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The overlooked cause of benign prostatic hyperplasia: prostatic urethral angulation
Medical Hypotheses (2008) 70, 532–535
http://intl.elsevierhealth.com/journals/mehy
The overlooked cause of benign prostatic hyperplasia: prostatic urethral angulation Kang Su Cho a, Joohan Kim b, Young Deuk Choi a, Jang Hwan Kim a, Sung Joon Hong a,* a
Department of Urology, Urological Science Institute, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, Seoul, Republic of Korea b Department of Mechanical Engineering, Seoul National University of Technology, Seoul, Republic of Korea Received 2 July 2007; accepted 3 July 2007
Summary Benign prostatic hyperplasia (BPH) is one of the most common problems faced by aging men and can be associated with bothersome lower urinary tract symptoms that affect quality of life by interfering with normal daily activities and sleep patterns. Despite the clinical importance of BPH, its pathogenesis is still poorly understood. Previously, our understanding of BPH was centered on bladder outlet obstruction being secondary to benign prostatic enlargement. However, prostate size itself is not correlated with the urine flow rate and symptomatology. The prostatic urethra is a bend tube and the increased prostatic urethral angulation shows a higher bladder neck on cystoscopic examination. Although some urologists suspected that the higher bladder neck might be a causal factor for BPH, the clinical significance of prostatic urethral angulation was previously underestimated. In this study, we propose a new hypothesis that prostatic urethral angulation is a causal factor for BPH. By applying the concept of fluid dynamics to the process of urination in the prostatic urethra, we show that the energy loss in this bending tube (the prostatic urethra) can occur during micturition and it increases proportionally to prostatic urethral angulation; this energy loss results in a decrease of the urine velocity and accordingly, the urine flow rate is inversely associated with prostatic urethral angulation. We also propose that BPH involves prostatic urethral angulation as well as the classical BPH triad of prostatic enlargement, bladder outlet obstruction, and symptomatology. Our hypothesis suggests that prostatic urethral angulation is an overlooked cause of bladder outlet obstruction and is a causal factor of BPH, and provides novel insight into the pathogenesis of BPH. Ultimately, the relationship between prostatic urethral angulation and urine flow rate, and other clinical factors including urodynamic parameters, the symptomatology, the response to treatment, and disease progression, need to be investigated in a clinical setting. c 2007 Elsevier Ltd. All rights reserved.
Background * Corresponding author. Tel.: +82 2 2228 2315; fax: +82 2 312 2538. E-mail address: [email protected] (S.J. Hong).
Benign prostatic hyperplasia (BPH) is one of the most common problems faced by aging men and can be associated with bothersome lower urinary
0306-9877/$ - see front matter c 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2007.07.012
The overlooked cause of benign prostatic hyperplasia: prostatic urethral angulation tract symptoms (LUTS) that affect quality of life by interfering with normal daily activities and sleep patterns. The prevalence of histopathologic BPH is age dependent, with initial development usually after 40 years of age [1]. By 60 years of age, its prevalence is greater than 50% and by age 85, it is as high as 90%. Similarly, the prevalence of bothersome urinary tract symptoms also increases with age; approximately half of all men with a histologic diagnosis have moderate to severe LUTS. Despite its clinical importance, the pathogenesis of BPH is still poorly understood. The triad of prostatic hyperplasia, which includes benign prostatic enlargement, bladder outlet obstruction, and LUTS, is the basis for the clinical diagnosis of BPH [2], but these items are not always present together, and very weak correlations have been found among these components [3,4]. Furthermore, the size of the prostate does not correlate with the degree of obstruction. Thus, other factors such as dynamic urethral resistance, the prostatic capsule and anatomic pleomorphism affect the clinical symptoms more than the absolute size of the gland [5–12]. The prostatic urethra runs through the prostate from the base to the apex, making an anterior angulation of 35 at the proximal part of verumontanum. This bend divides the urethra into proximal and distal portions [13]. The angulation tends to be greater than 35 in men with nodular hyperplasia, but it can also increase in men without prostatic hyperplasia. Upon cystoscopic examination, the increased prostatic urethral angulation shows a higher bladder neck in men without lateral and medial lobe enlargement. Although some urologists suspect that the higher bladder neck might be a causal factor for BPH, the clinical significance of prostatic
533
urethral angulation was previously underestimated. In this study, we propose a new hypothesis that prostatic urethral angulation could be a causal factor for BPH.
