The Natural History of Peyronie s Disease: An Ultrasonography-Based Study

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1 european urology 53 (2008) available at journal homepage: Sexual Medicine The Natural History of Peyronie s Disease: An Ultrasonography-Based Study Athanasios Bekos a, Mary Arvaniti b, Konstantinos Hatzimouratidis a, Kyriakos Moysidis a, Vasilios Tzortzis a, Dimitrios Hatzichristou a, * a Center for Sexual and Reproductive Health and 2nd Department of Urology, Papageorgiou General Hospital, Aristotle University of Thessaloniki, Greece b Department of Radiology, George Gennimatas General Hospital, Thessaloniki, Greece Article info Article history: Accepted July 9, 2007 Published online ahead of print on July 17, 2007 Keywords: Penile induration Ultrasonography Natural history Abstract Objectives: To define ultrasonographic patterns reflecting different states of Peyronie s disease (PD) and to use them to evaluate the natural history of the disease. Material and methods: Diagnosis of PD was based on medical and sexual history, physical examination, intracavernosal injection test, and penile ultrasonography. Patients with penile fracture history were excluded from the study. Three groups were formed according to ultrasonographic patterns: solitary hyperechoic lesion without acoustic shadow (group A), moderately hyperechoic multiple scattered calcified lesions with acoustic shadows (group B), dense calcified hyperechoic plaque with acoustic shadow (group C). All patients entered a watchful waiting protocol for 1 yr followed by a new penile ultrasonography. Results: Ninety-five 95 patients with PD were included in the study (mean age, yr; mean duration of disease, mo). Risk factors associated with cardiovascular disease were present in 79 of 95 patients (83.16%). Eleven (11.6%), 35 (36.8%), and 49 (51.6%) patients were classified into groups A, B and C, respectively. At the end of the study, in group A, reduction of fibrotic lesions and curvature angle was noticed in 9 of 11 (81.8%) patients, whereas plaque formation was noticed in 2 of 11 (18.2%) patients. In group B, plaque and curvature reduction was noticed in 15 of 35 (42.9%) and 12 of 35 (34.3%) respectively, whereas in the rest a dense calcified plaque was noticed. In group C, no ultrasonographic evidence of improvement was noticed; curvature angle was reduced in 4 of 49 (8.2%), owing to the extension of the plaque circumferentially. Significant hemodynamic changes were noticed at the two time points tested (30.53% diagnosed with vascular disease at baseline vs % at the end of the study, p = 0.03). Conclusions: Corporal ultrasonography in patients with PD allows objective evaluation and classification of disease. The density of echogenic areas and presence of acoustic shadows are predictors of disease stability. # 2007 Published by Elsevier B.V. on behalf of European Association of Urology. * Corresponding author. 77 Mitropoleos Str, Thessaloniki, Greece. Tel ; Fax: address: hatzichr@med.auth.gr (D. Hatzichristou) /$ see back matter # 2007 Published by Elsevier B.V. on behalf of European Association of Urology. doi: /j.eururo

2 european urology 53 (2008) Introduction Peyronie s disease is a connective tissue disorder, characterized by the formation of a fibrotic lesion or plaque in the tunica albuginea, which leads to penile deformity [1,2]. Although a benign condition, it affects sexual intercourse capabilities, predominantly in middle-aged men [3,4]. The natural history of the disease is poorly defined. Although initial reports presented a high spontaneous resolution rate of 50% [5], this finding was not confirmed by other studies [6,7]. In fact, spontaneous resolution seems to be uncommon, with the majority of patients experiencing disease progression. Although multiple conservative therapies have been offered for the treatment of the disease, their efficacy remains questionable because welldesigned, placebo-controlled trials have failed to demonstrate favorite results [8,9]. The main methodological problem of the published studies is the heterogeneity of the study samples, owing to the polymorphism of the lesions and the lack of a classification system for the disease. Surgical treatment on the other hand, the gold standard method for stabilized disease [10 12], suffers from the lack of robust data to provide objective criteria of