Textbook of Benign Prostatic Hyperplasia

cover

cover

next page >

Cover

title: author: publisher: isbn10 | asin: print isbn13: ebook isbn13: language: subject 

publication date: lcc: ddc: subject:

Textbook of Benign Prostatic Hyperplasia 2Nd Ed. Kirby, R. S. Informa Healthcare 190186555X 9781901865554 9780203640449 English Prostate--Hypertrophy, Prostate--Hypertrophy-Treatment, Prostatic Hyperplasia--diagnosis, Prostatic Hyperplasia--therapy, Adrenergic alpha-Antagonists-therapeutic use. 2005 RC899.T49 2005eb 616.6/5 Prostate--Hypertrophy, Prostate--Hypertrophy-Treatment, Prostatic Hyperplasia--diagnosis, Prostatic Hyperplasia--therapy, Adrenergic alpha-Antagonists-therapeutic use.

cover

next page >

file:///H|/...3%E8%FF/Textbook%20of%20Benign%20Prostatic%20Hyperplasia%202%20Ed%20Kirby%202005/start_here.html[09.07.2009 11:51:09]

page_i



Page i Second Edition TEXTBOOK OF BENIGN PROSTATIC HYPERPLASIA



file:///H|/...%E8%FF/Textbook%20of%20Benign%20Prostatic%20Hyperplasia%202%20Ed%20Kirby%202005/files/page_i.html[09.07.2009 11:51:10]

cover

cover

next page >

Cover

title: author: publisher: isbn10 | asin: print isbn13: ebook isbn13: language: subject 

publication date: lcc: ddc: subject:

Textbook of Benign Prostatic Hyperplasia 2Nd Ed. Kirby, R. S. Informa Healthcare 190186555X 9781901865554 9780203640449 English Prostate--Hypertrophy, Prostate--Hypertrophy-Treatment, Prostatic Hyperplasia--diagnosis, Prostatic Hyperplasia--therapy, Adrenergic alpha-Antagonists-therapeutic use. 2005 RC899.T49 2005eb 616.6/5 Prostate--Hypertrophy, Prostate--Hypertrophy-Treatment, Prostatic Hyperplasia--diagnosis, Prostatic Hyperplasia--therapy, Adrenergic alpha-Antagonists-therapeutic use.

cover

next page >

file:///H|/...3%E8%FF/Textbook%20of%20Benign%20Prostatic%20Hyperplasia%202%20Ed%20Kirby%202005/files/cover.html[09.07.2009 11:51:10]

page_ii



page_ii

next page >

Page ii This page intentionally left blank.



Page x This page intentionally left blank.



Page 1 I Basic Science



Page 2 This page intentionally left blank.



Page 112

30 cm3), a low peak uroflow (50 ml were also required. For a moderately restrictive definition requiring symptoms (I-PSS>7), prostatic enlargement (>30 cm3), and a moderately low peak uroflow (7 33 41 46 I-PSS>7, Q max7, Q max7, PVR>50 5 13 28 I-PSS>7, Q max50 7 24 37 I-PSS>7, Q max50 19 35 40 most logical gold standard, in some ways, would be the documented presence of histologic BPH, but its presence alone, along with symptoms, does not prove a causal relationship in individual cases (although its absence would presumably be a good indication that the symptoms had some other cause). The documentation of histologic BPH by biopsy, then, is a sensitive but not specific candidate gold standard. There are currently few or no published data correlating these various epidemiologic definitions with the presence or absence of histologic BPH, although the Medical Treatment of Prostatic Symptoms (MTOPS) trial should reveal this information, as a group of participants underwent prostate biopsies as part of a substudy.31 An alternative gold standard is the documentation of evidence of bladder outlet obstruction by simultaneous urodynamic measures of bladder pressure and uroflow.32 However, the poor correlation between symptom severity and degree of urodynamic obstruction (even among men with documented bladder outlet obstruction), and the fact that the great majority of men whom clinicians define as having symptoms due to BPH respond to treatment for BPH even in the absence of documented bladder outlet obstruction, at least suggest that this candidate gold standard, while specific, is not sensitive. It is reassuring that when clinicians make a diagnosis of symptomatic BPH, most of these men have urodynamic evidence of bladder outlet obstruction when studied, and even more respond to medical or surgical treatments aimed at BPH.33,34 Further definition of the mechanisms and pathways by which the histologic process of BPH leads to the development of LUTS will be necessary to arrive at a more optimal gold standard against which to judge more practical working epidemiologic definitions of this condition. Regarding the epidemiology of BPH, guidelines recently published by the AUA11 suggest that future research should focus on the following: • Establishment of an epidemiologic definition of BPH that is accepted worldwide. • Determination of outcome rates using established criteria in groups of BPH patients from different ethnic groups or environments stratified by age. • Identification of baseline parameters predictive of clinical outcome. • Study of the prevalence of concomitant conditions, both urologic (such as LUTS, erectile dysfunction and incontinence) and general (such as hypertension and vascular diseases) in the community. • Identification of familial and genetic aspects of BPH. • Means of preventing disease progression and/or development of BPH in high-risk patients and/or the population at large. Regarding the third point, the MTOPS trial has shown that prostate-specific antigen (PSA), Q max, PVR, and prostate volume at baseline correlate with disease progression and the need for BPH-related surgery.35 Community-based studies are needed to give further insight into this and the other aspects described above. Summary The histologic condition BPH is very common among older men around the developed world. Other manifestations of BPH, such as prostatic enlargement, depressed uroflow, and increased postvoid residual urine volume are likewise common, although in some cases these manifestations may be due to diseases other than BPH (even when histologic evidence of BPH is present). The clinical manifestations of BPH most important to patients, LUTS, are also extraordinarily common among older men, and their rising prevalence with aging is remarkably similar among men from many countries and of many ethnicities. Even if a substantial minority of these symptoms is caused



