanisms acting on the penile erectile tissue.
They are the result of relaxed sinusoidal smooth muscles, triggered by various reflexogenic and psychogenic stimuli. Central to this is nitric oxide-cyclic guanosine monophosphate (c-GMP) mechanism. Nitric oxide (NO) is a neurotransmitter synthesized from endogenous L-arginine by nitric oxide synthase (NOS). The NOS exits in three distinct forms: neuronal NOS (nNOS /NOS-1), induced NOS (iNOS/NOS-2), and endothelial NOS (eNOS/NOS-3).
The NOS-1 and NOS-3 are important in erection. Following sexual stimulation, there is local release of secondary messengers in the corpora cavernosa and
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adjacent endothelial cells. These include NO, vasoactve intestinal polypeptide (VIP), and prostaglandin-E1 (PGE1). Nitric oxide activates guanylate cyclase released from the smooth muscle cells of the sinusoids and blood vessels. The activated enzyme then catalyzes the formation of c-GMP from guanosine triphosphate (GTP). Vasoactive intestinal polypeptide and PGE1 activate adenylate cyclase which catalyzes the formation of cyclic-adenosine monophosphate (c-AMP) from adenosine triphosphate (ATP). The c-GMP and c- AMP then promote relaxation of the smooth muscles by activation of potassium channels. This causes hyperpolarization and closure of voltage-dependent calcium channels thus reduction of intracellular free calcium ion. There is succeeding net increase in blood flow which engorges cavernous spaces4,13,46-50. Neurogenic NO is considered the main factor responsible for the immediate relaxation of corpora cavernosa while endothlial NO is essential for maintaining relaxation4. As the cavernous spaces distend, they compress and obstruct the venules located beneath the tunica albugenia resulting in build-up of intracorporal pressure to give the penis rigidity. Erection is maintained until after ceasation of erotic stimulation or ejaculation. There is associated tonic sympathetic discharge which causes contraction of smooth muscles in the sinusoids and arterioles and diminishes blood flow to flaccid levels. About this period, orgasm may be achieved. This describes an intense and profoundly satisfying cerebral sensation that represents the explosive discharge of accumulated neuromuscular tensions46. Following this is detumescence. This is achieved by a combination of withdrawal of parasympathetic stimulation and active smooth muscle contraction mediated by the sympathetic nerves T10-L2.
The concentration of intracellular c-GMP is regulated by the cyclic nucleotide phosphodiesterase enzyme type-5 (PDE-5) which metabolizes it to 5I-guanosine monophosphate13,47-49. Intracellular calcium builds up, aiding active smooth muscle contraction. The result is reduction of arterial blood inflow and expulsion
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of venous blood to bring about flaccidity. A refractory period ensues, during which the male is unable to achieve full erection or repeat orgasm.
The state of erection can be divided into 6 phases: flaccid phase, latent or filling phase, tumescence phase, full erection phase, rigid/skeletal erection phase, and detumescence phase 46.In flaccid phase, there is minimal arterial and venous flow. A minimal amount of blood enters the cavernous tissue for nutrition. The cavernous arterial flow rates range from 15cm/sec to undetectable value. Latent or filling phase is a period of highest flow rate with a peak flow velocity of more than 30cm/sec. There is increased blood flow through the internal pudendal artery during both systolic and diastolic phases with associated penile elongation without change in the intracavernosal pressure (ICP).Tumescence phase describes period of maximal penile elongation and expansion. The ICP increases with gradual decrease in flow rate. At ICP above the diastolic pressure, blood flow occurs only during the systolic phase. In full erection phase, the ICP stabilizes at a value equal to 85% of the systolic blood pressure. Blood flow is slower than during the tumescence phase, yet greater than during the flaccid phase. The penile volume and pressure remains steady and venous flow equals arterial flow. Rigid or skeletal erection phase is a period the ICP rises well above that of systolic pressure due to contraction of the ischiocavernous muscle. There is no inflow of blood. Due to muscle fatigue, the duration of this phase is short.
This prevents tissue ischaemia and damage. Detumescence phase follows cessation of erotic stimuli (or ejaculation). There is tonic sympathetic discharge causing contraction of smooth muscle in the sinusoids and arterioles and diminished blood flow to flaccid level. This phase is further divided into initial, slow, and fast detumescence. Initial detumescence marks the beginning of smooth muscle contraction against closed venous system. It is characterized by transient increase in intracorporal pressure. The second phase shows a slow pressure decrease, suggesting a slow reopening of the venous channels with
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resumption of the basal level of arterial flow. The third phase shows a fast pressure decrease with fully restored venous outflow capacity.
