ISSUE 1 VOLUME 26 JANUARY - FEBRUARY - MARCH 2014 Hellenic Urology QUARTERLY PUBLICATION BY THE HELLENIC UROLOGICAL ASSOCIATION Reviews Original Articles Case Reports Hellenic UROLOGY QUARTERLY PUBLICATION BY THE HELLENIC UROLOGICAL ASSOCIATION JANUARY - FEBRUARY - MARCH 2014 ISSUE 1 - VOLUME 26 GR - ISSN 1105 - 1272 Hellenic Urology HELLENIC UROLOGY OFFICIAL JOURNAL OF THE H.U.A. ISSUE 1 VOLUME 26 JANUARY - FEBRUARY - MARCH 2014 EDITOR George Moutzouris President of H.U.A. EDITORIAL BOARD EDITOR-IN-CHIEF: Ioannis Varkarakis ASSISTANT EDITOR-IN-CHIEF: Andreas Skolarikos ASSOCIATE EDITORS: Nikolaos Ferakis Stilianos Giannakopoulos Athanasios Papatsoris ASSISTANT EDITORS: Ioannis Adamakis Iraklis Mitsogiannis Konstantinos Stamatiou MEMBERS: Charilaos Katsifotis Iraklis Poulias Grigorios Raptidis Distributed at no charge to all members of the Hellenic Urological Association INDEXED IN IATROTEK AND THE NATIONAL DOCUMENTATION CENTRE GR-ISSN 1105-1272 HELLENIC UROLOGY OFFICIAL JOURNAL OF THE H.U.A. Hellenic Urology Contents ISSUE 1 VOLUME 26 JANUARY - FEBRUARY - MARCH 2014 REVIEWS A. Bourdoumis, Th. Stasinou, Ath. G. Papatsoris Penile size and its correlation with other somatometric parameters 16-21 Ch. Komninos, I. C. Mitsogiannis Obstruction-induced pathological alterations within the urinary bladder due to Benign Prostate Hyperplasia (BPH). A review of the literature 22-29 ORIGINAL ARTICLES Ch. Asvestis, Th. Varvadesis, P. E. Maravelakis Greek Version of the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI), its linguistic adaptation and the pilot test of its validity (ÍÇÉ) 30-35 A.I. Archodakis, S. Bolometes Functional and ongological results of radical perineal prostatectomy for the management of clinically locally advanced prostate cancer. Single centre experience 36-44 M. Stavropoulos, P. Venetsanos, P. Anastasopoulos, C. Bouropoulos, N. Ferakis, I. Poulias Urodynamic findings in voiding symptoms after radical prostatectomy: Analysis of our experience 45-53 CASE REPORTS K. Stamatiou, G. Makris, D. Zavradinos, E. Geropappas, K. Fokas, Ath. Papatsoris Malakoplakia of the bladder associated with advanced obstructive uropathy 54-56 M. Stavropoulos, C. Bouropoulos, N. Ferakis, I. Poulias Emergency embolisation of a spontaneously ruptured angiomyolipoma in a solitary kidney 57-61 Ô Å Ë Å Õ ÔÁ É Á Í Å Á Ãíùìïäüôçóç ó÷åôéêÜ ìå ôçí áñìïäéüôçôá êáé ôéò ðñïûðïèÝóåéò ÷ïñÞãçóçò Üäåéáò ëåéôïõñãßáò éäéùôéêïý éáôñåßïõ ÁðÜíôçóç ôïõ Ãåí.ÃñáììáôÝá ôçò EAU ÁðÜíôçóç ôïõ Ãåí.ÃñáììáôÝá ôçò EAU, Êáèçãçôïý Ïõñïëïãßáò ê. Abrahamsson, ó÷åôéêÜ ìå ôï Ðñïó÷Ýäéï Íüìïõ ðïõ áöïñÜ ôçí ßäñõóç íÝùí Åðéóôçìïíéêþí Åôáéñåéþí ôùí Éáôñéêþí Åéäé... ÄéáäéêôõáêÝò ìåôáäüóåéò Óõíåäñéþí ÅÏÅ óôï ÍÉÌÔÓ Óáò åíçìåñþíïõìå üôé óõíå÷ßæïíôáé êáé ôï 2009 êáôÜ ôç äéÜñêåéá ôùí ìçíéáßùí óõíåäñéþí ôçò Åôáéñåßáò ìáò óôï ÍÉÌÔÓ, ïé äéáäéáêôõáêÝò ìåôáäüóåéò e-learning óôá Ðåñéöåñåé... «ÅéóáãùãÞ ÊùäéêïðïéÞóåùí ÉáôñéêÞò Ðëçñïöïñßáò» Êýñéïé, Ìå ôçí ðáñïýóá åðéóôïëÞ èá èÝëáìå íá óáò åíçìåñþóïõìå ãéá ôï Ýñãï «ÅéóáãùãÞ ÊùäéêïðïéÞóåùí ÉáôñéêÞò Ðëçñïöïñßáò», ôï ïðïßï õëïðïéåßôáé óôï ðëáßóéï ôïõ ÌÝôñïõ 2.7 ... 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Introduction to the electronic age, New York: E-Publishing Inc; 1999, p. 281–304. Note shortened form for last page number. e.g., 51–9, and that for more than 6 authors the first 6 should be listed followed by "et al." For further details you are referred to "Uniform Requirements for Manuscripts submitted to Biomedical Journals" (J Am Med Assoc 1997;277:927–934) (see also http://www.nlm.nih.gov/bsd/uniform_requirement s.html). REVIEW Penile size and its correlation with other somatometric parameters Andreas Bourdoumis1, Theodora Stasinou2, Athanasios G. Papatsoris3 1 Department of Urology, Royal London Hospital, Bartshealth NHS Trust, London, UK 2 Department of Urology, North Devon District Hospital, North Devon Healthcare NHS Trust, Barnstaple, UK 3 Second University Department of Urology, Sismanoglio General Hospital, Athens, Greece Corresponding Author: Andreas Bourdoumis Royal London Hospital, Whitechapel Road, E1 1BB, London, UK e-mail: [email protected] Summary The concept that penile size is related to various other body features is commonly encountered. In the current review, we seek evidence based results from studies investigating the correlation between the penile size and various other somatometric parameters. Parameters under investigation included penile circumference, flaccid and stretched penile lengths, age, height, weight, body mass index as well as shoe size and index finger length. The various investigated penile parameters were found to be positively correlated with somatometric parameters such as height, weight and body mass index. Key words Penile size, penile length, somatometric parameter Introduction Variations in penile shape and size may have considerable consequences in relationships and 1 quality of life . Concerns regarding the ideal penile size are commonly encountered in the male 2 population . Measurement of penile length is an important part in the assessment of microphalia and other external genitalia abnormalities3,4. Expert consultation and reassurance is often sought, driven by concern about adequacy of penile size, and this is also reinforced by the commercial campaigns from the industry (i.e. manufactures of condoms)5. The objective of this review was to highlight the evidence from the various studies in the literature that investigate the potential correlation of the average penile size to other somatometric parameters. 16 Hellenic UROLOGY Materials and Methods An electronic database (i.e. PubMed, E-medicine) literature search was performed by using relevant key words, such as penis, penile, size, penile length, somatometric parameter, penle enlargement, phalloplasty, microphalia, and micropenis syndrome (alone or in combination). Retrospective and prospective studies with more than one hundred male participants were analyzed. The selected journals were written in English, and the majority was published during the last decade. The impact of penile size There is a steady increase in the number of men who are not satisfied with their penile size and therefore seek penile enlargement2. In a recently published series of 250 patients complaining of a small-sized penis, 64% of them admitted that their anxiety arose after comparing their penis to their 6 friends during childhood . Penile size related anxiety may lead to negative affect disorders and 7 decreased self esteem . In an internet-based survey among 52,301 men and women, most men rated their penis as being of average size (66%) and only 12% rated their penis as small. In the same study, 85% of the female participants felt satisfied 8 with their partner's penile size . The results seem to be related to the subjective perception and selfesteem of the individual. Micropenis syndrome is considered to be a subjective perception of a small penis in flaccid state, despite a normal physical examination9. A psychological disorder known as dysmorphophobia is associated with an altered subjective perception of normal physical characteristics as Penile size and its correlation with other somatometric parameters inadequate or abnormal9. In a study conducted among 112 students, a subjective perception of a small sized penis was observed in 26% of participants and similar results were reported in another study from men serving in the military10,11. Also, it has also been postulated that most men who request penile augmentation surgery exaggerate as to the perception of what a normal penile size is. In a series of 67 men complaining for their size, none of the participants was proven to 2 actually have an objectively small penis . In the same cohort, 19 men (28.3%) continued to investigate the possibility of a surgical augmentation despite the detailed and scientifically 2 evidence based consultation provided . In other studies comprising of 331 volunteers, 67% was relatively satisfied with their penile size (mean: 13.6±2.3 cm) in flaccid length, although 62% believed that a larger penis would offer more 12,13 satisfaction to their female partners . However, women participants claimed that larger size is not 14 necessarily associated with sexual pleasure . Shortening of the penile shaft can be observed after prostate cancer treatment, in erectile dysfunction cases, after treatment of the Peyronie's disease or 15 in congenital penile deformity. Munding et al evaluated changes in the penile length after retropublic radical prostatectomy 3 months after the surgery. The authors reported a decrease in 71% of patients, with 48% measuring at least 1cm less in stretched measurement. Similarly, Savoie et 16 al reported a statistically significant reduction in 68% of the patients. Objective shortening is also reported following hormonal and external beam 17,18 radiation treatment of prostate cancer . Awwad 19 et al compared penile size lengths between normal adults and patients with erectile dysfunction. A statistically significant difference was demonstrated between the mean flaccid to the mean stretched length (9.3 cm vs. 7.7 cm and 13.5 cm vs. 11.6 cm, respectively) which was attributed to the inability of the tunica albuginea to expand. In patients with Peyronie's disease, postoperative measurements revealed a 30-50% shortening, especially following circumferential incision of the tunica albuginea and placement of a penile 20 implant . In cases who underwent a Nesbit operation that proportion was reported to be as high as 100% 21. True microphalia may be encountere as a result of defective gonadotropin secretion from the hypothalamus, or in mixed gonadal dysgenesis22-25. The epispadias-extrophy complex is also associated with penile shortening due to a relative 25 reduction in length of the copora cavernosa . Determination of normal penile length In a meta-analysis by Templer et al26 the average length of a normal range penis was identified to be 8.9cm in flaccid state and 15.2cm during erection. Although there is no standard technique for penile length measurement, some researchers prefer to measure penile dimensions from the pubic ramus to the distal tip of the glans penis on the dorsal 12,27 surface . During penile measurement, care should be taken to avoid pressure against the pubic fat pad, which may alter results. Measurements are generally made during flaccid, stretched and erect states. The first study about penile length is attributed to Loeb in 1899, and the average flaccid penile length as he measured it was 28 29 9.41 cm . Ponchietti et al conducted a study in 3300 men and managed to develop a nomogram including penile dimensions in percentiles during flaccid and erect state. Several studies have shown that there is a strong correlation between stretched 9, 27 penile length and erect length . As shown in Table 1, for a range between 8-10cm, flaccid length is usually 3-4cm shorter than the stretched penile length and 5-6cm shorter than the erect length. It is widely accepted that true microphalia corresponds in penile lengths which are shorter than the mean length at least at 2.5 standard deviations (SD) and it refers to penile length below 4cm in the flaccid state Hellenic UROLOGY 17 Andreas Bourdoumis, Theodora Stasinou, Athanasios G. Papatsoris 27 30 and under 7cm in stretched state . Brondil et al performed a study in 905 men and recorded measurements of 10.7cm and 16.74cm during flaccid and stretched state respectively. Their conclusion was that penile compliance is significantly decreased with aging. In other studies about microphalia it was appreciated that the shortest penile length sufficient for penetration and insemination was 4cm22, 23. Correlation to somatometric parameters The variability amongst measurements of penile size reflects the ethnic diversity of populations that were studied, the different age groups as well as the different measurement techniques that were applied. Somatometric parameters that were correlated with penile size in the studies included height, weight, ratio of circumference to waist/hip, 12, 29, 31, 32 shoe size and index finger length (Table 2) . 31 Shah et al reported that there was no correlation between shoe size and penile length. A study of 52 Greek males, aged 19–38, revealed that the penile length is weakly correlated inversely to age, weight, BMI and height/weight ratio, weakly correlated to height and directly statistically significant only with index finger length32. The largest relative study conducted by Ponchietti et al29 among 3300 Italian men demonstrated that penile measurements (length and circumference at the midshaft) correlated to height but no correlation between weight and the BMI. In a series of 1500 men, 4 Mehraban et al reported a significant positive correlation with age, height, index finger length, but not with waist/hip ratio or weight. In a Turkish study among 2247 men, weak positive correlations were identified between penile circumference, flaccid and stretched lengths and height and weight. Although those correlations were found between the mean circumference penile length and BMI, there were no correlations between length and BMI 33. In other words, there is enough evidence to suggest that penile size is positively correlated to the height and inversely correlated to the weight and BMI. In 18 Hellenic UROLOGY contrast to socially spread beliefs correlating index finger and shoe size length, such correlations are not supported by the current literature. For an accurate estimate of penile length, we recommend measurement starting at the pubopenile junction to the tip of the glans, during flaccid, stretched and 27 erect state . Surgical augmentation techniques The management of patients with microphalia should be multidisciplinary, including urological and psychological consultations. There are no clear recommendations for penile augmentation in the literature11. The respective surgical techniques are few, and the relative studies include only small numbers of patients and a short follow up. Liposuction can only provide a subjective visual lengthening effect. Skin enhancement techniques may lead to severe deformities and hypertrophic 34 scarring . Dissection of the penile suspensory ligament followed by postoperative penile stretching increases penile length by 1-2cm; however it may be followed by reduced erection angle and penile instability35, 36. There are few reports on the effect of circumcision on penile 37 size . A study showed a statistically important penile length difference between children submitted to circumcision compared to children who were not38. In the same study the penile length of the corpora cavernosa measured by ultrasound was not found to be statistically different 38. Conclusion During consultation for penile augmentation procedures, it is important for the urologists to be familiar with the respective range of normal penile length for the particular age and population group. In the present review, there were a few significant correlations among penile dimensions and other somatometric parameters, especially height, weight and BMI. Further studies are required to evaluate the safety and effectiveness of surgical augmentation techniques. Penile size and its correlation with other somatometric parameters Table1. Studies evaluating penile length (mean values) Year of publication Studies 28 Kinseyetal. Country 1948 29 Ajmanietal. 1985 Number of partici pants Age 2770 USA NIGERIA Stretched penile length (cm) Penile circumfe rence (cm) 2059 9,7 15,5 NR* 320 1723 8,16 NA 8,83 1 8,85 12,45 9,71 Bartshealth NHS Trust, London, UK Wessellsetal.20 1996 USA 80 Chenetal.23 2000 ISRAEL 55 2178 8,3 12,5 NA Ponchiettietal.9 2001 ITALY 3300 1719 9,0 12,5 10,0 200 2022 6,8 Spyropoulo 8 setal. 2002 GREECE 52 1939 7,76 12,18 8,68 Awwadetal.30 2005 JORDANIA 271 1783 9,3 13,5 8,98 Mehrabanetal.4 2007 IRAN 1500 2040 ÄÁ* 11,58 8,66 Promoduetal.31 2007 INDIA 301 1860 8,21 10,88 9,14 2010 TURKEY 1132 1930 9,3 13,7 NA 8,95 13,98 8,89 8,64 12,87 9,11 Söylemezet al. 2011 TURKEY 2276 1839 Average length in total of all studies. 19482011 UNIVE RSALLY 12 257 1783 1 ÁíäñåÜò Ìðïõñäïýìçò, 2Èåïäþñá Óôáóéíïý, 3 ÁèáíÜóéïò Ã. Ðáðáôóþñçò Department of Urology, Royal London Hospital, Department of Urology, North Devon District Hospital, North Devon Healthcare NHS Trust, Barnstaple, UK 2 TURKEY 25 óùìáôïìåôñéêÝò ðáñáìÝôñïõò 2 2002 Aslanetal.6 Ðåúêü ìåãÝèïò êáé óõó÷Ýôéóç ìå Üëëåò Flaccid penile length (cm) 2182 Sengezeretal.3 Ðåñßëçøç 12,7 NA Â' ÐáíåðéóôçìéáêÞ ÏõñïëïãéêÞ ÊëéíéêÞ, Óéóìáíüãëåéï Ãåíéêü Íïóïêïìåßï, ÁèÞíá Õðåýèõíïò åðéêïéíùíßáò: ÁíäñÝáò Ìðïõñäïýìçò Royal London Hospital,Whitechapel Road, E1 1BB, London, UK e-mail: [email protected] Ç áíôßëçøç ôïõ óõó÷åôéóìïý ôïõ ìåãÝèïõò ôïõ ðÝïõò ìå äéÜöïñåò Üëëåò óùìáôéêÝò ðáñáìÝôñïõò áðáíôÜôáé óõ÷íÜ óôïí áíäñéêü ðëçèõóìü. NA: Not Applicable Table 2. Studies correlating penile length to somatometric parameters Ï óêïðüò ìáò åßíáé ç áíáóêüðçóç ôçò âéâëéïãñáößáò þóôå íá äéåñåõíçèåß ç ðéèáíÞ óõó÷Ýôéóç ôïõ ìÝóïõ öáëëéêïý ìÞêïõò êáé Üëëùí óùìá- Studies Country Number of men Flaccid penile length (cm) Heigh Weight (cm) (kgr) BMI Index finger length (cm) Waist/ hip circum ference ôïìåôñéêþí ðáñáìÝôñùí. ÁíáóêïðÞèçêáí ìåëÝôåò ó÷åôéêÜ ìå ôç ðåñéöÝñåéá ôïõ ðÝïõò, ôï ìÞêïò êáôÜ ôç ÷áëáñÞ êáé ôåôáìÝíç öÜóç, ôçí çëéêßá, ôï 25 Söylemezet al. Ponchiettietal.9 TURKEY ITALY 2276 3300 8,95* 174,79* 69* 22,59* _ +/- +/- +/- +/- 1,04 5,44 6,93 1,97 9,0*** 175*** 69 22,53*** _ 179.4 82,5 25,7 9,6* +/- +/- +/- +/- 6,5 13 3,65 0,73 _ ýøïò, ôï âÜñïò, ôï äåßêôçò ìÜæáò óþìáôïò, ôï ìÝãåèïò ôçò Üêñáò ðïäüò êáé ôï ìÝãåèïò ôïõ äåß- _ êôç ôçò Üêñáò ÷åéñüò. Ïé äéÜöïñåò ðåúêÝò äéáóôÜóåéò ðïõ åîåôÜóôçêáí ðáñïõóßáóáí èåôéêÞ óõ- Spyropoulo GREECE setal.8 52 7,76*** 174,3*** Mehrabanetal. Promoduetal. 4 31 IRAN INDIA 1500 301 11,58 8,21 $ 78,67 +/- +/- 6,31 8,41 167,27 65,53** +/- +/- 6,91 10,8 ó÷Ýôéóç ìå óùìáôïìåôñéêÝò ðáñáìÝôñïõò, üðùò 0,89 ôï ýøïò, ôï âÜñïò êáé ôï äåßêôç ìÜæáò óþìáôïò. 