progress discontinuation [13]. The necessity of an objective classification system that can predict clinical outcome is apparent [14]. Several imaging techniques have been used to visualize the ultrastructural alterations associated with the disease. Ultrasonography, however, has been reported to be the method of choice because it is cost-effective and can determine both morphological patterns and corporal hemodynamic status [15,16]. The objective of the present prospective study was to develop a classification system by defining ultrasonographic patterns reflective of different states of the disease, which may predict clinical outcome. The overall aim was to assess this classification system to offer data on the natural history of Peyronie s disease. Fig. 1 Ultrasonographic type A: solitary existence of a hyperechoic lesion without acoustic shadow. The study was approved by the ethical committee and all patients signed an inform consent. Color Doppler ultrasonography was performed with the patient in the supine position by means of a 7.5 MHz transducer (Sonoline TM, General Electric) in transverse and longitudinal orientations by a trained radiologist who was blind to the patient symptoms. Penile vascular assessment included measurement of peak systolic (PSV) and end diastolic velocity (EDV) as well as calculation of the resistance index (RI). Arteriogenic ED was defined as PSV < 25 cm/s, and venoocclusive dysfunction as EDV > 5 cm/s and/or RI < 0.7. Ultrasonographic evaluation of size, location, and morphological patterns of the lesions was recorded. Patients were categorized into three groups on the basis of distinct ultrasonographic patterns: group A included patients with the existence of a solitary hyperechoic lesion without acoustic shadow (Fig. 1). Group B included patients with moderately hyperechoic, 2. Material and methods The study sample was formed from consecutive patients who visited our andrology outpatient clinic complaining of plaque formation within the corpora cavernosa and/or penile deviation. Diagnosis of Peyronie s disease was based on medical and sexual history, physical examination, intracavernosal injection (ICI) of a vasoactive agent (tri-mix: 30 mg/ml papaverine, 1 mg/ml phentolamine, and 10 mg prostaglandin E1), and penile ultrasonography under conditions of complete smooth muscle relaxation (a second injection of tri-mix was performed if necessary). Patients with history of penile fracture but not penile trauma were excluded from the study. Fig. 2 Ultrasonographic type B: moderately hyperechoic multiple scattered calcified lesions with acoustic shadows.

3 646 european urology 53 (2008) Results Fig. 3 Ultrasonographic type C: dense calcified hyperechoic plaque with acoustic shadow. multiple, scattered calcified lesions with acoustic shadows (Fig. 2). Finally, group C included patients with the presence of a dense calcified hyperechoic plaque with acoustic shadow (Fig. 3). All patients entered a watchful waiting protocol for 1 yr. Twelve-month follow-up included medical and sexual history, physical examination, and penile ultrasonography before and after ICI. Changes in plaque, penile curvature, ultrasonographic patterns, and vascular status were recorded. Ultrasonography was performed by the same radiologist who was blind to the category to which patients were assigned. Baseline and follow-up continuous parameters were compared statistically with the use of the two-tailed Student t test, whereas categorical variables were compared with the use of the chisquare test. A total of 95 patients with Peyronie s disease were included in the study (mean age, yr; range, 44 75). The mean duration of the disease was mo. Pain during erection was reported by 15 of 95 (15.8%) patients. The lesion was located in the dorsal, ventral, and lateral surface of the penis in 55 (57.9%), 24 (25.3%), and 16 (16.8%) patients, respectively. Plaque dimension in length ranged from 0.4 to 3.7 cm, and penile curvature ranged from 108 to 758. No association was noticed between the dimensions of the plaque and the angle of the curvature ( p = 0.17). Medical history revealed presence of or risk factors associated with cardiovascular disease (CVD) in 79 of 95 (83.16%) of the study sample (Table 1). Color Doppler ultrasonography revealed penile vascular disease in 29 of 95 (30.53%) of the patients (Table 2). Eleven (11.6%), 