Peyronie's Disease Plaque Research Articles

The Surgical Treatment of Peyronie's Disease: Replacement of Plaque by Free Autograft of Buccal Mucosa

Objectives: The aim of this work was the evaluation of clinical results of the use of buccal mucosa for replacement of Peyronie's disease plaque. Patients and methods: Twenty-six patients with Peyronie's disease were under observation. All the patients underwent the following investigations before and periodically within 3 years after the treatment: International Index of Erectile Function (IIEF-5), manual examination of plaque, autophotography of erect penis, conventional and power color Doppler sonography of penis, Peno-Brachial Index (PBI) before and its increase (IPBI) after the intracavernous injection of papaverin, Peak Systolic Velocity (PSV), end diastolic velocity (EDV), Resistance Index (RI), Sexual Encounter Profile questions (SEP-2 and SEP-3), measurements of penile length and curvature angle in the phase of rigidity. After stabilization in plaque's development (mean time 2.0 ± 0.1 years) the patients underwent a surgery by means of excision of plaque and its replacement by free autograft of buccal mucosa. Results: After the surgical treatment (with mean follow up observation of 3.2 ± 0.1 years) in 24 patients out of 26 (92.3%) the complete straightening of penis occurred, in two (7.7%) cases a residual curvature (<10°) remained, in four patients (15.4%) the shortening of penis (by 1 cm) and in two patients (7.7%) a partial reduction of erectile power were observed. Conclusion: Buccal mucosa showed high properties of adaptation and revascularization, good anatomical and functional clinical results by replacement of indurative plaque, it kept a stable elasticity without shrinkage; the method is simple and can be recommended for wide use in clinics for surgical treatment of Peyronie's disease.

Comparison of gene expression profiles between Peyronie's disease and Dupuytren's contracture

Objectives To compare the gene expression alterations in human Peyronie's disease (PD) and Dupuytren's disease (DD) to determine whether they share a common pathophysiology. Multiple mRNA expression profiles of human PD have previously shown that genes that regulate fibroblast replication, myofibroblast differentiation, collagen metabolism, tissue repair, and ossification are involved. DD, a palmar fascia fibrosis, may be associated with PD. Methods Total RNA samples from PD plaques, normal tunica albuginea, Dupuytren's nodules, and normal palmar fascia (nine samples per group) were subjected to differential gene expression profile analysis (Clontech Atlas DNA microarray) comparing PD with tunica albuginea and DD with normal palmar fascia. Changes of more than 2.0 in PD and DD compared with tunica albuginea and normal palmar fascia, respectively, were recorded. Reverse transcriptase-polymerase chain reactions were performed for some genes whose expression was altered in PD. Results Some of the gene families upregulated in both PD and DD were (a) collagen degradation: matrix metalloproteinase (MMP), with MMP2 and MMP9, and thymosins (MMP activators), with TMβ10 and TMβ4; (b) ossification: osteoblast-specific factors (OSFs) OSF-1 and OSF-2 (DD only); and (c) myofibroblast differentiation: RhoGDP dissociation inhibitor 1. The genes upregulated in PD only were decorin (an inhibitor of transforming growth factor-beta1 and a part of fibroblast replication/collagen synthesis) and early growth response protein. Reverse transcriptase-polymerase chain reaction confirmed these changes. Conclusions These data demonstrate that the pattern of alterations in the expression of certain gene families in PD and DD is similar, suggesting that they share a common pathophysiology and may be amenable to the same therapeutic regimens.

Gene transfer of inducible nitric oxide synthase complementary DNA regresses the fibrotic plaque in an animal model of Peyronie's disease.