8,97*** 25,87 +/- 0,91 ËÝîåéò åõñåôçñéáóìïý: Ðåúêü ìÝãåèïò, ðåúêü ìÞ- 0,89 23,5** _ _ êïò, óùìáôïìåôñéêÞ ðáñÜìåôñïò. *Positive correlation p<0.05 **Positive correlation p<0.01 ***Positive correlation p<0.001 Hellenic UROLOGY 19 Andreas Bourdoumis, Theodora Stasinou, Athanasios G. Papatsoris References 1. Diseth Th, Bjordal R, Schultz A, Stange M, Emblem R. Somatic function, mental health and psychosocial functioning in 22 adolescents with bladder exstrophy and epispadias. J Urol 1998; 159: 1684–1689; discussion 1689–1690. 2. Mondaini N, Ponchietti R, Gontero P, Muir Gh, Natali A, Caldarera E Et Al. Penile length is normal in most men seeking penile lengthening procedures. Int J Impot Res 2002; 14: 283–286. 3. Sengezer M, Ozturk S, Deveci M. Accurate method for determining functional penile length in Turkish young men. AnnPlastSurg 2002; 48: 381–385. 4. Mehraban D, Salehi M, Zayeri F. Penile size and somatometric parameters among Iranian normal adult men. Int J ImpotRes 2007; 19: 303–309. 5. Schneider T, Sperling H, Lummen G, Syllwasschy J, Rubben H. Does penile size in younger men cause problems in condom use? a prospective measurement of penile dimensions in 111 young and 32 older men. Urology 2001; 57: 314–318. 6. Ghanem H, Shamloul R, Khodeir F, Elshafie H, Kaddah A, Ismail I. Structured management and counseling for patients with a complaint of a small penis. J Sex Med 2007; 4: 1322–1327. 7. Alter Gj. Augmentation phalloplasty. UrolClin North Am 1995; 22: 887–902. 8. Lever J, Fredereicjk Da, Peplau La. Does size matter? Men's and women's views on penis size across the lifespan. Psychol Men Masculinity 2006; 3: 129–43. 9. Wylie Kr, Eardley I. Penile size and the 'small penis syndrome'. BJU Int 2007; 99: 1449–1455. 10. Lee Pa. Survey report: concept of penis size. J Sex Marital Ther1996; 22:131–5. 11. Son H, Lee H, Huh Js, Kim Sw, Paick Js. Studies on self-esteem of penile size in young Korean military men. Asian J Androl2003;5: 185–9. 12. Aslan Y, Atan A, Omur Aydin A, Nalcacioglu V, Tuncel A, Kadioglu A. Penile length and somatometric parameters: a study in healthy young Turkish men. Asian J Androl 2010; 13: 339–341. 20 Hellenic UROLOGY 13. Kuzgunbay B, Turunç T, Güvel S, Özkardeº H. The average penile size of the Turkish men and their opinions about the penile size. Turk J Urol 2007; 33: 290–293. 14. Francken Ab, Van De Wiel Hb, Van Driel Mf, Weijmar Schultz Wc. What importance do women attribute to the size of the penis? EurUrol 2002; 42: 426–431. 15. Munding Md, Wessells Hb, Dalkin Bl. Pilot study of changes in stretched penile length 3 months after radical retropubic prostatectomy. Urology 2001; 58: 567–569. 16. Savoie M, Kim Ss, Soloway Ms. A prospective study measuring penile length in men treated with radical prostatectomy for prostate cancer. J Urol 2003; 169: 1462–1464. 17. Haliloglu A, Baltaci S, Yaman O. Penile length changes in men treated with androgen suppression plus radiation therapy for local or locally advanced prostate cancer. J Urol 2007; 177: 128–130. 18. Hall Sj, Basile G, Bertero Eb, De Las Morenas A, Goldstein I. Extensive corporeal fibrosis after penile irradiation. J Urol 1995; 153: 372–377. 19. Awwad Z, Abu-hijleh M, Basri S, Shegam N, Murshidi M, Ajlouni K. Penile measurements in normal adult Jordanians and in patients with erectile dysfunction. Int J Impot Res 2005; 17: 191–195. 20. Porst H, Buvat J. Standard Practice in Sexual Medicine. Blackwell: Malden, MA, 2006. 21. Rigaud G, Berger Re. Corrective procedures for penile shortening due to disease. J Urol 1995; 153: 368–370. 22. Aaronson Ia. Micropenis: medical and surgical implications.J Urol 1994; 152: 4–14.I 23. Campbell Mf, Wein Aj, Kavoussi Lr. Campbell-Walsh Urology. editor-in-chief, Alan J, Wein; Louis R Kavoussi, et al.(eds), 9th edn. W.B. Saunders: Philadelphia, 2007 pp 3751–3754. 24. Moncada-irribaren I. Managing penile shortening after disease surgery. J Urol 2007; 177: 750A. Silver RI, Yang A, Ben Chaim J, Jeff RD, Gearheart JP. Penile length in adulthood after Penile size and its correlation with other somatometric parameters exstrophy reconstruction. J Urol 1997; 157: 999–1003. 25. Silver Ri, Yang A, Ben Chaim J, Jeff Rd, Gearheart Jp. Penile length in adulthood after exstrophy reconstruction. J Urol 1997; 157: 999–1003. 26. Templer D I. (2002). Is size important? Pittsburgh, PA: CeShore. 27. Wessells H, Lue Tf, Mcaninch Jw. Penile length in the flaccid and erect states: guidelines for penile augmentation. J Urol 1996; 156: 995–997. 28. Loeb H. Harnrohrencapacitat und Tripperspritzen. Munch Med Wochenschr 1899; 46: 17. 29. Ponchietti R, Mondaini N, Bonafe M, Di Loro F, Biscioni S, Masieri L. Penile length and circumference: a study on 3,300 young Italian males. EurUrol 2001; 39: 183–186. 30. Bondil P, Costa P, Daures Jp, Louis Jf, Navratil H. Clinical study of the longitudinal deformation of the flaccid penis and of its variations with aging. EurUrol 1992; 21: 284–286. 33. Söylemez H, Atar M, Sancaktutar Aa, Penbegül N, Bozkurt Y, Onem K. Relationship between penile size and somatometric parameters in 2276 healthy young men. Ént J Impot Res. 2012 MayJun;24(3):126-9. 34. Vardi Y, Gruenwald I. The status of penile enhancement procedures. CurrOpinUrol 2009; 19: 601–605. 35. Murtagh J. The 'small' penis syndrome. AustFamPhysician 1989; 18: 218, 220. 36. Li Cy, Kayes O, Kell Pd, Christopher N, Minhas S, Ralph Dj. Penile suspensory ligament division for penile augmentation: indications and results. EurUrol 2006; 49: 729–733. 37. Burgu B, Aydogdu O, Tangal S, Soygur T. Circumcision: Pros and cons. Indian J Urol 2010; 26: 12–15. 38. Smith Dp, Rickman C, Jerkins Gr. Ultrasound evaluation of normal penile (corporeal) length in children. J Urol 1995; 154(2 Part 2): 822–824. 31. Shah J, Christopher N. Can shoe size predict penile length? BJU Int 2002; 90: 586–587. 32. Spyropoulos E, Borousas D, Mavri-kos S, Dellis A, Bourounis M, Athanasiadis S. Size of external genital organs and somatometric parameters among physically normal men younger than 40 years old. Urology 2002; 60: 485–489; discussion 490–481. Hellenic UROLOGY 21 REVIEW Obstruction-induced pathological alterations within the urinary bladder due to Benign Prostate Hyperplasia (BPH) A review of the literature 1 2 Christos Komninos , Iraklis C. Mitsogiannis . 1 Department of Urology, Nikaia General Hospital, Athens, Greece 2 nd 2 Department of Urology, Sismanoglio Hospital, University of Athens Medical School, Athens, Greece. Corresponding Author: Iraklis C. Mitsogiannis 2nd Department of Urology, University of Athens Sismanoglio Hospital, 1 Sismanogliou str., 15126 Maroussi, Athens, Greece Tel: +30 2132058253, Fax: +30 2108044703 email: [email protected] Summary Introduction Benign prostatic hyperplasia (BPH) is a frequent cause of Bladder Outlet Obstruction (BOO) and Low Urinary Tract symptoms (LUTS). BPH process induces functional, biochemical and morphological alterations, in order for the urinary bladder to maintain a normal functionality. There is substantial evidence that detrusor blood flow significantly decreases in the presence of BOO. This review addresses the bladder response to BOO and focuses on the alterations and biochemical adaptability of the bladder wall in the presence of hypoxia. Methods A literature review of published articles has been performed, including both in vivo and in vitro studies on human and animal tissue. Results In the presence of obstruction and hypoxia, muscle enlargement and collagen deposition comes upon, mitochondria sustain damage, mitochondrial DNA deletions and decrease mitochondrial enzyme activity occur leading to a decreased oxidative metabolism and ATP synthesis. Anaerobic metabolism and probably glycogen deposit increase, in order for the muscle cells to find alternative energy supplies. As a result, lactic acid due to the anaerobic metabolism accumulates in the smooth muscle causing contractile dysfunction. Furthermore, hypoxia induces bladder wall denervation and reduces cholinergic nerve density. 22 Hellenic UROLOGY Conclusion BOO is a key factor in the aetiology of LUTS/BPH. Obstruction is associated with a variety of morphological, contractile and biochemical changes within the bladder. Key words Benign prostatic hyperplasia; bladder outlet obstruction; urinary bladder; detrusor muscle. Introduction BPH affects 50% to 90% of men between 50 and 85 years of age1. It is a common disorder of the male urogenital tract typically accompanied by LUTS (hesitancy, straining, weak urine flow, frequency, nocturia and urgency)2. BPH-related symptomatology is attributed to obstructed outflow (BOO), which results from either prostate enlargement (static component) and/or increased á-adrenergic activity at the level of bladder neck and prostatic urethra (dynamic component)3,4. BOO has been shown to be associated with a variety of morphological, contractile and biochemical changes within the bladder in both experimental and clinical studies. In general, the bladder modifies its structure to compensate the increased resistance to flow. Furthermore, it is known that in partial outlet obstruction significant hypoxia ensues because of the high resistance to flow and consequent high intravesical pressure. The present review addresses current data on the response of the bladder to BOO particularly Obstruction-induced pathological alterations within the urinary bladder due to Benign Prostate Hyperplasia (BPH). A review of the literature focusing on the bladder wall alterations and biochemical adaptability in the presence of hypoxia. Methods For this publication, both in vivo and in vitro studies on human and animal tissue were used to estimate the consequences of outlet obstruction on the bladder wall. A search of the PubMed using the terms “Benign Prostate Hyperplasia”, “Bladder Outlet Obstruction”, “bladder hypoxia” and “detrusor ischemia” was conducted. The search was limited to the period 1980-2013. Forty-six manuscripts were selected for their relevance to the subject of the review. Results Bladder response to outlet obstruction The urinary bladder often responds to BOO with hypertrophy, accompanied by an augmentation of connective tissue components and replacement of proteins of the contractile apparatus of the smooth muscle cell, with their non-muscle (embryonic) isoforms, such as non-muscle myosin heavy chain, a5-8 isoform of tropomyosyn, calponin, â- and ã-actin . High bladder pressure induces adaptive changes in the bladder structure, which, in the long term, are visible as muscle enlargement and collagen de9-11 position . The increase in connective tissue between muscle fibres and muscle bundles significantly decreases bladder elasticity and therefore 12 bladder compliance . Obstruction-induced smooth muscle remodelling and hypertrophy are compensatory responses aimed to produce the increased force required to expel urine against the obstruction. These compensatory changes are associated with altered expression of contractile proteins and various signalling and regulatory proteins such as calmodulin, Rho-activated kinase 13-15 and caveolins . Rho-kinase constitutes a main ++ pathway, which regulates detrusor Ca sensitisation, which is necessary for the detrusor 13 muscle to maintain contraction . Bladder outlet obstruction and the ensuing muscle hypertrophy and collagen deposition within the bladder wall results in a significant decrease in detrusor blood flow and hence impaired oxygen 16-23 diffusion to the tissues ; furthermore an increased expression of Hypoxia Inducible Factor-a 21 (HIF-a) is observed (Fig. A) . During obstruction, the detrusor reduces its own oxygen supply by producing pressures that compress the small 21-23 blood vessels . As a result to hypoxia, obstructed bladders appear hypervascular and partially denervated24 and exhibit alterations in the mito25 chondrial structure and function and the glycogen 26,27 content . Obstruction also induces protein oxidation in the detrusor smooth muscle28 and lactic acid due to the anaerobic metabolism accumulates 29 causing contractile dysfunction . These findings suggest that ischemia and hypoxia may be responsible for the development of bladder dysfunction in BOO17,18. It is not known whether this is mediated directly through an effect on the detrusor 30 smooth muscle or as a result of neuronal loss and 31 subsequent smooth muscle changes . Mitochondria-ATP-Glucose metabolism Mitochondrial enzyme activity is crucial in the energy production and contractility of detrusor muscle32 and it has been shown to increase with the severity of partial bladder outlet obstruction in the male33. As the obstruction progresses, increased oxidative stress in the detrusor muscle occurs, leading to a significantly higher incidence and 34 proportion of mitochondrial DNA deletions . Electron microscopy evaluation of the obstructed rabbit bladder showed that mitochondria within detrusor muscle cells become progressively more swollen. Six weeks post-obstruction, similarly swollen mitochondria are also present in other cell types within the bladder wall, such as fibroblasts, Schwann cells, endothelium and perivascular smooth muscle. These findings of mitochondrial damage have been interpreted as evidence of ischemic Hellenic UROLOGY 23 Christos Komninos, Iraklis C. Mitsogiannis damage of the bladder wall as a conse-quence of 35 outflow obstruction . Similar mitochondrial damage has been noted in human detrusor smooth muscle cells in biopsy samples removed from 12 patients with bladder outflow obstruction . Currently, many investigators consider mitochondrial alteration as a crucial factor in voiding dysfunction and hypothesise that severe and irreversible mitochondrial damage, marked by disruption of outer membrane, could explain the frequent persistence of symptoms after removal of bladder outlet obstruction in men36. Furthermore, during obstruction, mitochondrial enzyme activity subsides thus leading to impaired oxidative metabolism, as evidenced by specific decreases in the activity of citrate synthase (CS), 37 malate dehydrogenase and cytochrome oxidase . ATP provides most of the cellular energy required 38 for maintenance of cell function . Adequate cytosolic ATP concentration is maintained by anaerobic metabolism of glucose to pyruvate and subsequent oxidative metabolism of pyruvate to CO2 and H2O within the mitochondria through the tricarboxylic acid (TCA) cycle and respiratory chain pathway39. CS is the rate-limiting enzyme of the TCA cycle, which provides substrates for the respiratory chain. A reduction in respiratory chain substrates would lead to decreased oxidative phosphorylation (i.e., decreased ATP synthesis). Bladder biopsies from men with significant obstructive symptoms, secondary to BPH, have demonstrated a marked decrease in CS activity compared to bladder samples isolated from unobstructed men of the same age40. There is also evidence of reduced aerobic and increased anaerobic metabolism in obstructed bladders. Partial bladder outlet obstruction of the rabbit induces a shift from aerobic to anaerobic metabolism, as evidenced by the shift in glucose metabo41 lism from CO2 to lactic acid generation . Similarly, there is a marked decrease in the metabolism of 24 Hellenic UROLOGY 41 pyruvate to CO2. Glycogen content During obstruction, the bladder muscle reduces its own oxygen supply by producing pressures that 22,23 compress the small blood vessels . This prompts parts of the muscle to function anaerobically and glycogen may be used as an alternative energy supplier27. Upon chronic ischemic periods the bladder may adapt by increasing the amount of gly26 cogen stored in muscles cells . In an animal model, Bas W.D. de Jong et al showed that glycogen deposition in the bladder wall is directly 26 related to bladder function during obstruction ; the strongest glycogen deposition was found in bladders having experienced the highest pressures, lowest compliance and highest contractility. At first, little deposition occurred close to the serosal side of the detrusor layer and later on, strongest accumulation appeared throughout the whole de-trusor layer up to the urothelium. The authors concluded that glycogen content is a clear marker of the severity of the functional changes that urinary bladder has undergone during obstruction and claimed that analysing glycogen deposits may give insight in the severity of bladder damage and therefore contribute in making an accurate prognosis of bladder function26. Maintenance of normal detrusor function relies on sufficient oxygen and energy supplies and there is probably a crucial level below which hypoxia - induced muscle dysfunction ensues. In the compensated bladder, relief of the ischemia should result in an immediate restore of contractility. However, at some stage, ischemia-induced changes might become less reversible and the potential of the blad42 der to regenerate its function might be reduced . Denervation Several human bladder studies showed that there is a significant loss of innervation (denervation) associated with obstructive dysfunction secondary Obstruction-induced pathological alterations within the urinary bladder due to Benign Prostate Hyperplasia (BPH). A review of the literature to BPH24. Neurones are known to be very sensitive to hypoxic damage, with grey matter more easily 43 damaged than white . Denervation may arise because of damage to postganglionic parasympathetic neurones within the bladder wall and this damage may be caused by the transient bladder ischemia that occurs during obstructed micturi44 tion . Moreover, partial bladder denervation during BOO is more prominent on the cholinergic than on the sympathetic side of the system, as the 45 former is dominant in the bladder . Cumming et al, reported a 56% reduction in the number of acetylcholine-positive nerves in bladder biopsies obtained from obstructed compared to nonobstru46 cted men . Counts of nerve profiles confirmed reduced density of autonomic innervation and not merely decreased concentration of AchE. mage may become irreversible and this could explain the persistence of symptoms after relief of BOO in the male. Detrusor glycogen content could be probably used as a marker of the severity of alterations that have occurred within the bladder wall during obstruction. However, more studies in the human urinary bladder are required in order to confirm that hypothesis. Conclusion Bladder dysfunction secondary to BPH is a major affliction of aging men. Bladder modifies