Current Benign Prostatic Hyperplasia Treatment

Impact on Sexual Function and Management of Related Sexual Adverse Events

V. Mirone; A. Sessa; F. Giuliano; R. Berges; M. Kirby; I. Moncada

Int J Clin Pract. 2011;65(9):1005–1013 

Abstract and Introduction

Abstract

Benign prostatic hyperplasia (BPH) is a common disease in older men that can lead to lower urinary tract symptoms (LUTS). Male sexual dysfunction is also an age-related condition. Epidemiological studies have confirmed an association between BPH/LUTS and sexual dysfunction in ageing men that is independent of the effects of age, other co-morbidities and lifestyle factors. Proposed pathophysiological mechanisms for BPH/LUTS-associated sexual dysfunction include the nitric oxide/cyclic guanosine monophosphate (NO/cGMP) pathway, rho-kinase and endothelin-1 activity, autonomic nervous system overactivity and the metabolic syndrome, and pelvic organ atherosclerosis. Both BPH/LUTS and sexual dysfunction can have a substantial negative impact on a man's quality of life. However, urologists and primary care physicians appear to under-recognise sexual dysfunction in men with BPH/LUTS. Current guidelines recommend alpha-blockers and 5-alpha reductase inhibitors, either alone or in combination, among appropriate medical treatment options for BPH/LUTS. Randomised, controlled trials demonstrate that these therapies can be associated with sexual adverse effects (AEs) such as loss of libido, erectile dysfunction and ejaculatory disorders. Sexual dysfunction should be fully evaluated in men requiring treatment for BPH/LUTS using validated questionnaires. Management of sexual dysfunction in men treated for BPH/LUTS should involve assessment of co-morbidities and concomitant medications, consideration of lifestyle interventions such as weight loss and increased physical activity to improve risk factors and, if necessary, introduction of pharmacotherapies. In addition, physicians should provide patients with proper counselling on the possible sexual AEs of medical therapies for BPH/LUTS and their impact on sexual satisfaction, while being aware of the possibility that counselling in itself is likely to influence reported rates of sexual dysfunction.

Introduction

Benign prostatic hyperplasia (BPH) and benign prostatic enlargement (BPE) are common diseases in older men that can lead to lower urinary tract symptoms (LUTS).[1,2] The relationship between BPH/LUTS and ageing is well established. The characteristic histological changes of BPH are increasingly more common as men get older and found in 80–90% of men aged > 80 years.[3,4] Similarly, the prevalence of LUTS increases with age, from 14% for men in their fourth decade to more than 40% for men in their sixth decade.[3,4]

Male sexual dysfunction is also an age-related condition. For example, in the European Male Ageing Study of 3369 community-dwelling men aged 40–79 years (mean 60 ± 11 years), moderate or severe erectile dysfunction (ED) was reported by 6% of men in their forties, rising to 64% of men aged over 70 years.[5] Data on the natural history of ED indicate that the annualised incidence rate (new onset) of ED is 1.2%, 3.0% and 4.6% in men aged 40–49 years, 50–59 years and 60–69 years, respectively.[6] Ejaculatory disorders (EjD) also increase in prevalence as men age; in a community-based study of Dutch men aged 50–78 years, significant EjD increased from 3% in men aged 50–54 years to 26% in men aged 70–78 years.[7] Other studies have shown age to be a predisposing factor in reduced ejaculatory volume and anejaculation.[8]

Both BPH/LUTS and sexual dysfunction can have a substantial negative impact on a man's quality of life.[9–11] Studies show that moderate LUTS has the same negative impact on quality of life as potentially life-threatening conditions such as cancer, diabetes or hypertension,[10] while ED is commonly associated with depression and diminished quality of life.[11]

