New discoveries in the basic science understanding of Peyronie's disease
Department of Urology, University of California at Los Angeles, School of Medicine, Division of Urology, Research and Education Institute, Harbor-UCLA Medical Center, Torrance, CA 90509, USA. Current Urology Reports
(Impact Factor: 1.51).
12/2004; 5(6):478-84. DOI: 10.1007/s11934-004-0074-y
Peyronie's disease is an acquired benign condition representing localized fibrosis of the penis. The disease is caused by microvascular trauma to the penis, with subsequent fibrin deposition resulting in aberrant wound healing and possibly other etiologies. Histopathologic studies of the Peyronie's plaque have demonstrated the role of transforming growth factor-beta 1 in the pathologic development of penile plaque. Animal models have been developed to test pathophysiology and therapeutics. The role of inducible nitric oxide synthase and nitric oxide has been established to limit and counteract fibrosis. Differential gene expression studies have identified candidate up-regulated or down-regulated genes that are involved in the pathophysiology of Peyronie's disease.
Available from: Ralf Herwig
- "The underlying cause of Peyronie's disease is not well understood but is thought to be caused by trauma or injury to the penis usually through sexual activity although many patients often are unaware of any traumatic event or injury . After traumatic event, Peyronie's disease (PD) is a progressive fibrotic disorder of the penis that is characterized by formation of collagen plaques on the tunica albuginea of the penis that may result in penile deformity and pain (typically early in the disease course) and often occurs in conjunction with erectile dysfunction   . A possible underlying cause of trauma has not been investigated so far. "
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ABSTRACT: Peyronie's disease is a connective tissue disorder in the soft tissue of the penis. The underlying cause of Peyronie's disease is not well understood but is thought to be caused by trauma or injury to the penis during sexual intercourse. The purpose of the interdisciplinary cooperation between urological surgery and physics is the development of a physical simulation tool in order to give prognosis of possible tunica albuginea fibre rupture at a certain degree of deviation of the penis. For our group the first challenge was to translate the human organ of the penis into a physical model. Starting and marginal parameters had to be defined, whereby some of them had to be based on assumption, as physical data of the human living tissue have rarely been measured up to now. The algorithm and its dependencies had to be developed. This paper is a first step of a three-dimensional mathematical-physical simulation with the assumption of a 100% filled rigid penis. The calculation gives proof of the hypothesis that the fibre-load-angle of the penis is less than 12 degrees. Thus physical simulation is able to provide the surgeon with a simple instrument to calculate and forecast the risk of the individual patient.
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ABSTRACT: Peyronie's disease (PD) continues to be a major source of sexual dysfunction among the 3-9% of affected men. The challenge in treating PD is determining the natural history and clinical course for the individual patient. Currently, there exists no reliable means to predict whether a penile plaque of PD will progress, regress, or remain stable. This represents a significant deficiency in contemporary management, one that may be addressed with newer technologies such as proteomic profiling.
This review assesses the potential use of protein alterations measured by various novel technologies, to predict progression, regression, or stabilization of PD in an affected individual.
A comprehensive literature review of the past decade in the field of gene profiling and protein expression of PD was performed.
A critical analysis of the existing worldwide literature evaluating surface-enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF-MS or SELDI) and other proteonomic techniques.
SELDI and other technologies can provide the clinician with innovative data indicating the presence of unique individual factors that act to suppress or promote the fibrotic process in PD. Determining the clinical implications of altered protein expression in an individual is not yet defined.
The area of proteomics has begun to revolutionize the study of medicine in the postgenomic era, by allowing researchers to study the role that proteins play in health and disease. Applying this knowledge clinically has already led to innovative discoveries in early cancer detection in a number of malignancies, including prostate, ovarian, and bladder. Prior to the widespread use and acceptance of proteomic technology in PD, a critical assessment of its therapeutic and diagnostic value will be required.
Available from: dtic.mil
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ABSTRACT: This project aims to find a novel therapy to prevent or correct erectile dysfunction (ED) after radical prostatectomy (RP) for prostate cancer. This was done by determining in a rat model of bilateral cavernosal nerve resection (BCNR): a) the time course of the histological/biochemical alterations in the penile corpora cavernosa associated with corporal veno-occlusive dysfunction (CVOD), the type of ED that develops after RP; and b) whether continuous long-term treatment (CLTT) with PDE5 inhibitors (PDE5i) and/or nitric oxide (NO) generators oppose these changes by counteracting fibrosis, oxidative stress and the loss of smooth muscle cells (SMC) subsequent to nerve damage. We have shown that: a) apoptosis, SMC loss, fibrosis, and iNOS induction preceded CVOD; b) CLTT oral PDE5i (tadalafil and sildenafil; as previously vardenafil) at high doses, prevented these processes; c) oral sildenafil at a lower dose, + or - the NO generator molsidomine, also prevented CVOD, although the underlying histopathology was less ameliorated than with the higher dose, and the combination treatment did not improve efficacy; d) corporal implantation of muscle derived stem cells (MDSC) prevented CVOD, but the efficacy was not enhanced by sildenafil. We conclude that CVOD results indirectly from neuropraxia post-RP, and that an early CLTT with PDE5i, as opposed to on demand regimens, prevent CVOD through preservation of the corporal SM. This supports and drives the emerging clinical interest in preventing or "curing" post-RP ED ("penile rehabilitation") with CLTT PDE5i.
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