its structure in order to compensate the increased resistance to flow. As a result there is a significant decrease in detrusor blood flow, especially in the late period of the obstruction. During the obstruction and hypoxia period, six major alterations of bladder wall morphology and detrusor biochemistry may be recognised (Fig. B): 1) Muscle enlargement and collagen deposition, 2) mitochondrial DNA deletions, mitochondrial damage and reduced mitochondrial substrate (e.g. glucose) utilisation, 3) decreased mitochondrial enzyme activity which leads to decreased oxidative metabolism and ATP synthesis, 4) reduced aerobic and increased anaerobic metabolism which leads to lactic acid accumulation, 5) glycogen deposition, as an alternative energy supplier and 6) reduced cholinergic nerve density and denervation. In the case of long-lasting BOO, mitochondrial da- Fig. A,B. Pathophysiology of BPH and obstruction-induced alterations within the urinary bladder. BPH – benign prostate hyperplasia; BOO – bladder outlet obstruction; HIF-á – hypoxia induced factor á. Hellenic UROLOGY 25 Christos Komninos, Iraklis C. Mitsogiannis Ðåñßëçøç ÁðïôåëÝóìáôá: ÊáôÜ ôç äéÜñêåéá ôçò áðüöñáîçò êáé ôçò õðïîßáò åðÝñ÷åôáé ìõúêÞ õðåñ- ÐáèïöõóéïëïãéêÝò ìåôáâïëÝò óôçí ôñïößá, åíáðüèåóç êïëëáãüíïõ, âëÜâç óôá ïõñïäü÷ï êýóôç áðü ôçí õðïêõóôéêÞ ìéôï÷üíäñéá, äéáãñáöÝò ìéôï÷ïíäñéáêïý DNA êáé áðüöñáîç ðïõ ðñïêáëåß ç ÊáëïÞèçò ì å ß ù ó ç ô ç ò ì é ôï÷ï í ä ñ é á ê Þ ò å í æ õ ì é ê Þ ò Õðåñðëáóßá ôïõ ÐñïóôÜôç (ÊÕÐ). äñáóôçñéüôçôáò, ìå áðïôÝëåóìá ôïí ìåéùìÝíï Áíáóêüðçóç ôçò âéâëéïãñáößáò ïîåéäùôéêü ìåôáâïëéóìü êáé ôçí åëáôôùìÝíç Êïìíçíüò ×.1, ÌçôóïãéÜííçò Çñ.2 óýíèåóç ATP. Åðßóçò, ðáñáôçñåßôáé óôñïöÞ 1 ÏõñïëïãéêÞ ÊëéíéêÞ, Ãåíéêü Íïóïêïìåßï Íéêáßáò «´Áãéïò åíáðüèåóç ãëõêïãüíïõ, ðñïêåéìÝíïõ íá ÐáíôåëåÞìùí», 2´ ÏõñïëïãéêÞ ÊëéíéêÞ Ðáíåðéóôçìßïõ áíåõñåèïýí åíáëëáêôéêÝò ðçãÝò åíÝñãåéáò áðü ôá Áèçíþí, Óéóìáíüãëåéï ÃÍÁ ìõúêÜ êýôôáñá. ÁðïôÝëåóìá áõôþí ôùí Õðåýèõíïò Åðéêïéíùíßáò: ÇñáêëÞò ×. ÌçôóïãéÜííçò ïîÝïò óôéò ëåßåò ìõúêÝò ßíåò ëüãù ôïõ áíáåñüâéïõ ðñïò ôïí áíáåñüâéï ìåôáâïëéóìü êáé ðéèáíüí äéáäéêáóéþí åßíáé ç óõóóþñåõóç ãáëáêôéêïý ´ ÏõñïëïãéêÞ ÊëéíéêÞ Ðáíåðéóôçìßïõ Áèçíþí ìåôáâïëéóìïý, ç ïðïßá ðñïêáëåß óõóôïëéêÞ Óéóìáíüãëåéï ÃÍÁ äõóëåéôïõñãßá ôïõ åîùóôÞñá. Åðéðñüóèåôá, ç Óéóìáíïãëåßïõ 1, 15126 Ìáñïýóé, ÁèÞíá ôçë. +30 2132058253, fax: +30 2108044703 email: [email protected] õðïîßá ðñïÜãåé ôçí áðïíåýñùóç ôïõ ôïé÷þìáôïò ôçò êýóôçò êáé ôç ìåßùóç ôçò ðõêíüôçôáò ôùí ÷ïëéíåñãéêþí íåõñþíùí. Óêïðüò: Ç ÊáëïÞèçò Õðåñðëáóßá ôïõ Ðñï- ÓõìðÝñáóìá: Ç õðïêõóôéêÞ áðüöñáîç ó÷å- óôÜôç (ÊÕÐ) áðïôåëåß óõíÞèç áéôßá õðïêõóôéêÞò ôßæåôáé ìå ðïéêßëåò ìïñöïëïãéêÝò êáé âéï÷ç-ìéêÝò áðüöñáîçò êáé ðñüêëçóçò óõìðôùìÜôùí áðü ìåôáâïëÝò óôï ôïß÷ùìá ôçò êýóôçò ðïõ ôï êáôþôåñï ïõñïðïéçôéêü óýóôçìá (LUTS).Óôï åðçñåÜæïõí ôç óõóôáëôéêüôçôÜ ôçò. Ç ìáêñï- ôïß÷ùìá ôçò ïõñïäü÷ïõ êýóôçò óõìâáßíïõí ÷ñüíéá áðüöñáîç ìðïñåß íá ïäçãÞóåé óå ìç óçìáíôéêÝò ëåéôïõñãéêÝò, âéï÷çìéêÝò êáé áíáóôñÝøéìåò âëÜâåò óôïí åîùóôÞñá ìõ, ìå ìïñöïëïãéêÝò ìåôáâïëÝò êáôÜ ôçí åîÝëéîç ôçò ðáñáìïíÞ ôçò óõìðôùìáôïëïãßáò áêüìç êáé ìåôÜ ÊÕÐ, þóôå íá äéáôçñçèåß ç öõóéïëïãéêÞ ôçí Üñóç ôïõ êùëýìáôïò. ëåéôïõñãéêüôçôÜ ôçò. ÌåëÝôåò Ý÷ïõí êáôáäåßîåé ìåéùìÝíç áéìÜôùóç ôïõ åîùóôÞñá ìõüò üôáí õðÜñ÷åé õðïêõóôéêÞ áðüöñáîç. Ç ðáñïýóá óôÜôç, ÕðïêõóôéêÞ Áðüöñáîç, Éó÷áéìßá Åîù- áíáóêüðçóç ðáñïõóéÜæåé ôçí áðÜíôçóç ôçò óôÞñá, Óõìðôþìáôá Êáôþôåñïõ Ïõñïðïéçôéêïý. ïõñïäü÷ïõ êýóôçò êáôÜ ôçí õðïêõóôéêÞ áðüöñáîç êáé åóôéÜæåé óôéò ìåôáâïëÝò êáé âéï÷çìéêÝò ðñïóáñìïãÝò ôïõ êõóôéêïý ôïé÷þìáôïò ðáñïõóßá ôçò õðïîßáò. ÌÝèïäïò: ÐñáãìáôïðïéÞèçêå áíáóêüðçóç ôçò äçìïóéåõìÝíçò âéâëéïãñáößáò, ç ïðïßá óõìðåñéÝëáâå in vivo êáé in vitro ìåëÝôåò óå áíèñþðéíïõò êáé æùéêïýò éóôïýò. 26 ËÝîåéò ÊëåéäéÜ: ÊáëïÞèçò Õðåñðëáóßá Ðñï- Hellenic UROLOGY Obstruction-induced pathological alterations within the urinary bladder due to Benign Prostate Hyperplasia (BPH). A review of the literature References 1. Berry, S. J., Coffey, D. S., Walsh, P. C. and Ewing, L. L.: The development of human benign prostatic hyperplasia with age. J Urol, 1984;132: 474. 2. Shapiro, E. and Lepor, H.: Pathophysiology of clinical benign prostatic hyperplasia. Urol Clin North Am,1995; 22: 285. 3. Andersson KE. Storage and voiding symptoms: pathophysiologic aspects. Urology 2003;62:3-10. 4. Lepor H. Nonoperative management of benign prostatic hyperplasia. J Urol 1989;141:12839. 5. Madsen FA, Bruskewitz RC. Clinical manifestations of benign prostatic hyperplasia. Urol Clin North Am 1995;22:291-8. 6. Lu SH, Chang LS, Yang AH, Lin AT, Chen KK, Wei YH. Mitochondrial DNA deletion of the hu-man detrusor after partial bladder outlet obstru-ctioncorrelation with urodynamic analysis. Uro-logy 2000;55:603-7. 7. Lu SH, Wei YH, Chang LS, Lin AT, Chen KK, Yang AH. Morphological and morphometric analysis of human detrusor mitochondria with urodynamic correlation after partial bladder outlet obstruction. J Urol 2000;163:225-9. 8. Backhaus BO, Kaefer M, Haberstroh KM, et al. Alterations in the molecular determinants of bladder compliance at hydrostatic pressures less than 40 cm. H2O. J Urol 2002; 168:2600-4. 9. Yamaguchi O. Response of bladder smooth muscle cells to obstruction: signal transduction & the role of mechanosensors. Urology 2004;63:11-6. 10. Araki I, Du S, Kamiyama M, et al. Overexpression of epithelial sodium channels in epithelium of human urinary bladder with outlet obstruction. Urology 2004; 64: 1255-60. 11. Burkhard FC, Lemack GE, Zimmen Pe,et al. Contractile protein expression in bladder smo-oth muscle is a marker of phenotypic modulation after outlet obstruction in the rabbit model. J Urol 2001; 165:963-7. 12. Uvelius B, Arner A, Malmqvist U. Contractile and cytoskeletal proteins in smooth muscle during hypertrophy and its reversal.Am J Physiol 1991; 260:C1085-93. 13. Sjuve R, Haase H, Ekblad E, Malmqvist U, Morano I, Arner A. Increased expression of nonmuscle myosin heavy chain-B in connective tissue cells of hypertrophic rat urinary bladder. Cell Tissue Res 2001; 304:271–8. 14. Mannikarottu AS, Disanto ME, Zderic SA, Wein AJ, Chacko S. Altered expression of thin filament-associated proteins in hypertrophied urinary bladder smooth muscle. Neurourol Urodyn 2006; 25:78–88. 15. Lee SD, Akbal C, Jung C. Intravesical pressure induces hyperplasia and hypertrophy of human bladder smooth muscle cells mediated by muscarinic receptors. J Pediatric Urol 2006; 2:271-6. 16. Deveaud CM, Macarak EJ, Kucich U, et al. Molecular analysis of collagens in bladder fibrosis. J Urol 1998; 160:1518-27. 17. Levin R.M, Wein A.J, Butyan R, et.al: update on bladder smooth-muscle physiology. World J.Urol. 1994 12:226-232. 18. Robert M. Levin, Niels Haugaard, Laura O'Connor, Ralph Buttyan, Anurag Das, John S. Dixon, John A. Gosling. Obstructive Response of Human Bladder to BPH vs. Rabbit Bladder Response to Partial Outlet Obstruction: A Direct Comparison. Neurourology and Urodynamics 2000;19:609–629. 19. Bing W., Chang S., Hypolite J.A., DiSanto M.E., Zderic S.A., Rolf L., Wein A.J., Chacko S. Hellenic UROLOGY 27 Christos Komninos, Iraklis C. Mitsogiannis Obstruction-induced changes in urinary bladder smooth muscle contractility: a role for Rho kinase. Am J Physiol Renal Physiol. 2003;285:F990–F997. 20. Polyák E., Boopathi E., Mohanan S., Deng M., Zderic S.A., Wein A.J., Chacko S. Alterations in caveolin expression and ultrastructure after bladder smooth muscle hypertrophy. J Urol. 2009;182:2497–2503. 21. Boopathi E. et al.Transcriptional Repression of Caveolin-1 (CAV1) Gene Expression by GATA-6 in Bladder Smooth Muscle Hypertrophy in Mice and Human Beings. Am J Pathol. 2011 May; 178(5): 2236–2251. 22. Greenland JE, Brading AF.The effect of bladder out flow obstruction on detrusor blood flow changes during the voiding cycle in conscious pigs.J Urol 2001; 165:245-8. 23. Loran OB, Vishnevskii EL, Vishnevskii AE. The role of detrusor hypoxia in the pathogenesis of urination disorders in patients with benign prostatic hyperplasia. Urol Nefrol Mosk 1996; 6: 33-7. 24. Elbadawi A, Meyer S, Regnier CH. Role of ischaemia in structural changes in the rabbit detrusor following partial bladder outlet obstruction: a working hypothesis and a biomechanical/structural model proposal. Neurourol Urodyn 1989; 8: 151-62. 25. Macnab A., Stothers L.,Shadgan B. Monitoring detrusor oxygenation and hemodynamics noninvasively during dysfunctional voiding. Advances in Urology 2012 doi:10.1155/2012/676303. 26. Rosen R, Altwein J, Boyle P, Kirby RS, Lukacs B, Meuleman E,et al. Lower urinary tract symptoms and male sexual dysfunction: the multinational survey of the aging male (MSAM-7). Eur Urol. 2003;44:637-649. 27. Rosen RC, Giuliano F, Carson CC. Sexual dysfunction and lower urinary tract symptoms (LUTS) associated with benign prostatic hyperplasia (BPH). Eur Urol. 2005; 47: 824-837. 28 Hellenic UROLOGY 28. Koritsiadis G, Stravodimos K, Koutalellis G, Agrogiannis G, Koritsiadis S, Lazaris A, Constantinides C. Immunohistochemical estimation of hypoxia in human obstructed bladder and correlation with clinical variables.BJU Int. 2008 ;102(3):328-32. 29. Greenland JE, Hvistendahl JJ, Andersen H, et al. The effect of bladder outlet obstruction on tissue oxygen tension and blood flow in the pig bladder. BJU Int 2000;85:1109-14. 30. Azadzoi KM, Pontari M, Vlachiotis J, et al. Canine bladder blood flow and oxygenation: Changes induced by filling, contraction and outlet obstruction. J Urol 1996;155:1459-65. 31. Lin AT, Chen MT, Yang CH, et al. Blood flow of the urinary bladder: Effects of outlet obstruction and correlation with bioenergetic metabolism. Neurourol Urodyn 1995;14:285-92. 32. Chapple, C. R., Milner, P., Moss, H. E., & Burnstock, G. Loss of sensory neuropeptides in the obstructed human bladder. Br J Urol 1992;70, 373381. 33. Damaser MS, Haugaard N, Uvelius B. Partial obstruction of the rat urinary bladder: effects on mitochondria and mitochondrial glucose metabolism in detrusor smooth muscle cells. Neurourol Urodyn. 1997; 16(6):601-7. 34. Bas W.D. de Jong, Katja P. Wolffenbuttel, Jeroen R. Scheepe, Dirk J. Kok The detrusor glycogen content of a de-obstructed bladder reflects the functional history of that bladder during PBOO. Neurourology and Urodynamics 2008; 27, 454-460. 35. Pessina F, Solito R, Maestrini D, et al. Effect of anoxia-glucopenia and resuperfusion on intrinsic nerves of mammalian detrusor smooth muscle: Importance of glucose metabolism. Neurourol Urodyn 2005;24:389-96. 36. Siflinger-Birnboim A, Levin RM, Hass MA.Partial outlet obstruction of the rabbit urinary Obstruction-induced pathological alterations within the urinary bladder due to Benign Prostate Hyperplasia (BPH). A review of the literature bladder induces selective protein oxidation. Neurourol Urodyn.2008 ;27(6): 532-9. cular smooth muscle: quantitation of Na-pump activity and aerobic glycolysis. FASEB J 1988; 2:A755. 37. Alex Tong-Long Lin, Ming-Shi Shiao, ChingJu Chen, Luke S et.al. Energetics of detrusor contraction: Effects of outlet obstruction. Neurourology and Urodynamics 1992; 11: 605-614. 46. Siegman MJ, Butler TM, Mooers SU, Davies RE.Chemical energetics of force development, force maintenance, and relaxation in mammalian smooth muscle. J Gen Physiol 1980;76:609-29. 38. Zhao Y, Levin SS, Wein AJ, Levin RM. Correlation of ischemia/reperfusion or partial outlet obstruction-induced spectrin proteolysis by calpain with contractile dysfunction in rabbit bladder. Urology 1997; 49: 293-300. 47. Levin RM, Haugaard N, Mogavero L, Leggett RE, Das AK. Biochemical evaluation of obstructive bladder dysfunction in men secondary to BPH: a preliminary report. Urology 1999;53: 446-50. 39. Yokoyama O, Kawaguchi K, Hisazumi H. Denervation supersensitivity of the detrusor muscle due to bladder overdistension, with special reference to the relationship between supersensitivity, and changes in the connective tissue. Hinyokika Kiyo 1985; 31: 2127-34. 40. Lin AT, Chen KK, Yang CH, Chang LS. Effects of outlet obstruction and its reversal on mitochondrial enzyme activity in rabbit urinary bladders. J Urol 1998;160: 2258-62. 41. Gosling JA, Kung LS, Dixon JS, Horan P, Whitbeck C, Levin RM. 2000. Correlation between the structure and function of the rabbit urinary bladder following partial outlet obstruction. J Urol 163:1349-56. 42. Mirone V, Imbimbo C, Longo N, Fusco F. The detrusor muscle: an innocent victim of bladder outlet obstruction. Eur Urolog 2007;51:57-66. 43. Flameng W, Borgers M, Daenen W, Stalpaert G. Ultra-structural and cytochemical correlates of myocardial protection by cardiac hypothermia in man. J Thorac Cardiovasc Surg 1980;79:413-24. 48. Kato K, Lin AT-L, Wein AJ, Levin RM. Effect of outlet obstruction on glucose metabolism of the rabbit urinary bladder. J Urol 1990; 143:844-7. 49. De Jong BWD, Wolffenbuttel K., Arentshorst ME, et al. Detrusor Glycogen reflects the functional history of bladders with partial outlet obstruction . BJU Int 2007; 100: 846-52. 50. Haddad GG, Jiang C. O2 deprivation in the central nervous system: on mechanisms of neuronal response, differential sensitivity and injury. Prog Neurobiol 1993; 40: 277-318. 51. GelosoDA, Levin RM. Effect of partial outlet obstruction on the myogenic response to field stimulation. Gen Pharmacol 1998;31:291-5. 52. Martin C. Michel , Maurits M. Barendrecht. Physiological and pathological regulation of the autonomic control of urinary bladder contractility. Pharmacology & Therapeutics 2008;117:297-312. 53. Cumming JA, Chisholm GD. Changes in detrusor innervation with relief of outflow tract obstruction. Br J Urol 1992;69:7-11. 44. Hsu TH-S, Levin RM, Wein AJ, Haugaard N. Alterations of mitochondrial oxidative metabolism in rabbit urinary bladder after partial outlet obstruction. Mol Cell Biochem 1994;141:47-55. 45. Campbell JD, Agubosim S,Paul RJ. Compartmentation of metabolism and function in vas- Hellenic UROLOGY 29 ORIGINAL ARTICLE Greek Version of the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI), its linguistic adaptation and the pilot test of its validity (ÍÇÉ) 1 2 3 Charalambos Asvestis , Theodoros Varvadesis , Petros E. Maravelakis 1.Urologist-Andrologist. 2.Associate Professor, Department for Hygiene and Epidemiology, Medical School of Aristotle University, Thessaloniki. Corresponding Author: Charalambos Asvestis Tel: +30 2108948213 email: [email protected] 3.Lecturer, Department of Business Administration, University of Piraeus. Summary Introduction To formulate the Greek version of the National Institute of Health Chronic Prostatitis Symptom Index (NIH-CPSI), its linguistic adaptation and the pilot test of its validity. Methods The classical method of linguistic vali-dation was adopted. Seven patients with chronic prostatitis (CP) histologically confirmed parti-cipated in cognitive debriefing. The sample of the pilot study consisted of 45 CP patients based on clinical diagnosis according to symptoms and 42 healthy individuals aged 21 to 68 years old. In retest 22 of the above CP patients were included. Statistical analysis was carried out with the Statistical Package PASW Statistics 18. The statistical analysis was based on the chi-square, t and ANOVA tests. Internal consistency was examined by Cronbach's á and Pearson's r while for test-retest reproducibility k statistic and Wilcoxon test were used. Results Cultural adaptation was not required since the sample consisted of Greek citizens with common socio-religious characteristics. Cognitive debriefing revealed that the Greek version of the NIH-CPSI was easily understood and answered. During the pilot validation it was assured that the patients and healthy individuals were comparable regarding age, education and marital status. 