Hypothesis: Prostatic urethral angulation is a causal factor of BPH Weak urine stream is a typical symptom in patients with BPH and the urine flow rate is inversely proportional to urodynamically proven obstructions [14]. In general, a decrease in urine flow rate is due to bladder outlet obstruction that is secondary to prostatic enlargement. Prostatic enlargement can compress the prostatic urethra externally resulting in a luminal narrowing of the prostatic urethra. As previously mentioned, the prostatic urethra is a bend tube [13]. By applying fluid dynamics to the process of urination in the prostatic urethra, it has been demonstrated that the energy loss in the bending tube (the prostatic urethra) can occur during micturition as well as from friction in the urethra wall. The energy loss in the bending tube increases proportionally to the loss coefficient (k) at the bends, which can be calculated using the following equation [15]: k = 2.22 · 10 3h + 4.04 · 10 6h2.76, where 0 < h < 90. This formula shows that the energy loss increases with prostatic urethral angulation. This energy loss results in a decrease in the urine velocity and as a result, the urine flow rate is inversely associated with prostatic urethral angulation (Fig. 1). This suggests that prostatic urethral angulation is an overlooked cause of bladder outlet obstruction and a causal factor of BPH.
Figure 1 The relationship between prostatic urethral angulation and urine flow rate (sagittal view): (a) A strong urine flow rate in the prostatic urethra with mild angulation, (b) an intermediate urine flow rate in the prostatic urethra with moderate angulation, and (c) a weak urine flow rate in the prostatic urethra with severe angulation. As prostatic urethral angulation increases, the urine flow rate decreases in order of (a)—(c).
534
Cho et al.
A novel concept of benign prostatic hyperplasia The classical triad of BPH, which includes benign prostatic enlargement, bladder outlet obstruction, and lower urinary tract symptoms, cannot account for the pathogenesis of BPH. Specifically, it is unclear why a decrease in urine flow rate and severe voiding symptoms occur in patients with a mildly enlarged prostate or no prostatic enlargement. We propose that BPH pathogenesis can be better understood if we consider the involvement of prostatic urethral angulation as well as the classical triad (Fig. 2). Other anatomic factors such as dynamic urethral resistance, the prostatic capsule, anatomic pleomorphism, etc. should also be considered along with prostatic urethral angulation [5–12].
Discussion The degree of prostatic urethral obstruction is very important for determining treatment modalities and predicting responses to treatment in patients with BPH. Unfortunately, the total prostate volume (TPV) does not correlate well with the urine flow rate and the symptomatology [3,4], so urologists have been interested in other parameters, such as transition zone volume (TZV), transition zone index (TZI) and prostate configuration [6,7,9–12]. Kaplan et al. [6] maintained that TZI, but not TPV and TZV, was significantly correlated with the urine flow rate and the symptomatology. However, Lepor et al. [10] reported that TPV, TZV, and TZI were not directly related to the American Urological Association (AUA) symptom score and were only weakly related to the urine flow rate. Watanabe [11] introduced a new concept for BPH, the presumed circle area ratio (PCAR) theory, and he and his colleagues suggested that PCAR was more useful in assessing the severity of infravesical obstruction than other parameters, such as TPV, TZV, and TZI [7]. However, this theory also primarily focused on luminal
Figure 2 The diagrammatic concept of benign tatic hyperplasia: the classical concept (a) and a concept (b). BPE: benign prostatic hyperplasia, bladder outlet obstruction, LUTS: lower urinary symptoms, PUA: prostatic urethral angulation.