35 (36.8%), and 49 (51.6%) patients were classified into groups A, B, and C, respectively. No statistical significant differences for age or duration of disease were noticed between the three groups ( p = 0.43). Pain was reported by 3 of 11 (27.3%), 6 of 35 (17.14%), and 6 of 49 (12.24%) in groups A, B, and C, respectively. Inability for intercourse was reported by 4 of 11 (36.36%) patients in group A, 20 of 35 (57.14%) in group B, and 36 of 49 (73.47%) in group C. Patients were reassessed ultrasonographically after 12 mo. In group A, reduction of fibrotic lesions and curvature angle was noticed in 9 of 11 (81.8%) patients (Table 2). In 2 of 11 (18.2%) patients, a plaque had formed (typical for Peyronie s disease with the presence of acoustic shadow). In group B, plaque and Table 1 Cardiovascular risk factors in the study groups CV risk factors Overall Group A Group B Group C Diabetes 21/95 (22.1%) 1/11 (9.1%) 7/35 (20%) 13/49 (26.53%) Hypertension 32/95 (33.68%) 2/11 (18.18%) 12/35 (34.28%) 18/49 (36.73%) CVD 18/95 (18.95%) 0/11 (0%) 6/35 (17.14%) 12/49 (24.49%) Hypercholesterolemia 19/95 (20%) 2/11 (18.18%) 7/35 (20%) 10/49 (20.41%) Smoking history 67/95 (70.5%) 7/11 (63.63%) 27/35 (77.14%) 33/49 (67.35%) No risk factors 16/95 (16.84%) 4/11 (36.36%) 7/35 (20%) 5/49 (10.2%) CV, cardiovascular; CVD, cardiovascular disease. Table 2 Size of the plaque and curvature at baseline and follow-up Mean penile plaque size (range) Mean curvature (range) At baseline At 12 mo At baseline At 12 months Group A 0.9 cm ( ) 0.6 cm ( ) 208 ( ) 138 ( ) Group B 1.6 cm ( ) 2.1 cm ( ) 428 ( ) 368 ( ) Group C 2.2 cm ( ) 2.8 cm ( ) 538 ( ) 578 ( )

4 european urology 53 (2008) Table 3 Penile hemodynamic characteristics in the study groups Penile vascular disease Overall Group A Group B Group C At baseline 29/95 (30.53%) 1/11 (9.1%) 11/35 (31.43%) 17/49 (34.69%) At 12 mo 44/95 (46.32%) 2/11 (18.18%) 17/35 (48.57%) 25/49 (51%) curvature reduction was noticed in 15 of 35 (42.9%) and 12 of 35 (34.3%) patients, respectively (Table 2). All 12 patients with curvature reduction also showed a reduction in plaque size. In the remaining 20 of 35 (57.1%) patients, a dense calcified plaque was noticed. In group C, no ultrasonographic evidence of improvement was noticed. The plaque size remained unchanged or increased in all patients, whereas the curvature angle was reduced in 4 of 49 (8.2%) owing to the extension of the plaque circumferentially (Table 2). Significant penile hemodynamic changes were noticed (Table 3). At the end of the study, 44 of 95 (46.32%) patients were diagnosed as having penile vascular disease (Table 2) versus 29 of 95 (30.53%) at baseline ( p = 0.03). No prognostic factors were identified for disease progression, other than the presence of wellknown risk factors for CVD. 4. Discussion Although diagnosis of Peyronie s disease is relatively easy and is history-based, the exact pathogenesis and physical history of the disease remain questionable, creating therapeutic dilemmas, especially whether the indication for surgical correction is certain. Many theories have been proposed, including vitamin E deficiency, infections, arterial disease, use of beta-blocking agents, autoimmune cause, and genetic predisposition [8]. The most widely accepted theory, however, attributes the histological findings and symptoms to the effect of penile trauma during intercourse. Devine et al [1] proposed that either acute trauma or repetitive trauma during coitus might result in delamination between the layers of the tunica albuginea and microvascular injury, which causes hemorrhage into the intralaminar space. As the resulting clot is reabsorbed, fibrin remains in the injured tissue, activating fibroblasts and inflammatory mediators within the site. The final result is production and accumulation of collagen at the site of the injury. Tumor growth factor (TGF)-beta-1 seems to play an important role by regulating inflammatory immune responses and the tissue repair process. Autoinduction of TGF-beta-1, owing to environmental insults, has been described to be associated with the onset of the vicious cycle of tissue repair, a process that leads to fibrosis [17]. In analyzing the tunica albuginea from patients with Peyronie s disease and from impotent patients who had penile prosthesis surgery, El Sakka et al [18] found a TGF-beta-1 overexpression in the