Physiologically, erection is divided into psychogenic, reflexogenic and nocturnal erections46. These trace the etiology of erectile dysfunction.
Psychogenic erections are integrated in the medial preoptic area and paraventricular nucleus of hypothalamus. These areas are stimulated by audiovisual stimuli or fantasies. Impulses released modulate the spinal erection centers (T10– L2 and S2 – S4) to activate erection.
Reflexogenic erections are the result of local genital stimulation which set up a complex process involving the spinal erection centers, the higher centers and autonomic ganglion to produce erection.
Nocturnal erection occurs during Rapid Eye Movement (REM) sleep and the mechanism is not yet defined.
A B
Figure 2: The mechanism of penile erection
A: In the flaccid state the arteries, arterioles, and sinusoids are contracted. The intersinusoidal and
subtunical venular plexuses are wide open, with free flow to the emissary veins. B: In the erect state, the muscles of the sinusoidal wall and the arterioles relax allowing maximal flow to the compliant sinusoidal spaces. Most of the venules are compressed between the expanding sinusoids. Even the larger intermediary venules are sandwiched and flattened by distended sinusoids and the noncompliant tunica albuginea. This effectively reduces the venous capacity to a minimum.
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2.3 ERECTILE DYSFUNCTION(ED)
ED constitutes a component of sexual dysfunction which defines the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual intercourse1,11-15,36,51.
Aetiologies of erectile dysfunction are traceable to impairment in the complex interaction of the mechanism that mediates the normal erection. These include: psychogenic, vasculogenic, neurogenic, endocrine, organ failure, iatrogenic and drug induced causes46. However, Lizza and Rosen49 recommended a new classification of ED into psychogenic, organic and mixed types. The later being the commonest.
Psychogenic causes: Until about a decade ago, it was generally thought that 80 to 90% of ED was psychogenic and only 10% had an organic basis46. Recent studies have demonstrated that organic causes of ED are found in about 70 – 80% of patients. In less than a third of patients, the cause may be purely psychogenic46. However, Berrada et al22 and Melman et al53 reported the occurrence of psychogenic ED in up to 70% of men younger than 35 years and in approximately 10% of those older than 50years. Subtypes of psychogenic ED according to Lue classification are anxiety and fear of failure, depression (drug or disease induced), marital conflict, strained relationship, ignorance and religious beliefs, psychotic and personality disorders.
Vasculogenic causes: This results from direct or indirect thromboembolic occlusion, fibrosis, calcification, obliteration, scarring, and aneurysmal dilation of arterial supply to the penis or shunting away of blood as seen in pelvic steal syndrome. Alfredo et al36 and other workersnoted that ED is most commonly a vascular disorder14,54-58. Process of aging is associated with progressive obliteration of cavernosal arteries.
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Other risk factors related to vasculogenic ED include diabetes mellitus, hypertension, smoking, alcohol intake, hyperlipidemia, pelvic and perineal trauma4,12,28,29,32,39,59,60-63. Fedele et al63 found that the risk of ED increases with the duration of diabetes. This was also noted by other reports46,64. Deutsch and Sherman 65 reported that up to 12% of impotent men have unrecognized diabetes mellitus. The relationship between ED and smoking has been controversial.
Positive correlation of alcohol intake with ED was noted in some studies12,32,59 while negative correlation was noted in a study36. The health professional follow- up study found a lower prevalence of ED in moderate drinkers than in a non- drinker or heavy drinker66.However, Berrada et al22 and the Italian general practice-based study67 did not find any correlation. A population-based study done in Morocco by Berrada et al22 noted that ex-smokers had higher prevalence of ED than non-smokers. Shaeer et al14 reported that current smoking was associated with ED in age-adjusted bivariate analysis, but this was not significant in the multivariate model, in which over use of tobacco was associated with slightly lower prevalence of ED. The health professional follow-up study also corroborated positive association of current smoking with ED66. On the contrary, the Massachusetts Male Ageing Study (MMAS) found no association between ED and smoking12.
Neurogenic ED: This may be due to peripheral nerve, spinal cord or cerebral lesions. Conditions that may affect peripheral nerves include diabetes mellitus, uraemia and amyloidosis. Spinal cord lesions include spinal trauma, multiple sclerosis, tabes dorsalis, spina bifida, syringomyelia, cord compression from herniated disc and spinal tumors. Cerebral lesions that may cause ED include stroke, Parkinson’s disease, frontal lobotomy, Huntington’s chorea and electroconvulsive therapy (ECT)46.