file:///H|/...8%FF/Textbook%20of%20Benign%20Prostatic%20Hyperplasia%202%20Ed%20Kirby%202005/files/page_148.html[09.07.2009 11:52:29]

page_149



Page 149 by other diseases, BPH as a cause of LUTS clearly is responsible for substantial morbidity worldwide. Acknowledgment The epidemiologic analyses supporting this chapter were funded by the Agency for Health Care Policy and Research (Grant No HS 08397). References 1. Berry S J, Coffey D S, Walsh P C, Ewing L L. The development of human benign prostatic hyperplasia by age. J Urol 1984; 132:474–479 2. Isaacs J T, Coffey D S. Etiology and disease process of benign prostatic hyperplasia. Prostate 1989; 2(Suppl): 33–50 3. Gu F -L, Xia T -L, Kong X -T. Preliminary study of the frequency of benign prostatic hyperplasia and prostatic cancer in China. Urology 1994; 44:688–691 4. Bosch J L H R, Hop W C J, Niemer A Q H J et al. Parameters of prostate volume and shape in a community based population of men 55 to 74 years old. J Urol 1994; 152:1501–1505 5. Masumori N, Tsukamoto T, Kumamoto Y et al. Japanese men have smaller prostates but comparable urinary flow rates relative to American men: results of community based studies in 2 countries. J Urol 1996; 155:1324–1327 6. Girman C J, Panser L A, Chute C G et al. Natural history of prostatism: urinary flow rates in a community-based study. J Urol 1993; 150:887–892 7. Bruskewitz R C, Iversen P, Madsen P O. Value of postvoid residual urine determination in evaluation of prostatism. Urology 1982; 20:602–604 8. Kolman C, Girman C J, Jacobsen S J, Lieber M M . Distribution of post-void residual volume in randomly selected men. J Urol 1999; 161:122–127 9. Mebust W, Kozio R, Shroeder F, Villers A. Correlations between pathology, clinical symptoms and the course of the disease. In: Cockett A T K, Aso S, Chatelain C et al. (eds). The international consultation on benign prostatic hyperplasia (BPH). Jersey, Channel Islands: Scientific Communication International Ltd, 1991:51–62 10. Barry M J, Fowler F J, O’Leary M P et al. The American Urological Association symptom index for benign prostatic hyperplasia. J Urol 1992; 148:1549–1557 11. AUA BPH Guideline Update Panel. The Management of BPH, 2003. https://shop.auanet.org/timssnet/products/guidelines/bph_management.cfm 12. Sagnier P -P, Macfarlane G, Richard F et al. Results of an epidemiologic survey using a modified American Urological Association symptom index for benign prostatic hyperplasia in France. J Urol 1994; 151:1266–1270 13. Badia X, Garcia-Losa M, Dal-Re R. Ten-language translation and harmonization of the International Prostate Symptom Score: developing a methodology for multinational clinical trials. Eur Urol 1997; 31:129–140 14. Barry M J, Adolfsson J, Batista J E et al. Measuring symptoms and health impact of benign prostatic hyperplasia and its treatments. In: Denis L, Griffiths K, Khoury S et al. (eds). Fourth international consultation on BPH. Plymouth: Plymbridge Distributors, 1998:265–321 15. Oishi K, Boyle P, Barry M J et al. Epidemiology and natural history of BPH. In: Denis L, Griffiths K, Khoury S et al. (eds). Fourth International Consultation on BPH. Plymouth: Plymbridge Distributors, 1998; 23–59 16. Homma Y, Kawabe K, Tsukamoto T et al. Epidemiologic survey of lower urinary tract symptoms in Asia and Australia using the International Prostate Symptom Score. Int Urol 1997; 4:40–46 17. Bosch J L H R, Hop W C J, Kirkels W J, Schroder F H . The International Prostate Symptom Score in a community-based sample of men between 55 and 74 years of age: prevalence and correlation of symptoms with age, prostate volume, flow rate and residual urine volume. Br J Urol 1995; 75:622–630 18. Nacey J N, Morum P, Delahunt B. Analysis of voiding symptoms in Maori, Pacific Island, and Caucasian New Zealand men. Urology 1995; 46:506–511 19. Tan H Y, Choo W C, Archibald C, Esuvaranathan K. A community-based study of prostatic symptoms in Singapore. J Urol 1997; 157:890–893 20. Hunter D J W, Berra-Unamuno A, Martin-Gordo A . Prevalence of urinary symptoms and other urological conditions in Spanish men 50 years old or older. J Urol 1996; 155:1965–1970 21. Chicharro-Molero J A, Burgos-Rodriquez R, SanchezCruz J J et al. Prevalence of benign prostatic hyperplasia in Spanish men 40 years old or older. J Urol 1998; 159: 878–882 22. Chute C G, Panser L A, Girman C J et al. The prevalence of prostatism: a population-based survey of urinary symptoms. J Urol 1993; 150:85–89 file:///H|/...8%FF/Textbook%20of%20Benign%20Prostatic%20Hyperplasia%202%20Ed%20Kirby%202005/files/page_149.html[09.07.2009 11:52:29]