30 Hellenic UROLOGY Key Words Greek Version of the National Insti-tutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI). Introduction The chronic prostatitis is the most frequent cause for visiting a urologist for primary care2. Epidemiological data from other countries such as the United States of America3, Italy4, Germany and China5 have shown different rates of occurrence of the disease in these different populations. The questionnaires have been widely used, as tools of epidemiological study, aids to diagnosis and monitoring of the effectiveness of treatments and instruments of evaluation of the quality of life caused by various diseases as well. In urology, the most widely used questionnaires are that of the benign hyperplasia of the prostate (AUA-SI)6, erectile dysfunction (IIEF) 7 and premature ejaculation (IELTs) 8. The use of such questionnaires, appropriately translated into different languages, allows comparative studies between different population groups. The Diagnostic Questionnaire for Chronic Prostatitis- Chronic Pelvic Pain of the American National Health Institute has already been translated into the Italian4, German9, Spanish10, Japanese11, and French languages12 and studies have been made in many countries as in Australia13, Korea14, China15, Turkey16 and in all those countries mentioned above. Standardized methodology for cultural adjustment Greek Version of the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI), its linguistic adaptation and the pilot test of its validity (ÍÇÉ) and control of linguistic validity was used. The original questionnaire in English language was translated into the Greek language by two professional translators with their native language being Greek. The two translators worked independently without any contact between them. Then the scientific coordinator made the comparison between the two translations. After the required clarifications requested by the two translators, the first draft Greek questionnaire was completed. This questionnaire was then translated into English by a professional translator with English as a native language. The reverse English translation has been checked with the original English questionnaire in order to confirm the conceptual match. After the clarifications requested by the translator the second draft Greek questionnaire was completed. Then the text was corrected and edited to maintain the same form as the English original. The next step was that of the cognitive testing of the chronic prostatitis/chronic pelvic pain questionnaire on seven patients who had undergone Multiple transrectal ultrasound guided biopsies of the prostate gland due to high measure of the Prostatic-Specific Antigen (PSA) and in whom inflammatory infiltrate been found histologically, which conforms to the histological diagnosis of prostatitis. ction of the text. The next step was the pilot study for the validity of the final questionnaire (Appendix I). Patients were chosen from a private andrology clinic who had been diagnosed with prostatitis, on the basis of clinical symptomatology. The ages of the patients ranged from 59 to 80 years. The recruitment of participants was joined with a detailed explanation of the objective of the research, the assurance of anonymity and of course oral consent was obtained. For each patient selected for the pilot study the next patient that came to the clinic with any diagnosis other than prostatitis that belonged to the same age group was added to the control group. If someone chose not to take part, the next patient was chosen. Every third participant from each group (ill-healthy) responded to the questionnaire at the next appointment which had been arranged for about 10 days later. The collection of data occurred during the period between October 2011 and February 2012. The process of approaching patients for the test included detailed reference to the purpose of the investigation, as well as absolute assurances of anonymity17 with a view to obtaining oral consent. These patients were given the questionnaire with written instructions and stated that it should be read and that no consideration should be given to the grade (after completing the questionnaire) because the objective of our study at this stage is the degree of understanding and not evaluation of the medical condition. In this group there were 45 patients (approaching 50-degree response 90 %) and the control group were 42 patients (also approaching 50-degree response 84 % ). Each participant answered the questionnaire anonymously. The questionnaire consisted of demographic questions and questions regarding pain, urination and quality of life. Pain was assessed using the sum of questions 1a, 1b, 1c, 2a, 2b, 3 and 4. Urination symptomatology was assessed using the sum of questions 5 and 6. Effects on quality of life were assessed via the sum of questions 7,8 and 9. For each patient the completion time for the questionnaire was measured and then followed by personal interview to investigate whether the patient understood the questionnaire (questions, instructions for its completion, response scales, understanding concepts, level of difficulty). After the completion of this stage there were further amendments which led to the third draft of the questionnaire. There was further detailed corre- After completion the questionnaire was codified and the data was entered on a computer. For the statistical analysis the statistical package PASW Statistics 18 was used. The statistical analysis used the checks chi-squares, t and ANOVA. The Cronbach alpha coefficient was calculated for the assessment of internal consistency. The Pearson coefficient was calculated for which the lowest acceptable value was set to 0.7 for the Hellenic UROLOGY 31 Charalambos Asvestis, Theodoros Varvadesis, Petros E. Maravelakis reliability test, (test/retest reliability). Results The average age of the respondents in the group who suffered from prostatitis was 68.2+/- 6.3 years and the control group was 63.4+ /-8.3 years. The observed statistical significance was p=0,109, showing that there was no statistically significant difference between the two groups. The assessment of pain the average value of the sum for the group of patients was 4.5+ /-0.9 and for the control group was 0.8+ / -0.5. The observed statistical significance was p=0,007 showing that there was a statistically significant difference between the two groups. Regarding urinary symptomatology it was found that the average value of the sum for the group of patients was 6.5+ /-1.2 and for the control group was 1.1+ / -0.7. The observed statistical significance was p=0,006 showing that there was a statistically significant difference between the two groups. For the impact on the quality of life it was found that the average value of the sum for the group of patients was 1.9+ /-0.6 and for the control group was 0.5+ / -0.4. The observed statistical significance was p=0,012 stating that there was a statistically significant difference between the two groups. The scores for pain, urinary symptomatology and the impact on the quality of life were not found to have a statistically significant correlation with age, marital status and education (all observed significance levels is greater than 0.05). Next the reliability of the questionnaire was checked for internal consistency. Cronbach's alpha was for the whole sample was 0.89. The value for the group of patients was 0.71 and for the control group was 0.77. Discussion From its first publication1 in 1999, the questionnaire for Chronic Prostatitis/ Chronic Pelvic Pain by the National Institute of Health United has received wide acceptance in many countries, and many studies, in particular of an epidemiological nature, have been based on its application. It is important that two teams from the United 18,19 20 States and Germany reevaluated its effectiveness as a tool for the diagnosis of Chronic Pro- 32 Hellenic UROLOGY statitis/ Chronic Pelvic Pain. With the translation of the Greek text we hope it will offer to Greek urologists the possibility of conducting comparative studies with other countries in order to better understand the disease. Ðåñßëçøç ÌåôÜöñáóç óôçí ÅëëçíéêÞ Ãëþóóá êáé ÐéëïôéêÞ ÌåëÝôç Åãêõñüôçôáò ôïõ Äéáãíùóôéêïý Åñùôçìáôïëïãßïõ ×ñüíéáò Ðñïóôáôßôéäïò-Óõíäñüìïõ ×ñüíéïõ Ðõåëéêïý ¢ëãïõò ôïõ ÁìåñéêÜíéêïõ Åèíéêïý Éíóôéôïýôïõ Õãåßáò (ÍÇÉ) ×áñÜëáìðïò ÁóâÝóôçò1, Èåüäùñïò ÄáñäáâÝóçò2, ÐÝôñïò Å. ÌáñáâåëÜêçò 3 1. Ïõñïëüãïò-Áíäñïëüãïò 2. ÁíáðëçñùôÞò ÊáèçãçôÞò, ÅñãáóôÞñéï ÕãéåéíÞò, ÉáôñéêÞ Ó÷ïëÞ ÁñéóôïôÝëåéïõ Ðáíåðéóôçìßïõ Èåóóáëïíßêçò 3. ËÝêôïñáò, ÔìÞìá ÏñãÜíùóçò êáé Äéïßêçóçò Åðé÷åéñÞóåùí, ÐáíåðéóôÞìéï Ðåéñáéþò Õðåýèõíïò åðéêïéíùíßáò: ×áñÜëáìðïò ÁóâÝóôçò ôçë: +30 2108948213 - email: [email protected] Óêïðüò: Ç äçìéïõñãßá ôïõ Åëëçíéêïý Äéáãíùóôéêïý Åñùôçìáôïëïãßïõ ×ñüíéáò Ðñïóôáôßôéäïò-×ñüíéïõ Ðõåëéêïý ¢ëãïõò (ÅÄÅ×ÐÁ), ç ãëùóóéêÞ ðñïóáñìïãÞ ôïõ êáé ç ðéëïôéêÞ áîéïëüãçóç ôçò åãêõñüôçôáò ôïõ âáóéæüìåíïé óôï äéáãíùóôéêü Åñùôçìáôïëüãéï ×ñüíéáò Ðñïóôáôßôéäïò-×ñüíéïõ Ðõåëéêïý ¢ëãïõò ôïõ ÁìåñéêÜíéêïõ 1 Åèíéêïý Éíóôéôïýôïõ Õãåßáò (ÍÇÉ) . ÌÝèïäïò: ×ñçóéìïðïéÞèçêå ç êëáóéêÞ ìåèïäïëïãßá ãëùóóéêÞò ðñïóáñìïãÞò óôçí ÅëëçíéêÞ ãëþóóá. ÅðôÜ áóèåíåßò ìå ÷ñüíéá ðñïóôáôßôéäá åðéâåâáéùìÝíç éóôïëïãéêÜ ðÞñáí ìÝñïò óôïí ãíùóôéêü Ýëåã÷ï. Ôï äåßãìá ãéá ôçí ðéëïôéêÞ ìåëÝôç áðïôÝëåóáí 45 áóèåíåßò ìå ÷ñüíéá ðñïóôáôßôéäá ðïõ âÜóåé ôçò êëéíéêÞò äéÜãíùóçò óôçñéæüìåíïé óôçí óõìðôùìáôïëïãßá êáé óáí ïìÜäá åëÝã÷ïõ 42 õãéåßò Üíäñåò çëéêßáò áðü 21 Ýùò 68 åôþí. Óôïí åðáíÝëåã÷ï óõììåôåß÷áí 22 áðü ôïõò ðáñáðÜíù ðÜó÷ïíôåò óõììåôÝ÷ïíôåò. Ç óôáôéóôéêÞ åðåîåñãáóßá Ýãéíå ìå ÷ñÞóç ôïõ Greek Version of the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI), its linguistic adaptation and the pilot test of its validity (ÍÇÉ) óôáôéóôéêïý ðáêÝôïõ PASW Statistics 18. Óôçí óôáôéóôéêÞ áíÜëõóç ÷ñçóéìïðïéÞèçêáí ïé Ýëåã÷ïé ÷é-ôåôñÜãùíï, t êáé ANOVA. Ç áîéï-ðéóôßá åëÝã÷èçêå ùò ðñïò ôçí åóùôåñéêÞ óõíÝðåéá ìå ôïõò óõíôåëåóôÝò Cronbach's á êáé Pearson's r åíþ ùò ðñïò ôçí áíáðáñáãùãéêü-ôçôá óôïí åðáíÝëåã÷ï ìå ôï óôáôéóôéêü k êáé ôïí Ýëåã÷ï ôïõ Wilcoxon. ÁðïôåëÝóìáôá: ÐïëéôéóôéêÞ ðñïóáñìïãÞ ôïõ åñùôçìáôïëïãßïõ äåí áðáéôÞèçêå åðåéäÞ ôï äåßãìá Þôáí ¸ëëçíåò õðÞêïïé ìå êïéíÜ êïéíùíéêüèñçóêåõôéêÜ ÷áñáêôçñéóôéêÜ. Ï ãíùóôéêüò Ýëåã÷ïò Ýäåéîå üôé ôï ÅÄÅ×ÐÁ Ýãéíå åýêïëá êáôáíïçôü êáé ïé áðáíôÞóåéò Þôáí åýêïëï íá äïèïýí. Óôçí ðéëïôéêÞ ìåëÝôç åãêõñüôçôáò äéáóöáëßóôçêå üôé ïé áóèåíåßò êáé ïé õãéåßò Þôáí óõãêñßóéìïé üóïí áöïñÜ ôçí çëéêßá, ôçí åêðáßäåõóç êáé ôçí ïéêïãåíåéáêÞ êáôÜóôáóç. ËÝîåéò Åõñåôçñéáóìïý: Åëëçíéêü Äéáãíù-óôéêü Åñùôçìáôïëüãéï ×ñüíéáò Ðñïóôáôßôé-äïò×ñüíéïõ Ðõåëéêïý ¢ëãïõò (ÅÄÅ×ÐÁ). References 4. Giubilei G. Mondaini N. Crisci A. Raugei A. Lombardi G. Travaglini F. Del Popolo G. Bartoletti R. The Italian Version of the National Institutes of Health Chronic Prostatitis Symptom Index. European Urology 47. 805-811. 2005. 5. Liang C.Z. Zhang X.J. Zong Y.H. Qiang H. Wang K.X. Prevalence of sexual dysfunction in Chinese men with chronic prostatitis. BJU INTERNATIONAL 93.568-570. 2004. 6. Barry M.J. Fowler F. J. Jr. O'leary M. P. Bruskewitz R.C. Logan H.H. Mebust K. W. Cockett A. T. K. and the measurement comitte of the American Urological Association. The American urological association symptom index for benign prostatic hyperplasia.The Journal of Urology Vol.148, 15491557. 1992. 7. Ê.Xáôæçìïõñáôßäçò, Æ.Ôóéìôóßïõ, Á.ÊáñáíôÜíá, Ä.×áôæç÷ñÞóôïõ. ÐïëéôéóìéêÞ êáé ãëùóóïëïãéêÞ áîéïëüãçóç ôïõ ÄéåèíÞ Äåßêôç Ëåéôïõñãßáò (ÄÄÓË) óôçí åëëçíéêÞ ãëþóóá. ÅëëçíéêÞ ÏõñïëïãéêÞ Åôáéñåßá. 13:313-321. 2001. 1. Litwinm.s. Mc Naughton-collins M. Fowler F.j. Jr., Nickel C. J. Calhoun E.a. Pontari M.a. Richard B. A. Farrar J.t. O'leary M.p. And The Chronic Prostatitis Collaborative Research Network. The national institutes of health chronic prostatitis symptom index: development and validation of a new outcome measure. The Journal of Urology. Vol. 162, 369-375. 1999 2. Collins Mc Naughton M. Stafford S.r.o'leary P.m. Barry J.m. Distingishing chronic prostatitis and benign prostatic yperplasia symptoms: results of a national survey of physician visits. Adult Urology 53 (5). 1999. 3. Clemens Q.j. Meenan R.t. Maureen C. Rosetti O.K. Gao S.Y. Brown S.O. Calhoun E.A. Prevalence of prostatitis-Like Symptoms in a Managed Care Population. Volume 176, issue 2, pages 593-596. 2006. 8. Althofs. PHD. Rosen R. PHD. Symonds T.PHD.Mundayat, R.Msc.May, K.PHD. Abraham L. Msc. Development and Validation of a new Questionnaire to Assess Sexual Satisfaction, Control, and Distress Accosiated with Premature Ejaculation. J. Sex Med; 3:465-475. 2006. 9. Hochreiter W. Ludwig M. Weidner W. et al. National Institutes of Health (NIH) Chronic pro-statitis Symptom Index. The German version (in German). Urologe A 40:16-7. 2001. 10. Collins MM, O'leary MP, Calhoun EA, Pontari MA, Adler A, Eremenco S, Chang Ch, Odom L, Litwin MS. The Spanish National Institutes of Health-Chronic Prostatitis Symptom Index: translation and linguistic validation. J Urol. 2001 Nov;166(5):1800-3. 11. Koichi M. Masaya T. Yuko N. Eiichi A. Hiromi K. Ajapanese. Version of the National Insti-tutes of Health Chronic Prostatitis SymptomIndex (NIH-CPSI, Okayama version) and the clinical eva-luation Hellenic UROLOGY 33 Charalambos Asvestis, Theodoros Varvadesis, Petros E. Maravelakis ofcernitin pollen extract for chronic non-bacte-rial prostatitis. Nihon HinyokikaGakkaiZasshi. 2002 May ;93 (4):539-47. 12. Karakiewicz PI, Perrotte P, Valiquette L, Benard F, Mccormack M, Menard C, Mcnaughton Collins M, Nickel JC. French-Canadian linguistic validation of the NIH Chronic Prostatitis Symptom Index.Can J Urol. 2005 Oct:12(5):2816-23. 13. Ferris Ja. Pitts Mk. Richters J. et al. National prevalence of urogenital pain and prostatitis-like symptoms in Australian men using the National Institutes of Health Chronic Prostatitis Symptom Index. BJU Int. 2009. 105:373-9. 14. Ahn Sg, Kim Sh, Chung Ki, Park Ks, Cho Sy, Kim Hw. Depression, anxiety, stress perception, and coping strategies in Korean military patients with chronic prostatitis/chronic pelvic pain syndrome. Korean J Urol. 2012 Sep: 53(9):643-8. 15. Liang Cz. Li Hj. Wang Zp.et al. The prevalence of prostatitis-like symptoms in China. J. Urol 2009. 182:558-63 34 Hellenic UROLOGY 16. Yalcinkaya A. R. Gokce A. Davarci M. Guven E. O. Inci M. Kartal S. B. Ayyildiz A. Balbay M. D.The impact of NIH-IV prostatitis on early post-operative outcomes of transurethral resection of the prostate in patients with symptomatic benign prostate hyperplasia. TurkJMedSci. 2011: 41 (3) 515-519. 17.http://www.ncbi.nlm.nih.gov/pubmed?term=Ch ronic%20Prostatitis%20Collaborative%20Research% 20Network%5BCorporate%20Author%5D.ÄÁËËÁÂÏ ÑÃÉÁÐ. Áðüññçôç êáé ÉáôñéêÞ ¸ñåõíá: ÍïìéêÜ êáé çèéêÜ èÝìáôá êáôÜ ôç ÷ñÞóç éáôñéêþí óôïé÷åßùí óôçí åðéäçìéïëïãéêÞ Ýñåõíá. ÄéáôñéâÞ åðß äéäáêôïñßáò: ÐáíåðéóôÞìéï Áèçíþí. ÁèÞíá 1983: 45-75. 18. Litwinms. A review of the development and validation of the National Institutes of Health Chronic Prostatitis Symptom Index. Urology. 2002. 60:14-8. 19. Turner Ja, Ciol Ma, Von Korff M, Berger R. Validity and responsiveness of the national institutes of health chronic prostatitis symptom index. J Urol. 2003 Feb: 169(2):580-3. 20. Schneider H. Brahler E. Ludwig M. et al. Two year experience with the German-translated version of the NIH-CPSI in patients with CP/CPPS. Urology. 2004. 63:1027-30 Greek Version of the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI), its linguistic adaptation and the pilot test of its validity (ÍÇÉ) PROSTATITIS SYMPTOMS QUESTIONNAIRE/ CHRONIC PELVIC PAIN SYNDROME. 1. In the last week, have you experienced any pain or 6. How often have you had a sensation of not emptying discomfort in the following areas? your bladder completely after youfinish urinating, over the a) Area between rectum and testicles (perineum) (crotch). YES 1 b) Testicles YES NO 1 Less than 1 to 5 times 0 c) Tip of the penis (not related to urination). YES 1 NO 1 NO Less than half the time About half the time 0 d) Below your waist, in your bladder or pubic area . YES 0 Not at all 0 NO last week? 2 3 More than half the time 4 5 Almost always 0 1 2. In the last week have you experienced: a) Pain or burning during urination? YES 1 NO things you would usually do, overthe last week? 0 b) Pain or discomfort during or after ejaculation? YES 1 NO 7. How much have your symptoms kept you from doing 0 None 1 Only a little 0 2 Some 3. How often have you had pain or discomfort in any of A lot 3 these areas over the last week? Never 0 Rarely 1 8. How much did you think about your symptoms, over the last week? Sometimes Often 4 Always 5 A lot days that you had it, over the last week? 1 2 3 4 2 Some 4.Which number describes your pain or discomfort on the 0 1 Only a little 3 Usually 0 None 2 5 6 7 8 9 10 No pain Excruciating pain. 3 9.If you were to spend the rest of your life with your symptoms just the way they have beenduring the last week, how would you feel about that? 0 Delighted Pleased 1 Mostly satisfied 2 Mixed (about equally satisfied and unsatisfied) 5. How often have you had the sensation of not emptying your bladder completely after you finish urinating, over the last week? Never Disappointed Unhappy Miserable 3 4 5 6 0 Less than 1 to 5 times Less than half the time About half the time 5 Pain: Total of questions 1a, 1b, 1c, 2a, 2b, 3 êáé 4 = 2 3 More than half the time Almost always 1 Urinary symptoms:total of questions 5 êáé 6= 4 Evaluation of life quality: total of questions 7, 8 êáé 9= Hellenic UROLOGY 35 ORIGINAL ARTICLE Functional and ongological results of radical perineal prostatectomy for the management of clinically locally advanced prostate cancer. Single centre experience Athanasios I. Archodakis, Stefanos Bolometes Department of Urology, 401 Genaral Military Hospital of Athens Corresponding Author: Athanasios I. Archodakis Department of Urology, 401 General Military Hospital of Athens Tel: +30 2107494179 email: [email protected] Summary Introduction Radical prostatectomy is considered to be the best choice for managing localized prostate cancer. There is increased evidence that a surgical approach has an important role to play as a method of treatment for locally advanced prostate cancer. According to the European Association of Urology (EAU), radical prostatectomy is an option for properly chosen patients with locally advanced prostate cancer. The aim of our study is to evaluate the oncological and functional results of radical perineal prostatectomy for the management of patients with clinically locally advanced prostate cancer. Methods Between 1993 and 2012, 627 patients underwent radical perineal prostatectomy for histologically confirmed prostate cancer. Eighty three out of 627 patients had clinically advanced disease. Perioperative morbidity, functional results and early oncological outcomes were examined and compared between the two groups. Results There was no statistically significant difference between the two groups regarding operation time, intraoperative blood loss, length of hospital stay and duration of catheterization. The rate of complications was also similar, with the exception of two rectal injuries in the locally advanced group, 36 Hellenic UROLOGY though these were successfully repaired at the same time. In the locally advanced group, 17.3% of the clinically advanced patients had pathologically confined disease. Out of the patients 99.8% remained continent and 36.1% remained potent in the locally advanced group. In the organ confined group the rates were 100% and 62.5%, respectively. Between the two groups there was no significant difference regarding the cancer-specific survival rate. Conclusion Radical perineal prostatectomy is considered to be the best choice for treating locally advanced disease, provided patients are fully informed and that they consent to undergo this treatment. Key Words Radical perineal prostatectomy, locally advanced prostate cancer. Introduction Treatment of clinically locally advanced prostate cancer is considered to be a medical challenge for a urologist. Even today, selecting an appropriate treatment is a subject of research. Surveys show that a greater overall benefit results from combined treatment (radiotherapy together with hormone therapy) instead of monotherapy (using only radiotherapy). However, no study has ever proved that combined treatment is a better choice than radical prostatectomy1. Functional and ongological results of radical perineal prostatectomy for the management of clinically locally advanced prostate cancer. Single centre experience In the past, surgical treatment of locally advanced 2 prostate cancer was not often resorted to due to an increased risk of positive surgical margins, and 3,4 also due to existence of lymph node metastases . Nowadays there is an increasing number of reports in the literature that support radical prostatectomy as a legitimate solution to manage locally adva5-10 nced disease . This has led the European Association of Urology (EAU) to consider radical prostatectomy as a potential option to a selective range of patients with locally advanced disease. 