majority of patients with Peyronie s disease. These data suggest that although the etiology of Peyronie s disease remains controversial, activation of the TGF-beta-1 molecular pathway may be the pathogenetic mechanism of the disease [19]. The disease process includes sparse fibrotic lesions followed by fibrotic plaque formation, whereas the calcification process starts later on different distinct areas of the fibrotic plaque [20]. Complete calcification of the plaque is considered a sign of chronic stabilized disease state. The majority of patients with Peyronie s disease usually give an accurate description of their deformity, and penile palpation commonly confirms the diagnosis [2]. Photographs taken by the patients and pharmacological erection are useful to objectively determine the degree of penile deviation. Most of the plaques, as our study confirmed, are situated in the dorsal surface of the penis, rendering palpation easier [21]. Several imaging techniques, including X-ray, computed tomography (CT), and magnetic resonance imaging (MRI), have been used in an effort to distinguish different disease stages, especially stabilization of the disease, thus allowing a urologist to consider surgical management [22]. Ultrasonography has been used in the present study because it is capable of identifying minimal lesions as well as signs of stabilized disease. CT does not seem to have an important role in diagnosis, whereas MRI can provide additional information about inflammation status and plaque formation at penile basis but not calcification. Therefore, ultrasonography is considered the method of choice in the diagnosis and follow-up evaluation of patients with Peyronie s disease [15,22 24]. Furthermore, color Doppler ultrasonography before and after ICI provides a dynamic, minimally invasive, functional assessment of penile vasculature to evaluate potency status of the patients [25,26]. In the present study, ultrasonographic findings were evaluated in an attempt to identify the different stages of the disease and to correlate them with the natural history of the disease and therefore treatment outcome. The classification was based on the lesions echoic characteristics analysis: (1)

5 648 active phase consisting of painful erections and a gradual bending of the penis. However, pain may not be the presenting clinical sign in most patients with Peyronie s disease. Whether the onset of deformity associated with the active phase is gradual or sudden, the pain resolves and the pathologic process seems to stabilize after mo. A secondary phase follows, which is characterized by painless stable deformity [6]. Williams and Thomas [5] reported spontaneous resolution of penile plaques in 50% of patients (only 12 patients included in the study), whereas pain was resolved in all 3 men who reported pain between 7 and 24 mo after presentation. The natural history of Peyronie s disease was also evaluated in 97 men by Gelbard et al [6]. Disease duration ranged from 3 mo to 8 yr. Approximately 40% of the patients found pain, bending, ability for intercourse, and overall effects to be unchanged during the course of the disease. Bending and ability for intercourse worsened in 40% of the patients during the same interval, whereas only 6% had worsening of pain. Overall, 13% of the patients believed the disease to be one of gradual resolution, 47% believed there had been little or no change, and 40% believed that the disease pattern was one of gradual progression. The authors concluded that there was no significant association between disease duration and spontaneous improvement in penile bending. However, this study was based on patient self-reports using a nonvalidated questionnaire. In a retrospective study of 63 of 307 men who presented with the acute phase of Peyronie s disease, Kadioglu et al [7] reported progression in 30.2%, stabilization in 66.7%, and spontaneous resolution in 3.2% without any treatment after a mean of 8.4 mo. The duration of Peyronie s disease in this study was mo. Recently, Mulhall et al [28] presented an analysis of the natural history of Peyronie s disease in a cohort of 246 patients who were followed a mean of 14.5 mo. Penile pain resolved in the majority of patients (89%) by 12 mo after presentation. However, curvature improved in only 12% of patients, whereas 40% remained stable and 48% had worsened at