page_149

23. Garraway W M, McKelvie G B, Russell E B A et al. Impact of previously unrecognized benign prostatic hyperplasia on the daily activities of middle-aged and elderly men. Br J Gen Pract 1993; 43:318–321 24. Girman C J, Jacobsen S J, Tsukamoto T et al. Health-related quality of life associated with lower urinary tract symptoms in four countries. Urology 1998; 51:428–436 25. McKelvie G B, Collins G N, Hehir M, Rogers C N. A study of benign prostatic hyperplasia—a challenge to British Urology. Br J Urol 1993; 71:38–42



file:///H|/...8%FF/Textbook%20of%20Benign%20Prostatic%20Hyperplasia%202%20Ed%20Kirby%202005/files/page_149.html[09.07.2009 11:52:29]

page_150



Page 150 26. Jolleys J V, Donovan J L, Nanchahal K et al. Urinary symptoms in the community: how bothersome are they? Br J Urol 1994; 74:551–555 27. Girman C J, Jacobsen S J, Guess H A et al. Natural history of prostatism: relationship among symptoms, prostate volume, and peak urinary flow rate. J Urol 1995; 153: 1510–1515 28. Garraway M, Collins R, Lee R. High prevalence of benign prostatic hypertrophy in the community. Lancet 1991; 338:469–471 29. Bosch J L H R, Hop W C J, Kirkels W J, Schroeder F H . Natural history of benign prostatic hyperplasia: appropriate case definition and estimate of its prevalence in the community. Urology 1995; 46(Suppl 3A): 34–40 30. Jacobsen S J, Girman C J, Guess H A et al. New diagnostic and treatment guidelines for benign prostatic hyperplasia. Arch Intern Med 1995; 155:477–481 31. Bautista O M, Kusek J W, Nyberg L M et al for the MTOPS Research Group. Study design of the Medical Therapy of Prostatic Symptoms (MTOPS) trial. Control Clin Trials 2003; 24:224–243 32. Abrams P. In support of pressure-flow studies for evaluating men with lower urinary tract symptoms. Urology 1994; 44:153–155 33. McConnell J D. Why pressure-flow studies should be optional and not mandatory studies for evaluating men with benign prostatic hyperplasia. Urology 1994; 44: 156–158 34. Jepsen J V, Bruskewitz R C. Comprehensive patient evaluation for benign prostatic hyperplasia. Urology 1998; 51(Suppl 4A): 13–18 35. McConnell J D, Roehrborn C G, Slawin K M et al. Baseline measures predict the risk of benign prostatic hyperplasia clinical progression in placebo-treated patients. J Urol 2003; 169 (Suppl 4): abstract 1287



