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Dermatologic Manifestations of Peyronie Disease

  • Author: Anne Elizabeth Laumann, MBChB, MRCP(UK), FAAD; Chief Editor: Dirk M Elston, MD  more...
Updated: Nov 20, 2015


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.

Lateral view demonstrates vertical curvature. Lateral view demonstrates vertical curvature.
Superior view shows a full erection. Superior view shows a full erection.

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.[1] 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.




United States

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.

Contributor Information and Disclosures

Anne Elizabeth Laumann, MBChB, MRCP(UK), FAAD Professor of Dermatology, Chief of General Dermatology, Director of the Collagen Vascular Disorders Clinic, Northwestern University, The Feinberg School of Medicine

Anne Elizabeth Laumann, MBChB, MRCP(UK), FAAD is a member of the following medical societies: American Academy of Dermatology, Association of Professors of Dermatology, British Association of Dermatologists, Chicago Dermatological Society, Chicago Medical Society, Illinois Dermatological Society, Illinois State Medical Society, Medical Dermatology Society, Society for Investigative Dermatology, Women's Dermatologic Society

Disclosure: Nothing to disclose.


Gregory Bales, MD Associate Professor, Department of Surgery, Section of Urology, University of Chicago

Gregory Bales, MD is a member of the following medical societies: American Urological Association

Disclosure: Nothing to disclose.

Victoria Godinez-Puig, MD Resident Physician, Department of Dermatology, Northwestern University, The Feinberg School of Medicine

Victoria Godinez-Puig, MD is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Joseph J Pariser, MD Resident Physician, Department of Urology, The University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American College of Rheumatology

Disclosure: Received income in an amount equal to or greater than $250 from: XOMA; Biogen/IDEC; Novartis; Janssen Biotech, Abbvie, CSL pharma<br/>Received honoraria from UpToDate for author/editor; Received honoraria from JAMA Dermatology for associate editor and intermittent author; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for i inherited these trust accounts; for: Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Jay W Zimmerman, MD, FAAD Consulting Physician, Berman Skin Institute, Palo Alto

Jay W Zimmerman, MD, FAAD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, California Medical Association

Disclosure: Received consulting fee from Allergan for consulting; Received consulting fee from Centocor for consulting; Received consulting fee from Galderma for consulting; Received consulting fee from Coria Labs for consulting.

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Lateral view demonstrates vertical curvature.
Superior view shows a full erection.
Postoperative picture after surgical repair demonstrates a straight erection.
Intraoperative picture of an artificial erection demonstrating lateral curvature.
Intraoperative picture after penile plication demonstrating a straight erection.
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