Endocrine and metabolic causes: The overall incidence of endocrinopathy in ED patients is estimated to be 17.5% with diabetes mellitus
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leading as the single most frequent cause of ED in United States46. Endocrinopathy causes include hypergonadotropic hypogonadism. This may result from congenital defects, Klinefelter’s syndrome, chemotherapeutic agents, and radiation therapy. Hypogonadotrophic hypogonadism resulting from failure of primary luteinizing hormone (LH) secretion by the anterior pituitary may also be a cause. Congenital hypogonadotrophic hypogonadism is associated with Kallmann’s, Prader-Willi and Laurence-Moon-Biedl syndromes. Other causes include hyperprolactinemia, thyroid disorder, and dialyzed patients. These are related to changes in testosterone levels46.
End organ factors: Pathological conditions of the penis, prostate or seminal vesicles may cause ED either directly or indirectly. Congenital problems like extrophy/epispadias complex, micropenis, severe penile chordees can make erection and penetration difficult while Peyronie’s disease, prostatitis and seminal vesiculitis can cause pain on arousal or ejaculation thus indirectly cause ED by feedback inhibition from higher center. Priapism with corporal scarring can also cause ED46.
Iatrogenic causes and Drug induced ED: Surgical procedures known to cause ED include vascular pelvic/penile surgeries, transplant and radical pelvic surgeries, surgeries for priapism and pelvic irradiation. Spinal cord and brain procedure can also be causes. These may cause direct or indirect neuronal or vascular injury to the systems that coordinate erection. The resulting impaired nervous coordination or tissue ischemia may lead to ED46.
Various drugs can cause ED by interfering with either central neuroendocrine or local neurovascular control of penile smooth muscle. Common examples include alcohol, recreational drugs, antihypertensive (especially sympatholytic agents like methyldopa, clonidine, and reserpine), antidepressants, and psychotropic drugs46.
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2.4 LOWER URINARY TRACT SYMPTOMS (LUTS)
The symptoms related to bladder outlet obstruction (BOO) due to BPH have in the past arbitrarily been described as a group as “Prostatism” and further categorized as obstructive or irritative68. Obstructive group include impairment in the size or force of the urinary stream, hesitancy and/or abdominal straining, intermittent or interrupted flow or sensation of incomplete emptying, and terminal dribbling. Irritative symptoms include nocturia, daytime frequency, urgency and urge incontinence. LUTS is a rubric, introduced by Abrams, to replace the term “prostatism” which implied that the prostate was responsible for most (or all) symptomatic voiding complaints in men68. LUTS with its subdivision, filling-storage phase symptoms, and voiding (emptying) phase symptoms, have replaced as well the terminology of “irritative” and “obstructive”
symptoms, both rather imprecise terms that imply an etiology that may be incorrect. BPH is the most common aetiology of significant voiding dysfunction seen by the urologist68. Symptoms are however what bring the patient to the doctor and their progression/regression/stability over time is important in determining the need for treatment and the aggressiveness of treatment once instituted. LUTS have classically formed the initial database on which to formulate evaluation of potential BOO, indications for active treatment when obstructive BPH is present, and evaluation of the results of treatment.
2.5 RELATIONSHIP BETWEEN ERECTILE DYSFUNCTION AND LOWER URINARY TRACT SYMPTOMS.
The conventional opinion among urologists has long been that there was no relationship between LUTS and sexual dysfunction, except their greater occurrence with ageing4. Little evidence supporting the connection was available until the mid 1990s when several epidemiological studies assessing the
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prevalence of BPH and associated QoL issues suggested that LUTS by themselves could affect sexual functions4. Lukacs et al69 first reported in 1996 that impairment of patients’ perceived sexuality was related to both age and severity of LUTS. Subsequently, some workers noted that erectile dysfunction is frequently present in patients who presented with LUTS5,6,27,28,59. Other studies showed that severity of LUTS is a crucial risk factor for sexual dysfunction independent of age and co-morbidities8,59,71-73. Mario et al7 observed that severe LUTS were associated with higher rate of ED and was supported by other studies4,39,71,72,74. Elliott et al90 found that voiding phase LUTS were better predictors of ED than storage/filling phase LUTS.
