Presentation Authors: Jeffrey Campbell*, London, Canada, Uros Milenkovic, Leuven, Belgium, Dorota J. Hawksworth, Xiaopu Liu, Baltimore, MD, Maarten Albersen, Leuven, Belgium, Arthur L. Burnett, Trinity J. Bivalacqua, Baltimore, MD
Introduction: Peyronie's disease (PD) is a connective tissue disorder of the tunica albuginea (TA) that results in penile deformity and has a high association with erectile dysfunction (ED). The mechanism of cavernosal dysfunction and subsequent ED is not well understood. Using human corpora cavernosa tissue, we explored the pathophysiology of ED in PD patients to determine if erectile tissue fibrosis occurs in a similar fashion as in the TA.
Methods: Human corpora cavernosa tissues were removed during inflatable penile prosthesis implantation. Four patient groups were categorized as: (1) no PD and no ED (N=3), (2) PD and no ED (N=7), (3) PD and mild ED (N=7) and (4) PD and severe ED (N=7). Diagnosis of PD was based on patient history and clinical examination. ED was categorized by penile Doppler-ultrasound findings as peak systolic velocity (PSV) â‰¤25mmHg/s (severe), between 25-35mmHg/s (mild) or PSV â‰¥35mmHg/s (no ED). Immunohistochemistry (IHC) for Î±-smooth muscle actin (Î±-SMA), Masson's trichrome and immunofluorescence (IF) for neuronal nitric oxide synthetase (nNOS) and CD34 (endothelial marker) were performed. Gene expressions of transforming growth factor (TGF)-Î²1, nNOS, endothelial NOS, inducible NOS, and Rho-GDI were measured by quantitative polymerase chain reaction (qPCR). RNA extracted from tissue samples was assayed by Nanostring nCounter ultra-high-throughput gene expression system for 255 inflammatory gene sets, including the common genes associated with TA fibrosis in PD.
Results: There were no significant differences in baseline clinical or demographic characteristics. Using IHC and IF we did not observe a significant difference in markers for smooth muscle, fibrosis, or endothelial content, suggesting an absence of generalised penile corporal fibrosis. There was no significant difference in our gene expression by qPCR analysis (p=0.8). Nanostring bioinformatical analysis did not show a significant difference in any of the 255 inflammatory genes between the 4 groups.
Conclusions: This is the first study that examines ED using human erectile tissue from PD patients. Gene expression analysis of corpora cavernosa did not demonstrate the fibrosis or inflammation typically observed in the TA of PD. Our findings suggest that PD-related ED should not be attributed to inflammation or fibrosis in the corpora cavernosa and as such, favors a mechanical etiology of ED.