Download Peyronies disease

World J Urol (2001) 19: 244±250
Ó Springer-Verlag 2001
FREE PAPER
Hari Siva Gurunadha Rao Tunuguntla
Management of Peyronie's disease ± a review
Abstract Peyronie's disease is an uncommon condition
involving middle-aged men and probably resulting from
penile trauma. The injury causes an in¯ammation in the
tunica and ultimately scarring and penile curvature
develop. It may also occur due to nonspeci®c in¯ammation. The use of medications such as b-blockers can
sometimes result in Peyronie's disease. In Peyronie's
disease, the normal elastic tissue of the tunica is replaced
by scar tissue. The penile plaque, or scar tissue in this
condition, is not elastic but hard and will not stretch with
erection. The side that does not stretch results in penile
curvature to the side of the scar. One third of men with
Peyronie's disease have painful erections. A low percentage of men with Peyronie's disease develop erectile
dysfunction. Because in¯ammation is initially associated
with the scar tissue, some amount of discomfort occurs
during erection. Most patients with early stage Peyronie's disease can continue to function sexually with the
curvature in the penis. Others with a severe penile deformity will have diculty in sexual intercourse. Literature regarding the e€ectiveness of conservative therapy
in the early phase with pain and in¯ammation is limited,
with only modest and at times anecdotal bene®ts. The
commonly used agents include 400 units of vitamin E
(vitamin E promotes healing and prevents scarring),
ibuprofen (anti-in¯ammatory) and Colchicine (useful for
pain during erection). Fexofenadine is recently being
used in the early phase of Peyronie's disease for its antiin¯ammatory e€ect. Radiation and ultrasound are not
usually very helpful. When the disease process stops,
there is usually some residual distortion of the penis but
H. S. G. R. Tunuguntla
1624, SW 40th Terrace, Apt. D, Gainesville,
FL 32607±4086, Florida, USA
e-mail: [email protected]
Tel.: +1-352-3841817
H. S. G. R. Tunuguntla
North Florida Urology Research Institute,
6440, West Newberry Road, Suite 410, Gainesville,
FL 32605, USA
the majority of patients are able to have satisfactory
sexual intercourse. However, if there is severe penile
distortion interfering with intercourse, surgery is indicated. Surgical techniques for Peyronie's disease include
tightening or plication (Nesbit's tuck) of the penis
opposite the curvature to produce straightening. This
usually results in some small loss of length. The other
type of surgery consists of incision of the plaque or scar
tissue and patching with a vein (saphenous vein graft)
or dermal graft. Laser therapy is occasionally used. A
penile prosthesis is the treatment of choice in patients
with Peyronie's disease and erectile dysfunction.
Peyronie's disease (PD) is a localized connective tissue
disorder of the tunica albuginea of the penis, which results
in a severe curvature of the erect penis. The cause of this
condition is not completely understood at present [29].
The condition was named after FrancËois Gigot de la
Peyronie, the personal physician of King Louis XVI of
France. Common presenting complaints of PD include
palpable penile plaque, painful erections, and curvature
of the penis. It is a psychologically debilitating problem,
and a‚icted men demonstrate a signi®cantly reduced
quality of life. Studies are currently underway regarding
the exact cause of this disorder.
A minor bend (about 10°) in the erect penis is normal.
A signi®cant percentage of patients with Peyronie's
disease have erectile dysfunction either as a result of the
Peyronie's disease or in association with it. In some
patients with Peyronie's the penis can form a J or a
corkscrew, making intercourse impossible.
Statistics [41]
Statistically, PD shows the following:
± Occurs in 0.38%±3% of the adult male (40±60 years)
population.
245
± Occurs in 1.5% in men in the 30±39-year age group.
± Occurs in 6.5% in men older than 70 years.
± Approximately 40% of men with PD have some
evidence of erectile dysfunction
Characteristics of PD in young men include a past history of trauma during sexual intercourse and painful
erections. Medical therapy is commonly used for painful
erections in this subset of patients, although it is not
e€ective in all patients.
Structure of the penis [27]
The penis is composed of three cylindrical structures,
two on the dorsum, called the corpora cavernosa (cavernous spaces, blood-®lled spaces which expand and
trap the blood during erection), and one on the ventrum,
the corpus spongiosum (along with the urethra). The
corporal bodies are surrounded by an elastic covering
called the tunica albuginea. The nerves and blood vessels
(dorsal artery and veins) of the penis are located on the
dorsal aspect of the corpora cavernosa.