The goal of the present study was to investigate the antifibrotic role of inducible nitric oxide synthase (iNOS) in Peyronie's disease (PD) by determining whether a plasmid expressing iNOS (piNOS) injected into a PD-like plaque can induce regression of the plaque. A PD-like plaque was induced with fibrin in the penile tunica albuginea of mice and then injected with a luciferase-expressing plasmid (pLuc), either alone or with piNOS, following luciferase expression in vivo by bioluminescence imaging. Rats were treated with either piNOS, an empty control plasmid (pC), or saline. Other groups were treated with pC or piNOS, in the absence of fibrin. Tissue sections were stained for collagen, transforming growth factor (TGF) beta1, and plasminogen-activator inhibitor (PAI-1) as profibrotic factors; copper-zinc superoxide dismutase (CuZn SOD) as scavenger of reactive oxygen species (ROS); and nitrotyrosine to detect nitric oxide reaction with ROS. Quantitative image analysis was applied. Both iNOS and xanthine oxido-reductase (XOR; oxidative stress) were estimated by Western blot analysis. Luciferase reporter expression was restricted to the penis, peaked at 3 days after injection, but continued for at least 3 wk. In rats receiving piNOS, iNOS expression also peaked at 3 days, but expression decreased at the end of treatment, when a considerable reduction of plaque size occurred. Protein nitrotyrosine, XOR, and CuZn SOD increased, and TGFbeta1 and PAI-1 decreased. The piNOS gene transfer regressed the PD plaque and expression of profibrotic factors, supporting the view that endogenous iNOS induction in PD is defense mechanism by the tissue against fibrosis.

1437: Phosphodiesterase 4 (PDE4) is Expressed in the Normal Tunica Albuginea and in the Peyronie's Disease Plaque

1437: Phosphodiesterase 4 (PDE4) is Expressed in the Normal Tunica Albuginea and in the Peyronie's Disease Plaque

1428: Osteogenic Progenitor Cells in the Peyronie's Disease Plaque may be Responsible for Plaque Ossification

1428: Osteogenic Progenitor Cells in the Peyronie's Disease Plaque may be Responsible for Plaque Ossification

Peyronie's disease fibroblasts demonstrate tumorigenicity in the severe combined immunodeficient (SCID) mouse model.

Peyronie's disease is a localized connective tissue disorder, caused by trauma to the erect penis, which results in cellular proliferation and excess extracellular matrix production within the tunica albuginea of the penis. We have previously demonstrated that cells derived from Peyronie's disease plaque tissue demonstrate increased cell growth, increased S-phase on flow cytometry, stabilization and inactivation of p53, and consistent morphologic transformation, all suggesting that these cells are biologically transformed. Severe combined immunodeficient (SCID) mice have been used extensively to study the pathobiology of malignant and benign tissue and cells. This study was undertaken to determine if Peyronie's derived fibroblasts had the potential to demonstrate tumorigenicity in the SCID mouse model, thus confirming their biologically transformed nature. Cultured fibroblasts were derived from three sources, namely, plaque tissue excised from men with Peyronie's disease, tunical tissue excised from young men with congenital penile curvature and neonatal foreskins. BALB/C SCID mice were divided into three groups and each group was inoculated with cultured fibroblasts from each of the three different sources. All animals were evaluated regularly and maintained in isolation for a period of 3 months following inoculation. All SCID mice inoculated with cells derived from Peyronie's disease plaque tissue (n=10) developed subcutaneous nodules at a mean time period of 2.5+/-0.5 months following injection. The mean maximum dimension and weight of the nodules at the time of killing the animal was 1.1+/-0.2 cms and 0.6+/-0.2 g, respectively. Histologically, the nodules were composed of large pleomorphic epithelioid cells with a high mitotic activity, which were negative for cytokeratin but positive for vimentin. None of the SCID mice inoculated with cells cultured from either normal tunica (n=5) or foreskin (n=5) developed subcutaneous nodules. In conclusion, the tumorigenic nature of Peyronie's disease plaque-derived fibroblasts sheds further light on the pathobiologic characteristics of these cells. Specifically, these data confirm that cells cultured from Peyronie's disease plaque are biologically transformed. Future refinement and study of this animal model may permit a more complete understanding of the pathophysiology of Peyronie's disease and fibromatoses in general. Furthermore, such an animal model may, in the future, allow a more ready evaluation of the therapeutic interventions for Peyronie's disease.