file:///H|/...8%FF/Textbook%20of%20Benign%20Prostatic%20Hyperplasia%202%20Ed%20Kirby%202005/files/page_150.html[09.07.2009 11:52:30]

page_151



Page 151 10 Descriptive epidemiology of benign prostatic hyperplasia H A Guess C J Girman Introduction A thorough understanding of benign prostatic hyperplasia (BPH) requires a knowledge not only of its pathophysiology but also of its epidemiology. Until recently, most epidemiologic information about BPH had come from studies involving only men who had sought treatment for BPH. Such studies make it difficult to separate factors related to seeking treatment from factors related to other measures of disease progression. In addition, they do not provide information on the full spectrum of disease or of early findings, since they are limited to men in whom the clinical manifestations have progressed far enough to lead them to seek medical attention, To provide more complete information requires population-based studies, which involve representative sampling from a geographically defined population. Population-based studies of BPH can contribute to medical knowledge in at least three areas.1 First, there is the need to establish community-based normal ranges of symptom scores and commonly used diagnostic tests. A proper evaluation of any test requires that the study population include a sufficiently broad spectrum of diseased and nondiseased individuals.2 Studying only men seen in urology clinics can lead to optimistic estimates of sensitivity and specificity that are later proven to be incorrect when the test is applied to men with milder disease in a general practice setting.2,3 Studies to establish community-based normal ranges of tests also provide information on the community prevalence of symptoms and other measures of BPH. This information is useful in characterizing the amount of morbidity attributable to BPH. Second, it is important to determine how symptoms and other factors influence both the decision to seek treatment and the choice of treatment. Barry et al. have shown that differences in individual patient preferences are important in making rational choices of treatments.4 Such information is also useful in estimating how practice guidelines may affect utilization of medical services.5 A third potential contribution of long-term community-based studies is to provide information on outcomes from a representative sample of a defined population rather than only from patients treated at particular health-care facilities. What may appear to be intervention-related or hospital-related variation in outcomes may be variation in the magnitude and form of patient-selection bias. Selection bias in nonpopulation-based studies is often impossible to control by co-morbidity adjustments, because factors which bring patients to a particular facility or which lead to the choice of one type of treatment over another are often not adequately reflected in medical records or in any other readily available data source.6–9 It is the lower potential for selection bias which makes community-based studies of disease natural history preferable to natural history studies conducted in referral populations.10 Studies of BPH natural history are discussed in a subsequent chapter. In this chapter we will review a number of populationbased studies of urinary symptoms and health status related to BPH that have been conducted recently. Several of these studies are still ongoing and further publications of results will be forthcoming in the next few years. This chapter will acquaint readers with the designs of such studies and some of the cross-sectional and longitudinal results recently available from these studies. An overview of the sampling methods is given in the Appendix. Most of these studies were cross-sectional studies, with data collected at a single point in time. The earliest large community-based studies of BPH were conducted in the US and Scotland, and both of these studies were longitudinal in nature. Later studies involved a national survey of urinary symptoms and quality of life among French men, and community-based studies in Denmark, Japan, and The Netherlands. After introduction of a standard symptom assessment tool,11 a number of cross-sectional surveys were conducted in Europe, Asia, and worldwide.12–33 Several published community surveys have used instruments other than the American Urological Association Symptom Index or International Prostate Symptom Score (I-PSS),33–39 making it difficult to compare with studies using the more recent standard tools. A few of these studies assessed urological measurements in addition to frequency of urinary symptoms, including prostate volume and urinary flow rates. These include the studies conducted in the US, Scotland, Japan, Korea, The Netherlands, Norway, and Spain. For more comprehensive reviews of BPH epidemiology the reader is referred to a number of review articles.40–47



file:///H|/...8%FF/Textbook%20of%20Benign%20Prostatic%20Hyperplasia%202%20Ed%20Kirby%202005/files/page_151.html[09.07.2009 11:52:30]