prosnovel BOO: tract
narrowing of the prostatic urethra as measured by a horizontal sonogram of the prostate. Chia et al. [5] demonstrated that intravesical prostatic protrusion (IPP) was a better and more reliable predictor of bladder outlet obstruction than age, symptoms, urine flow rate, postvoid residual urine volume or prostate volume. They suggested that IPP, as determined by transabdominal ultrasonography, was useful for non-invasive assessments of bladder outlet obstruction. IPP causes a ‘ball-valve’ type obstruction, disrupting the funneling effect of the bladder neck and causing dyskinetic movement of the bladder during voiding [8]. Enlargement of the median lobe causes an increase in the prostatic urethral angulation and the increased prostatic urethral angulation is thought to contribute to factors other than dyskinetic movement. Namely, it has been suggested that increased prostatic urethral angulation can contribute to aggravation of bladder outlet obstruction in patients with benign prostatic obstructions. Martinez-Borges [16] applied fluid dynamics to urine flow in the urethra and determined that turbulent urinary flow in the urethra could be a causal factor for BPH. This current study is the first trial to investigate the impact of prostatic urethral angulation on the urine flow rate using a fluid dynamics approach, and we demonstrated that prostatic angulation is inversely associated with urine flow rate. BPH patients with small prostates can be successfully treated with a transurethral resection or incision in the prostate (bladder neck) [17–20]. Our hypothesis provides a theoretical basis for the transurethral resection or incision of the prostate (bladder neck) in such patients. BPH is a very complex clinical syndrome. Urethral and detrusor functions as well as various anatomical factors of the prostate are also important in the pathogenesis of BPH [21,22]. Nevertheless, the current hypothesis suggests that prostatic urethral angulation is an overlooked cause of bladder outlet obstruction and a causal factor of BPH and this hypothesis provides novel insights into the pathogenesis of BPH. Ultimately, the relationship between prostatic urethral angulation and urine flow rate, and other clinical factors such as urodynamic parameters, symptomatology, response to treatment, and disease progression, need to be investigated in a clinical setting.
References [1] Berry SJ, Coffey DS, Walsh PC, Ewing LL. The development of human benign prostatic hyperplasia with age. J Urol 1984;132:474–9.
The overlooked cause of benign prostatic hyperplasia: prostatic urethral angulation [2] Hald T. Urodynamics in benign prostatic hyperplasia: a survey. Prostate Suppl 1989;2:69–77. [3] Andersen JT, Nordling J, Walter S. Prostatism I. The correlation between symptoms, cystometric and urodynamic findings. Scand J Urol Nephrol 1979;13:229–36. [4] Barry MJ, Cockett AT, Holtgrewe HL, McConnell JD, Sihelnik SA, Winfield HN. Relationship of symptoms of prostatism to commonly used physiological and anatomical measures of the severity of benign prostatic hyperplasia. J Urol 1993;150:351–8. [5] Chia SJ, Heng CT, Chan SP, Foo KT. Correlation of intravesical prostatic protrusion with bladder outlet obstruction. BJU Int 2003;91:371–4. [6] Kaplan SA, Te AE, Pressler LB, Olsson CA. Transition zone index as a method of assessing benign prostatic hyperplasia: correlation with symptoms, urine flow and detrusor pressure. J Urol 1995;154:1764–9. [7] Kojima M, Ochiai A, Naya Y, Ukimura O, Watanabe M, Watanabe H. Correlation of presumed circle area ratio with infravesical obstruction in men with lower urinary tract symptoms. Urology 1997;50:548–55. [8] Kuo HC. Clinical prostate score for diagnosis of bladder outlet obstruction by prostate measurements and uroflowmetry. Urology 1999;54:90–6. [9] Kurita Y, Masuda H, Terada H, Suzuki K, Fujita K. Transition zone index as a risk factor for acute urinary retention in benign prostatic hyperplasia. Urology 1998;51:595–600. [10] Lepor H, Nieder A, Feser J, O’Connell C, Dixon C. Total prostate and transition zone volumes, and transition zone index are poorly correlated with objective measures of clinical benign prostatic hyperplasia. J Urol 1997;158:85–8. [11] Watanabe H. New concept of BPH: PCAR theory. Prostate 1998;37:116–25. [12] Witjes WP, Aarnink RG, Ezz-el-Din K, Wijkstra H, Debruyne EM, de la Rosette JJ. The correlation between