11 (cT3) . The literature refers to retropubic radical prostatectomy and perhaps for the first time in this study we attempt to promote the significant role of perineal access to deal with pre-operatively diagnosed, locally advanced prostate cancer. In our clinic (Department of Urology 401 G.M.H.A) since 1993, radical perineal prostatectomy has been not only the method of choice, but the only surgical method of access to prostate cancer. In our given material we do not have any other method, and for that reason in this study we attempt to compare our results to other authors, as these are found in the international literature. Material and methods This study refers to 627 radical perineal prostatectomies that were conducted in the Department of Urology in the 401 Military Hospital of Athens, between 1993 and 2012. Diagnosis of this disease was conducted with a transrectal ultrasonographically guided prostate biopsy. Typically, 5 or 6 tissue blocks were extracted from each lobe and also from suspicious areas detected in a digital examination or in the transrectal ultrasound, regarding either intraprostatic fat, or the seminal vesicles. Clinical staging was accomplished through digital examination, transrectal ultrasound and CT scan, and showed 83 patients with locally advanced disease. There was no patient selection in reference to prostate size or somatometric measurements, while 35 of the patients had already been submitted to pre-operative hormonal manipulation to achieve shrinking of the tumor. Properties of each group are shown in Table 1. Table1 Characteristics of the patients treated with radical perineal prostatectomy Average age (years) 62,7 (51-73) Gleason score biopsy 7 (4-9) PSA 13,38 (3,5-42) Laparoscopic Lymphadenectomy 77,1% Unilateral preservation of Neurovascular bundle (NVB) 43,3% Follow up (months) 37 (8-62) Evaluation of lymph node metastasis was achieved through CT scans, and bone metastasis was evaluated using bone scintigraphy. The first postoperative measurement of PSA occurred after six weeks. During the first year follow up examination took place every three months, during the second and third year, every fourth-month, and later every six months. Patients with positive surgical margins were submitted to adjuvant radiotherapy, while those with lymph node metastases were submitted to hormonal 12 manipulation . As for biochemical relapse, the EAU guidelines were followed, based on whether PSA doubling time (PSADT) showed local relapse or distant metastasis. To be more specific, if an increase of PSA was noted after the third postoperative year, PSA DT was >11months, and the specimen Gleason score was <6, then it would be considered as a local relapse and automatically followed by radiotherapy. On the other hand, if an increase of PSA was noted within the first postoperative year PSA DT was <6 months and the specimen Gleason score was 8-10, then it would be considered as a systematic relapse and the patient would undergo hormonal therapy. In the case of preservation of neurovascular bundles, patients received post-operative phosphodiesterase inhibitors. Selection of patients who underwent Hellenic UROLOGY 37 Athanasios I. Archodakis, Stefanos Bolometes laparoscopic lymphadenectomy, which has been practiced since 1994, was based on the preoperative PSA value and the biopsy Gleason score. Patients with PSA lower than 10 and a Gleason 13 score <7 (19 patients) were excluded. For the statistical analysis, we used Pearson chisquared test for independence. Due to the zerofrequency of some parameters (no appearance), the calculation of p-value (observed statistic level of importance) for this test was not asymptotic (that is, with the use of the chi-squared distribution), but was calculated with the use of a Monte-Carlo simulator. The result was considered to be statistically significant when p-value was less than 0,05(the level of statistical significance). Results Average duration of the operation was 175min, including the average 60min duration time of laparoscopic lymphadenectomy for the locally advanced group. Average blood loss was 280ml. In comparison to the 544 patients with localized disease, the difference was statistically insignificant (pvalue=0.150)(168min and 250ml. respectively). There was also an insignificant difference in postoperative complications as well, with the exception of two intraoperative rectal injuries in the group of locally advanced disease, which were successfully repaired. Also in one patient from the locally advanced group, the formation of a urinary fistula was observed. The removal of the penrose drain was difficult, possibly being caught on the stitches of the pelvic musculature. st After penrose drain removal, on the 1 post-operative day, an outflow of urine was observed through the wound that continued for 2 weeks, when a small penrose drain remnant was spontaneously rejected. The urinary incontinence was successfully resolved via additional catheterization for the following 2 weeks, without any further intervention (table 2). 38 Hellenic UROLOGY Erectile Function was tested 12 months postoperatively. 36.1% of the patients reported erection capable of vaginal penetration in the group of locally advanced disease (30 patients), significantly lower than the respective rate of localized disease Table 2 Complications after radical perineal prostatectomy LOCAL DISEASE LOCALLY disease Death rate 0 0 Bowel injury 0 2 (2,4%) Pulmonary Embolism 0 0 Lymphocele 0 0 Anastomotic stricture 11 (2%) 2 (2,4%) Compartment Syndrome 1 (0,18%) 0 Urinary Fistula 0 1 (1,2%) ADVANCED (62.5%) (P-value<0, 05). This is due to the unilateral preservation of neurovascular bundle only in 43.3% of the patients with clinically locally advanced disease, due to local extention of the disease. In a single patient with invasion of the prostate apex, incontinence persisted 12 months postoperatively which was resolved with implantation of an artificial urinary sphincter. As for the oncological results, pathologic down staging was observed in 16.8% of the patients with clinically diagnosed, locally advanced disease (p-value<0, 05)(Table 3). Table 3: Pathological stage distribution after radical perineal prostatectomy pT2 16,8% pT3a 48,2% pT3b 31,4% pT4 3,6% Positive surgical margins were found in 14.4% of the group with clinically advanced disease in comparison to 12.5% of the group with the localized disease. Positive lymph nodes were detected in 10 out of 83 patients with clinically locally advanced disease (12%). The preoperative CT scan evaluation showed no sign of lymphnode metastasis. In the first case patients underwent adjuvant Functional and ongological results of radical perineal prostatectomy for the management of clinically locally advanced prostate cancer. Single centre experience radiotherapy while in the second case they underwent hormonal deprivation. During the follow-up period, 28.1% of the patients received adjuvant or salvage radiotherapy due to positive surgical margins or biochemical relapse, indicative of local relapse, and 33.7% received hormonal therapy due to lymphatic metastasis or biochemical relapse indicative of systemic disease. The disease specific survival in the first three years was 93.9% in the group of clinically locally advanced disease and 96% in the group of localized disease. Discussion Selection of the therapeutic treatment of clinically advanced cancer is a challenge for the urologist14.The goals of treatment should include: healing; extension of life, although this should be achieved without any metastasis; localized control of the tumor; and improvement of quality of life. The therapeutic choices for the achievement of the above are various. Prognosis varies widely, and the choice of treatment depends on predictive factors such as PSA value, Gleason score and tumor size. According to the EAU guidelines, watchful waiting may be conducted even inpatients without symptoms, with well-or moderately-differentiated T3 disease, and life expectancy of less than 10years, who are not able to undergo surgery or radiation treatment. Radical prostatectomy is considered an option in a selective range of patients with T3a, PSA<20ng/ml, biopsy Gleason score <8 and life expectancy lower than 10 years. According to the EAU, those patients should be aware that radical prostatectomy is related to increased risk of positive surgical margins and lymph-node metastasis, which need adjuvant radiotherapy or hormonal therapy, respectively. Amongst the patients with clinically diagnosed, locally advanced disease in the study, 16.8% were eventually diagnosed with pT2 disease and as a result it was not necessary to follow adjuvant treatment. If we take into consideration the low rate of intraoperative complications and the satisfactory functional results, these patients benefited from undergoing an operation of lower severity such as perineal prostatectomy, which in our experience allows for the preservation of critical structures, just as much in the case of locally advanced disease, as in that of localized. During the follow-up the percentage of patients who received treatment was 28.1% and 33.7% for local radiotherapy and hormonal therapy respectively. In the literature there are not series of patients with clinical locally, advanced cases of the disease who underwent radical perineal prostatectomy, and therefore comparisons can be made only with series which have undergone retropubic prostatectomy. The reported results in those cases arise from strictly selected cases; such selection did not occur in our study for the reasons explained above. Downstaging in clinical locally advanced disease in 15-19 pT2, ranges in the literature from 13-27% . Those patients have an increased chance of a cure by means of radical prostatectomy only. Also, the 5year disease specific survival rate varies from 85100%19-22. An additional benefit of surgical treatment is the prevention of local complications that relate to the tumor but also to the fact that it is easier to follow up and diagnose relapse in comparison to radiotherapy. Pre-operative hormonal therapy, despite the fact that it improves pathological - anatomical parameters, such as positive surgical margins, does not affect biochemical or clinical progress of the 24 disease and does not improve survival rates . The EORTC 22911 survey presented a distinct survival benefit without disease progress and with improved local control of the disease in patients with positive surgical margins or PT3 disease, Hellenic UROLOGY 39 Athanasios I. Archodakis, Stefanos Bolometes when radical prostatectomy was combined postoperatively with radiotherapy23. In a recent 17 study , the 5-year, 10-year and 15-year diseasefree survival and disease specific survival incT3 disease in patients who had undergone radical prostatectomy, where the majority received adjuvant radio -or hormone- treatment, were 85%, 73% and 67%, and 95%,90% and 79%, respectively. Radical prostatectomy is an option even to high risk patients with locally advanced disease, without increasing morbidity11. A recent study from the USA showed that patients submitted to radical prostatectomy for cT4 disease, had an improved survival rate in comparison to those who received radiotherapy or hormonal therapy as monotherapy, and similar survival rates to those who received 24 combined therapy (RT and HT) . Despite many reports in the literature, where survival rates of radical prostatectomy with or without additional treatment, are comparable to those of combined therapy, more randomized prospective studies are required to compare surgical treatment to the combination of radio- and hormonal therapy. The latter is considered by many as the treatment of choice to manage locally advanced prostate cancer. This was reinforced by the EORTC 22863 survey, showing that 5-year disease free survival improved from 79% to 94% and overall survival improved from 62% to 78% 23 when combined treatment was utilized . Hormonal therapy contributes to improved results of radiotherapy by suppressing or probably eliminating the latent systematic disease. Moreover, the above combination seems to have additional effects on local control with the promotion of apoptosis invarious clone cancer cells24, 25. In our opinion this provides another advantage of surgical removal of the affected organ in cases of locally advanced prostate cancer. Removal of these different cancer cell clones 40 Hellenic UROLOGY possibly changes the natural progress of the disease, combined when necessary with adjuvant radio- or even hormonal- therapy. This should constitute a subject of study in further research, which will compare radical prostatectomy, supplemented when necessary with radio- or hormonal- therapy, with the combined treatment for the management of clinically locally advanced prostate cancer. In the present study, all the prostate cancer cases underwent perineal prostatectomy, and as a result the comparison between perineal prostatectomy results and retropubic prostatectomy was not possible in patients within a single centre. However, comparison with published results from centers experienced in retropubic prostatectomy may lead to safer conclusions regarding the effectiveness of the two treatment approaches. Also, despite the fact that pre-surgical selection of patients participating in similar clinical surveys is appropriate, long-term experience in the particular technique and the volume of patients that underwent surgery have led us to the conclusion that preoperative selection is not mandatory when perineal prostatectomy is applied, and actually the non-necessity of the preoperative selection should be considered as an important advantage of perineal prostatectomy in comparison to retropubic prostatectomy. Until the publication of results from further studies, modern data, from both the literature and also from our study show that radical prostatectomy, combined when necessary with radiotherapy or hormonal therapy, has results comparable to those of combined therapy whilst avoiding localized complications related to the tumour. Improvement of quality of life is the result. The avoidance of morbidity related to the surgical procedure is also of great importance, something Functional and ongological results of radical perineal prostatectomy for the management of clinically locally advanced prostate cancer. Single centre experience which is also shown by our results with perineal access, as also occurs in localized disease. The low rate of positive surgical margins in our study, 28-32 relative to that of the international literature , is attributable to the fact that perineal access allows the affected organ and the extent of neoplasms to be removed in total without dissection of the prostate. remains a relevant choice in the face of new challenges in modern oncological surgery. This is verified by the low rates of positive surgical margins and complications, and also by the satisfactory functional results relative to those of other surgical approaches in the existing literature. Conclusion Radical perineal prostatectomy is a safe option for well-informed patients with clinically diagnosed, locally advanced prostate cancer. The combination of the technique, when necessary, with adjuvant radiotherapy and hormonal therapy contributes to better control of the disease with lower morbidity and maintenance of good quality of life. Ðåñßëçøç Despite the fact that there was no strict preoperative patient selection there were comparable results to those in patients with clinically localized disease that underwent similar surgery, not only relating to postoperative complications but also to positive surgical margins and urinary incontinence. The markedly low rates of preservation of erectile function are a result of local tumor extension to neurovascular tissue blocks unilaterally or bilaterally. The latest imaging methods of detailed representation of localized tumor extension may also further increase chances of preservation of neurovascular bundles and increase as a result the rates of erectile function maintenance. ÏõñïëïãéêÞ ÊëéíéêÞ, 401 ÃÓÍÁ More prospective, randomized studies are required to compare surgery with other methods of treatment, but also to compare various different surgical techniques between themselves, in relation to oncological outcomes and complications, and patient quality of life for those patients with clinical locally advanced prostate cancer. It appears that radical perineal prostatectomy, although it remains the oldest form of surgical access to the prostate, ËåéôïõñãéêÜ êáé ïãêïëïãéêÜ áðïôåëÝóìáôá ôçò ñéæéêÞò ðåñéíåúêÞò ðñïóôáôåêôïìÞò óôçí áíôéìåôþðéóç ôïõ êëéíéêÜ ðñï÷ùñçìÝíïõ ôïðéêÜ êáñêßíïõ ðñïóôÜôç. Ç Åìðåéñßá ôçò ïõñïëïãéêÞò êëéíéêÞò ôïõ 401 ÃÓÍÁ Á.É. Áñ÷ïíôÜêçò, Ó. Ìðïëïìýôçò Õðåýèõíïò åðéêïéíùíßáò: Á.É. Áñ÷ïíôÜêçò Tçë: +30 2107494179 email:[email protected] ÅéóáãùãÞ. Ç ñéæéêÞ ðñïóôáôåêôïìÞ èåùñåßôáé ùò ç èåñáðåßá åêëïãÞò óôïí åíôïðéóìÝíï êáñêßíï ôïõ ðñïóôÜôç. Ôá ôåëåõôáßá ÷ñüíéá ðëçèáßíïõí ïé âéâëéïãñáöéêÝò áíáöïñÝò ðïõ õðïóôçñßæïõí ðùò ç ÷åéñïõñãéêÞ áíôéìåôþðéóç Ý÷åé èÝóç óôçí áíôéìåôþðéóç ôçò, ôïðéêÜ, ðñï÷ùñçìÝíçò íüóïõ. Óýìöùíá ìå ôéò ïäçãßåò ôçò ÅõñùðáúêÞò ÏõñïëïãéêÞò Åôáéñåßáò, ç ñéæéêÞ ðñïóôáôåêôïìÞ èåùñåßôáé ðñïáéñåôéêÞ (optional) åðéëïãÞ óå êáëÜ åðéëåãìÝíïõò áóèåíåßò ìå, ôïðéêÜ, ðñï÷ùñçìÝíç íüóï. Óêïðüò ôçò ðáñïýóáò åñãáóßáò åßíáé íá áíáäåßîåé ôïí ñüëï ôçò ðåñéíåúêÞò ðñïóðÝëáóçò óå áóèåíåßò ìå, ôïðéêÜ, ðñï÷ùñçìÝíï êáñêßíï ðñïóôÜôç. Õëéêü êáé ìÝèïäïò. Ìåôáîý 1993 êáé 2012, 627 áóèåíåßò ìå êáñêßíï ðñïóôÜôç õðïâëÞèçêáí óå ñéæéêÞ ðåñéíåúêÞ ðñïóôáôåêôïìÞ. Áðï ôïõò áóèåíåßò áõôüõò 83 åß÷áí êëéíéêÜ, Hellenic UROLOGY 41 Athanasios I. Archodakis, Stefanos Bolometes ôïðéêÜ, ðñï÷ùñçìÝíç íüóï. Óõãêñßíáìå ôç ìåôåã÷åéñçôéêÞ ðïñåßá êáé ôá ðñþéìá ïãêïëïãéêÜ áðïôåëÝóìáôá ìåôáîý ôùí äýï ïìÜäùí. 