page_152



Page 152 French national survey Sagnier et al. conducted a survey of urinary symptoms and quality of life in a nationally representative probability sample of 2011 French men 50–80 years old, using a French translation of the American Urological Association Symptom Index (AUASI).11,48–51 This French translation has been accepted as the French language version of the I-PSS.50 In the initial article describing prevalence of symptoms,18 the authors referred to their symptom score as the AUASI. In a subsequent article describing the impact of symptoms on quality of life,51 the same symptom score was referred to as the International Prostate Symptom Score. For the sake of consistency we will henceforth refer to their symptom score as the International Prostate Symptom Score. In the survey, information was collected by household interview, in which 12525 dwellings had to be contacted to obtain the above sample size. The authors noted that a calculation of the true response rate in this study is not possible, since the sampling unit (dwellings) and the reporting units (subjects) were different and the eligibility status of subjects who were not at home at the time of the initial contact is not known. However, one accepted definition of response rate is the ratio of the number of completed interviews divided by the number of known eligible units in the sample.52 By that definition the response rate was 53%. After exclusion of patients with prostate cancer, 7% of the subjects reported having undergone prostate surgery and an additional 8% reported having received a diagnosis of BPH. Among those with no history of surgery or prostate cancer, 19% had no symptoms, 67% had mild symptoms (I-PSS in the range 1– 7), 13% had moderate symptoms (I-PSS: 8–19), and 1% had severe symptoms (I-PSS: 20+). The proportion with moderate to severe symptoms approximately doubled with each decade of age. Nocturia and repeat voiding within 2 hours were the most prevalent symptoms. The index formed by the American Urological Association (AUA) questions on bother due to urinary symptoms (also known as the Symptom Problem Index,53 referred to here as the AUA Bother Score) was the best determinant of each subject’s level of worry about urinary conditions and the degree to which urinary symptoms interfered with daily life. Urgency was by far the most bothersome symptom among men who reported one or more urinary symptoms, followed by wet underclothes, revoiding within 10 minutes, and nocturia. Intermittency and weak stream appeared to be less bothersome. The AUA Bother Score was highly correlated to the I-PSS ( r=0.85, p 30 ml 3.0 1.0–9.0 Flow rate* 2.5 0.70   Transition zone index‡ >0.65 0.924   *Jacobsen et al.22; †Roehrborn et al.23; ‡Kurita et al.24; IPSS, international prostate symptoms score; PSA, prostate-specific antigen. The placebo arms of trials of pharmaceutic treatments for BPH provide useful epidemiologic data and have demonstrated that PSA, prostate volume, and symptom severity significantly affect the risk of AUR.23,27–29 The largest study was a 4-year, double-blind randomized trial of 3040 men comparing the treatment of BPH with finasteride or placebo. Receiver operating characteristic (ROC) curve analyses showed that serum PSA and prostate volume were powerful predictors of the risk of AUR in placebotreated patients (area under the curve 0.70 and 0.81, respectively).23 The transition zone index (TZI=transition zone volume/total prostate volume) as measured with TRUS has been suggested as an accurate predictor for acute retention (area under the ROC curve 0.924).24 The authors concluded that patients with a TZI greater than 0.65 have a high risk of developing AUR. Quality of life As AUR usually involves an emergency admission to hospital and insertion of a catheter, it is perhaps not surprising that some patients may find the event traumatic. There have been a few studies which have looked at the impact of an episode of AUR on the patient, but this has remained a relatively neglected aspect of the management of this condition. A recent retrospective study of the management of patients with AUR in one surgeon’s practice over a 23-year period showed that 90% of patients were discharged home with a catheter to await surgery.30 While at home, 72% of patients experienced some complication, 69% found the catheter uncomfortable, and 65% found it inconvenient, particularly with respect to finding adequate toilet facilities. Another group prospectively evaluated the impact of discharging patients with AUR home with a catheter by means of a self-completion questionnaire (93% response rate).31 One hundred and one patients were seen with AUR and discharged home immediately with a catheter. Unlike the previous group, the majority of patients (87%) did not find that their activities were limited in any way although all of them had experienced at least one complication. The questionnaire used was not a validated measure, however it did show that despite having complications from the catheter most of the patients still found having a catheter at home acceptable. This study challenges the perception of most clinicians that patients do not like having a catheter. Treatment Catheterization The initial management of AUR is prompt relief of retention and pain by catheterization of the bladder. This can be achieved via the urethral or suprapubic route, each of which has its merits. Depending on the cause of the episode of AUR, local policy, the patient’s physical condition, and social circumstances, they may then be discharged with the catheter or admitted into hospital. Urethral catheterization is performed more commonly than suprapubic due to concern regarding the potential complications of inserting a suprapubic catheter and because the personnel (i.e. accident and emergency staff, family practitioners) who first see the patient are generally more familiar with the urethral route.32,33 A prospective study of 86 patients with AUR who were catheterized described a significantly lower incidence of urinary tract infection (18% vs 40%) and stricture formation (0 vs