The tunica of the corpus cavernosum is a 2-layered
structure. The inner layer, with its circularly oriented ®bers, has supportive function and surrounds the cavernous tissue. Intracavernosal pillars (ICPs) radiate inwards
from the inner layer and augment the support provided
by the septum (the main structure providing support to
the erectile tissue of the corporal bodies). The ®ber bundles of the outer layer are oriented longitudinally extending from the glans penis to the proximal crura and
insert into the inferior pubic ramus. These ®ber bundles
are, however, are absent at the 6 o'clock positions.
The tunica albuginea consists of elastic ®bers forming
an irregular network of elastic ®bers and collagen ®bers.
Emissary veins travel between the inner and outer layers
and obliquely pierce the outer ®bers. The tunica a€ords
great ¯exibility, rigidity and tissue strength to the penis
during erection, with its outer layer compressing the
veins.
Branches of the dorsal artery of the penis travel
within the penis in a perpendicular direction, surrounded by a periarterial ®brous sheath.
The corpus spongiosum is a low-pressure structure
during erection due to the absence of an outer investing
layer and the intracorporeal struts, speci®c to the corpora cavernosa.
Internal pudendal artery (a branch of the hypogastric artery) is the main arterial supply to the penis
and becomes the common penile artery after giving o€
the perineal branch in Alcock's canal. The penile artery gives 3 branches: bulbourethral artery (which
supplies the urethral bulb, the spongiosum and the
glans penis), cavernous (deep or central) artery of the
penis (which supplies the erectile tissue of the corpora
cavernosa) and the dorsal artery (which supplies the
glans penis, penile skin and subcutaneous tissue).
Collaterals among the cavernosal, dorsal, and urethral
arteries run along the length of the penis. Proximal to
the glans, the three arteries converge to form a vascular ring.
Accessory pudendal arteries sometimes originate
from vesical, obturator or external iliac arteries, which
may explain the postoperative vascular impotence following radical cystectomy and prostatectomy.
In the ¯accid penis, most of the penile arterioles are in
a constricted state (30 lm in diameter). The sinusoids
and their interconnecting channels are also in a constricted state due to contracted cavernous muscles. The
intrinsic tone, coupled with the sympathetic innervation
is believed to contribute to the cavernous muscle contraction in the ¯accid penis.
Regarding venous drainage, the emissary veins of the
corpora cavernosa drain into four groups of veins:
dorsal, right lateral, left lateral and ventral. These
groups of veins form circum¯ex, deep dorsal, cavernous,
and crural veins. The deep dorsal vein primarily drains
the glans penis, whereas in the mid and distal shaft, the
emissary veins either empty directly into the deep dorsal
vein or drain through ®ve to ten sets of circum¯ex veins
into the deep dorsal vein (which subsequently drains
into the periprostatic venous plexus). The base and hilum of the corpora cavernosa drain into many cavernous and crural veins, which join the periurethral vein
and form the internal pudendal vein. The super®cial
dorsal vein primarily drains the skin and subcutaneous
tissue of the penis. Communications exist between the
super®cial dorsal, deep dorsal, and cavernous veins of
the penis.
Venous drainage of the penis begins as tiny venules
from sinusoidal spaces, which merge into the subtunical
venous plexus. The emissary veins (approximately
100 lm) then originate from the subtunical venous
plexus.
Physiology of erection [27]
The sinusoids become distended during erection from
the arterioles and capillaries. The arterioles open directly
into the sinusoidal spaces and the capillaries supply the
connective tissue framework. In the ¯accid state, the
terminal arterioles are tortuous and contracted, whereas
during erection the arterioles and the main cavernous
artery become dilated and straight.
In the ¯accid state, the venous channels remain open
due to the constricted sinusoids. During erection, on the
other hand, the expanded sinusoids compress the tiny
venules in the trabeculae between them. With increasing
tumescence, expansion of the sinusoidal system against
the noncompliant tunica albuginea further compresses
the subtunical venous plexuses. At full erection, the
unequal stretch of the inner circular and outer longitudinal tunical layers further reduce the venous ¯ow to a
minimum.
246
Risk factors
Local penile trauma during aggressive sexual intercourse
is a well-identi®ed cause for PD. The presence of the
HLA antigen, DRW 52 (commonly found in patients
with certain autoimmune disorders) has been found to
be associated with PD. PD has been found to be associated with certain autoimmune diseases such as SjoÈgren's syndrome, BehcËet's disease, systemic sclerosis,
and systemic lupus erythematosus (SLE).