[13] [14]
[15] [16]
[17]
[18]
[19]
[20]
[21]
[22]
535
prostate volume, transition zone volume, transition zone index and clinical and urodynamic investigations in patients with lower urinary tract symptoms. Br J Urol 1997;80:84–90. McNeal JE. The prostate and prostatic urethra: a morphologic synthesis. J Urol 1972;107:1008–16. Comiter CV, Sullivan MP, Schacterle RS, Yalla SV. Prediction of prostatic obstruction with a combination of isometric detrusor contraction pressure and maximum urinary flow rate. Urology 1996;48:723–9 [discussion 29–30]. Schetz JA, Fuhs AE. Handbook of fluid dynamics and fluid machinery. New York: John Wiley & Sons; 1996. Martinez-Borges AR. Turbulent urinary flow in the urethra could be a causal factor for benign prostatic hyperplasia. Med Hypotheses 2006;67:871–5. Li MK, Ng AS. Bladder neck resection and transurethral resection of the prostate: a randomized prospective trial. J Urol 1987;138:807–9. Katz PG, Greenstein A, Ratliff JE, Marks S, Guice J. Transurethral incision of the bladder neck and prostate. J Urol 1990;144:694–6. Riehmann M, Knes JM, Heisey D, Madsen PO, Bruskewitz RC. Transurethral resection versus incision of the prostate: a randomized, prospective study. Urology 1995;45: 768–75. Orandi A. Transurethral incision of prostate (TUIP): 646 cases in 15 years – a chronological appraisal. Br J Urol 1985;57:703–7. Nakai H, Yamanishi T, Yasuda K, Kitahara S, Suzuki T. Correlation between lower urinary tract symptoms and urethral function in benign prostatic hyperplasia. Neurourol Urodyn 2004;23:618–22. Ameda K, Sullivan MP, Bae RJ, Yalla SV. Urodynamic characterization of nonobstructive voiding dysfunction in symptomatic elderly men. J Urol 1999;162:142–6.
Available online at www.sciencedirect.com
http://intl.elsevierhealth.com/journals/mehy
The overlooked cause of benign prostatic hyperplasia: prostatic urethral angulation Kang Su Cho a, Joohan Kim b, Young Deuk Choi a, Jang Hwan Kim a, Sung Joon Hong a,* a
Department of Urology, Urological Science Institute, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, Seoul, Republic of Korea b Department of Mechanical Engineering, Seoul National University of Technology, Seoul, Republic of Korea Received 2 July 2007; accepted 3 July 2007
Summary Benign prostatic hyperplasia (BPH) is one of the most common problems faced by aging men and can be associated with bothersome lower urinary tract symptoms that affect quality of life by interfering with normal daily activities and sleep patterns. Despite the clinical importance of BPH, its pathogenesis is still poorly understood. Previously, our understanding of BPH was centered on bladder outlet obstruction being secondary to benign prostatic enlargement. However, prostate size itself is not correlated with the urine flow rate and symptomatology. The prostatic urethra is a bend tube and the increased prostatic urethral angulation shows a higher bladder neck on cystoscopic examination. Although some urologists suspected that the higher bladder neck might be a causal factor for BPH, the clinical significance of prostatic urethral angulation was previously underestimated. In this study, we propose a new hypothesis that prostatic urethral angulation is a causal factor for BPH. By applying the concept of fluid dynamics to the process of urination in the prostatic urethra, we show that the energy loss in this bending tube (the prostatic urethra) can occur during micturition and it increases proportionally to prostatic urethral angulation; this energy loss results in a decrease of the urine velocity and accordingly, the urine flow rate is inversely associated with prostatic urethral angulation. We also propose that BPH involves prostatic urethral angulation as well as the classical BPH triad of prostatic enlargement, bladder outlet obstruction, and symptomatology. Our hypothesis suggests that prostatic urethral angulation is an overlooked cause of bladder outlet obstruction and is a causal factor of BPH, and provides novel insight into the pathogenesis of BPH. Ultimately, the relationship between prostatic urethral angulation and urine flow rate, and other clinical factors including urodynamic parameters, the symptomatology, the response to treatment, and disease progression, need to be investigated in a clinical setting. c 2007 Elsevier Ltd. All rights reserved.