follow-up. The duration of Peyronie s disease in this study was mo. Penile vascular disease was common in our study group because it was expected owing to the presence of cardiovascular risk factors or diseases in most of our patients. Our findings suggest that significant hemodynamic changes were noticed at the two time points tested (12 mo apart). Because the known mechanisms for penile vascular damage associated with Peyronie s disease are either obstruction of the cavernosal arteries by the plaque formation or site-specific veno-occlusive dysfunceuropean urology 53 (2008) intensity of the echogenicity; (2) existence of acoustic shadow; and (3) density of echogenic areas. Three distinct ultrasonographic patterns were identified, which correspond to three different stages of Peyronie s disease. Ultrasonographic type A described patients with hyperechoic lesions without any acoustic shadow, reflective of a fibrotic process before solid plaque formation and calcification. The usual course of Peyronie s disease has two distinct phases: an early phase in which the plaque is new, still in formation with associated inflammation, and a late phase in which the plaque is relatively stable with extensive fibrosis and finally calcification. Although it is unknown if this was an initial lesion, this pattern seems to correspond to the initial phase of Peyronie s disease. After 12 mo, reduction of fibrotic lesions and angle of curvature was noticed in 81.8% of the patients; in therest, a plaque typical for Peyronie s disease, with the presence of acoustic shadow, was demonstrated. Our findings clearly suggest that, in patients with such ultrasonographic characteristics, an observational period is mandatory because there is a potential to reverse ultrastructure alterations and therefore penile deviation [27]. Ultrasonographic type B described patients with a rather solid hyperechoic lesion, which might have contained scattered calcified lesions with acoustic shadows. After 12 mo, reduction in plaque and curvature was noticed in 12 of 35 (34.3%), whereas, in 3 more patients, plaque reduction was noticed but without improvement in the angle of the deviation. In the remaining 20 of 35 (57.1%) patients in this group, a dense calcified plaque was noticed. Our results suggest that prediction in patients with scattered calcified lesions is uncertain, and other pathogenetic factors and environmental insults will determine either disease progression or remission. In this group of patients, an observational period is also mandatory, even though patients may be informed that, in most cases, progression will be noticed. Finally, ultrasonographic type C described patients with a dense calcified hyperechoic lesion with acoustic shadow. After 12 mo, no ultrasonographic evidence of improvement was noticed. The plaque size remained unchanged in all but 4 patients (4 of 49, 8.2%), whereas the curvature angle was reduced owing to the extension of the plaque circumferentially (ring-type lesion). This pattern reflects the final stage of Peyronie s disease with disease stabilization. In such patients, observation seems irrational and surgical intervention must be considered earlier. The natural history of Peyronie s disease is poorly defined. In most cases, onset is associated with an

6 european urology 53 (2008) allows objective evaluation and classification of disease. The density of echogenic areas and the presence of acoustic shadows are predictors of the disease s stability. Spontaneous resolution may be highly expected in only the acute phase, before solid plaque formation and calcification. This classification system may also be used to predict clinical outcome after treatment. Conservative treatment, if there is a role, may be exclusively offered in the acute phase, whereas surgical intervention seems necessary in stabilized disease. Conflicts of interest The authors have nothing to disclose. Fig. 4 Proposed management strategy for Peyronie s disease based on the proposed ultrasonographic classification system. tion at the fibrotic site of the tunica albuginea, it is postulated that the main factor determining penile hemodynamics was the high prevalence of cardiovascular risk factors in our study sample, rather than alterations due to ultrastructural changes within the corporal body [29]. The present study is the first study to offer data on