Gene expression profiles and effects of transforming growth factor-beta1 intervention in Peyronie's disease

To demonstrate molecular insight into the pathology of Peyronie's disease (PD). A preliminary profile of differential gene expression between the PD plaque and control tunica albuginea was obtained with DNA microarrays. Also, to investigate the effect of intervention in PD cells, transforming growth factor-beta1 (TGF-beta1) was recruited to treat PD cell lines. Three PD plaques and control tunica albugineas were constructed and studied. cDNA probes were prepared from RNA isolated from those cells and hybridized with the Clontech Atlas 3.6 Array. Relative changes of greater than 2.0 defined up-regulation and down-regulation, respectively. The expression of selected individual gene MCP-1 and the effect of TGF-beta1 on MCP-1 were analyzed by reverse transcriptase-polymerase chain reaction. Some up-regulated genes in the PD plaque detected by the Clontech assay were screened, one of them was monocyte chemotactic protein. One involved the pathogenesis of PD as a downstream gene and responded to the TGF-beta1 treatment but not CTGF. The results were also confirmed by TR-PCR in all the types of cell. The cell lines from plaque tissue and normal tunica from men with PD were successfully established. The findings indicate a potential role for MCP-1 over expression in the pathogenesis of PD as a downstream gene regulated by some genes and could be a new therapeutic target in PD. The information may allow a better understanding of the basic mechanisms involved in the etiology and pathogenesis of PD. Furthermore, it may permit some strategies of therapeutic interventions combine routine methods with Chinese herbal medicine.

Human Cadaveric Pericardial Graft for the Surgical Correction of Peyronie’s Disease

In patients with stable penile deformity secondary to Peyronie's disease (PD) penile straightening can be achieved with plaque incision or partial excision and grafting. We present our experience with human cadaveric pericardium for tunica albuginea grafting for men undergoing penile reconstruction for Peyronie's disease. We retrospectively reviewed our experience with 40 men with PD who underwent penile straightening with partial plaque excision and grafting using human cadaveric pericardium from January 1999 to January 2003. All 40 men were evaluable for preoperative, operative and postoperative characteristics. Mean postoperative followup was 22.0 months. Mean preoperative penile curvature was 69.1 degrees. Subjectively 36 of the 40 patients (90%) graded preoperative erection as sufficiently rigid for coitus and 100% had sufficiently rigid erection for coitus following intracorporeal papaverine injection. Mean pericardial graft size was 4.9 x 4.8 cm. Postoperatively 39 of the 40 patients (98%) had successful penile straightening, 38 (95%) achieved coitus, 28 (70%) achieved full, unaided erection and 12 (30%) had some degree of erectile dysfunction (ED) requiring pharmacological assistance for intercourse. There were no significant differences in ED risk factors, plaque location, graft size or complications in men who did and did not have ED postoperatively (p >0.05). There were no major complications or graft related adverse events. Human cadaveric pericardium is a safe, readily available and pliable tissue for tunica albuginea grafting following PD plaque incision or partial excision. Careful patient selection must be emphasized and particular attention must be given to deformity stability and preoperative erectile function to maximize surgical outcome.

Radiation Increases Fibrogenic Cytokine Expression by Peyronie’s Disease Fibroblasts

Peyronie's disease is a crippling penile deformity that results from fibrosis in the tunica albuginea. To our knowledge its cause is unknown and empirical therapies are used extensively. A factor involved in the development of Peyronie's disease is fibrogenic cytokine over expression. Radiation therapy is an empirical therapy for this condition and, while some data suggest a role for it, no literature exists on the effects of radiation on tunical tissue or cells derived from this tissue. We evaluated the effect of radiation on fibrogenic cytokine production in cells cultured from Peyronie's disease plaque tissue. Using a well established cell culture model cells derived from Peyronie's disease plaque tissue and neonatal foreskins were irradiated with 5 Gy (treatment group) or left nonirradiated (control group). At 24 hours cells were harvested and the supernatant was analyzed using enzyme-linked immunosorbent assay to determine the levels of the 2 fibrogenic cytokines basic fibroblast growth factor and platelet-derived growth factor-AB. Four Peyronie's disease plaque derived cultures and 2 neonatal foreskin derived cultures were analyzed. All plaque derived fibroblasts demonstrated significant elevations in basic fibroblast growth factor and platelet-derived growth factor-AB compared with foreskin derived fibroblasts. These data suggest that radiation may in fact increase the production of fibrogenic cytokines, which may promote the fibrotic process involved in Peyronie's disease. Further study is aimed at defining the effect of irradiation on plaque tissue.