Current guidelines recommend alpha-blockers and 5-alpha reductase inhibitors (5ARIs), either alone or in combination, as appropriate medical treatment options for BPH/LUTS.[2,12] It is well recognised that these treatment options may have an impact on sexual function.[13] In June 2010, GlaxoSmithKline convened an expert panel of urologists and primary care physicians, chaired by Professor Vincenzo Mirone, to discuss key topics and issues related to current medical therapies for BPH/LUTS and related sexual adverse effects. Participants were selected under the direction of the meeting Chair. GlaxoSmithKline contributed to the meeting agenda, although the expert panel retained final control of both the agenda and presentations. A key objective of the meeting was to develop the current manuscript (which all participants agreed to author, with support from a medical writer funded by GlaxoSmithKline), the purpose of which is to provide physicians with a greater understanding of topics such as the epidemiology of BPH/LUTS and sexual dysfunction, possible common pathophysiological mechanisms, and the impact of medical treatments for BPH/LUTS on sexual function. In addition, the manuscript provides recommendations for evaluation and management of sexual dysfunction in men requiring treatment for BPH/LUTS.

Epidemiology: The Association Between Age, BPH/LUTS and Sexual Dysfunction

Over the last decade, population- and practice-based studies have provided consistent evidence of an association between BPH/LUTS and sexual dysfunction in ageing men that is independent of the effects of age, other co-morbidities (e.g. hypertension, diabetes, dyslipidaemia and coronary heart disease) and lifestyle factors.[14,15] One such study is the Cologne Male Survey, in which responses of 4489 men to questionnaires on ED and voiding symptoms [International Prostate Symptom Score (IPSS)] were assessed.[16] The overall prevalence of ED and LUTS was 19.2% and 31.2%, respectively. The prevalence of LUTS in men suffering from ED was 72.2% compared with 37.7% in men with normal erectile function (odds ratio 2.11) and further analysis identified LUTS as a risk factor for ED independent of age.

The Multinational Survey of the Ageing Male (MSAM-7), one of the largest population-based studies of ageing men yet conducted, evaluated the associations between age, LUTS, concomitant comorbidities and male sexual dysfunction in > 12,000 men in the United States and Europe.[17] In MSAM-7, the overall prevalence of LUTS was 90%, while the overall prevalence of ED and EjD was 49% and 46%, respectively.[17] The rate of both ED and EjD was significantly dependent on age and correlated highly with the severity of LUTS (Figure 1); similar results were reported for sexual desire. These associations were independent of other factors such as comorbidities and tobacco use. In addition, LUTS were a stronger predictor of sexual dysfunction than diabetes, heart disease or hypertension.[17]

Figure 1.

 

Erectile dysfunction (A) and ejaculatory dysfunction (B) according to age and lower urinary tract symptoms (LUTS) severity(17). Reprinted with permission from Elsevier. (A) Base: total sample. (B) Base: men who have erections

The EpiLUTS study assessed the impact of LUTS on sexual health among more than 11,000 men aged at least 40 years (mean age 56.1 years) in the USA, UK and Sweden, 71% of whom reported being sexually active.[18] There was a significant inverse correlation (r = −0.28; p < 0.001) between the Erectile Function (EF) domain of the International Index of Erectile Function (IIEF) and the IPSS, suggesting that increasing ED severity was associated with increasing severity of LUTS. In addition, men with voiding, storage and postmicturition LUTS had the highest proportion of EjD and were more likely to experience premature ejaculation.[18] The EpiLUTS study also showed that LUTS are associated with decreased enjoyment of sexual activity.

Another study assessed the impact of voiding and storage LUTS on recorded diagnosis of sexual dysfunction in men from 333 UK general practice clinics.[19] Men with a diagnosis of storage or voiding LUTS, or both conditions, had a significantly increased prevalence of all types of sexual dysfunction compared with men with no recorded LUTS. The odds ratio for ED in men with storage LUTS relative to those with no LUTS was 3.0 (95% CI 2.61–3.40); for voiding LUTS, the odds ratio for ED was 2.6 (95% CI 2.44–2.69).[19] It is possible that storage LUTS have a bigger impact on erectile function than voiding LUTS;[20] interrupted sleep as a result of nocturia, for example, may contribute to ED. Another potential mechanism for the link between nocturia and ED is interruption of nocturnal erections, which may reduce oxygenation of cavernosal tissue.