Though epidemiologically, there is a link between ED and LUTS, Kevin4 noted that widespread acceptance is made possible if causal relationship is shown to have biological plausibility. He further highlighted the currently existing theories that support biological plausibility. These include the nitric oxide synthase (NOS)/Nitric oxide (NO) theory, the autonomic hyperactivity and metabolic syndrome hypothesis, the Rho-kinase activation/endothelial pathway and pelvic atherosclerosis. NOS/NO theory attempts to explain the link between ED and LUTS by the reduced production of NOS/NO in the pelvis, which includes the penis, bladder, and prostate. The role of NOS/NO in normal penile erection has been highlighted in section 2.2. Conditions associated with reduced function of nerves and endothelium can cause circulatory and structural changes in penile tissues, resulting in ED. NOS/NO theory also suggests that reduced NOS/NO results in smooth muscle proliferation, which may result in structural changes in the prostate and simultaneous increased contraction which affects outlet resistance and bladder compliance, leading to LUTS. In autonomic hyperactivity and metabolic syndrome hypothesis, it was hypothesized that noradrenaline and alpha 1-adrenoceptors, that mediate adrenergic contraction of smooth muscle in the prostate, bladder neck, urethra and the corpus cavernosa,
17
constitute the common link between LUTS and ED. Rho-kinase pathway is a regulatory mechanism thought to modify the sensitivity of contractile and regulatory proteins to calcium, leading to a smooth muscle contraction without changing intracellular calcium concentration. Rho-kinase activity and consequently increased calcium sensitivity of contractile machinery has been demonstrated in prostatic tissue and detrusor muscle of animals thus leaving speculation that the common link between LUTS and ED in humans is increased Rho-kinase activity. Pelvic atherosclerosis induces pelvic ischemia with consequences compatible with all theories mentioned above.
2.6 ASSESSMENT METHODS OF ERECTILE DYSFUNCTION AND LOWER URINARY TRACT SYMPTOMS
ED and LUTS are usually subjective symptoms that depend majorly on patient’s perception for clinical assessment. The validated self-administered questionnaires have been found useful in clinical assessment of patients with these complaints. These provide useful information on the prevalence, progression and bothersomeness of these conditions in community or hospital populations and impact of treatment39. Commonly used tools are discussed below.
ED ASSESSMENT
International index of erectile function (IIEF)
IIEF is a 15-item self - reported questionnaire developed and validated psychometrically to assess the efficacy of pharmacological treatment of ED39,42. It assesses five domains of sexual functioning: erectile function, orgasmic function, sexual desire, intercourse satisfaction and overall satisfaction. An abridged five-item version known as Sexual Health Inventory for Men (SHIM) has also been developed and validated39,40. This abridged version will be used in
18
this study. This is justified by its validity, applicability, and ease of use. The subject answers five questions on erection and sexual satisfaction. Each is scored on a five-point scale 1 to 5, where lower values represent poorer erectile function.
The possible scores range from 1 to 25. A score above 21 is considered a normal erectile function and at or below this cut-off, ED. Based on this scale, ED is further classified into four categories: severe ED (scores 1 to 7), moderate (8-11), mild to moderate (12 to 16), mild (17 to 21). No sexual activity over the past 4 weeks is scored zero and given a separate column on the questionnaire form for convenience40.
IIEF however has some limitations. It provides no information on the ejaculatory component, partner relationship or her sexual functioning and focuses exclusively on vaginal intercourse. This makes this tool inappropriate for use in men who are not heterosexual.
The brief sexual function inventory
This is an 11-item self-administered questionnaire validated psychometrially39,75. It evaluates sexual drive, erectile function, ejaculation, bother associated with sexual symptoms and overall satisfaction with sexual life.
However, the erectile function and ejaculatory domains are only partially evaluated by this tool.
Urolife scale
This is a validated tool for assessing health related QoL associated with BPH/LUTS. Its initial version consisted of 20 self-administered items in form of a visual analogue scale which assessed various aspects of physical and mental health, social life and overall health39,76. An abridged version has been developed and validated. This focuses on well-being, BPH-specific interference with
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activities and sexual life. The sexual life domain evaluates erection, sexual desire and satisfaction with sexual life 39,77.
Its limitations in clinical practice are partial evaluation of sexual function, and lack of identified sexual dysfunction severity classes.
The Danish prostatic symptoms score sex (DAN-PSSsex) and the International Continence Society sex (ICSsex)
The DAN-PSSsex assesses the severity and bothersomeness of stiffness of erection, amount of ejaculates and pain/discomfort on ejaculation39,78. This is scored in weighted score rated 0 to 9 by increasing severity of sexual symptom.