Background * Corresponding author. Tel.: +82 2 2228 2315; fax: +82 2 312 2538. E-mail address: [email protected] (S.J. Hong).
Benign prostatic hyperplasia (BPH) is one of the most common problems faced by aging men and can be associated with bothersome lower urinary
0306-9877/$ - see front matter c 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2007.07.012
The overlooked cause of benign prostatic hyperplasia: prostatic urethral angulation tract symptoms (LUTS) that affect quality of life by interfering with normal daily activities and sleep patterns. The prevalence of histopathologic BPH is age dependent, with initial development usually after 40 years of age [1]. By 60 years of age, its prevalence is greater than 50% and by age 85, it is as high as 90%. Similarly, the prevalence of bothersome urinary tract symptoms also increases with age; approximately half of all men with a histologic diagnosis have moderate to severe LUTS. Despite its clinical importance, the pathogenesis of BPH is still poorly understood. The triad of prostatic hyperplasia, which includes benign prostatic enlargement, bladder outlet obstruction, and LUTS, is the basis for the clinical diagnosis of BPH [2], but these items are not always present together, and very weak correlations have been found among these components [3,4]. Furthermore, the size of the prostate does not correlate with the degree of obstruction. Thus, other factors such as dynamic urethral resistance, the prostatic capsule and anatomic pleomorphism affect the clinical symptoms more than the absolute size of the gland [5–12]. The prostatic urethra runs through the prostate from the base to the apex, making an anterior angulation of 35 at the proximal part of verumontanum. This bend divides the urethra into proximal and distal portions [13]. The angulation tends to be greater than 35 in men with nodular hyperplasia, but it can also increase in men without prostatic hyperplasia. Upon cystoscopic examination, the increased prostatic urethral angulation shows a higher bladder neck in men without lateral and medial lobe enlargement. Although some urologists suspect that the higher bladder neck might be a causal factor for BPH, the clinical significance of prostatic
533
urethral angulation was previously underestimated. In this study, we propose a new hypothesis that prostatic urethral angulation could be a causal factor for BPH.
Hypothesis: Prostatic urethral angulation is a causal factor of BPH Weak urine stream is a typical symptom in patients with BPH and the urine flow rate is inversely proportional to urodynamically proven obstructions [14]. In general, a decrease in urine flow rate is due to bladder outlet obstruction that is secondary to prostatic enlargement. Prostatic enlargement can compress the prostatic urethra externally resulting in a luminal narrowing of the prostatic urethra. As previously mentioned, the prostatic urethra is a bend tube [13]. By applying fluid dynamics to the process of urination in the prostatic urethra, it has been demonstrated that the energy loss in the bending tube (the prostatic urethra) can occur during micturition as well as from friction in the urethra wall. The energy loss in the bending tube increases proportionally to the loss coefficient (k) at the bends, which can be calculated using the following equation [15]: k = 2.22 · 10 3h + 4.04 · 10 6h2.76, where 0 < h < 90. This formula shows that the energy loss increases with prostatic urethral angulation. This energy loss results in a decrease in the urine velocity and as a result, the urine flow rate is inversely associated with prostatic urethral angulation (Fig. 1). This suggests that prostatic urethral angulation is an overlooked cause of bladder outlet obstruction and a causal factor of BPH.
Figure 1 The relationship between prostatic urethral angulation and urine flow rate (sagittal view): (a) A strong urine flow rate in the prostatic urethra with mild angulation, (b) an intermediate urine flow rate in the prostatic urethra with moderate angulation, and (c) a weak urine flow rate in the prostatic urethra with severe angulation. As prostatic urethral angulation increases, the urine flow rate decreases in order of (a)—(c).
534
Cho et al.
