Peyronie’s disease (PD) is characterized by the formation of fibrous, inflexible plaques within the tunica albuginea of the penile corpus cavernosum. These plaques can cause pain, penile bending during erections, and/or penile deformities such as an hourglass shape in an erect penis. Severe PD can lead to complications such as painful intercourse, the inability to have intercourse due to the severity of the curve of the penis, and erectile dysfunction (ED).
Although estimates on the prevalence of PD vary widely, multiple studies put the range at somewhere between 0.3% to 13% worldwide. This prevalence may further increase in certain subpopulations. For example, the prevalence of PD is higher in men who have had a radical prostatectomy.
In the same vein, there are several known risk factors for PD. A history of genital and/or perineal injuries, transurethral prostatectomy, cystoscopy, diabetes mellitus, hypertension, lipoma, propranolol in therapy, a history of Dupuytren's contracture, smoking, alcohol consumption, fibromatous lesions on the genital tract of the sexual partner, and surgical intervention on the genital tract of the partner were among the PD risk factors identified by multiple case-control studies.
The exact pathophysiology of PD is more difficult to define. Given the complex nature of the condition, it is generally understood that the pathophysiology of PD is multifactorial. In almost all cases, PD is likely to be caused by a combination of genetic and environmental factors.
At this time, there is no known population that is genetically predisposed to PD. Nevertheless, this does not necessarily mean that there is no genetic component to PD. Some experts have theorized that a proportion of men may be more likely to respond to microvascular trauma to the penis with a hyperactive healing response – resulting in an increased risk of the formation of PD plaques. Currently, this is just a theory.
Another theory is that the arrangement of the blood vessels in the tunica albuginea, (wherein the arteries are cushioned by a cuff of loose connective tissue and the veins come in direct contact with the fibrous tunica,) creates a trapped inflammatory response when the tunica is damaged by blunt trauma. This trapped response might then facilitate the production of collagen fibers within the tunica albuginea, which would be the aforementioned PD plaques.
Further research is needed to determine the true pathophysiology of PD, and these theories may be good starting points for studies. Knowing the prevalence, risk factors, and possible pathophysiology of PD may help health care providers who are diagnosing and treating PD patients.
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