Pathophysiological Mechanisms for BPH/LUTS-associated Sexual Dysfunction

Four pathophysiological mechanisms have been put forward to explain the association between BPH/LUTS and sexual dysfunction. For each of the mechanisms, most of the evidence is from laboratory studies and almost exclusively relates to an association between BPH/LUTS and ED as a result of impaired relaxation of smooth muscle fibres from both the lower urinary tract and erectile tissue. It is important to note that while each of the possible explanations is biologically plausible, causality has not been proven for any.

Nitric Oxide/Cyclic Guanosine Monophosphate Pathway

The rationale behind the NO/cGMP theory is that production of NO synthase (NOS) and NO in the pelvis (including the penis, the prostate and the bladder) is reduced in the presence of various systemic factors that are also risk factors for ED (diabetes, smoking, dyslipidaemia and hypertension). Reduced levels of NOS/NO in the penis lead to ED; reduced levels in the prostate and bladder increase smooth muscle tone of the bladder neck and urethra and may stimulate prostatic smooth muscle cell proliferation that results in increased outlet resistance.[21] In support of this theory, NOS activity has been demonstrated in tissue from human urethra, corpus cavernosum, prostate, vas deferens and bladder neck.[22] In addition, a relaxing effect of NO donors and phosphodiesterase-5 (PDE5) inhibitors on human prostate tissue and bladder neck has been shown.[23–26] In vitro models have also shown an antiproliferative effect of NO donors on prostatic smooth muscle cells.[27]

Rho-kinase and Endothelin-1 (ET-1) Activity

The rho-kinase pathway is the major mechanism regulating calcium sensitivity (and hence contraction) of smooth muscle, while ET-1 is a potent vasoconstrictor that affects the rho-kinase pathway.[28] The theory behind a role for rho-kinase and ET-1 in the development of BPH/LUTS and ED involves rho-kinase-induced changes in the calcium sensitivity of smooth muscle. ET-1, which is a factor in the increased smooth muscle activity observed in LUTS and ED, exerts its effects via rho-kinase. In animal models, blocking the activity of rho-kinase has been shown to inhibit proliferation and adrenergic contraction of prostatic smooth muscle cells,[29] while ET-1 has been shown to mediate smooth muscle contraction and stimulate smooth muscle cell proliferation in normal prostate.[28] Other experimental studies have shown rho-kinase expression and activity is increased in the corpus cavernosum of bladder-obstructed rats, suggesting involvement of this pathway in the pathogenesis of LUTS-associated ED.[30]

Overactivity of the Autonomic Nervous System and the Metabolic Syndrome

It has been proposed that LUTS secondary to BPH may be part of the metabolic syndrome, a condition which also includes risk factors for ED (e.g. obesity, insulin resistance, dyslipidaemia and hypertension).[31,32] Epidemiological studies have observed an association between LUTS and the metabolic syndrome.[33] A possible link between LUTS/BPH and the metabolic syndrome is the autonomic nervous system.[34] The metabolic syndrome results in autonomic sympathetic overactivity through complex mechanisms that are not completely understood,[35] while animal studies support a link between overactivity of the autonomic nervous system and the development of LUTS; growth of the prostate gland is profoundly affected by autonomic innervation of the pelvis, while spontaneously hypertensive rats develop BPH and ED following autonomic nervous system hyperactivity.[36–39]

Autonomic nervous system hyperactivity is also associated with BPH/LUTS in humans. A study of tilt-table testing (a measure of autonomic tone and reactivity) in 38 men with BPH/LUTS showed a significant association between increased sympathetic tone and the level of LUTS.[40] This association remained after controlling for other factors known to influence sympathetic tone, such as age, body mass index, abdominal obesity, insulin levels and physical inactivity.