The value is calculated by multiplying symptom severity (0 – 3) by the bother severity (0 – 3)39. The ICSsex assesses the domains as above in DAN-PSSsex and includes the degree to which the respondent’s sexual life has been impaired by LUTS39,79.
However, these tools do not assess some aspects of sexual function like orgasm, sexual desire and satisfaction with sexual life.
LUTS ASSESSMENT
The close attachment of LUTS to prostatic disease has previously been mentioned. Following same trend is the assessment of LUTS. The concept of a symptom score or severity table for BPH was first developed by an ad hoc group formed by the Food and Drug Administration (FDA) in 1975; the initial recommendations were published in 197768. Over the years, investigators have evaluated several factors with such scoring tables to develop improved tool for assessment of LUTS
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The American Urological Association Symptoms Index (AUA-SI)/
The International Prostate Symptom Score (IPSS)
AUA-SI was a fallout of BPH guideline panel meeting during which AUA formed a measurement committee that formulated indices that addressed the issues relevant to symptom scores and produced a validated symptom index that became widely utilized. They concluded that AUA-SI has a correlation with severity of symptoms80,81. In 1994, the WHO adopted the AUA-SI as the IPSS82. The IPSS is a modification of AUA-SI, which includes a single question assessing the QoL or bother score based on the patient’s perception of the problem83. Patient is scored 0 to 6 corresponding to “delighted” and “terrible”
respectively. With the aid of other well structured questions, subjects are asked to indicate how often over the last one month they had incomplete bladder emptying, frequency, intermittency, urgency, weak stream, straining on micturation or nocturia. Scores of 0 to 5 are assigned corresponding to “not at all” and “almost always” respectively. The scores are summed up to create a score of 0 to 35. This is further categorized into three groups: mild symptoms (0 to 7), moderate symptoms (8 to 19), and severe symptoms (≥20).
Other tools for assessment of LUTS of historical importance include AUA- 784, the Maine Medical Assessment Program Score85, the Boyarsky score86, the Madsen-Iverson score87 and the Danish Prostatic Symptom Score88.
In this study, the IPSS will be used. This is based on its validity, correlation with severity of symptoms, wide utilization, and ease of use.
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CHAPTER THREE
3.0 PATIENTS AND METHODS
3.1 STUDY DESIGN AND SETTING
This was a descriptive cross-sectional study to determine the incidence and correlation of ED among adult male patients who presented with LUTS at the urology clinics of Nnamdi Azikiwe University Teaching Hospital (N.A.U.T.H).
NAUTH is a Tertiary Health Institution located in Nnewi, an industrial city of Anambra State, South-East of Nigeria, with estimated land mass area of 72km2 and total population of 157,569 people (2006 population census)89. The people are ethnically Igbos, the major language is Igbo, and they are predominantly Christians. The study centre receives referral for health problems with catchment areas spanning all through the state and its neighbourhood including Imo, Abia, Enugu, Ebonyi, Kogi and Delta States. Sometimes, farther areas may be involved because of nearness to patient’s relatives and people on business trips. The catchment areas have recorded a progressive increase in population from 22,658,410 in 2001 to 25,430,493 in 2005 with average annual growth of 3.5%89.
3.2 STUDY POPULATION AND SAMPLE SIZE
This study was a hospital-based study with emphasis on urological outpatient clinic. The cohort comprised of new patients ≥40 years that attended the urology clinic with LUTS. The sample size was calculated based on the statistical formula as shown below90.
nf = n 1+ n
N
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Where: nf = the desired sample size when population is less than 10,000 n = the desired sample size when population is more than 10,000
N = the estimate of the population size which is averagely 281. This was derived from a retrospective review of the cohort over a one year period. This figure justifies the choice of the statistical formula for calculation of the sample size (nf).
But:
n = z2pq d2
p = Prevalence rate i.e. estimate of % of key proportion to be measured. Value 13% (0.13) was chosen. This was estimated retrospectively by calculating the percentage of patients that are likely to have LUTS among all new patients attending the urology clinic over a one year period.
i.e 281 × 100 =12.997 2162
q = the remaining proportion not likely to have LUTS q = 1.0-p (i.e. 0.87)
d = Absolute precision i.e. the value required (in percentage points) which in actual term describes the maximum difference between the population rate and the sample rate that can be tolerated. 5% (.05) is taken for this study.
z = confidence level. Usually corresponds to 95% level of significant.
