In 1587, Guilio Cesare Aranzi was the first to formally describe Peyronie disease (PD) in his book Tumores praeter naturam. He called Peyronie disease "a rare affection of the genitals in people with excessive sexual intercourse: a little penile tumor palpable like a bean in the flaccid penis causing a deformity similar to a ram horn during erection." The disease was not given its current name until 1743, when Francoise de La Peyronie described the cases of 3 men with fibrous thickening of the penile shaft, painful erections, and penile curvature, as demonstrated in the images below.
Medscape Reference's Urology article, Peyronie Disease, also may be helpful.
Although the exact etiology of Peyronie disease is not clear, trauma may cause perivascular inflammation.  In ordinary tissue, the rupture of blood vessels leads to coagulation and fibrin deposition. Fibrinolysis of the deposited fibrin occurs as tissue cells proliferate to close the site of injury. In Peyronie disease, the tunica albuginea may initially undergo microvascular trauma during sexual intercourse. Adequate postinjury fibrinolysis is prevented because the tunica albuginea is hypovascular.
After multiple microvascular traumas, large quantities of fibrin accumulate in the form of a plaque, generally along the dorsal and ventral midline aspects of the penile shaft. This deposition appears to be immune mediated. Some people may be genetically predisposed to this reaction. The plaque prevents the adequate expansion of the tissue during erection, leading to penile curvature and pain. The relationship of this condition to other fibromatoses suggests a predisposition to fibrous proliferation. Although these microtraumatic events are implicated in the current theory of the pathogenesis of Peyronie disease, no etiology is proven.
Results of animal studies indicate that transforming growth factor-beta (TGF-beta) may be involved in the formation of the plaques via early inflammatory reactions. When TGF-beta analogs are injected into rat tunica albuginea, they form collagen bundles that are morphologically similar to those in Peyronie disease.
Peyronie disease starts in 1 of 2 ways. Most patients report the acute onset of pain accompanied by a lump in the shaft of the penis, followed by gradually increasing curvature with or without pain. Alternatively, a minority of the patients report curvature of the penile shaft that occurs suddenly, seemingly overnight, and remains stable once it occurs.
In the progressive form, the cycle of trauma, fibrin deposition, and attempts at fibrinolysis continue to escalate. Remodeling of the fibrin deposits can take as long as 2 years in the absence of further traumatic events.
The rate for Peyronie disease is 0.3-4% among white men.
Peyronie disease is less common in men of African or Asian heritage.
Peyronie disease is well documented in whites. Peyronie disease may occur in black men, often in the presence of preexisting diabetes mellitus and erectile dysfunction.
Peyronie disease predominantly occurs in men aged 40-60 years. The age range of affected persons is 30-80 years.
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