Fibrin as an inducer of fibrosis in the tunica albuginea of the rat: a new animal model of Peyronie's disease.

To investigate the role of fibrin in inducing fibrosis in the tunica albuginea (TA) of the rat penis, to develop a new animal model for Peyronie's disease (PD). The TA of rats (five per group per period) were injected with either saline, fibrin, transforming growth factor-beta1 (TGF-beta1) or TGF-beta1 plus fibrin; the rats were killed at 1, 3, and 6 weeks after injection. Images were analysed quantitatively from tissue sections stained for collagen (Masson trichrome), fibrin (Verhoeff's stain) and elastin (Hart's stain), and immunostained for TGF-beta1, inducible nitric oxide synthase (iNOS), heme oxygenase 1 (HO1), alpha-smooth muscle actin (ASMA), apoptosis (TUNEL) and plasminogen activator inhibitor (PAI). Collagen fibre organization was characterized by electron microscopy. Human PD plaque tissue and normal human TA were assayed for fibrin by immunohistochemistry in nine samples. At 1 week after injection of fibrin into the rat TA, only oedema was present; at 3 weeks, the oedema developed into a characteristic fibrotic PD-like plaque. The injection of TGF-beta1 into the TA also induced oedema in the TA at 1 and 3 weeks but there was very little evidence of a recognisable plaque at either time. Injection with TGF-beta1 plus fibrin resulted in oedema at 1 week but at 3 weeks there was a smaller plaque than with fibrin only. At 6 weeks the induced plaques in the fibrin-only and fibrin + TGF-beta1 groups persisted, and were comparable with those elicited at this time by TGF-beta1 alone. The control animals showed no pathology at any of the sample times. At 3 weeks the PD plaque induced by injection with fibrin alone had not only greater expression of TGF-beta1 than the TA of the animals receiving TGF-beta1 alone, but also greater levels of other markers of fibrosis, e.g. HO1 (reactive oxygen species), ASMA (presence of myofibroblasts), apoptosis, and PAI (inhibitor of fibrinolysis). iNOS, a known antifibrotic agent, was also increased. In human PD plaque tissue, fibrin was detected by immunohistochemistry in all nine specimens. These results suggest that fibrin, when introduced into the TA of the rat penis, acts as a potential profibrotic protein, possibly via the local release of TGF-beta1, and induces a plaque not only histologically similar to that induced by TGF-beta1 but to that of the human condition. Because fibrin can extravasate from the blood into the human TA after an injury to the TA, and because fibrin persists in the plaque tissue, we hypothesise that fibrin may play a key role in the pathogenesis of human PD.

Tunica Albuginea Tissue Analysis After Electromotive Drug Administration

To minimize patient discomfort electromotive drug administration has been used as noninvasive transdermal therapy for Peyronie's disease. We directly measured the tissue concentration of verapamil after electromotive drug administration to investigate whether this treatment modality is an effective drug delivery system. A total of 19 tunica albuginea samples from 16 men undergoing surgical treatment for Peyronie's disease were used for analysis. Of these 16 men 14 underwent electromotive drug administration, including 12 with 10 mg. verapamil and 2 with 10 mg. verapamil plus 0.05 mg. epinephrine. In 2 men partial plaque excision was performed and the tunica albuginea samples were directly injected with verapamil. Another 3 men who served as controls had no exposure to verapamil. Electromotive drug administration was performed at an output of 2 mA. for 20 minutes. Tissue analysis was done using liquid chromatography-tandem mass spectrometry. Control tunica albuginea samples showed a verapamil level that was undetectable up to 109 ng./gm. The 14 verapamil electromotive drug administration treated specimens demonstrated undetectable to 37,510 ng./gm. verapamil. Overall 10 of the 14 electromotive drug administration treated tunica albuginea specimens (71.5%) contained measurable levels of verapamil. Adding epinephrine to the drug solution did not appear to enhance drug delivery. The concentration of verapamil in the 2 direct verapamil injection tunica albuginea samples was 166,898 and 118,411 ng./gm., respectively. There were no surgery or electromotive drug administration related complications. Electromotive drug administration is a safe and noninvasive treatment modality. Verapamil was detected in 71.5% of tunica albuginea specimens after electromotive drug administration with a wide range of verapamil levels. To our knowledge whether these levels affect change in Peyronie's disease plaque, resulting in improvement in penile deformity, is unknown and requires further placebo controlled trials.