Pelvic Organ Atherosclerosis

A number of risk factors for vascular disease are also risk factors for ED, such as hypertension, smoking, diabetes and hypercholesterolaemia. These risk factors have been proposed to contribute to LUTS by reducing pelvic arterial blood flow, resulting in smooth muscle loss from the bladder, prostate fibrosis and increased urethral resistance.[21,41] A similar process occurring in the penis would cause loss of smooth muscle cells and contribute to the development of ED. In animal models, atherosclerosis-induced chronic ischaemia has been shown to cause bladder and penile fibrosis.[42] Chronic ischaemia has also been shown to induce fibrosis in the prostate, along with impaired neurogenic relaxation.[43,44] Pelvic atherosclerosis may also induce autonomic nervous system hyperactivity, reduce NOS expression and upregulate rho-kinase[21]

Impact of Medical Treatments for BPH/LUTS on Sexual Function: Evidence From Clinical Trials

Randomised, controlled trials demonstrate that standard medical therapies for BPH/LUTS are associated with sexual adverse effects (AEs) such as decreased or loss of libido, ED and EjD.[45,46] The rates of sexual AEs reported in these trials vary, most likely reflecting differences in study treatment, study duration, AE reporting method, adjudication and AE classification. Such differences make it difficult to compare the rate of sexual AEs across studies and treatments.

5-alpha Reductase Inhibitors

While treatment with 5ARIs (finasteride and dutasteride) is generally well tolerated, side effects related to sexual function do occur (). The profile and incidence of sexual AEs is similar for both treatments. The precise mechanisms of 5ARI-induced sexual dysfunction are not known, although it may be related to the inhibition of androgen-stimulated NOS expression.[49] Evidence from a number of studies suggests that the likelihood of new sexual AEs with 5ARI treatment decreases with longer duration of therapy. Analysis of 4-year data from PLESS demonstrated that, compared with placebo, men treated with finasteride experienced new drug-related sexual AEs with an increased frequency only during the first year of therapy.[50] Similarly, the incidence of drug-related sexual AEs decreased with longer duration of therapy in an analysis of the 4-year safety and tolerability of dutasteride.[51]

Table 1.  Sexual adverse events reported in various clinical trials of medical therapies for BPH/LUTS

ED (%) EjD (%) Decreased libido (%)
Alpha-blockers (12)
   Alfuzosin 3 1
   Doxazosin 4 0 3
   Tamsulosin 4 10
   Terazosin 5 1 3
   Placebo 4 1 3
   Silodosin (52)* 28
Dutasteride (47)†
   Dutasteride 7.3 2.2 4.2
   Placebo 4.0 0.8 2.1
Finasteride (48)†
   Finasteride‡ 8.1 4.5 6.4
   Placebo‡ 3.7 0.9 3.4

*Treatment-emergent adverse events. Data from pooled results of two phase III, 12-week studies. †Drug-related adverse events reported in year 1 of study. ‡EjD includes decreased ejaculate volume and ejaculation disorder; ED reported as 'impotence'. ED, erectile dysfunction; EjD, ejaculatory dysfunction.

Alpha-blockers

There are five alpha-blockers available in Europe for the treatment of BPH/LUTS (alfuzosin, doxazosin, tamsulosin, terazosin and silodosin) with differences between the drugs in terms of the uroselectivity of their action and the associated risk of sexual AEs (). In particular, alpha-blockers are associated with an increased risk of EjD, with the different agents appearing to differ in their likelihood of causing EjD.[53,54] The exact mechanisms underlying sexual dysfunction induced by alpha-blocker therapy are not clear. One suggestion is that these agents, particularly those selective for the α1A-adrenoceptor that is widely distributed in organs involved in the emission phase of ejaculation, may effect this first phase of the ejaculation process.[13] A second hypothesis involves an effect of alpha-blockers on the central nervous system, possibly via binding to serotonin and/or dopamine receptors, to block signals controlling ejaculation.[13,49]

Table 1.  Sexual adverse events reported in various clinical trials of medical therapies for BPH/LUTS