the natural history of Peyronie s disease in terms of ultrastructural changes as they appear by time using ultrasonography, as well as penile hemodynamic changes over time. It is a well-documented imaging modality for Peyronie s disease used to objectively define different morphological patterns of the disease. The three ultrasonographic patterns described reflect different stages of the disease from the acute phase to the stabilized one. Although spontaneous resolution may be expected in the acute phase, this is not the case in stabilized disease. This objective classification system also may be able to predict clinical outcome. Patients in the acute phase may benefit from conservative therapy, whereas, in patients with stabilized disease, the only treatment option may be surgical intervention (Fig. 4). These data may explain the wide discrepancy in the results of several conservative treatments published in the literature. 5. Conclusions This is the first ultrasonographic study on the natural history of Peyronie s disease. Corporal ultrasonography in patients with Peyronie s disease References [1] Devine Jr CJ, Somers KD, Jordan SG, Schlossberg SM. Proposal: trauma as the cause of the Peyronie s lesion. J Urol 1997;157: [2] Pryor J, Akkus E, Alter G, et al. Peyronie s disease. J Sex Med 2004;1: [3] Mulhall JP, Creech SD, Boorjian SA, et al. Subjective and objective analysis of the prevalence of Peyronie s disease in a population of men presenting for prostate cancer screening. J Urol 2004;171: [4] Sommer F, Schwarzer U, Wassmer G, et al. Epidemiology of Peyronie s disease. Int J Impot Res 2002;14: [5] Williams JL, Thomas GG. The natural history of Peyronie s disease. J Urol 1970;103:75 6. [6] Gelbard MK, Dorey F, James K. The natural history of Peyronie s disease. J Urol 1990;144: [7] Kadioglu A, Tefekli A, Erol B, Oktar T, Tunc M, Tellaloglu S. A retrospective review of 307 men with Peyronie s disease. J Urol 2002;168: [8] Greenfield JM, Levine LA. Peyronie s disease: etiology, epidemiology and medical treatment. Urol Clin North Am 2005;32: [9] Hauck EW, Diemer T, Schmelz HU, Weidner W. A critical analysis of nonsurgical treatment of Peyronie s disease. Eur Urol 2006;49: [10] Ralph D. For the motion: surgery is the best choice for Peyronie s disease. Eur Urol 2006;49:1127, discussion 9. [11] Ralph DJ. The surgical treatment of Peyronie s disease. Eur Urol 2006;50: [12] Kadioglu A, Akman T, Sanli O, Gurkan L, Cakan M, Celtik M. Surgical treatment of Peyronie s disease: a critical analysis. Eur Urol 2006;50: [13] Hauck EW. Against the motion: surgery is the best choice for Peyronie s disease. Eur Urol 2006;49:1128. [14] Levine LA, Greenfield JM. Establishing a standardized evaluation of the man with Peyronie s disease. Int J Impot Res 2003;15(Suppl 5):S [15] FornaraP, Gerbershagen HP. Ultrasound inpatients affected with Peyronie s disease. World J Urol 2004;22:365 7.

7 650 european urology 53 (2008) [16] Kendirci M, Nowfar S, Gur S, Jabren GW, Sikka SC, Hellstrom WJ. The relationship between the type of penile abnormality and penile vascular status in patients with peyronie s disease. J Urol 2005;174:632 5, discussion 5. [17] Davila HH, Ferrini MG, Rajfer J, Gonzalez-Cadavid NF. Fibrin as an inducer of fibrosis in the tunica albuginea of the rat: a new animal model of Peyronie s disease. BJU Int 2003;91: [18] El-Sakka AI, Hassoba HM, Pillarisetty RJ, Dahiya R, Lue TF. Peyronie s disease is associated with an increase in transforming growth factor-beta protein expression. J Urol 1997;158: [19] Hauck EW, Hauptmann A, Schmelz HU, Bein G, Weidner W, Hackstein H. Prospective analysis of single nucleotide polymorphisms of the transforming growth factor beta-1 gene in Peyronie s disease. J Urol 2003;169: [20] Vande Berg JS, Devine Jr CJ, Horton CE, et al. Mechanisms of calcification in Peyronie s disease. J Urol 1982;127:52 4. [21] Smith CJ, McMahon C, Shabsigh R. Peyronie s disease: the epidemiology, aetiology and clinical evaluation of deformity. BJU Int 2005;95: [22] Hauck EW, Hackstein N, Vosshenrich R, et al. Diagnostic value of magnetic resonance imaging in Peyronie s disease a comparison both with palpation and ultrasound in the evaluation of plaque formation. Eur Urol 2003;43: [23] Andresen R, Wegner HE, Miller K, Banzer D. Imaging modalities in Peyronie s disease. An intrapersonal comparison of ultrasound