Prospective Analysis of Single Nucleotide Polymorphisms of the Transforming Growth Factor β-1 Gene in Peyronie’s Disease

The detection of increased expression of transforming growth factor beta-1 (TGF-beta1) in Peyronie's disease plaques and the possibility of initiating a Peyronie's disease-like condition by intratunical injection of a synthetic heptopeptide with TGF-beta-like activity in an animal model has provided evidence for the central role of this cytokine in the pathogenesis of this entity. Recently 2 defined single nucleotide polymorphisms in the coding region of the TGF-beta1 gene have been described that are associated with different levels of TGF-beta1 production. Based on these data we prospectively investigated the genetic association of distinct TGF-beta1 genotypes with Peyronie's disease. DNA samples from 111 consecutive patients with idiopathic Peyronie's disease and 100 controls were genotyped for the 2 defined dimorphic single nucleotide polymorphisms T869C and G915C in the coding region of the TGF-beta1 gene using allele specific polymerase chain reaction. We found an increased frequency of the homozygous genotype of the single nucleotide polymorphism G915C in patients with Peyronie's disease compared with healthy controls (89.2% versus 79%, p = 0.04). However, there were no significant differences in allele frequencies of the single nucleotide polymorphism T869C. Experimental data from other investigators have shown that TGF-beta1 has an important role in the etiopathology of Peyronie's disease. Our results indicate that the homozygous wild type of the G915C single nucleotide polymorphism in the coding region of the TGF-beta1 gene, which was recently associated with elevated TGF-beta1 production and pulmonary fibrosis, may influence the predisposition to Peyronie's disease. However, it does not represent a major genetic risk factor.

Penile scintigraphy with 99mTc-human immunoglobulin G: a novel method for distinguishing the unstable and stable phases of Peyronie's disease.

To investigate the value of penile scintigraphy using 99mTc-human immunoglobulin G (IgG) to differentiate the unstable (acute) and stable (chronic) phases of Peyronie's disease (PD). Thirty-two consecutive patients (25 with PD and seven without) were evaluated using a detailed sexual history, serum chemistry panel, colour Doppler ultrasonography during simultaneous intracavernosal injection of 50 mg papaverine and stimulation, and 99mTc-IgG scanning. When indicated, nocturnal penile tumescence monitoring, dynamic infusion cavernosometry, cavernosonography and cavernosal artery systolic occlusion pressure were measured. After administering 370 MBq of 99mTc-IgG, images were taken at 30 min, 1, 2, 3 and 4 h. The scans were considered positive if there was any focal accumulation of radiopharmaceutical consistent with PD plaque formation. Eleven of the 25 patients with PD (mean age 56 years, sd 8) were in the unstable phase, the remaining 14 being in the stable phase. There was a localized increase in 99mTc-IgG activity in 10 patients who had unstable PD. There was complete resolution of increased activity in two patients at 12 and 13 months of follow-up. Of the 14 patients in the stable phase, 12 (at > 1 year) showed neither increased nor decreased 99mTc-IgG activity. In the remaining two patients there was increased activity on the plaque side. There was no local increase in activity in the control group. Inflammatory reactions can develop at various intervals during the unstable phase of PD. Medical methods should be used during the unstable phase and surgery delayed until the stable phase of the disease begins. An objective method of differentiating between the phases is therefore important. Penile 99mTc-IgG imaging is a new diagnostic approach for confirming the unstable phase of PD.

Gene expression in Peyronie's disease.