4. Boccon-Gibod L, Bertaccini A, Bono AV, et al. Management of locally advanced prostate cancer: a European Consensus. Int J ClinPract 2003 Apr;57(3):187-94. ÁðïôåëÝóìáôá. Äåí ðáñáôçñÞèçêå äéáöïñÜ üóïí áöïñÜ óôï ìÝóï ÷åéñïõñãéêü ÷ñüíï, ôçí áðþëåéá áßìáôïò , ôçí ðáñáìïíÞ óôï íïóïêïìåßï êáé ôç äéÜñêåéá êáèåôçñéáóìïý ìåôáîý ôùí äýï ïìÜäùí. Äåí õðÞñ÷å óôáôéóôéêÜ óçìáíôéêÞ äéáöïñÜ óôéò ìåôåã÷åéñçôéêÝò åðéðëïêÝò êáé 2 äéåã÷åéñçôéêÝò ôñþóåéò ïñèïý óôçí ïìÜäá ôçò ôïðéêÜ ðñï÷ùñçìÝíçò íüóïõ áðïêáôáóôÜèçêáí óå ðñþôï ÷ñüíï, åðéôõ÷þò. Óôçí ïìÜäá ôçò ôïðéêÜ ðñï÷ùñçìÝíçò íüóïõ õðÞñîå ðáèïëïãïáíáôïìéêÞ õðïóôáäéïðïßçóç óôï 17,3% ôùí ðåñéðôþóåùí. Ôï 99,8% äéáôÞñçóáí ôçí åãêñÜôåéá ôïõò êáé ôï 36,1 % ôçí óôõôéêÞ ôïõò ëåéôïõñãßá Ýíáíôé 100 êáé 62,5% óôçí ïìÜäá ôçò åíôïðéóìÝíçò íüóïõ. Äåí õðÞñîå óôáôéóôéêÜ óçìáíôéêÞ äéáöïñÜ óôçí åéäéêÞ ôçò íüóïõ åðéâßùóç ìåôáîý ôùí äýï ïìÜäùí. 5. Yamada AH, Lieskovsky G, Petrovich Z, et al. Results of radical prostatectomy and adjuvant therapy in the management of locally advanced, clinical stage TC, prostate cancer. Am J ClinOncol 1994 Aug;17(4):277-85. 6. Hsu CY, Joniau S, Oyen R, et al. Outcome of surgery for clinical unilateral T3a prostate cancer: a single-institution experience. EurUrol 2007 Jan;51(1):121-8; discussion 128-9. 7. Gerber GS, Thisted RA, Chodak GW, et al. Results of radical prostatectomy in men with locally advanced prostate cancer: multi-institutional pooled analysis. EurUrol 1997;32(4):385-90. 8. Ward JF, Slezak JM, Blute ML, et al. Radical prostatectomy for clinically advanced (cT3) prostate cancer since the advent of prostate-specific antigen testing: 15-year outcome. BJU Int 2005 Apr;95(6): 751-6. References 1. Bolla M, Collette L, Blank L, et al. Long-term results with immediate androgen suppression and external irradiation in patients with locally advanced prostate cancer (an EORTC study): a phase III randomised trial. Lancet 2002 Jul;360(9327):103-6. 2. Hodgson D, Warde P, Gospodarowicz M. The management of locally advanced prostate cancer. UrolOncol 1998;(4):3-12. 3. Fallon B, Williams RD. Current options in the management of clinical stage C prostatic carci-noma. UrolClinNorthAm 1990 Nov;17(4):853-66. 42 Hellenic UROLOGY 9. Isorna Martinez de la Riva S, BelónLópezTomasety J, Marrero Dominguez R, et al. [Radical prostatectomy as monotherapy for locally advanced prostate cancer (T3a): 12 years follow-up]. ArchEspUrol 2004 Sep;57(7):679-92. [ArticleinSpanish] 10. Van den Ouden D, Hop WC, Schröder FH. Progression in and survival of patients with locally advanced prostate cancer (T3) treated with radical prostatectomy as monotherapy. J Urol 1998 Oct; 160(4):1392-7. 11. A. Heidenreich (chairman), P.J. Bastian, J. Bellmunt, M. Bolla, S. Joniau, M.D. Mason, V. Functional and ongological results of radical perineal prostatectomy for the management of clinically locally advanced prostate cancer. Single centre experience Matveev, N. Mottet, T.H. van der Kwast, T. Wiegel, F. Zattoni. EAU GuidelinesonProstateCancer 2012. 12. Koutsilieris M, et al. Combination of somatostatin analogues and dexamethasone (antisurvival-factor concept) with luteinizing hormonereleasing hormone in androgen ablation-refractory prostate cancer with bone metastasis. BJU Int. 2007 Jul;100 Suppl 2:60-2. 13. S. Joniau, C. Y. Hsu, E. Lerut et al., “A pretreatment table for the prediction of final histopathology after radical prostatectomy in clinical unilateral T3a prostate cancer,” European Urology, vol. 51, no. 2, pp. 388–394, 2007. 14. S.G.Fletcher and D. Theodorescu, “Surgery or radiation:what is the optimal management for locally advanced prostate cancer?” The Cana-dianjournalofurology, vol. 12, no. 1, supplement 1, pp. 58–61, 2005. 15. S. E. Lerner,M. L. Blute, and H. Zincke, “Extended experience with radical prostatectomy for clinical stage T3 prostate cancer: outcome and contemporary morbidity,” Journal of Urology, vol. 154, no. 4, pp. 1447–1452, 1995. 16. W. R. Morgan, E. J. Bergstralh, and H. Zincke, “Long-term evaluation of radical prosta-tectomy as treatment for clinical stage C (T3) prostate cancer,” Urology, vol. 41, no. 2, pp. 113–121, 1993. 17. J. F. Ward, J. M. Slezak, M. L. Blute, E. J. Bergstralh, and H. Zincke, “Radical prostatectomy for clinically advanced (cT3) prostate cancer since the advent of prostate-specific antigen testing: 15-Year outcome,” BJU International, vol. 95, no. 6, pp. 751–756, 2005. 18. K. A. Roehl, M. Han, C. G. Ramos, J. A. V. Antenor, and W. J. Catalona, “Cancer progression and survival rates following anatomical radical retropubic prostatectomy in 3,478 consecutive patients: long-term results,” Journal of Urology, vol. 172, o. 3, pp. 910–914, 2004. 19. D. Van den Ouden, P. J. T. Davidson, W. Hop, and F. H. Schroder, “Radical prostatectomy as a monotherapy for locally advanced (stage T3) prostate cancer,” Journal of Urology, vol. 151, no. 3, pp. 646–651, 1994. 20. H. Van Poppel, H. Goethuys, P. Callewaert, L. Vanuytsel, W. Van De Voorde, and L. Baert, “Radical prostatectomy can provide a cure for well-selected clinical stage T3 prostate cancer,” European Urology, vol. 38, no. 4, pp. 372–379, 2000. 21. G. S. Gerber, R. A. Thisted, G. W. Chodak et al., “Results of radical prostatectomy in men with locally advanced prostate cancer:multi-institutional pooled analysis,” European Urology, vol. 32, no. 4, pp. 385–390, 1997. 22. S. M. de la RivaIsorna, L.-T. J. Belon, D. R. Marrero, C. E. Alvarez, and B. P. Santamaria, “Radical prostatectomy asmonotherapy for locally advanced prostate cancer (T3a): 12 years follow-up,” ArchivosEspa˜noles de Urolog´ýa, vol. 57, no. 7, pp. 679–692, 2004. 23. M. Bolla, H. Van Poppel, L. Collette et al., “Postoperative radiotherapy after radical prostatectomy: a randomised controlled trial (EORTC trial 22911),”The Lancet, vol. 366, no.9485, pp. 572–578, 2005. 24. Shelley MD, Kumar S, Wilt T, et al. A systematic review and meta-analysis of randomised trials of neoadjuvant hormone therapy for localised and locally advanced prostate carcinoma. Cancer TreatRev 2009 Feb;35(1):9-17. Hellenic UROLOGY 43 Athanasios I. Archodakis, Stefanos Bolometes 25. Johnstone PA, Ward KC, Goodman M, et al. Radical prostatectomy for clinical T4 prostate cancer. Cancer 2006 Jun;106:2603-9. 26. Zietman AL, Prince EA, Nakfoor BM, et al. Androgen deprivation and radiation therapy: sequencing studies using the Shionogi in vivo tumour system. Int J RadiatOncolBiolPhys 1997 Jul;38(5):1067-70. 27. Joon DL, Hasegawa M, Sikes C, et al. Supraadditive apoptotic response of R3327-G rat prostate tumours to androgen ablation and radiation. Int J RadiatOncolBiolPhys 1997 Jul;38(5):1071-7. 28. C. Obek, S. Sadek, S. Lai, F. Civantos, D. Rubinowicz, and M. S. Soloway, “Positive surgical margins with radical retropubic prostatectomy: anatomic site-specific pathologic analysis andimpact on prognosis,” Urology, vol. 54, no. 4, pp. 682–688, 1999. 29. R. B.Watson, F. Civantos, and M. S. Solo-way, “Positive surgical margins with radical prostatectomy:detailed pathological analysis and prognosis,” Urology, vol. 48, no. 1, pp. 80–90, 1996. 44 Hellenic UROLOGY 30. D. I. Quinn, S. M. Henshall, A. M. Haynes et al., “Prognostic significance of pathologic features in localized prostate cancer treated with radical prostatectomy: Implications for staging systems and predictive models,” Journal of Clinical Onco-logy, vol. 19, no. 16, pp. 3692–3705, 2001. 31. S. S. Connolly, G. C. O'Toole, K. J. O'Malley et al., “Positive apical surgical margins after radical retropubic prostatectomy, truth or artefact?” ScandinavianJournalofUrologyandNephrology, vol. 38, no. 1, pp. 26–31, 2004. 32. S. R. Bott, A. A. Freeman, S. Stenning et al., “Radical prostatectomy: pathology findings in 1001 cases compared with other major series and over time,” BJU International, vol. 95, no. 1, pp. 34–39, 2005. ORIGINAL ARTICLE Urodynamic findings in voiding symptoms after radical prostatectomy: Analysis of our experience M. Stavropoulos, P. Venetsanos, P. Anastasopoulos, C. Bouropoulos, N. Ferakis, I. Poulias. Hellenic Red Cross Hospital.Department of Urology, Athens, Greece. Corresponding Author: Constantinos Bouropoulos Hellenic Red Cross Hospital Department of Urology 11526, Athens e-mail: [email protected] Summary Introduction To determine and assess urodynamic findings in patients with persistent post-radical prostatectomy (R.P) voiding symptoms. Furthermore, the purpose of the study is to estimate the effect of age, body mass index (B.M.I) and nerve sparing techniques on the presence of these symptoms. Methods A total of 45 patients reported incontinence or lower urinary tract symptoms, at least 12 months following radical retropubic prostatectomy (R.P) were enrolled in the study. All patients underwent clinical evaluation and standardized urodynamic test. Patients with urinary tract infections, anastomotic strictures, hormonal or radiation therapy were excluded. Results The mean patient age was 68.5 years (59-74). 2 Mean B.M.I was 27.5kg/m and the mean follow-up period after R.P was 15.3 months. Stress urinary incontinence was the most common urodynamic finding, occurring in 26 patients (57.8%). Detrusor overactivity was identified in 14 patients (31, 3%). However, in 15 patients (33.3%) complaining of urgency, involuntary detrusor contractions were not recorded during urodynamic study. In 9 cases (20%) reduced bladder compliance was noted. Four (4) patients (8.9%) were diagnosed with detrusor hypocontractility, who were also found to have symptoms of obstruction. Moreover, B.M.I was found to be significantly correlated with stress urinary incontinence, detrusor hypocontractility and bladder outlet obstruction (p<0.001, p=0.038 and p=0.038 respectively). Old age was significantly related to stress urinary incontinence (p=0,019). Conclusion There is a large variety of urodynamic findings after radical prostatectomy with stress urinary incontinence being the most common. Most of the patients' complain of urgency but involuntary detrusor contractions are recorded in only half of the cases. Increased B.M.I is associated with stress urinary incontinence, bladder outlet obstruction and detrusor hypocontractility. Detrusor deficiency is a prevalent medical problem in older patients. Key words Radical prostatectomy, stress urinary incontinence, urodynamic testing. Introduction It is well-known that radical prostatectomy is considered to be the treatment of choice for patients with prostate cancer. The widespread application of PSA measurement has led to an 1-3 increase in early-stage diagnosis of the disease . This fact, in combination with better understanding of male pelvic anatomy, as well as developments in surgical techniques have led to a rapid increase in the number of patients who undergo both open and minimally-invasive surgery1-3. However, despite the developments in surgical techniques, urinary incontinence remains a relatively frequent complication of radical prostatectomy which may have negative effects on patients' quality of life1-4. Furthermore, after RP further complications may be observed, apart from urinary incontinence, such as overactive bladder, detrusor hypocontractility, poor bladder control, and bladder outlet voiding Hellenic UROLOGY 45 M. Stavropoulos, P. Venetsanos, P. Anastasopoulos, C. Bouropoulos, N. Ferakis, I. Poulias 1-12 symptoms . Urodynamic findings observed in patients with urinal incontinence complaints after radical prostatectomy are described and evaluated in the present study. Material and Methods 45 Patients, who had undergone radical prostatectomy and complained of persistent disturbances in urination, such as irritative of obstructive bladder problems, as well as urinary incontinence were included in the study. As urinary incontinence was considered according to International Continence Society guidelines- the involuntary urine loss or urine leakage (ICS) 13. Minimum follow-up period postoperatively was 12 months. None of these patients reported recurrence or development of the disease and no one required adjuvant radiotherapy or hormonal therapy. All patients were examined with cystourethroscopy in order to exclude the possibility of the urethral anastomosis narrowing. Also patients with comorbid diseases such as diabetes, neuron disease or infections detected in the urinalysis were excluded from the study. Patients were stratified according to the stage of the disease, localization of the tumor, age and pre-surgical erectile function as indicated by the questionnaire of the International Index of Erectile Function (IIEF-5). They underwent non-nerve sparing or nerve sparing open retropubic radical prostatectomy. The nerve sparing technique was conducted with intrafascial or an interfascial access, but also with extrafascial access with a partial preservation of neurovascular bundles. Doctors recorded the medical history and performed a physical examination of all patients prior to evaluating the urodynamic test outcomes. Urodynamic tests included cystomanometry, voiding pressure-flow test and intravesical pressure and flow measurement (UVJ). We used a double lumen catheter with a 6FCh diameter and a rectal catheter with a 16Ch diameter. UVJ was measured during the filling phase with a volume of 200ml, with the patient in an upright position, and by increasing the 46 Hellenic UROLOGY intraversical pressure either with cough or Valsalva maneuver. UVJ levels of <60cm H2O were indicative of an Intrinsic Sphincter Deficiency. At full capacity, the patient is asked to urinate and maximum urinary flow rate is measured (Qmax), the detrusor pressure during maximum flow (Pdetmax) and the post voiding residual volume. Bladder outlet obstruction and detrusor contractility were quantified according to the Schafer Nomogram. Categories 0-2 included nonobstructive patients whereas categories 3-6 included obstructive patients. Furthermore the nomogram was applied to distinguish between normal and reduced detrusor contractility. The four categories of overactive bladder reviewed in this study are related to urodynamic assessment of the patients with an overactive detrusor as described 15 by Blaivas JG et al. Regression analysis was performed to delineate threshold between patients' clinical characteristics and urodynamic findings. Tvalue indicates the risk factors whereas p values greater 0, 05 were statistically insignificant. Results The mean patient age was 68.5 years (59-74). Mean BMI was 27.3 ± 2.8 kg/m2 and mean followup period after radical prostatectomy was 15.3 months (Table 1). Stress urinary incontinence was the most common urodynamic finding, occurring in 26 patients (57, 8%) (Table 2). Twety nine patients (64, 4%) complained of urgency, however, during the urodynamic testing involuntary detrusor contractions (types II, III, IV), were observed in 14 patients (31.1%). Although intrinsic sphincter deficiency was the most common urodynamic finding in the present study, it was recorded as a primary disorder in only 7 patients (15.5%). In the remaining patients it co-existed with functional bladder disorders. Urinal urgency in combination with overactive detrusor was exclusively found in 15% patients (33.3%). In most of these cases it was diagnosed overactive detrusor type I without involuntary contractions. A statistically significant correlation (p<0.001) was found between high BMI and stress urinary incontinence and detrusor hypocontractility and bladder outlet obstruction as Urodynamic findings in voiding symptoms after radical prostatectomy: Analysis of our experience well. Older age was significantly correlated to stress urinary incontinence (p=0.019). No statistically significant correlation was observed between the nerve-sparing techniques and the patients' urodynamic disorders (Tables 3, 4). Discussion It has been shown by many authors that the elimination of prostatic obstruction during radical prostatectomy following the excision of the prostate gland may lead to an improvement of voiding symptoms especially in patients with severe voiding symptoms pre-surgically (high IPSS 10 values) . However during radical prostatectomy apart from the removal of the prostate, the separation of the bladder trigone from the anterior of the urethra at the level of the bladder neck may 1-3,10 cause innervational and vascular disorders . As a result, symptoms of the urinary tract system and the related reduction of the quality of life may not be improved1-4. In the present study, urodynamic findings of stress incontinence (UVJ< 60 cm H2O), indicating intrinsic sphincter deficiency (ISD) were reported in 26 patients. Currently, the underlying mechanism of urinary incontinence following RP is not fully understood. Anatomical changes that take place after radical prostatectomy seem to play an important role. More specifically, damage to the sphincter may occur either as a result of direct injury during the excision of the prostate apex or during suturing of the cysteourethral anastomosis or indirectly as a result of its innervation damage. In fact, several nerves responsible for urinary continence are located in the neurovascular bundles and may be damaged in non-nerve 1, 2 sparing radical prostatectomy . Furthermore an injury in the pelvic plexus which is located on the lateral sidewall of the rectum and provides innervation to the pelvic organs may occur during the excision of the apex of seminal vesicles 1, 2, 16. Loss of continuity of the smooth bladder muscles and the reduction of the circumferential sphincter lining of muscles and fascias seems also to play an important role1,2. For this reason, disruption of the innervation of the sphincter which originates from the pelvic branch of the pudendic nerve as well as of the branches of the lower hypogastric plexus, and the muscular components surrounding the sphincter should be avoided. In fact, the above disruptions lead to loss of support from a stable point of the sphincter, and lead to its relaxation and insufficient contraction1, 2. Some authors consider that the frequency of urinary incontinence after radical prostatectomy seems to correlate with the reduction of the 1,2 functional length of the urethra length . Finally, preservation of the bladder neck increases the rate of premature continence without affecting the long17 term results . Other investigators concluded that the age of the patient is an independent prognostic factor for the radical prostatectomy induced incontinence19.. The above observation