ED (%) EjD (%) Decreased libido (%)
Alpha-blockers (12)
   Alfuzosin 3 1
   Doxazosin 4 0 3
   Tamsulosin 4 10
   Terazosin 5 1 3
   Placebo 4 1 3
   Silodosin (52)* 28
Dutasteride (47)†
   Dutasteride 7.3 2.2 4.2
   Placebo 4.0 0.8 2.1
Finasteride (48)†
   Finasteride‡ 8.1 4.5 6.4
   Placebo‡ 3.7 0.9 3.4

*Treatment-emergent adverse events. Data from pooled results of two phase III, 12-week studies. †Drug-related adverse events reported in year 1 of study. ‡EjD includes decreased ejaculate volume and ejaculation disorder; ED reported as 'impotence'. ED, erectile dysfunction; EjD, ejaculatory dysfunction.

In controlled clinical trials with tamsulosin, an alpha1A-selective alpha-blocker, the proportion of patients reporting EjD varied between 4% and 26% depending on the dose of tamsulosin used and study duration.[55,56] Also in clinical studies, the proportion of patients reporting EjD with silodosin was 28%.[52] By contrast, the reported incidence of EjD related to the use of doxazosin, terazosin and alfuzosin (non-selective alpha-blockers) is generally < 1.5%.[12] Data from clinical studies and experience from clinical practice support the notion that EjD occurs more commonly with tamsulosin and silodosin.[15,52]

Combination Therapy: 5ARI Plus Alpha-blocker

In both the MTOPS and CombAT studies, the incidence of sexual AEs was higher with combination therapy than with monotherapies (). For EjD, the rate reported in the combination therapy arms was higher than the sum of the rates reported in the monotherapy arms. Despite this, in both studies the discontinuation rates in the combination therapy arms were similar to those in the monotherapy arms.[45,46] This suggests that drug-related sexual dysfunction does not represent a clinically significant cause of treatment withdrawal, or that the benefits of therapy outweigh the impact of drug-related sexual AEs.

Table 2.  Sexual adverse event rates for 5ARIs, alpha-blockers and the combination reported in randomised, controlled trials

Patients with AE (%)
5ARI Alpha-blocker Combination therapy
CombAT (45)*; dutasteride and tamsulosin
   Decreased libido 3 2 4
   ED 7 5 9
   Semen volume decreased < 1 < 1 2
   Retrograde ejaculation < 1 1 4
MTOPS (46) †; finasteride and doxazosin
   Decreased libido 2.36 1.56 2.51
   ED 4.53 3.56 5.11
   EjD (abnormal ejaculation) 1.78 1.10 3.05

*Drug-related adverse events. †Reported among the 10 most frequent adverse events; data expressed as rate per 100 person-years (incidence density). 5ARIs, 5-alpha reductase inhibitors; AE, adverse effect; ED, erectile dysfunction; EjD, ejaculatory dysfunction.

Impact of Medical Treatments for BPH/LUTS on Sexual Function: Perceptions in Clinical Practice

Data from a survey of urologists and primary care physicians (PCPs) suggest that doctors under-recognise sexual dysfunction in men with BPH/LUTS.[57] In this study, physicians were sent a 12-question survey to gain an understanding of how they treat patients with LUTS/BPH and of the occurrence of sexual dysfunction with and without medical therapy in these patients. Urologists (n = 1087) estimated that 19% of their patients experienced sexual dysfunction because of LUTS, while PCPs (n = 177) estimated that 27% of their patients had impaired sexual function because of LUTS. These estimates contrast sharply with data from epidemiological studies, which suggest prevalence rates of ED and EjD in excess of 50% in men with BPH/LUTS.[58]

Data from a cross-sectional study in four European countries is informative with regard to patients' willingness to continue treatment in the face of potential adverse events.[9] The study showed that 50–60% of patients would not agree to treatment, even in return for complete suppression of urinary problems, if ED or EjD was inevitable. However, these proportions were no higher (and in some examples lower) than for other potential AEs such as nasal congestion (56%), itching (66%), significant headache (70%), nausea (74%) and digestive disorders (74%).