Pathophysiology and mechanism
of injury [2, 10, 15, 20, 36]
PD has a multifactorial etiology. Repetitive microtrauma of the penis during sexual intercourse is thought to
incite a local autoimmune reaction in genetically susceptible individuals.
Penile trauma acts as an initiating factor in the majority of young men with PD [4]. Abnormal healing of
tissue injury along with progressive chromosomal instability then results in PD. Altered composition of
certain tissue proteins in the extracellular matrix (such as
decorin, biglycan, ®bromodulin, gelatinase A, and collagenase II) in the tunica albuginea of men with PD has
been identi®ed, suggesting an abnormal remodeling
process following tissue injury [2, 10, 15, 36].
Some studies have found that levels of the enzyme,
nitric acid synthase (NOS) are also diminished in the
cavernous tissue of the penis in patients with PD. Normal
levels of this enzyme are essential for normal penile
erection. Diminished local concentration of this enzyme
may be one of the causes of erectile dysfunction in PD [29].
The disease is thought to result when blood leaks
(from penile trauma during intercourse/penile fracture)
from the corpora cavernosa during erection and accumulates between the layers of the tunica albuginea, resulting in excessive scar tissue production, and a plaque
formation [20]. This leakage of blood most often occurs
where the septal ®bers attach to the under surface of the
tunica albuginea, and this accounts for the most frequent location of the plaque in the dorsal midline and
along the septum.
Young men have strong elastic tissues that resist injury. Old men have weak tunica that tears, but their
erections are also weak and consequently injury does not
occur. In contrast, middle-aged men begin to lose the
elastic strength of their corporeal tissues and at the same
time maintain fairly strong erections making injury
likely. Injury may occur suddenly (in 1/3 of patients). In
the other two-thirds of cases injury may occur gradually
over a period of time, and these patients have a more
gradual onset and slow progression of the disease
(classical PD).
Men who sustain traumatic rupture of the tunica albuginea (fractured penis) experience sudden pain when
the penis is forcibly bent during erection. They then have
penile swelling and ecchymosis (local collection of clotted blood). If the defect in the tunica albuginea is not
repaired surgically, it will heal but a large scar or plaque
forms. This post-penile fracture penile plaque is located
laterally at the base of the penis.
Plaque distribution
The most common location for plaque in PD is the
dorsal midline resulting in an upward bend of the erect
penis. The next most common site is a dorsal midline
plaque with septal extension. The plaque may also extend from the dorsal midline circumferentially around
the corporeal bodies. Rarely, the plaque may be seen
between the corpus spongiosum and the ventral surface
of the corpora cavernosa. A dorsal plaque and a ventral
plaque may connect through septal extensions to form
an I-beam.
Peyronie's disease and erectile dysfunction
A signi®cant percentage of patients with PD have erectile dysfunction. The erectile dysfunction may be a result
of PD or may be occurring simultaneously. The causes
of erectile dysfunction in PD include psychological factors (performance anxiety), penile pain and deformity
(especially if it is ventral or lateral) preventing coitus,
¯ail penis/lack of tumescence due to cavernosal ®brosis
and penile vascular (arterial and/or venous) disease.
Diminished elastic ®ber content of the tunica along with
increased type III (immature) collagen may contribute to
veno-occlusive dysfunction in PD [7, 42].
In the acute in¯ammatory phase, patients su€er from
pain during ¯accidity and/or during erection and sexual
intercourse. In addition to pain, a predominantly dorsal
penile deviation is the main symptom; in later stages it is
often associated with erectile dysfunction and/or distal
¯accidity [47].
The anxiety associated with PD may trigger functional impotence; these patients may be referred to a sex
therapist and/or be treated with sildena®l citrate. In
addition, a mild erectile deformity may precipitate some
mechanical diculties during coitus. The patient should
be given reassurance and suggestions such as the use of a
water-soluble lubricant, elevation of the partner's hips
on a pillow, and manual guidance of the penis for
vaginal penetration.
Diagnosis
The ability of the patient to obtain and maintain an
erection should be determined, and any problems with
vaginal penetration or thrusting should be noted [1, 17,
22, 25, 35, 37]. If chordee (curvature) is present, the
247
patient should be asked to describe the direction and
extent (estimated in degrees). Any other erectile deformity should also be noted. This is best achieved with a
polaroid picture when the patient gets an erection.