Its desired value from the normal distribution table is 1.96 n = (1.96)2 (0.13) (0.87)
(0.05)2 =173.79
*Value rounded up to 174.
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Thus, nf = 174 1+ 174
281 = 174
1.619217 =107.5 ≈ 108
3.3 PATIENT SELECTION
Patient selection was by purposive criterion sampling method. This entailed picking all the subjects who met some specific criteria. The subjects included in the study were all new patients attending the urology clinic of N.A.U.T.H with clinical features suggestive of LUTS without the under listed exclusion criteria, and who also gave their consent to take part in the study.
Exclusion criteria included
1. Patients already on treatment for ED or LUTS 2. Patients with clinical features of UTI
3. Patients with major psychiatric disorders 4. Patients with penile anatomical disorders 5. Patients who were not heterosexuals.
3.4 STUDY PERIOD
The study was conducted over a one year period.
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3.5 ETHICAL ISSUES
All protocol and informed consent procedures were approved by the research and ethical committee of the NAUTH (Appendix I).
Written informed consents, (Appendix II) were obtained from subjects who met the inclusion criteria.
3.6 OUTCOME MEASURES (DATA COLLECTION & QUALITY CONTROL)
All patients who consented and met the inclusion criteria were recruited for the study.
Each subject was interviewed by me using a standard proforma (Appendix III) to obtain information about his biodata, major co- morbidities, family history, social life style and past surgical history. Subjects were also screened for lower urinary tract infection, undiagnosed diabetes mellitus, renal tuberculosis, schistosomiasis, prostatitis and painful bladder syndrome by specific questions.
LUTS was assessed using the validated 7-item IPSS questionnaire form (Appendix IV) and ED with IIEF-5 questionnaire form (Appendix V). LUTS and ED QoL were assessed with the QoL section of IPSS questionnaire. However, ED QoL was assessed by replacing urinary condition with erectile condition.
To ensure quality control, all subjects were interviewed by the same interviewer (the researcher) who also assisted in filling the questionnaires. The subjects were interviewed in a separate room with guarantee of absolute confidentiality in order to aid free flow of information.
3.7 DATA PROCESSING AND ANALYSIS.
Data collected were analyzed using multipurpose computer Statistical Package for Social Sciences version 17 (SPSS v 17) with the help of a statistician. Results obtained were expressed using tables and charts where
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necessary. The data were subjected to linear regression and Chi square tests where applicable. The statistical significance was set at p-value ≤ 0.05.
3.8 SCOPE AND STUDY LIMITATIONS
The scope was to determine the incidence of ED and evaluate the correlations of ED and LUTS among adult Nigerian male patients who presented with LUTS at the urology clinics of N.A.U.T.H. The prevalence of common associated co- morbidities and effect on Quality of Life (QoL) was also assessed.
The limitations:
The IPSS and IIEF were designed to be self-administered. However, many of the subjects were illiterate and semiliterate, thus the researcher resorted to slight modification of the IIEF without alteration in its main structure. The researcher also assisted in the filling of the questionnaire. This could introduce observer bias to the study.
In the study, the co-morbidities were self-reported. No attempts were made to validate respondents’ answers with their medical records. Also, single screening for conditions like diabetes and hypertension may not be enough to exclude them. These medical conditions may be asymptomatic and unknown to the subject and thus may be underreported
The study population was also selective. Thus the findings may not be directly applicable to the general population.
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CHAPTER FOUR RESULTS
A total of 110 patients were studied. The age ranged from 43 years to 80 years with a mean age of 65.8 ± 7.95 years. The peak age group was in age range 71 to 75 years with 34 patients. Other basic characteristics of the patients were also noted (Table 1, Figure 3).
Table 1 Baseline characteristics of patients (n = 110).
Characteristics Range Mean ± SD
Age (yrs) 43.0-80.0 65.8 ± 7.95
Height (m) 1.60-1.81 1.68 ± 0.04
Weight (Kg) 46.0-98.0 69.61 ± 10.66
BMI (Kg/m2) 16.9-34.72 24.59 ± 3.55
SBP (mmHg) 110.0-192.0 141.6 ± 19.98
DBP (mmHg) 60.0-110.0 81.45 ± 10.86
Figure 3: The distribution of LUTS according to age groups (n=110).
n=6 n=34
n=22
n=14 n=24
n=2 n=4 n=4
0 5 10 15 20 25 30 35
40-45 46-50 51-55 56-60 61-65 66-70 71-75 76-80 AGE GROUPS (YRS)
FREQUENCY(%)
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Body mass index (BMI) ranged from 16.9 to 34.7 with mean BMI of 24.59 ± 3.55. The peak BMI was within the 18.5 to 24.9 group representing 47.3% (Figure 4). This means that most of the patients had normal body weight.
