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What is Peyronie’s Disease?

In order to understand the variations of Peyronie’s disease, it is best to first be familiar with some basic anatomy of the penis and physical changes during an erection.


The innermost portion of the penis, the corpus cavernosa, consists of two cigar-shaped chambers consisting of sponge-like tissue with many tiny blood vessels. The corpus cavernosa fills with blood and hardens during an erection. These chambers are surrounded by a layer of connective tissue called the tunica albuginea. This tissue remains rather elastic when the penis is flaccid, however when maximally stretched, interlaced connective tissue fibers allow it to become rigid. The tunica albuginea coordinates internal filling with structural rigidity, which helps determine the shape of the erect penis and controls expansion.1

Peyronie’s disease is an inflammatory disease related to the tunica albuginea. Microvascular trauma, which can result from injury or wear and tear on particularly vulnerable areas, initiates the wound healing process with the accumulation of fibrin on the tunica albuginea. In someone with Peyronie’s, the healing mechanisms are abnormal and inflammation remains persistent. In some cases, this inflammation is somewhat reversible. However, in severe cases, the fibrin deposit becomes a hardened plaque. This plaque reduces the elasticity of the erectile tissue, can cause the penis to bend or arc during erection, and may be painful.2

In some, physical trauma or injury to the penis is evident; however, for many, it is difficult to identify a specific occurrence. It is believed that typical use in sexually active men can cause microvascular damage which may initiate inflammation and fibrin deposition. The reason for an overreaction of the inflammatory response in some men remains unknown. There are a number of factors that can contribute to poor wound healing and may play a role in Peyronies disease. These include:

  • Vasculitis: inflammation of blood or lymphatic vessels, which can lead to the formation of scar tissue
  • Connective tissue disorders: disorders such as Dupuytren’s contracture (thickening of connective tissue in hands) increase the risk of developing disorders in other parts of the body
  • Heredity: having a relative with Peyronie’s increases the risk of developing the disorder

Also, men with diabetes have been seen to be at greater risk because it can contribute to impaired wound and connective tissue healing.

Peyronie’s disease symptoms may appear gradually or happen suddenly. The most common symptoms are:

  • Formation of scar tissue nodule under the skin
  • Bend in the penis with erection (most commonly upward)
  • Narrowing or shortening of the penis with erection
  • Pain during an erection, intercourse or orgasm

Curvature may gradually worsen during the first 6 to 18 months after symptoms begin. Deformity will not worsen after a certain point in time, but it will continue to reoccur with erections.

Peyronie’s disease worsens over time. Complications include:

  • Inability to have sex
  • Difficulty achieving or maintaining an erection (erectile dysfunction)
  • Anxiety or stress about the appearance of the penis
  • Stresses on the relationship with one’s sexual partner

Peyronie’s disease can be treated surgically or non-surgically. Surgical correction options are invasive and pose a greater risk of impotency, so they are typically reserved for severe cases of Peyronie’s. The most common surgical methods include:

  • Shortening of the unaffected side
  • Lengthening of the affected side
  • Removal of plaque and skin grating
  • Penile implants

Non-surgical methods include:

  • Oral medications: potassium aminobenzoate (Potaba), Vitamin E
  • Radiation therapy
  • Shock wave lithotripsy
  • Penile injections (in fibrous tissue): corticosteroids, Verpamil, Interferon, collagenase
References:
1. Creed KE, Carati CJ, Keogh EJ. The physiology of penile erection. Oxf Rev Reprod Biol. 1991; 13:73-95.
2. Moreland RB, Nehra A. Pathophysiology of Peyronie’s disease. J Sexual Med. 2002; 14(5):406-410.
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