sonography, X-ray in mammography technique, computerized tomography, and nuclear magnetic resonance in 20 patients. Eur Urol 1998;34: [24] Mander A, Palleschi G, Gentile V, et al. Early echographical assessment of minimal lesions of cavernosum corpora and tunica albuginea in subjects with erectile dysfunction, suggestive of La Peyronie s disease. Int J Impot Res 2006;18: [25] Levine LA, Coogan CL. Penile vascular assessment using color duplex sonography in men with Peyronie s disease. J Urol 1996;155: [26] Schaeffer EM, Jarow Jr JP, Vrablic J, Jarow JP. Duplex ultrasonography detects clinically significant anomalies of penile arterial vasculature affecting surgical approach to penile straightening. Urology 2006;67: [27] Dohle G. Peyronie s disease: can we prevent disease progression? Eur Urol 2006;49: [28] Mulhall JP, Schiff J, Guhring P. An analysis of the natural history of Peyronie s disease. J Urol 2006;175:2115 8, discussion 8. [29] Deveci S, Palese M, Parker M, Guhring P, Mulhall JP. Erectile function profiles in men with Peyronie s disease. J Urol 2006;175: Editorial Comment on: The Natural History of Peyronie s Disease: An Ultrasonography-Based Study Kevin T. McVary Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA k-mcvary@northwestern.edu Peyronie s disease is an acquired disease of the tunica albuginea surrounding the corpus cavernosa of the penis that has a highly variable course and the affects approximately 3% of the male population. It is this variable clinical course that this paper attempts to address with the use of penile ultrasonography to differentiate those who are likely to progress and those unable to improve versus those with more transient disease [1]. Because of this variable presentation, course, and progression, Peyronie s disease has been the unfortunate victim of multiple untested therapies of dubious quality. It is this inability to predict who improves, who stabilizes, and who progresses that has allowed the charlatan s creep of quasi-medicine into the treatment armamentarium of Peyronie s disease. The authors are to be commended for their attempts to make better sense of patient stratification using ultrasonic appearance as one identifiable marker of progression. It is apparent that the follow-up of those with the worst disease at baseline have little prospect of improvement. This is useful to the practitioner because surgical treatment should be advised earlier rather than the typical delay prior to any definitive intervention. It is surprising to read the marked amount of vascular disease in the three cohort groups. One explanation is that this patient population has an unrecognized progressive vasculopathy that puts them at risk for Peyronie s disease in the first place. Another possibility is that Doppler measurements have inherent inaccuracies leading to over-read vasculopathy. The true utility of this investigation is to address how the ultrasound alterations correlated to clinical improvement of curvature. Without such knowledge of clinical outcome then the ultrasound tool becomes more of a radiographic curiosity with no clinical impact. The authors identified a reduction in fibrotic lesions and curvature in > 80% of men in group A. A more modest reduction in plaque and curve was found in 43% of group B and, of course, group C had no ultrasonographic improvement and likewise more progressive disease. These results support the concept that ultrasound appearance at presentation might allow an algorithm to stratify risk of progression or remission and improve patient flow and outcome.

8 european urology 53 (2008) The authors believe that the ultrasonographic pattern in men in group A with hyperechoic lesions and no acoustic shadow suggest a fibrotic process occurring before solid plaque formation and calcification. This is a logical explanation but the reader should be aware that it does not confirm that an early lesion progresses to plaque formation. The implications for plaque calcification are not fully elucidated, but it remains possible that the ultrasonic pattern noted in group A may, in fact, be the initial phase of the Peyronie s disease. Reference [1] Bekos A, Arvaniti M, Hatzimouratidis K, Moysidis K, Tzortzis V, Hatzichristou D. The natural history of Peyronie s disease: an ultrasonography-based study. Eur Urol 2008;53: DOI: /j.eururo DOI of original article: /j.eururo