A novel concept of benign prostatic hyperplasia The classical triad of BPH, which includes benign prostatic enlargement, bladder outlet obstruction, and lower urinary tract symptoms, cannot account for the pathogenesis of BPH. Specifically, it is unclear why a decrease in urine flow rate and severe voiding symptoms occur in patients with a mildly enlarged prostate or no prostatic enlargement. We propose that BPH pathogenesis can be better understood if we consider the involvement of prostatic urethral angulation as well as the classical triad (Fig. 2). Other anatomic factors such as dynamic urethral resistance, the prostatic capsule, anatomic pleomorphism, etc. should also be considered along with prostatic urethral angulation [5–12].
Discussion The degree of prostatic urethral obstruction is very important for determining treatment modalities and predicting responses to treatment in patients with BPH. Unfortunately, the total prostate volume (TPV) does not correlate well with the urine flow rate and the symptomatology [3,4], so urologists have been interested in other parameters, such as transition zone volume (TZV), transition zone index (TZI) and prostate configuration [6,7,9–12]. Kaplan et al. [6] maintained that TZI, but not TPV and TZV, was significantly correlated with the urine flow rate and the symptomatology. However, Lepor et al. [10] reported that TPV, TZV, and TZI were not directly related to the American Urological Association (AUA) symptom score and were only weakly related to the urine flow rate. Watanabe [11] introduced a new concept for BPH, the presumed circle area ratio (PCAR) theory, and he and his colleagues suggested that PCAR was more useful in assessing the severity of infravesical obstruction than other parameters, such as TPV, TZV, and TZI [7]. However, this theory also primarily focused on luminal
Figure 2 The diagrammatic concept of benign tatic hyperplasia: the classical concept (a) and a concept (b). BPE: benign prostatic hyperplasia, bladder outlet obstruction, LUTS: lower urinary symptoms, PUA: prostatic urethral angulation.
prosnovel BOO: tract
narrowing of the prostatic urethra as measured by a horizontal sonogram of the prostate. Chia et al. [5] demonstrated that intravesical prostatic protrusion (IPP) was a better and more reliable predictor of bladder outlet obstruction than age, symptoms, urine flow rate, postvoid residual urine volume or prostate volume. They suggested that IPP, as determined by transabdominal ultrasonography, was useful for non-invasive assessments of bladder outlet obstruction. IPP causes a ‘ball-valve’ type obstruction, disrupting the funneling effect of the bladder neck and causing dyskinetic movement of the bladder during voiding [8]. Enlargement of the median lobe causes an increase in the prostatic urethral angulation and the increased prostatic urethral angulation is thought to contribute to factors other than dyskinetic movement. Namely, it has been suggested that increased prostatic urethral angulation can contribute to aggravation of bladder outlet obstruction in patients with benign prostatic obstructions. Martinez-Borges [16] applied fluid dynamics to urine flow in the urethra and determined that turbulent urinary flow in the urethra could be a causal factor for BPH. This current study is the first trial to investigate the impact of prostatic urethral angulation on the urine flow rate using a fluid dynamics approach, and we demonstrated that prostatic angulation is inversely associated with urine flow rate. BPH patients with small prostates can be successfully treated with a transurethral resection or incision in the prostate (bladder neck) [17–20]. Our hypothesis provides a theoretical basis for the transurethral resection or incision of the prostate (bladder neck) in such patients. BPH is a very complex clinical syndrome. Urethral and detrusor functions as well as various anatomical factors of the prostate are also important in the pathogenesis of BPH [21,22]. Nevertheless, the current hypothesis suggests that prostatic urethral angulation is an overlooked cause of bladder outlet obstruction and a causal factor of BPH and this hypothesis provides novel insights into the pathogenesis of BPH. Ultimately, the relationship between prostatic urethral angulation and urine flow rate, and other clinical factors such as urodynamic parameters, symptomatology, response to treatment, and disease progression, need to be investigated in a clinical setting.
References [1] Berry SJ, Coffey DS, Walsh PC, Ewing LL. The development of human benign prostatic hyperplasia with age. J Urol 1984;132:474–9.