Currently, surgical intervention is the only efficacious treatment for Peyronie's disease (PD), a fibromatosis of the tunica albuginea of the penis. Therapies based on the molecular pathways for this disease could provide alternatives to surgical treatment but only recently has the pathophysiology of the Peyronie's disease plaque been investigated at the molecular level. In this review, we examine the current knowledge of gene expression in the PD plaque and the relationship of PD with other fibrotic conditions such as Dupytren's disease. TGFbeta1, along with other growth factors, pro-fibrotic genes, and collagen, are expressed in fibroblasts and myofibroblasts. Myofibroblasts are normally involved in wound contracture and largely eliminated via apoptosis during the late stages of wound remodeling. In the PD plaque, however, these cells persist and may play an important role in the PD plaque fibrosis. The expression levels of TGFbeta1 and pro- and anti-fibrotic gene products, along with the nitric oxide/reactive oxygen species (NO/ROS) ratio in the tunica albuginea, appear to be essential for the formation and progression of the PD plaque and effect the expression of multiple genes. This can be assessed with the recently developed DNA-based chip arrays and results with the PD plaque have been encouraging. OSF-1 (osteoblast recruitment), MCP-1 (macrophage recruitment), procollagenase IV (collagenase degradation), and other fibrotic genes have been identified as being possible candidate regulatory genes. Finally, possible therapeutic avenues for gene-based therapy in the treatment of PD are discussed that may eventually reduce the need for surgical intervention.

Peyronie's disease cell culture models: phenotypic, genotypic and functional analyses.

Peyronie's disease is a fibromatosis of the tunica albuginea. While trauma is believed to be the inciting event, the exact pathophysiology of this condition is unknown. In vitro analysis of cell biology can shed light on the pathogenesis of medical conditions and has been used for many decades as a research tool. We have established a cell culture model, which we have used to study the pathobiology of cells derived from Peyronie's disease plaque tissue. In 10 separate cell cultures derived from different individuals, these cells have demonstrated consistent phenotypic, genotypic and functional alterations. In neither of the control cell cultures, neonatal foreskin fibroblasts and normal tunica-derived fibroblasts have any of the above aberrations been demonstrated. The cells studied have been shown to be fibroblasts in nature with a sub-population of myofibroblasts present in culture. The Peyronie's disease plaque tissue-derived fibroblasts have demonstrated (i) consistent morphologic transformation (ii) increased S-phase on flow cytometry (iii) decreased dependence on culture medium (iv) cytogenic instability (v) excess production of fibrogenic cytokines and (vi) stabilization and dysfunctionalization of p53. Further refinement of this model and future analyses may permit an increased understanding of the pathogenesis of this condition and allow the development of therapeutic strategies.

Antifibrotic Role of Inducible Nitric Oxide Synthase

Long-term treatment in rats with l-NAME, an isoform-non-specific inhibitor of nitric oxide synthase (NOS), leads to fibrosis of the heart and kidney, suggesting that nitric oxide (NO) may play a role in preventing tissue fibrosis. In this process, a likely target of NO is the quenching of reactive oxygen species (ROS) through peroxynitrite formation, and one possible source for this NO is inducible NOS (iNOS). Using Peyronie's disease (PD) tissue from both human specimens and from a rat model of PD as the source of fibrotic tissue, we investigated if NO derived from iNOS could act as such an antifibrogenic defense mechanism by determining whether: (a) tunical ROS and iNOS are increased in PD; and (b) the long-term inhibition of iNOS activity decreases the NO/ROS balance in the tunica albuginea thereby promoting collagen deposition. It was determined that in the human PD plaque, iNOS mRNA and protein, ROS, collagen, and the peroxynitrite marker, nitrotyrosine, were all increased in comparison to the normal tunica. In the rat model of PD, the fibrotic plaque also showed significant increases in iNOS mRNA and protein, nitrotyrosine, ROS as measured by heme oxygenase-1, and collagen when compared with the normal control tunica. When a selective inhibitor of iNOS, L-NIL, was given to rats with the PD-like plaque, this resulted in a decrease in nitrotyrosine levels but intensified ROS levels and collagen deposition. These data demonstrate that: (a) iNOS induction occurs in both the human and rat PD fibrotic plaque; and (b) that the NO derived from iNOS appears to counteract ROS formation and collagen deposition. Because the inhibition of iNOS activity leads to a decrease in the NO/ROS ratio, thereby favoring the development of fibrosis, it is proposed that iNOS induction in this tissue may be a protective mechanism against fibrosis and abnormal wound healing.