Figure 4: The incidence of LUTS according to the level of adiposity (n=110).
Ninety-four patients (85.5%) were married and had their wives alive while 16 patients (14.5%) were widowed. One hundred and eight (98.2%) were Christians while 2 (1.8%) were traditionalists. Sixty (54.5%), 20 (18.2%) and 30 (27.3%) patients had up to primary, secondary and post secondary levels of education respectively. Thus there is a tendency towards illiteracy or semi- illiteracy. The life-style patterns of the patients are also represented in table 2.
n=6 n=46
n=52
n=6 0
5 10 15 20 25 30 35 40 45 50
<18 18-24.9 25-29.9 30-34.9
ADIPOSITY LEVEL BY BMI (KG/M2)
FREQUENCY(%)
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Table 2 Frequencies of other characteristics and life-style of patients
Frequency Percentage
Marital Status Married Widowed Total
94 16 110
85.5*
14.5 100 Religion
Christianity Traditionalist Total
108 2 110
98.2*
1.8 100 Highest Level of
Education Primary Secondary Post-secondary Total
60 20 30 110
54.5*
18.2 27.3 100 Smoking Habit
Smokers Non-smokers Total
8 102 110
7.3 92.7*
100 Alcohol Intake
Yes No Total
22 88 110
20 80*
100
* Option with the highest frequency amongst respondents
The mean total LUTS and ED scores were 15.81 ± 7.52 and 16.90 ± 6.45 respectively. Other graded LUTS scores and QoL scores are represented in table 3.
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Table 3 LUTS, ED and Quality of life scores for patients (n = 110).
Range Mean ± SD
LUTS Score (Voiding phase)
0-19 7.6 ± 5.11
LUTS Score (Filling &
Storage phase)
1-15 8.12 ± 3.67
Total LUTS Score 2-33 15.81 ± 7.52
ED Score 8-25 16.90 ± 6.45
LUTS Quality of life score
1-6 4.05 ±1.07
ED Quality of life score 3-6 4.18 ± 1.22
The number of LUTS patients that had sexual intercourse within the preceding one month was 44 (40%) while the number of those that did not have sexual intercourse was 66 (60%).We did not assess the possible reasons for the greater number of patients that did not attempt sexual intercourse within the preceding one month. However, using ED scores to assess the LUTS patients that had sexual intercourse, 16 (36.4%) had normal sexual function (ED score >21), 8 (18.2%) had mild ED (ED score 17 to 21), 8 (18.2%) had mild to moderate ED (ED score 12 to 16), 12 (27.2%) had moderate ED (ED score 8 to 11) while none had severe ED (≤ 7). Thus a total of 28 (63.6%) LUTS patients who had attempted sexual intercourse had some form of ED without any severe ED (figure 5).
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Figure 5: Distribution of ED among LUTS patients who had sex (n=44)
RELATIONSHIP BETWEEN SEVERITY OF ED AND LUTS
A linear regression between ED scores and LUTS scores indicated a significant relationship between ED scores and voiding phase, filling-storage phase, and total LUTS scores respectively (table 4, figures 6-8).
Table 4: Pearson’s bivariate correlation test between ED scores and LUTS scores ED Score vs. Regression Coefficient P-value
Voiding phase LUTS Score
0.388 0.009
Filling-storage phase LUTS Score
0.428 0.004
Total LUTS Score 0.445 0.002
n=0 n=12
n=8 n=8
n=16
0 5 10 15 20 25 30 35 40
NORMAL MILD ED MILD TO MODERATE
ED
MODERATE ED
SEVERE ED
INCIDENCE OF ED
FREQUENCY(%)
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Figure 6: Scatter plot between voiding phase LUTS and ED (n=44)
32
Figure 7: Scatter plot between filling-storage phase LUTS and ED (n=44)
33
Figure 8: Scatter plot between total LUTS and ED (n=44)
This positive correlation thus shows that the higher the LUTS scores (voiding phase, filling-storage phase and total), the higher the ED scores. However Pearson’s chi-square analysis of severity of ED and graded LUTS score revealed no significant association between the severity of ED and that of voiding phase and filling-storage phase LUTS. Conversely, severity of ED was significantly related (p = 0.0001) to the severity of total LUTS score (Table 5).
