Implications of Calcification in Peyronie’s Disease

[madman]

A common characteristic of Peyronie’s Disease (PD) is plaque calcification, which is associated with decreased response to treatments and higher rates of surgical intervention. Despite its prevalence in the PD population, the literature on plaque calcification is limited. While the diagnosis of PD is mostly clinical, imaging modalities such as ultrasound can be used to identify plaque calcification. The proper identification of plaque calcification is crucial for guiding management and setting therapeutic expectations for patients with PD. Herein we discuss what is known about PD plaque calcification, including epidemiology, etiology, diagnosis, and management.




Peyronie’s disease (PD) is a benign condition characterized by acquired penile deformity often accompanied by pain and sexual dysfunction. PD curvature results from abnormal scarring and fibrous collagen buildup (plaque) in the tunica albuginea (TA) of the corpora cavernosa. 1 PD is estimated to have a worldwide prevalence of 0.3%-13.1%, with greater occurrence in men with risk factors such as diabetes, smoking, and alcohol consumption. 2,3 PD’s pathophysiology has not been fully elucidated. Both genetic and environmental factors, such as microtrauma to the penis during intercourse, may be involved. A subset of men will develop calcification within the PD plaque. Calcification is associated with worse treatment outcomes and a greater need for surgical intervention. 4,5 However, little is known about the mechanisms of PD plaque calcification. In this review, we will discuss what is known about PD plaque calcification and how calcification affects treatment and outcomes.




*EPIDEMIOLOGY

*GENETICS

*PATHOPHYSIOLOGY

*DIAGNOSIS

*CLINICAL IMPLICATIONS




CONCLUSION

Despite ongoing research, the pathophysiology of PD remains undefined, especially as it pertains to plaque calcification. Calcification could have substantial implications on the natural history and treatment options for PD. Regardless of the true pathophysiology of calcification in PD, it remains apparent that it is predictive of a patient’s clinical course and treatment outcomes. PD patients with calcification respond poorly to CCH, the only medication currently FDA approved for the treatment of PD, and they undergo surgery at higher rates than those without calcification. For this reason alone, we argue that imaging to evaluate calcification is an essential component of evaluation for PD patients. Currently the American Urological Association and European Association of Urology do not strongly recommend US in the evaluation of patient’s with PD, even though US is safe and can be of high diagnostic value for detecting calcification.

 

[madman]

Figure 1. The development of Peyronie’s disease plaques appears to involve an increased local concentration of TGF-b1 and PDGF causes differentiation of fibroblasts into myofibroblasts and deposition of aberrant collagen in the extracellular matrix. Additionally, there is a decrease in the removal of ECM by matrix metalloproteinases (MMPs) and an increase in tissue inhibitors of metalloproteinases (TIMP). Taken together, this leads to plaque formation, tissue contraction and penile curvature. (Color version available online.)

 

[madman]

Figure 2. A representative image of Ultrasound detected Peyronie’s disease plaques in 2 patients. Left, a noncalcified plaque without acoustic shadowing. Right, a calcified plaque with posterior acoustic shadowing. (Color version available online.)

 

[madman]

Table 1. Summary of calcification systems used to describe the severity of calcified plaques in PD patients

 

[madman]

Table 2. Comparison of patients who had >20% improvement in curvature after at least 2 cycles of collagenase clostridium histolyticum with encouraged penile traction for 1-3 hours daily, calcified versus noncalcified plaque