There is also evidence to suggest that counselling on sexual AEs generates a higher rate of sexual dysfunction being reported than no counselling. In a study of 120 sexually active men with a clinical diagnosis of BPH, blinded administration of finasteride was associated with a significantly higher proportion of sexual dysfunction in men informed about potential sexual side effects compared with those who were not counselled (Figure 2).[59] This so-called nocebo effect (an adverse effect that is not a direct result of the specific pharmacological action of the drug) has also been reported in other settings; for example, reporting of ED has been shown to be related to knowledge of side effects among patients receiving beta-blockers for cardiovascular disease.[60] Several factors have been identified that appear to be associated with this phenomenon, including a patient's expectations of adverse effects at the start of treatment, psychological characteristics such as anxiety and depression and a patient's susceptibility to suggestions of possible adverse effects associated with treatment.[61]

Figure 2.

 

Impact of counselling on reports of sexual dysfunction in men receiving finasteride (59)

Evaluation of Sexual Dysfunction in Men Requiring Treatment for BPH/LUTS

It is likely that a substantial proportion of men who present with BPH/LUTS will already have some degree of sexual dysfunction. It is therefore important to thoroughly assess sexual function before initiating pharmacotherapy for BPH/LUTS (Figure 3). In the same way that LUTS should be assessed using the IPSS, sexual function should be assessed using validated questionnaires. The IIEF is a 15-question tool that has been validated for the assessment of erectile function.[62] A validated abbreviated version, the IIEF-5, is also available,[63] although use of the full version is recommended whenever possible. The IIEF covers erectile function, orgasmic function, sexual desire, intercourse satisfaction and overall satisfaction, but does not adequately address EjD; therefore an additional tool is required. A four-item version of the Male Sexual Health Questionnaire has been developed and validated for the assessment of EjD[64] and is suitable for use in the clinical practice setting.

Figure 3.

 

Proposed algorithm for the management of sexual dysfunction in men treated for benign prostatic hyperplasia/lower urinary tract symptoms (BPH/LUTS)

Some physicians, especially in the primary care setting, may not have sufficient time during a single consulation to administer the full IIEF along with the IPSS and a tool for assessing EjD. One solution to this problem is to make the assessments over several consultations. The questionnaires for assessing LUTS and sexual function are suitable for self-administration by patients, so the relevant questionnaires could be provided to patients to complete at home when they first present with LUTS, and a follow-up appointment made during which the completed questionnaires are evaluated and any treatment decisions taken. Abbreviated questionnaires that have been validated psychometrically, including the IIEF-5 mentioned previously, are available. Another shorter questionnaire is the Male Sexual Function-4 (MSF-4), a 4-item questionnaire that covers interest in sex, quality of erection, achievement of orgasm and achievement of ejaculation ().[65,66]

Table 3.  Male Sexual Function-4 item (MSF-4) questionnaire (65). Reprinted with permission from John Wiley and Sons

How would you rate the following aspects of your life? (Circle one answer for each question)
Very strong Strong Moderate Weak Very weak None
1. Your interest in sex 0 1 2 3 4 5
2. The quality of your erection 0 1 2 3 4 5
3. Achieving orgasm 0 1 2 3 4 5
4. Achieving ejaculation 0 1 2 3 4 5

Management of Sexual Dysfunction in Men Treated for BPH/LUTS

There are a number of elements to consider when managing sexual dysfunction in men receiving treatment for BPH/LUTS, regardless of whether the sexual problems are co-morbid conditions or an adverse effect of the medication for BPH/LUTS. It is important to understand the impact of any sexual dysfunction on the patient and their partner; the impact is likely to be less in men who are not sexually active and in men whose LUTS are most serious and bothersome.

It is also important to obtain information on comorbidities and concomitant medications, and be aware of medications that can affect erectile capacity. Many men with ED will also have hypertension and some antihypertensive drugs (e.g. thiazide diuretics) have ED as a potential side effect; in such cases, switching to a medication that is less likely to cause ED (e.g. angiotensin receptor blocker) may help to alleviate the problem.[67] Other drug classes that can interfere with male sexual function include antihistamines, psychotherapeutics, Parkinson's disease drugs and muscle relaxants, as well as recreational drugs such as alcohol.