is in accordance with the statistically significant correlation between patients' age and in the frequency of urodynamic findings of urinary stress incontinence found in the present study. Reasons explaining this fact are not well known. However, it is reported that older patients who underwent radical prostatectomy have more severe voiding symptoms18 and tend to suffer by comorbident diseases which possibly affects the pre-operative level of urinary continence1,2,19. On the other hand, nerve-sparing techniques are performed less often in older than in younger patients. Moreover, age related histological changes of the bladder muscolar and connective tissue are less likely to adapt changes of urodynamic parameters introduced by the radical prostatectomy. Therefore, the patients' age should be taken into consideration during the data evaluation concerning functional outcomes after radical prostatectomy. In the present study patients with a high BMI showed increased urinary stress incontinence and detrusor hypocontractility. Several studies on large series of patients who underwent both laparoscopic and open radical prostatectomy (via either the transperineal or suprapubic approach) or robotically assisted radical prostatectomy, have shown that increased BMI is significantly related to increased post-operative rates of morbidity and more frequent complications20-25. In fact, increased deposition of adipose tissue, adds difficulty in the access to the pelvic organs, and therefore renders the operation more difficult. Conclusively, these pa- Hellenic UROLOGY 47 M. Stavropoulos, P. Venetsanos, P. Anastasopoulos, C. Bouropoulos, N. Ferakis, I. Poulias tients have a greater chance of reporting negative functional results, and a longer period of time is required for them to return to original levels of continence. Post radical prostatectomy urinary complications may also occur due to detrusor dysfunction (such as involuntary detrusor contractions, reduced bladder contractility, detrusor hypocontractility) or bladder outlet obstruction. Data related to bladder 1-12 dysfunctions vary and are often contradictory . They are usually found in combination with stress urinary incontinence and as a single urodynamic finding in a small number of cases. It is possible that these dysfunctions occur in a pre-existing, urinary obstruction, although several authors report that they may occur de novo as a result of denervation and ischemic alterations which occur during radical 1-12 prostatectomy . Urodynamic testing is a fundamental tool for the detection and accurate description of the above disorders even in the absence of incontinence or other symptoms as indicated by the patient. The present study presents certain limitations, apart from its retrospective nature. It includes uro- dynamic findings from a selective group of patients who underwent radical prostatectomy. Those patients complained of persistent urinary dysfunction for more than one year while their urodynamic preoperative data was not available. However, our study reflects the current clinical practice that not include the urodynamic evaluation for the radical prostatectomy candidates as a routine examination. Conclusion In conclusion despite the radical development of surgical techniques urinary incontinence remains one of the most frequent complications of the radical prostatectomy procedure significantly affecting patient quality of life. Besides intrinsic sphincter deficiency which is the most common urodynamic finding after radical prostatectomy a variety of bladder complications may be observed. Several patients complain of urinary urgency but involuntary detrusor contractions are not recorded in all cases. Stress urinary incontinence may occur in overweight and elderly patients. Table 1. Demographic Characteristics of Patients Patients(n) 45 Age (yrs)1 68,33 (59-74) Age > 68,5 yrs 28 (62,22%) Age < 68,5 yrs 17 (37,78%) 2 2 BMI (kgr/m ) 27,34+2,83 BMI > 27,5 kgr/m2 22 (48,89%) 2 23 (51,11%) BMI < 27,5 kgr/m 1 48 Hellenic Nerve-sparing radical prostatectomy (n%) 24 (53,33%) Non Nerve-sparing radical prostatectomy (n%) 21 (46,67%) Follow up (months)3 15,33+2,39 Average value (åýñïò) UROLOGY 2,3 Average value ± Standard deviation Urodynamic findings in voiding symptoms after radical prostatectomy: Analysis of our experience Table 2. Urodynamic findings in voiding symptoms after radical prostatectomy. 15 (33,33%) Detrusor Overactivity Type I (n, %) Detrusor Overactivity Type II, III, IV (n, %) 14 (31,1%) Stress Urinary Incontinence (n, %) 26 (57,77%) Reduced Bladder Compliance (n, %) 9 (20%) Detrusor Hypocontractility (n, %) 4 (8,88%) Bladder Outlet Obstruction (n, %) 4 (8,88%) Stress Urinary Incontinence single (n, %) 7 (15,55%) Detrusor Overactivity Single / all Types (n, %) 15 (33,33%) Reduced Bladder Compliance Single (n, %) 0 (0%) Detrusor Hypocontractility / Bladder Outlet Obstruction 1 (2,22%) Single (n, %) Stress Urinary Incontinence + Detrusor overactivity (n, %) 9 (20%) Stress Urinary Incontinence + Detrusor overactivity 7 (15,55%) +Reduced Bladder Compliance (n, %) Stress Urinary Incontinence + Reduced Bladder Compliance (n, %) 1 (2,22%) Stress Urinary Incontinence + Detrusor Hypocontractility 2 (4,44%) / Bladder Outlet Obstruction (n, %) Hellenic UROLOGY 49 M. Stavropoulos, P. Venetsanos, P. Anastasopoulos, C. Bouropoulos, N. Ferakis, I. Poulias Table 3. Urodynamic Findings and Demographic characteristics of patients. Urodynamic Age < 68,5 BMI > 27,5 BMI < 27,5 kgr/m2 kgr/m2 years N.P1 N.N.P2 Age > 68,5 years Detrusor overactivity Type I 10(66,7%) 5(33,3%) 3(20%) 12(80%) 3(20%) 12(80%) Detrusor overactivity Type ÉÉ,ÉÉÉ,ÉV 3(21,4%) 11(78,6%) 13(92,9%) 1(7,1%) 10(71,4%) 4(28,6%) Stress Urinary Incontinence 9(34,6%) 17(65,4%) 24(92,3%) 2(7,7%) 22(84,6%) 4(15,4%) 1(11,1%) 8(88,9%) 9(100%) 0(0%) 7(77,8%) 2(22,2%) Detrusor Hypocontractility 0(0%) 4(100%) 4(100%) 0(0%) 1(25%) 3(75%) Bladder Outlet Obstruction 0(0%) 4(100%) 4(100%) 0(0%) 1(25%) 3(75%) Findings Reduced Bladder Compliance 1 Nerve sparing radical prostatectomy 2 Non-nerve sparing radical prostatectomy Table 4. Correlation among demographic characteristics of the patients and urodynamic findings D.O1 TYPE I Demographic Characteristics D.O1 TYPE I,III,IV Stress Urinary Incontinence Reduced Bladder Compliance Detrusor Hypocontractility Bladder Outlet Obstruction value p value t value p value t value p value t value p value t value p value t value p value t Operation type2 0,092 1,722 0,819 -0,229 0,630 -0,456 0,089 -1,740 0,389 -0,869 0,389 -0,869 Age 0,633 -0,480 0,867 0,167 0,019 2,423 0,980 0,025 0,204 1,290 0,204 1,290 BMI 0,604 0,522 0,739 -0,334 <0,001 6,871 0,282 -1,080 0,038 2,136 0,038 2,136 1 Detrusor Overactivity 2 nerve-sparing or non nerve-sparing 50 Hellenic UROLOGY Urodynamic findings in voiding symptoms after radical prostatectomy: Analysis of our experience Ðåñßëçøç ÏõñïäõíáìéêÞ åõñÞìáôá óôéò äéáôáñá÷Ýò ôçò ïýñçóçò ìåôÜ áðü ñéæéêÞ ðñïóôáôåêôïìÞ: ÁíÜëõóç ôçò åìðåéñßáò ìáò Ì. Óôáõñüðïõëïò, Ö. ÂåíåôóÜíïò, Ð. Áíáóôáóüðïõëïò, Ê. Ìðïõñüðïõëïò, Í. ÖåñÜêçò, Ç. Ðïýëéáò ÏõñïëïãéêÞ ÊëéíéêÞ Íïóïêïìåßïõ Åëëçíéêïý Åñõèñïý Óôáõñïý Õðåýèõíïò åðéêïéíùíßáò: Ìðïõñüðïõëïò Êùíóôáíôßíïò Íïóïêïìåßï Åëëçíéêïý Åñõèñïý Óôáõñïý ÏõñïëïãéêÞ ÊëéíéêÞ, 11526 ÁèÞíá tel:2106414000 - email: [email protected] Óêïðüò: Ï êáèïñéóìüò êáé ç áîéïëüãçóç ôùí ïõñïäõíáìéêþí åõñçìÜôùí óå áóèåíåßò ìå åðßìïíåò äéáôáñá÷Ýò ôçò ïýñçóçò ìåôÜ áðü ñéæéêÞ ðñïóôáôåêôïìÞ (ÑÐ). ÅðéðëÝïí, óêïðüò ôçò ìåëÝôçò åßíáé íá åêôéìçèåß åðßäñáóç ôçò çëéêßáò, ôïõ áõîçìÝíïõ äåßêôç ìÜæáò óþìáôïò (ÄÌÓ) êáé ôùí íåõñïðñïóôáôåõôéêþí ôå÷íéêþí óôçí ðáñïõóßá ôùí äéáôáñá÷þí áõôþí. Õëéêü êáé ìÝèïäïò: ÓõíïëéêÜ 45 áóèåíåßò ðïõ åìöÜíéóáí áêñÜôåéá ïýñùí ç óõìðôùìáôïëïãßá áðü ôï êáôþôåñï ïõñïðïéçôéêü, ôïõëÜ÷éóôïí 12 ìÞíåò ìåôÜ ôçí ïðéóèïçâéêÞ ÑÐ óõìðåñéëÞöèçóáí óôç ìåëÝôç. ¼ëïé ïé áóèåíåßò áîéïëïãÞèçêáí êëéíéêÜ êáé õðïâëÞèçêáí óå ïõñïäõíáìéêü Ýëåã÷ï. Áóèåíåßò ìå ëïßìùîç ôïõ ïõñïðïéçôéêïý, óôÝíùìá ôçò ïõñçèñïêõóôéêÞò áíáóôüìùóçò, éóôïñéêü ïñìïíïèåñáðåßáò, ç áêôéíïâïëßáò áðïêëåßóèçêáí áðü ôç ìåëÝôç. èçóçò ôùí áóèåíþí ìåôÜ ôçí ÑÐ 15.3 ìÞíåò. ÁêñÜôåéá áðü ðñïóðÜèåéá ðáñïõóéÜóèçêå óå 26 áóèåíåßò (57.8%) êáé Þôáí ôï ðéï óõ÷íü ïõñïäõíáìéêü åýñçìá. Õðåñëåéôïõñãéêüò åîùóôÞñáò äéáðéóôþèçêå óå 14 áóèåíåßò (31.3%). Ùóôüóï, óå 15 áóèåíåßò (33.3%) ðïõ ðáñáðïíÝèçêáí ãéá åðéôáêôéêÞ ïýñçóç äåí êáôáãñÜöçêáí áêïýóéåò óõóðÜóåéò ôïõ åîùóôÞñá êáôÜ ôïí ïõñïäõíáìéêü Ýëåã÷ï. Óå 9 ðåñéðôþóåéò (20%) ðáñáôçñÞèçêå ìåéùìÝíç ðñïóáñìïóôéêüôçôá ôçò ïõñïäü÷ïõ êýóôçò. Õðïóõóôïëéêüò åîùóôÞñáò äéáãíþóèçêå óå 4 áóèåíåßò (8.9%), ïé ïðïßïé âñÝèçêáí åðßóçò íá Ý÷ïõí êáé áðïöñáêôéêÜ óõìðôþìáôá. ÅðéðëÝïí, äéáðéóôþèçêå óçìáíôéêÞ óõó÷Ýôéóç ôïõ õøçëïý ÄÌÓ ìå ôçí áêñÜôåéá ðñïóðáèåßáò, ôïí õðïóõóôïëéêü åîùóôÞñá êáé ôçí áðïöñáêôéêÞ ïýñçóç (p<0.001, p=0.038 êáé p=0.038 áíôßóôïé÷á). Ç ìåãÜëç çëéêßá ó÷åôßóèçêå óçìáíôéêÜ ìå ôçí áêñÜôåéá áðü ðñïóðÜèåéá (p=0.019). ÓõìðÝñáóìá: ÌåôÜ áðü ÑÐ ðáñáôçñåßôáé ìåãÜëç ðïéêéëßá ïõñïäõíáìéêþí åõñçìÜôùí, ìå ôçí áêñÜôåéá áðü ðñïóðÜèåéá íá åßíáé ôï ðéï óõ÷íü. Ïé ðåñéóóüôåñïé áóèåíåßò ðáñáðïíïýíôáé ãéá åðéôáêôéêüôçôá, ùóôüóï áêïýóéåò óõóðÜóåéò ôïõ åîùóôÞñá êáôáãñÜöïíôáé ìüíï óôïõò ìéóïýò áðü áõôïýò. Ï õøçëüò ÄÌÓ ó÷åôßæåôáé ìå áêñÜôåéá áðü ðñïóðÜèåéá, õðïóõóôïëéêüôçôá ôïõ åîùóôÞñá êáé áðïöñáêôéêÞ ïýñçóç. Ç åíäïãåíÞò áíåðÜñêåéá ôïõ óöéãêôÞñá åìöáíßæåôáé ðéï óõ÷íÜ óå ðéï çëéêéùìÝíïõò áóèåíåßò. ËÝîåéò åõñåôçñéáóìïý: ÑéæéêÞ ðñïóôáôåêôïìÞ, áêñÜôåéá áðü ðñïóðÜèåéá, ïõñïäõíáìéêüò Ýëåã÷ïò. ÁðïôåëÝóìáôá: Ç ìÝóç çëéêßá ôùí áóèåíþí Þôáí 68.5 Ýôç (59-74 Ýôç). Ï ìÝóïò ÄÌÓ Þôáí 2 27.5 kg/m êáé ï ìÝóïò ÷ñüíïò ðáñáêïëïý- Hellenic UROLOGY 51 M. Stavropoulos, P. Venetsanos, P. Anastasopoulos, C. Bouropoulos, N. Ferakis, I. Poulias References 1. Giannantoni A, Mearini E, Zucchi A, Constantini E, Mearini L, Bini V et al. Bladder and urethral sphincter function after radical retropubic prostatectomy: a prospective long-term study. Eur Urol 2008, 54: 657664. 2. Porena M, Mearini E, Mearini L, Vianello A, Giannantoni A. Voiding dysfunction after radical retropubic prostatectomy:more than external urethral sphincter deficiency. Eur Urol 2007, 52: 38-45. 3. Bauer RM, Bastian PJ, Gozzi C, Stief CG. Postprostatectomy incontinence: all about diagnosis and management. Eur Urol 2009, 55: 322-333. 4. Alivizatos G, Skolarikos A. Incontinence and erectile dysfunction following radical prostatectomy: a review. Sci World J 2005, 13: 747-58. 5. Groutz A, Blaivas JG, Chaikin DC, Weiss JP, Verhaaren M. The pathophysiology of post-radical prostatectomy incontinence: a clinical and video urodynamic study. J Urol 2000, 163: 1767-70. 6. Kleinhans B, Gerharz E, Melekos M, Weingartner K, Kalble T, Riedmiller H. Changes of urodynamic findings after radical retropubic prostatectomy. Eur Urol 1999, 35: 217-21. 7. Namiki S, Ishidoya S, Saito S, Satoh M, Tochigi T, Ioritani N et al. Natural history of voiding function after radical retropubic prostatectomy. Urology 2006, 68: 142-7. 8. Dubbelman Y, Groen J, Wildhagen M, Rikken B, Bosch R. Quantification of changes in detrusor function and pressure-flow parameters after radical prostatectomy: relation to postoperative continence status and the impact of intensity of pelvic floor muscle exercises. Neurourol Urodyn 2012, 31: 637-41. 52 Hellenic UROLOGY 9. Kielb SJ, Clemens JQ. Comprehensive urodynamics evaluation of 146 men with incontinence after radical prostatectomy. Urology 2005, 66: 392-6. 10. Song C, Lee J, Hong Jh, Choo Ms, Kim Cs, Ahn H. Urodynamic interpretation of changing bladder function and voiding pattern after radical prostatectomy: a long-term follow-up. BJU Int 2010, 106: 681-6. 11. Huckabay C, Twiss C, Berger A, Nitti Vw. A urodynamics protocol to optimally assess men with post-prostatectomy incontinence. Neurourol Urodyn 2005, 24: 622-6. 12. Chung D, Dillon B, Kurta J, Maschino A, Cronin A, Sandhu J. Detrusor underactivity is prevalent after radical prostatectomy: a urodynamic study including risk factors. Can Urol Assoc J 2013, 7: E33-E37. 13. Thuroff Jw, Abrams P, Andersson KE, Atribani W, Chapple CR, Drake MJ et al. EAU guidelines on urinary incontinence. Eur Urol 2011, 59: 389-400. 14. SCHAFER W. Principles and clinical application of advanced urodynamic analysis of voiding function. Urol Clin North Am 1990, 17: 553-66. 15. Blaivas JG, Flisser AJ, Wamsley K. Urodynamic classification of patients with symptoms of overactive bladder. J Urol 2003, 169: 529–533. 16. John H, Hauri D. Seminal vesicle-sparing radical prostatectomy: a novel concept to restore early urinary continence. Urology 2000, 55: 820-4. 17. Grasso M, Torelli F, Lania C, Blanco S. The role of bladder neck preservation during radical prostatectomy: clinical and urodynamic study. Arch Ital Urol Androl 2012, 84: 1-6. 18. Deliveliotis C, Liakouras C, Delis A, Skolarikos Urodynamic findings in voiding symptoms after radical prostatectomy: Analysis of our experience A, Varkarakis J, Protogerou V. Prostate operations: long-term effects on sexual and urinary function and quality of life. Comparison with an agematched control population. Urol Res 2004, 32: 283-9. 22. Wolin Ky, Luly J, Sutcliffe S, Andriole Gl, Kibel AS. Risk of urinary incontinence following prostatectomy: the role of physical activity and obesity. J Urol 2010, 183: 629-33. 19. Eastham JA, Kattan MW, Rogers E, Goad JR, Ohori M, Boone TB et al. Risk factors for urinary incontinence after radical prostatectomy. J Urol 1996, 156: 1707-13. 23. Herman Mp, Raman Jd, Dong S, Samadi D, Scherr DS. Increasing body mass index negatively impacts outcomes following robotic radical prostatectomy. JSLS 2007, 11: 438-42. 20. Ahlering TE, Eichel L, Edwards R, Skarecky DW. Impacts of obesity on clinical outcomes in robotic prostatectomy. Urology 2005, 65: 740-4. 24. Yates J, Munver R, Sawczuk I. Robot-assisted laparoscopic radical prostatectomy in the morbidly obese patient. Prostate Cancer 2011. 21. Ampeggi A, Xylinas E, Ploussard G, Ouzaid I, Fabre A, Allory Y et al. Impact of body mass index on perioperative morbidity, oncological, and functional outcomes after extraperitoneal laparoscopic radical prostatectomy. Urology 2012, 80: 576-84. 25. Bae JJ, Choi SH, Kwon TG, Kim TH. Advantages of robot-assisted laparoscopic radical prostatectomy in obese patients: comparison with the open procedure. Korean J Urol 2012, 53: 536-40. Hellenic UROLOGY 53 CASE REPORT Malakoplakia of the bladder associated with advanced obstructive uropathy Konstantinos Stamatiou1, Georgios Makris1, Dimitris Zavradinos1, 1 1 2 Eleutherios Geropappas , Konstantinos Fokas , Athanasios Papatsoris . 1. Urology Department, Tzaneio General Hospital, Piraeus, Greece nd 2. 2 Department of Urology, University of Athens, Athens, Greece Corresponding Author: Konstantinos Stamatiou Urology Department, Tzaneio General Hospital, Piraeus, Greece Salepoula 2, 18536, Piraeus - Tel: +30 2104592387 e-mail: [email protected] Summary Malakoplakia is an inflammatory condition that rarely occurs in the urogenital tract. The most frequently affected organ is the urinary bladder, while involvement of the testis is extremely rare. This condition has the features of a granulomatous inflammation. In this article we present a case of bladder malakoplakia associated with advanced obstructive uropathy. Key Words Malakoplakia, inflammatory disease, urinary bladder, kidney failure. Introduction Malakoplakia is a granulomatous inflammation which was originally described in 1902 by Michaelis and Gutmann. Malakoplakia most often occurs in patients above 40 years old, and usually in women. Symptoms in the affected bladder are not specific and are similar to cystitis1. The pathogenesis of malakoplakia remains poorly understood, though it is speculated to be caused by defective macrophage elimination of bacteria. Defective macrophage killing results in an accumulation of bacterial degradation products and a granulomatous reaction, which clinically manifests as the formation of a papule, plaque or ulceration. It is hypothesized that the disease occurs in patients with history of E. coli infections, immunosuppression (usually connected to kidney transplantation and in rare cases due to lymphoma or cancer), diabetes, and chronic steroid use, although the relationship has not been clearly described. Macroscopically, on the internal surface of the affected organ, yellow- soft plaques are detected, whilst microscopically the disease is characterized by the presence of large macrophages (foamy hystiocyotic cells-also known as von Hansemann cells) containing pathognomonic Michaelis-Gutmann bodies. 