file:///H|/...8%FF/Textbook%20of%20Benign%20Prostatic%20Hyperplasia%202%20Ed%20Kirby%202005/files/page_183.html[09.07.2009 11:52:46]

page_184



Page 184 16.7%) with suprapubic versus urethral catheters.34 It was also commented that trial without catheter was easier as it merely required clamping and unclamping of the suprapubic catheter. The relatively high stricture rate may be explained in part by the now outdated use of latex catheters by this group; however, the incidence is still likely to be higher than when the suprapubic route is used. The lower infection rate with suprapubic catheterization was also reported by a group who randomized patients to urethral versus suprapubic catheterization.35 In addition, they noted that patients found the suprapubic catheter was more comfortable and easier to manage. Despite these findings, the majority of patients with AUR are still managed with a urethral catheter, probably due to the continuing perception of suprapubic catheterization as a potentially hazardous procedure.36 A novel suggestion by one group is that patients with AUR can be managed by clean intermittent selfcatheterization (CISC),37 The authors found that the CISC group had a higher rate of spontaneous voiding (56% vs 25%) and lower infection rate (32% vs 75%) compared with the indwelling catheter group, They concluded that patients found CISC acceptable and manageable and experienced fewer complications than do those with an indwelling catheter. There is significant variation among studies in the timing of removal of a catheter (trial without catheter or TWOC). Some investigators have found no difference in success rates at 24 and 48 hours.38 Others have suggested a benefit to waiting longer, particularly in men with large residual volumes >1 liter.39 It has recently been suggested that prostate size >27.5 g, residual volume >1 liter and age >75 years may significantly reduce the chance of successfully voiding after a TWOC.40 It has also been suggested that the use of an α-blocker may improve the success rate of a TWOC.41 Pharmacotherapy There has been an increasing trend towards the use of drugs in both the prevention and treatment of AUR due to BPH. The two main classes of drugs used are α-block-ers and 5α-reductase inhibitors. α-Blockers act by relaxing the smooth muscle in the bladder neck and prostate, thereby decreasing the resist-ance to urinary flow. The potential role of α-blockers in the treatment and prevention of AUR was first described over 25 years ago.42 Since then, different types of α-block-ers have been produced and reported to have differing side-effect profiles.43 The impact of some of these in the prevention of AUR has been compared with placebo. A double-blind study of 2084 patients randomized to terazosin or placebo reported no difference in the incidence of AUR in each group during the 1-year follow-up period.44 In contrast, a study of 81 patients with AUR randomized to receive either alfuzosin or placebo for 48 hours prior to trial without catheter showed after 24 hours that those patients on alfuzosin had a significantly increased chance of passing a trial without catheter: 55% versus 28% ( p =0.03). This effect was sustained over 18 months of follow-up, although the study group was relatively small.45 Finasteride is at present the only 5α-reductase inhibitor available, although newer agents such as dutasteride are under evaluation.46 They act by selective inhibition of 5α-reductase responsible for the conversion of testosterone to dihydrotestosterone.47 In a large, doubleblind, randomized placebocontrolled trial 3040 men with moderate to severe lower urinary tract symptoms and enlarged prostates were recruited.48 Over a 4-year period they were treated daily with either 5 mg finasteride or placebo. Acute urinary retention developed in 99 (7%) of men in the placebo group versus 42 (3%) in the finasteride group. This represents over a 50% risk reduction for developing AUR. However, because of the relatively rarity of AUR, 15 men would have to be treated for 4 years to avoid one episode of AUR. Similar reductions in the risk of events such as heart attack or stroke occur with statins and antihypertensive medication.49 A pooled analysis of three randomized trials comprising 4222 men with moderately symptomatic BPH treated with either finasteride or placebo for 2 years reported 81 episodes of AUR (24/2113 finasteride group, 57/2109 placebo group).47 The hazard ratio for the occurrence of AUR was consistent amongst the studies, with a 57% decrease in the hazard rate for patients treated with finasteride compared with placebo ( p 1500 ml, lack of detrusor instability, detrusor pressure at maximum fill of 1.2 SD in only three of the 32 voids (9%). However, variation of flow in patients with bladder outlet symptoms is often a feature of their history. Home uroflowmetry with multiple voids in more normal surroundings may give a better indication.15 Golomb et al.16 studied flow rate variations by home uroflowmetry in 32 men with symptoms of obstruction who did a mean of 14.9 tests, and 16 controls without symptoms, by a mean of 6.25 tests. They found that the men with obstruction varied their flow rates by >1 SD in 87.5% and by >2 SD in 47%. The normal men had flows showing less variation but which still varied by >1 SD in 50% and by >2 SD in 12.5%. In an elderly population of incontinent men and women who underwent two urodynamic studies 2–4 weeks apart, the between-session variability of the flow rate was ±4.7 ml/s and the correlation coefficient was 0.44.17 Similarly, the URA, which is a measure of obstruction, varied by ±11.7 with a correlation coefficient of 0.61.18 The results suggest there is substantial long-term variability in voiding function, including urethral resistance. Diurnal variation Many patients say their flow is worse at night, and this was borne out in the study done by Golomb et al.16 In their study the adjusted flow rate was lower in the home flowmetry studies done between midnight and noon than in the subsequent half-day. This variation was not seen in younger men.19