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Table 5: Relationship between the severity of ED and graded LUTS scores Severity of ED vs. Pearson’s Chi2 P-value
Graded voiding phase LUTS score
6.33 0.096
Graded filling-storage phase LUTS score
7.11 0.068
Graded Total LUTS score 26.15 0.0001
EFFECTS OF ED AND LUTS ON QoL:
The range and mean values of LUTS and ED QoL scores are as previously reported in table 3. One hundred (90.9%) of LUTS patients were worried about their LUTS while 10 (9.1%) were not worried. Among 44 (40%) of LUTS patients that had sexual intercourse, 22 (50%) were worried about their sexual function while same number of patients were not. Twenty-two of LUTS patients were worried about both LUTS and ED. Among these, 10 (45.5%) found LUTS more worrisome while 8 (36.3%) found ED more worrisome. In 4 (18.2%) of LUTS patients, both ED and LUTS were found worrisome (Table 6).
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Table 6 Assessment of the quality of life of patients
Frequency Percentage Attempted Sex (n=110)
Yes No Total
44 66 110
40 60 100 Worried about LUTS (n=110)
Yes No Total
100 10 110
90.9 9.1 100 Worried about ED among sex
attempted group (n=44) Yes
No Total
22 22 44
50 50 100 Which is more worrisome (n=22)
ED LUTS Both Total
8 10 4 22
36.3 45.5 18.2 100
Pearson’s Chi-square analysis showed no significant relationship between severity of filling-storage phase and total LUTS scores and QoL of patients with LUTS. Conversely, QoL shows a significant relationship (P<0.05 and P<0.01) between severity of voiding phase LUTS and severity of ED (Table 7).
Table 7: Relationships of severity of LUTS and ED with the Quality of Life Pearson’s Chi2 P-value
Severity of voiding phase LUTS vs. QoL
8.36 0.015
Severity of filling- storage phase LUTS vs.
QoL
1.20 0.548
Severity of Total LUTS vs. QoL
5.48 0.242
Severity of ED vs. QoL 10.16 0.006
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This indicates that the more severe the voiding phase LUTS or ED, the poorer the QoL and vice versa.
CO-MORBIDITIES AND OTHER CLINICAL FINDINGS
There was low incidence of co-morbidities and their family history among LUTS patients (Table 8).
Table 8: Prevalence of Co-morbidities in patients
Frequency Percentage Hypertension
Yes No Total
30 80 110
27.3 72.7*
100 Diabetes
Yes No Total
16 94 110
14.5 85.5*
100 Heart disease
Yes No Total
4 106 110
3.6 96.4*
100 Stroke
Yes No Total
4 106 110
3.6 96.4*
100 Previous surgeries
Yes No
No response Total
34 58 18 110
30.9 52.7*
16.4 100
* Option with the highest frequency amongst respondents.
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CHAPTER FIVE DISCUSSION
DEMOGRAPHY
The peak age range of 71years to 75 years and mean age of 65.8 ± 7.95 years in this study supports the predominance of LUTS among the ageing population as reported by other studies2,91,92. Kupelian et al2 in a Boston community health survey reported peak age range 60 years to 69 years. He studied the prevalence of lower urinary tract symptom and effect on quality of life in a racially and ethnically diverse random sample. Elliott et al91 did a hospital based study to find the correlation between obstructive LUTS and ED.
They noted peak age range of 70 years to 80 years with mean age of 68.2 years.
Hoesl et al92 reported mean age of 63.4 ± 8.5 years. They studied ED prevalence, bothersomeness and diagnosis in patients consulting urologists for benign prostatic syndrome (PBS)
THE INCIDENCE OF ED
The incidence of ED in this study was 63.6%. This incidence is slightly higher than the finding by Berrada et al22. They worked on the prevalence of ED and its correlates among Moroccan men residing in Casablanca. The age range was 25years to 85 years. They reported ED incidence of 53.6%. Spector et al93 also reported a lower incidence of 53% among 109 United Kingdom men aged 16years to 65 years. They worked on the prevalence and perceived aetiology of male sexual problems in a non-clinical sample. This study was among older patients in whom ED incidence is expected to be higher. This study was also restricted to patients who had LUTS, a compounding issue for ED. Thus it is
expected that ED incidence would be higher among them.