The overlooked cause of benign prostatic hyperplasia: prostatic urethral angulation [2] Hald T. Urodynamics in benign prostatic hyperplasia: a survey. Prostate Suppl 1989;2:69–77. [3] Andersen JT, Nordling J, Walter S. Prostatism I. The correlation between symptoms, cystometric and urodynamic findings. Scand J Urol Nephrol 1979;13:229–36. [4] Barry MJ, Cockett AT, Holtgrewe HL, McConnell JD, Sihelnik SA, Winfield HN. Relationship of symptoms of prostatism to commonly used physiological and anatomical measures of the severity of benign prostatic hyperplasia. J Urol 1993;150:351–8. [5] Chia SJ, Heng CT, Chan SP, Foo KT. Correlation of intravesical prostatic protrusion with bladder outlet obstruction. BJU Int 2003;91:371–4. [6] Kaplan SA, Te AE, Pressler LB, Olsson CA. Transition zone index as a method of assessing benign prostatic hyperplasia: correlation with symptoms, urine flow and detrusor pressure. J Urol 1995;154:1764–9. [7] Kojima M, Ochiai A, Naya Y, Ukimura O, Watanabe M, Watanabe H. Correlation of presumed circle area ratio with infravesical obstruction in men with lower urinary tract symptoms. Urology 1997;50:548–55. [8] Kuo HC. Clinical prostate score for diagnosis of bladder outlet obstruction by prostate measurements and uroflowmetry. Urology 1999;54:90–6. [9] Kurita Y, Masuda H, Terada H, Suzuki K, Fujita K. Transition zone index as a risk factor for acute urinary retention in benign prostatic hyperplasia. Urology 1998;51:595–600. [10] Lepor H, Nieder A, Feser J, O’Connell C, Dixon C. Total prostate and transition zone volumes, and transition zone index are poorly correlated with objective measures of clinical benign prostatic hyperplasia. J Urol 1997;158:85–8. [11] Watanabe H. New concept of BPH: PCAR theory. Prostate 1998;37:116–25. [12] Witjes WP, Aarnink RG, Ezz-el-Din K, Wijkstra H, Debruyne EM, de la Rosette JJ. The correlation between
[13] [14]
[15] [16]
[17]
[18]
[19]
[20]
[21]
[22]
535
prostate volume, transition zone volume, transition zone index and clinical and urodynamic investigations in patients with lower urinary tract symptoms. Br J Urol 1997;80:84–90. McNeal JE. The prostate and prostatic urethra: a morphologic synthesis. J Urol 1972;107:1008–16. Comiter CV, Sullivan MP, Schacterle RS, Yalla SV. Prediction of prostatic obstruction with a combination of isometric detrusor contraction pressure and maximum urinary flow rate. Urology 1996;48:723–9 [discussion 29–30]. Schetz JA, Fuhs AE. Handbook of fluid dynamics and fluid machinery. New York: John Wiley & Sons; 1996. Martinez-Borges AR. Turbulent urinary flow in the urethra could be a causal factor for benign prostatic hyperplasia. Med Hypotheses 2006;67:871–5. Li MK, Ng AS. Bladder neck resection and transurethral resection of the prostate: a randomized prospective trial. J Urol 1987;138:807–9. Katz PG, Greenstein A, Ratliff JE, Marks S, Guice J. Transurethral incision of the bladder neck and prostate. J Urol 1990;144:694–6. Riehmann M, Knes JM, Heisey D, Madsen PO, Bruskewitz RC. Transurethral resection versus incision of the prostate: a randomized, prospective study. Urology 1995;45: 768–75. Orandi A. Transurethral incision of prostate (TUIP): 646 cases in 15 years – a chronological appraisal. Br J Urol 1985;57:703–7. Nakai H, Yamanishi T, Yasuda K, Kitahara S, Suzuki T. Correlation between lower urinary tract symptoms and urethral function in benign prostatic hyperplasia. Neurourol Urodyn 2004;23:618–22. Ameda K, Sullivan MP, Bae RJ, Yalla SV. Urodynamic characterization of nonobstructive voiding dysfunction in symptomatic elderly men. J Urol 1999;162:142–6.
Available online at www.sciencedirect.com