New advances in Peyronie's disease.

The formation of Peyronie's disease plaques is a process that seems to involve a cascade of genetic, structural and immunologic events. Clinical manifestations include penile deformity and possible erectile dysfunction. Rational strategies have been forthcoming, with both minimally invasive and surgical treatments of Peyronie's disease available. This article reviews and updates current scientific and clinical advances in Peyronie's disease.

Prevalence of Peyronie's disease in men over 50-y-old from Southern Brazil.

The pathogenesis of Peyronie's disease still remains an enigma and few epidemiological studies are available. The purpose of this study was to determine the prevalence of Peyronie's disease in males older than 50 y. From 26 to 30 July 1998, 1071 men attended the 'Prostate Cancer Awareness Week of Santa Casa Hospital, Porto Alegre, Brazil'. In the prostate exam they also consented to be screened for Peyronie's disease. They underwent the 5-item International Index of Erectile Function (IIEF-5) questionnaire for evaluation of the erectile condition. The presence of a well-defined plaque in the penis was the diagnostic criterion for Peyronie's disease. The men were examined by five senior residents, under supervision by the staff Urologist. Men younger than 50 y as well as patients under intracavernous injection therapy for erectile dysfunction were excluded from the study. Chi2 test was used for statistical analysis. Nine hundred and fifty-four (89.1%) out of the 1071 men with a mean age of 62 y (ranging from 52 to 77) were included in the study. Peyronie's disease plaques were found in 35 men (3.67%). Eight hundred and forty-five (88.6%) were Caucasians. There was no significant statistical difference regarding age (P > 0.05). The presence of erectile dysfunction in the men with Peyronie's disease and without this condition, was 68.6% and 53.5%, respectively (P > 0.05). From this data we can conclude that the prevalence of Peyronie's disease is higher than in formerly reported studies. Further observations should be carried out in different communities and in other groups of patients in order to confirm our results.

Fibrin Deposition in Peyronie's Disease Plaque

Peyronie's disease is a pathological fibrosis characterized by excessive deposition of collagen in the plaque. Although the etiology of Peyronie's disease is unknown, trauma has been hypothesized as the inciting event. In an effort to obtain more insight into the pathogenesis of Peyronie's disease plaque tissue was examined for collagen, elastic fiber, and fibrin content and distribution. Plaque tissue specimens from 33 patients with Peyronie's disease, control penile tissue and nodular tissue from 8 patients with Dupuytren's contracture were analyzed histochemically for collagen staining and elastic fiber structure and distribution. Plaque tissue from 19 Peyronie's disease patients, control tissue and nodular tissue from Dupuytren's disease were also analyzed for the presence of fibrin by histochemical staining and immunoblotting. Aberrantly stained collagen was detected in 32 of 33 plaque specimens (97%) and disrupted elastic fibers in 31 of the same specimens (94%). Fibrin deposition was detected histochemically in plaque tissue from 18 of 19 patients (95%) but it was not detectable in normal or scarred tunica from control patients. The presence of authentic fibrin accumulation in plaque tissue was confirmed by immunoblot analysis but fibrin was not detected in dermal tissue extracts from the same patient. Aberrant collagen staining and fibrin deposition were detected in nodular tissue from 7 of 8 Dupuytren's contracture patients (88%) and altered elastic fibers in 5 of the same patients (63%). Deposition of fibrin in plaque tissue is consistent with the hypothesis that repetitive microvascular injury results in fibrin deposition in the tissue space and has served to provide insights into the pathophysiology of Peyronie's disease. We propose a model that accounts for the clinical and biological features of Peyronie's disease.

Fibrin Deposition in Peyronie's Disease Plaque

Fibrin Deposition in Peyronie's Disease Plaque