file:///H|/...8%FF/Textbook%20of%20Benign%20Prostatic%20Hyperplasia%202%20Ed%20Kirby%202005/files/page_228.html[09.07.2009 11:53:09]

page_228



file:///H|/...8%FF/Textbook%20of%20Benign%20Prostatic%20Hyperplasia%202%20Ed%20Kirby%202005/files/page_228.html[09.07.2009 11:53:09]

page_229



Page 229 Bladder volume The flow rate depends on volume voided and is slower than representative with volumes less than 150– 200 ml.20 Older men often have greater difficulty holding on to do this volume and hence volumes of 100 ml are not uncommon. When they do hold on deliberately, it does not always result in a representative voiding rate, and after going home they often have marked frequency. In the ICS BPH study,9 the voided volume was less than 150 ml and therefore bladder outlet obstruction was diagnosed in 72% of cases, compared to 56% in men in whom the voided volume was greater than 150 ml. Because of this, some centers have developed ‘flow clinics’, at which patients are asked to drink plenty and to do three or four tests. In this way, the proportion of men voiding less than 150 ml fell from 59% to 21%.21 Several workers studying flow patterns have developed nomograms and volume-independent variables. First, Drake22 developed the idea of a ‘corrected’ peak flow rate derived by dividing maximum flow rate by the square root of bladder volume itself measured as a sum of the volume voided and the residual urine volume. Second, the importance of using the initial bladder volume, rather than the voided volume alone, which would disregard the PVR, was emphasized by Siroky et al.14 Use of voided volume would result in an overestimate of voiding ability. Despite this, the measurement of PVR is considered unnecessary in the majority of cases unless the flow rate is normal or borderline. Siroky et al.14 constructed a nomogram of flow rate against volume in a small group of young men, and expressed the variance in terms of a mean and standard deviation which paralleled the mean. None of the normals had values below −2 SD, whereas in a group of 53 men considered obstructed on clinical grounds, 52 had values below −2 SD.23 The clinical diagnosis of obstruction was not validated by urodynamic studies, however. Lim et al.24 compared the reliability of the Bristol and Siroky nomograms against the objective criteria of obstruction using a URA of >29. They showed that the Siroky nomogram had poor specificity (30%) but good sensitivity in diagnosing obstruction (91%). The Bristol nomogram had a specificity of 70% and a sensitivity of 53%. They concluded that if a precise diagnosis of obstruction is required, then pressure/flow studies must be performed. Schafer et al.25 reported that only 75% of men considered obstructed in the Siroky nomogram were proven to be obstructed on pressure/flow studies. Flow rates were slower with higher volumes in several studies.11,20 Haylen et al.13 constructed a Liverpool nomogram based on a large number of men and women. They found a strong correlation with voided volume of both maximum and average flow rate, but did not see any deterioration of flow rate in either sex with higher voided volumes. Pooling the results from 12 studies in 817 men aged 25–60 years showed the relation between flow rate and voided volume displayed in Fig. 16.1.26 For voided volumes of