54 Hellenic UROLOGY Case report description A male, 72 years old was brought to the Emergency Department (E.R) reporting inability to urinate and fever. He also reported weakness, fatigue and dysuria all starting a month ago. The patient's medical history was relevant for diabetes, hypertension and peripheral vascular disease. His past surgical history was relevant for a transvesical prostatectomy 3 years ago, due to urinary retention. This occurred after a significant history of recurrent urinary tract infections. During their evaluation a bladder biopsy of a membranous mucosal lesion was performed indicating nonspecific inflammation. Upon admission the patient presented with increased creatinine and glucose levels (21mg/dl, 300 mg/dl respectively). Anemia (Hct: 19%) with a normal white cell count however was noted. Ultrasound of the urinary system revealed bilateral hydronephrosis due to obstructive uropathy indicated by bladder wall thickening and trabeculation. Nevertheless bladder capacity was minimal with no residual urine observed (Image 1). Image 1.Transabdominal ultrasonography: abnormally thick bladder wall with the presence of exophytic lesion Urine analysis indicated hematuria, pyuria and microorganisms. Digital rectal examination Malakoplakia of the bladder associated with advanced obstructive uropathy revealed a small benign prostate. After immediate antibiotic initiation and fluid replacement the patient underwent initially hemodialysis due to the presence of hyperkalemia, following nephrostomy tube placement, which successfully stabilized renal function. Cystoscopic evaluation depicted atypical polypoid lesions of the mucosa and scattered red-yellow nodules sized 2 to 3.5cm in the trigone, left and posterior bladder wall. A transurethral resection of the lesions followed. Histology revealed malakoplakia of the urinary bladder (image 2-5). Despite initial patient stabilization the patient died 8 months later due to renal failure and complications of the cardiovascular system since he continued to present with urinary tract infections and chronic hydronephrosis. bioptic material with an absence of microscopic pathognomonic findings such as acidophilic foamy hystiocytic cells, or Michaelis-Gutmann bodies. In these cases the emergence of positive results for CD68 immunohistochemical staining confirms the 5 clinical hypothesis . This disease is frequently considered an auto-immune disorder or a type of 5. immunodeficiency Even though this inflammatory disease is chronic, in certain cases progresses acutely. Image 3. Malakoplakia with the use of a PAS stain in von Hausemann Çystiocyotic cells. Image 2. Pathognomonic histological image of malakoplakia of the urinary bladder. (HEX 100). Discussion Malakoplakia is a benign self-limiting disease that 3 usually has a benign course . Initial management consists of treating aggressively associated urinary tract infections and transurethral removal of the lesion mainly for histologic diagnosis. Few incidents of renal impairment, caused by multifocal malakoplakia, are reported in the literature. Indeed, when the symptoms are severe, the disease is 4 promptly diagnosed . The reason for the delayed diagnosis in the present case remains unknown. As the symptoms were chronic, we hypothesize that the bladder was already affected during the first biopsy. Failure to diagnose the disease may have occurred due to an insufficient amount of In summary, malakoplakia of the bladder should be carefully examined in patients with persistent infections of the urinary system and the presence of a tumor-like mass in the cystoscopy. A numerous of potential complications can be avoided with earlystage diagnosis and immediate antibiotic treatment. Image 4. Malakoplakia of the Urinary Bladder Hellenic UROLOGY 55 K. Stamatiou, G. Makris, D. Zavradinos, E. Geropappas, K. Fokas, A. Papatsoris Ðåñßëçøç Ç ìáëáêïðëáêßá åßíáé ìéá öëåãìïíþäçò êáôÜóôáóç ðïõ óðÜíéá åìöáíßæåôáé óôïí ïõñïãåííç- Ìáëáêïðëáêßá ôçò ïõñïäü÷ïõ êýóôçò óõíäåüìåíç ìå ðñï÷ùñçìÝíç áðïöñáêôéêÞ ïõñïðÜèåéá. Kùíóôáíôßíïò Óôáìáôßïõ1, Ãåþñãéïò ÌáêñÞò1, 1 1 ÄçìÞôñçò Æáâñáäéíüò , ÅëåõèÝñéïò Ãåñüðáððáò , 1 2 Êùíóôáíôßíïò ÖùêÜò , ÁèáíÜóéïò Ðáðáôóþñçò ôéêü óýóôçìá. Óõ÷íüôåñá ðñïóâáëëüìåíï üñãáíï åßíáé ç ïõñïäü÷ïò êýóôç, åíþ åßíáé åîáéñåôéêÜ óðÜíéá ç åìðëïêÞ ôïõ üñ÷åïò. Ç ðÜèçóç Ý÷åé ôá ÷áñáêôçñéóôéêÜ ìéáò êïêêéùìáôþäïõò öëåãìïíÞò. Óôï ðáñüí Üñèñï ðáñïõóéÜæïõìå Ýíá ðåñéóôáôéêü ìáëáêïðëáêßáò ôçò ïõñïäü÷ïõ êýóôçò 1 ÏõñïëïãéêÞ KëéíéêÞ, ÔæÜíåéï Ãåíéêü Íïóïêïìåßï ÐåéñáéÜ óõíäåüìåíçò ìå ðñï÷ùñçìÝíç áðïöñáêôéêÞ ïõ- 2  ÐáíåðéóôçìéáêÞ ÏõñïëïãéêÞ ÊëéíéêÞ, Óéóìáíüãëåéï ñïðÜèåéá. Ãåíéêü Íïóïêïìåßï Áìáñïõóßïõ Õðåýèõíïò åðéêïéíùíßáò: Kùíóôáíôßíïò Óôáìáôßïõ ÏõñïëïãéêÞ êëéíéêÞ, Ôæáíåéï ãåíéêü Íïóïêïìåßï ÐåéñáéÜ Óáëåðïýëá 2, 18536 ÐåéñáéÜò ôçë: 2104592387 - e-mail: [email protected] ËÝîåéò Åõñåôçñéáóìïý: Ìáëáêïðëáêßá, öëåãìïíþäçò íüóïò, ïõñïäü÷ïò êýóôç, íåöñéêÞ áíåðÜñêåéá. References 1. Ballesteros Sampol JJ. Urogenital malacoplakia. Report of 4 cases and review of the literature. ArchEsp Urol. 2001;54(8):768-76. 2. Gupta R, Mahajan A, Atri S, Gupta CL. Recurrent painless hematuria secondary to malacoplakia of the urinary bladder: a case report and review of literature. Urol J. 2013;10(1):821-3. 3. Bessim S, Heller DS, Dottino P, Deligdisch L, Gordon RE. Malakoplakia of the female genital tract causing urethral and ureteral obstruction. A case report. J Reprod Med. 1991;36(9):691-4. 56 Hellenic UROLOGY 4. Bylund J, Pais VM Jr. A case of acute renal failure caused by bilateral, multifocal malacoplakia lesions of the bladder and ureters. NatClinPract Urol. 2008;5(9):516-9. 5. Ristiæ-Petroviæ A, Stojnev S, Jankoviæ-Velickoviæ L, Marjanoviæ G. Malakoplakia mimics urinary bladder cancer: a case report. VojnosanitPregl. 2013;70(6): 606-8. CASE REPORT Emergency embolisation of a spontaneously ruptured angiomyolipoma in a solitary kidney Marios. Stavropoulos, Constantinos Bouropoulos, Nikolaos Ferakis, Iraklis Poulias Urological Clinic, Hellenic Red Cross Hospital Corresponding Author: Constantinos Bouropoulos Hellenic Red Cross Hospital Urological Clinic Athens 11526 - Tel: +30 2106414000 e-mail: [email protected] Summary Angiomyolipoma of the kidney is one of the most common causes of spontaneous renal bleeding. Here we present the case of a middle aged female patient, who presented with automatic rupture of a large angiomyolipoma in a solitary kidney. The patient was treated with selective angioembolisation (SAE), and was discharged in good condition with unaltered renal function. SAE provides an efficient control of haemorrhage in the acute stage, but it has limited value in long-term treatment of angiomyolipomas. In contrast, surgical treatment allow the full removal of the tumour, however it is associated with significant complications. Description of the case At admission, the patient was complaining of acute, sudden pain in the left lumbar region without any reference to prior injury. The patient did not present macroscopic haematuria and the urinalysis was normal. She had signs of hypobolaemic shock (pallor, sweating and coldness of the extremities). The medical history of the patient included nephrectomy of the right kidney following a diagnosis of renal cancer 5-years priory to the admission. Furthermore, she reported an 8 cm AML in the left kidney for which she was under surveillance with regular imaging tests (Fig. 1). Keywords Angiomyolipoma, Wunderlich syndrome, embolisation. Introduction The spontaneous, non-traumatic renal haemorrhage, also known by the term Wunderlich syndrome, was described for the first time in the middle of the 19th century1. It comprises an urgent clinical situation, which requires immediate treatment. The causes of automatic renal haemorrhage vary, with angiomyolipoma (AML) being the most common14. AMLs are mesenchymal neoplasms found almost exclusively in the kidney and are comprised of atypically developed blood vessels that are prone to the formation of aneurysms, smooth muscle fibbers and fatty tissue1. We describe the case of a 50-year-old patient with a history of previous right nephrectomy, which was presented to the emergency department with automatic rupture of an angiomyolipoma of the left kidney. Figure 1. CT Scan of the upper and lower abdomen after the application of intravenous contrast. The characteristic radiological image of a large angiomyolipoma with a largest diameter of 8 cm, is visible on the upper pole of the left kidney. (Image from an older CT scan, in the course of regular observation of the patient). Upon examination, the patient had a pulse of 110 bpm, systolic arterial pressure of 80mmHg and was non-feverish. Palpation of the left lumbar region resulted in intense sensitivity and pain. Laboratory test showed an 8.8g/dl and 26% levels of haemoglobin and haematocrit count respectively. Hellenic UROLOGY 57 M. Stavropoulos, C. Bouropoulos, N. Ferakis, I Poulias Serum creatinine level was at 1.2 mg/dl. Revitalisation took place immediately, with intravenous administration of fluids and colloidal solutions and transfusion. When the the patient's hemodynamic status was stabilized she underwent a CT scan of the upper and lower abdomen. The imaging test displayed the presence of a large retroperotoneal haematoma extended as far as the left iliac fossa, and the presence of a sizable AML on the upper pole of the left kidney (Fig. 2). Figure 2. CT scan of the upper and lower abdomen after the application of intravenous contrast. A sizable mass lesion resembling angiomyolipoma can be seen on the upper pole of the left kidney, and signs of haemorrhaging around the formation and the kidney. For diagnostic and therapeutical purposes, the patient was submitted to angiography: under local anaesthesia the right femoral artery was catheterised and under the guidance of an angiographic hydrophilic wire, a Cobra type angiographic catheter was placed. Via the catheterization of the left renal artery, and the subsequent angiogram, signs of haemorraging were found, the control of which was achieved with the appropriate placement of coils (Fig. 3). The patient was transfused with a total of two units of blood, and the treatment was not accompanied by any particular complications. The first hours after the embolisation the patient complained of mild pain located in the right abdominal area and presented low grade fever. Finally, the patient was discharged in a generally good condition three 58 Hellenic UROLOGY days later with a haemocrit at 36%, haemoglobin at 12.2 g/dl and serum creatinine at 1.0 mg/dl. The patient received instructions for retesting with a new angiogram and CT scan of the abdomen, and was scheduled for partial nephrectomy. Discussion AML are rarely malevolent tumours of the kidney. Their frequency in the community is less than 0.5%1. Approximately 20% of these tumours grow in patients with tuberous sclerosis1. However, the majority of AMLs (80%) appear as sporadic 1,3 tumours in the general population . Sporadic AML is more frequent in women (male to female ratio of 1:4) and especially those of middle and old age, and are usually solitary and contralateral1,3. In contrast, AMLs related to tuberous sclerosis appear at a younger age and are usually bilateral, multiple, and larger in size. AMLs displaying a large percentage of atypical blood vessels, those related with which tuberous sclerosis and large AMLs, are in higher risk of spontaneous rupture and perirenal 1-4 haemorrhage . CT scans of the abdomen are currently considering the imaging test of choice for the detection of perirenal haemorrhaging, with sensitivity as precise as 100%. CT scan is also highly accurate in the diagnosis of Wunderlicht syndrome attributable to 2 spontaneous ruptures of AMLs . Figure 3. Angiography of the left renal artery after embolisation. Spirals (as shown by the arrows) can be seen, as well as the blockage of the feeder vessels of the neoplasm. Emergency embolisation of a spontaneously ruptured angiomyolipoma in a solitary kidney Wunderlich syndrome constitutes a potentially fatal complication of the AML rupture. It can occur in up to 50% of patients and more precisely in those with tumours larger than 4 centimetres in diameter. Of note, 33% of patients with AML related renal blee4 ding may suffer from hypobolaemic shock . The clinical picture involves the three classic symptoms, such as pain in the lower lumbar region, sensitivity during palpation and signs of hypobolae1,2 mic schock (Lenk's triad) . Patients with AML that display symptoms such as pain and haemorrhaging, or those for whom there is a suspicion of malevolence, require therapeutic treatment. Prophylactic intervention is excusable for large tumours (usually larger than 4 centimetres, although the size is disputed), in woman of reproductive age and in cases of insufficient provision of emergency medical care or regular 5 check-ups . Non-symptomatic AMLs with a diameter of up to 4 centimetres are usually placed under active surveillance with imaging techniques. Several authors suggest the same treatment for patients with nonsymptomatic AML greater than 8 centimetres in diameter and those with symptomatic tumours 1,3,5,6 greater than 4 centimetres . The two main therapeutic choices for the treatment of spontaneous renal bleeding associated with automatic rupture of angiomyolipomas involve 5,6 surgery and selective angioembolisations (SAE) . Most usual methods of surgical treatment are the conventional open nephrectomy and the partial nephrectomy. Less invasive techniques such as laparoscopic or robotically-assisted partial nephrectomy, high-frequency thermotherapy (RF), cryotherapy, as well as conservative methods such as the administration of antiangiogenic agents (mTOR inhibitors) have been developed over the 1,3,4,5 last few years . However, the ideal therapeutic method is not known. In fact, few randomized or prospective comparative studies examining surgical treatment and SAE exist in the international literature. Furthermore, guidelines regarding this specific subject are somehow unclear and therefore the choice of the right treatment is difficult. Many factors such as the effectiveness and the morbidity of each method, the renal function of the patient, the characteristics of the tumour and the preferences of the patient and the surgeon must all be taken into consideration. The benign nature of AML suggests the adoption, of -as much as possible- nephron sparing interventions. Under the light of this evidence, SAE constitutes the least invasive method with commonly a shorter treatment period than that is required with the conventional surgical treatments 5-8. Nowadays, SAE is considered as the first line treatment of acute haemorrhaging after an AML rupture since it can safely control bleeding stabilizing thus the patient quickly. Besides, the related to SAE blood loss is limited. SAE can lower the risk of AML haemorrhage without placing the renal function in danger, even in 5-8 patients with pre-existing renal insufficiency . The presence of multiple nutrient vessels renders the embolisation of the tumour more difficult technically and increases the risk of healthy renal tissue damage6. Finally, SAE can be performed preoperatively in cases of large AMLs in order to lower the loss of blood during surgery, while it could be offered in large AML in which partial nephrectomy it is not possible 3,5. SAE can be effective in the control of acute haemorrhaging from AML, although it has limited value as a long-term treatment. In fact, the tumour continues to exist after embolisation, despite its sizable reduction (about 40-50%)5. Tumours relapse (increase in size, or haemorrhage) may occur, mainly in patients with tuberous sclerosis and thus, further embolisation may be required. Consequently, such patients require long-term observation. Complications of SAE usually involve symptoms after embolisation (pain, fever, nausea), which are the most common, being found in 85% of cases, whilst necrosis of tissue and the formation of Hellenic UROLOGY 59 M. Stavropoulos, C. Bouropoulos, N. Ferakis, I Poulias abscesses is rarer. The frequency of complications 5-8 is independent of the materials used . On the other hand, surgical forms of treatment offer the possibility of a complete removal of the tumour and present exceptionally low rates of relapse. The observation period for these patients is shorter than that required after embolisation, a fact that is favourable, especially for younger patients4,5. However, the complications of surgical intervention, whilst they are rare, are more serious, a fact that is extremely important if we consider that surgery treats a benign illness. These includes renal haemorrhage, injury of the renal pelvis, urinoma and the formation of fistulas. Generally, radical nephrectomy for the removal of AML should be avoided where possible. In the limited cases where radical nephrectomy is considered, it is either because the AML comprise a large component of the renal tissue; when nephron sparing techniques are not available or due to the 5,8 strong suspicion of malevolence in the AML . In conclusion, it is worth mentioning that therapeutic treatment of AML is a complex process, especially when regards large or multiple tumours. Surgical forms of treatment, along with SAE, comprise the cornerstone of treatment of AML. SAE offers effective control of haemorrhaging in the acute phase, but has limited value in the long term treatment of AML. In contrast, partial nephrectomy is accompanied by exceptionally low rates of relapse of the illness and offers a more radical treatment. Although it presents more complications than SAE, we believe that it should comprise the method of choice when the specific characteristics of the illness allow it. Prospective, randomized comparative studies between the two methods are required, in order to determine their effects with precision. 60 Hellenic UROLOGY Ðåñßëçøç Åðåßãùí åìâïëéóìüò ìåôÜ áðü ñÞîç áããåéïìõïëéðþìáôïò óå ìïíÞñç íåöñü Ì. Óôáõñüðïõëïò, Ê. Ìðïõñüðïõëïò, Í. ÖåñÜêçò, Ç. Ðïýëéáò ÏõñïëïãéêÞ ÊëéíéêÞ Íïóïêïìåßïõ Åëëçíéêïý Åñõèñïý Óôáõñïý Õðåýèõíïò åðéêïéíùíßáò: Ìðïõñüðïõëïò Êùíóôáíôßíïò Íïóïêïìåßï Åëëçíéêïý Åñõèñïý Óôáõñïý ÏõñïëïãéêÞ ÊëéíéêÞ, 11526 ÁèÞíá Tçë: +30 2106414000 - email: [email protected] Ôï áããåéïìõïëßðùìá ôïõ íåöñïý áðïôåëåß ìéá áðü ôéò ðéï óõ÷íÝò áéôßåò ðïõ ìðïñïýí íá ðñïêáëÝóïõí áõôüìáôç ðåñéíåöñéêÞ áéìïññáãßá. ÐáñïõóéÜæïõìå ôçí ðåñßðôùóç ìéáò ãõíáßêáò áóèåíïýò, ìÝóçò çëéêßáò, ðïõ ðáñïõóéÜóèçêå ìå áõôüìáôç ñÞîç åíüò ìåãÜëïõ áããåéïìõïëéðþìáôïò óå ìïíÞñç íåöñü. Ç áóèåíÞò áíôéìåôùðßóèçêå ìå åêëåêôéêü áããåéáêü åìâïëéóìü (ÅÁÅ) êáé åîÞëèå óå êáëÞ êáôÜóôáóç ìå áíåðçñÝáóôç íåöñéêÞ ëåéôïõñãßá. Ï ÅÁÅ ðñïóöÝñåé áðïôåëåóìáôéêü Ýëåã÷ï ôçò áéìïññáãßáò óôçí ïîåßá öÜóç, áëëÜ Ý÷åé ðåñéïñéóìÝíç áîßá óôçí ìáêñïðñüèåóìç áíôéìåôþðéóç ôùí ÁÌË. Ïé ÷åéñïõñãéêÝò ìïñöÝò áíôéìåôþðéóçò åðéôñÝðïõí ôçí ðëÞñç áöáßñåóç ôïõ üãêïõ, áëëÜ åìöáíßæïõí óçìáíôéêüôåñåò åðéðëïêÝò. ËÝîåéò åõñåôçñéáóìïý: áããåéïìõïëßðùìá, óýíäñïìï Wunderlich, åìâïëéóìüò Emergency embolisation of a spontaneously ruptured angiomyolipoma in a solitary kidney References 1. Óôáõñüðïõëïò Ì, Ìðïõñüðïõëïò Ê, Ðïýëéáò Ç. Áõôüìáôç ñÞîç íåöñïý: áéôéïëïãßá, äéÜãíùóç êáé èåñáðåõôéêÞ áíôéìåôþðéóç. ÅëëçíéêÞ Ïõñïëïãßá 2012, 24:247-54. 5. Faddegon S, SO A. Treatment of angiomyolipoma at a tertiary care centre: the decision between surgery and angioembolization. Can Urol Assoc J 2011, 5: 138-141. 2. Parameswaran B, Khalid M, Malik N. Wunderlich syndrome following rupture of a renal angiomyolipoma. Ann Saudi Med 2006, 26:310-12. 6. Chatziioannou A, Gargas D, Malagari K, Kornezos I, Ioannidis I, Primetis E, et al. Transcatheter arterial embolization as therapy of renal angiomyolipomas: the evolution in 15 years of experience. Eur J Radiol 2012, 81:2308-12. 3. Coskuner E R, Ozkan B, Yalcin V. The role of partial nephrectomy without arterial embolization in giant renal angiomyolipoma. 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