An algorithm to improve sexual dysfunction in men who may require medical therapy for BPH/LUTS is proposed in Figure 3. Sexual function should be assessed thoroughly before initiating medical therapy for BPH/LUTS. If sexual dysfunction is identified, non-pharmacological interventions such as lifestyle changes should be considered. For example, ED is associated with modifiable risk factors such as obesity, physical inactivity and the metabolic syndrome, which can be addressed to a degree through lifestyle changes.[68,69] As well as improving erectile function, interventions such as weight loss and increased physical activity may have a positive impact on LUTS as well as improving overall cardiovascular health. If drug therapy is considered necessary, PDE5 inhibitors are a highly effective treatment option.

If sexual dysfunction emerges after initiation of pharmacotherapy for BPH/LUTS, the options available depend on the type of sexual dysfunction and the BPH/LUTS treatment regimen. In men who present with ED, PDE5 inhibitors should be considered. Recent studies suggest that PDE5 inhibitors may also improve LUTS because of BPH irrespective of the presence of comorbid ED,[70,71] although these agents are not yet approved for this indication. EjD is more difficult to manage than ED; if medical therapy for BPH/LUTS is thought to be contributing to EjD, switching to an alternative drug (such as a 5ARI or an alternative alpha-blocker) may be an option.

Adequate and appropriate counselling is a key element of the management of sexual dysfunction in men with BPH/LUTS. Good clinical practice dictates that physicians provide patients with proper counselling on the safety and tolerability of medical therapies for BPH/LUTS. However, physicians should be aware that counselling in itself is likely to influence reporting of sexual dysfunction; this should be taken into account when medical therapy is used to manage BPH/LUTS. Patients should also be counselled on the likely impact of sexual AEs on their sexual satisfaction. A discussion of the impact on sexual satisfaction of possible changes in ejaculation (such as reduced force, reduced volume and retrograde ejaculation) should take place before commencement of treatment.

Conclusion

BPH/LUTS and sexual dysfunction are common in older men. Epidemiological studies have confirmed an association between BPH/LUTS and sexual dysfunction in ageing men that is independent of the effects of age, other comorbidities and lifestyle factors. Physicians (urologists and PCPs) appear to under-recognise sexual dysfunction in men with BPH/LUTS, highlighting the need for improved awareness of the relationship between BPH/LUTS and sexual dysfunction, and the importance of evaluating fully sexual function in men with BPH/LUTS. This is particularly relevant in patients who will receive medical therapy for BPH/LUTS, to enable proper assessment of whether any subsequent sexual dysfunction is likely to be drug-related. Management of sexual dysfunction in men treated for BPH/LUTS should involve assessment of co-morbidities and concomitant medications, intervention to improve risk factors for ED and, if necessary, introduction of pharmacotherapies. In addition, physicians should provide patients with proper counselling on the possible sexual AEs of medical therapies for BPH/LUTS and their impact on sexual satisfaction, while being cogniscent of the possibility that counselling in itself may influence reported rates of sexual dysfunction.

Sidebar

Review Criteria

Relevant English-language articles were identified from Medline searches (2000–2010), the 'related citations' function of Medline, and from reference lists of articles identified as relevant. Search terms included benign prostatic hyperplasia, lower urinary tract symptoms, epidemiology, sexual dysfunction, erectile dysfunction, ejaculatory dysfunction, alpha-blockers, 5-alpha reductase inhibitors and treatment.

Message for the Clinic

Sexual dysfunction should be fully evaluated in men requiring treatment for BPH/LUTS using validated questionnaires. Physicians managing sexual dysfunction in men treated for BPH/LUTS should assess co-morbidities and concomitant medications, consider lifestyle interventions such as weight loss and increased physical activity to improve risk factors and, if necessary, consider pharmacotherapies. Patients should receive proper counselling on the possible sexual adverse events with pharmacotherapies for BPH/LUTS and their impact on sexual satisfaction.

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