On physical examination the penis should be stretched out and a careful examination for plaque should be
performed. The number, size, and location of plaques
are recorded, and whether the plaques are sharply demarcated. Intracorporal injections of vasoactive drugs
(Prostaglandin E1, Papaverine) are used to produce
erections, and if a full erection is not obtained after injection, visual sexual stimulation (VSS) can be used. This
allows the urologist to examine the erect penis and to
note the type and extent of erectile deformities (Fig. 1).
If an erection cannot be produced in the oce, the
clinician can ask the patient to make a polaroid photo of
his erect penis at home. Penile ultrasound can be useful
in determining the location and extent of plaque; however, not all plaque is readily visualized by ultrasound
and magnetic resonance imaging (MRI) may be better in
this regard. Contrast-enhanced MRI is especially useful
for a detailed assessment of the plaque prior to surgical
intervention in extensive PD.
Objective evaluation of erectile function is achieved
by assessment of penile arterial in¯ow (and arterial
collaterals), venous out¯ow and resistive indices (factors
useful in selecting patients with PD who can bene®t from
surgery for erectile dysfunction) by nocturnal penile
tumescence (NPT) testing and duplex ultrasound (after
injection of 10 mcg of PG-E1) [1, 17, 25, 35, 37]. In a
study by Kadioglu and associates, color Doppler ultrasonography (CDU) revealed penile vascular abnormalities in 76.5% of patients with PD. Veno-occlusive
dysfunction (VOD) was observed in 40% of men with
normal erection (based on history), whereas mixed (arterial + venous) vascular disease was diagnosed in 10%
[22]. In those who presented with erectile dysfunction,
penile vascular disease was detected in 87.5% patients
(VOD in 28%, arterial disease in 9.3% and mixed vascular disease in 50%). The prevalence of arterial disease
on CDU among PD patients with erectile dysfunction
(59.3%) was found to be signi®cantly higher than that
among patients with normal erection (10%). The prev-
alence of pure VOD was, however, similar in those with
or without erectile dysfunction. Penile vascular abnormalities were observed in 76.5% of PD patients by CDU
and this ratio increased to 87.5% in patients with erectile
dysfunction by history. In addition, arterial disease accounted for much of the diminished rigidity in those
with PD.
Careful documentation of the type and extent of
erectile deformity is important not only to plan therapy
but for medicolegal reasons as well. NPT studies, color/
duplex ultrasound examinations of the penile arteries
and MRI of the plaque are, therefore, helpful in identifying PD patients most likely to bene®t from the different surgical options currently available, such as penile
plaque excision, penile straightening procedures, and
penile prostheses. For example, patients with penile deformity combined with vasculogenic erectile dysfunction
are best treated by implantation of penile prosthesis.
Treatment
Many patients with PD may not have symptoms and
reassurance that the palpable lesion is not cancer is all
that is necessary. Treatment is indicated only when
penile pain (an indication of early disease) or deformity
is troublesome.
Medical treatment
Stabilization of the condition may require approximately 6 months [8, 12, 14, 16]. There is, therefore, a
waiting period between diagnosis and the decision to
start de®nitive surgical treatment. The condition usually
evolves over a period of time and in some patients it can
resolve or improve spontaneously without treatment.
Remission of PD in the early stage has been reported in
approximately 40%, overall spontaneous regression in
13%, stable disease in 47%, and progression in 40% of
patients [12, 14, 36].
Nonoperative treatment of Peyronie's disease
Fig. 1 Penile curvature (chordee) in Peyronie's disease
Conservative treatment is useful during the early in¯ammatory and painful stage of the disease. No causal
therapy is currently available due to the lack of concrete
knowledge regarding its etiology. Nonoperative treatment is mainly symptom-directed and mostly of questionable ecacy as no placebo controlled double blind
trials are available to date [8].
Agents tried include vitamin E, p-aminobenzoate,
orgotein (super oxide dismutase), clostridial collagenase,
procarbazine, dimethylsulfoxide (DMSO), parathyroid
hormone, b-aminopropionitrile, a-chymotrypsin, colchicines, tamoxifen, nonspeci®c antihistamines such as
terfenadine and fexofenadine, and systemic steroids
248
[11, 17, 31, 37, 44]. However, only vitamin E and potassium p-aminobenzoate were found to be useful [48].
Vitamin E is the traditional treatment of choice for
PD. It is easy to take, cheap, free of side e€ects and
better than placebo for treating the pain. It is used in a
dose of 400 mg twice daily. Vitamin E acts by its free
radical scavenging e€ect [3, 5, 37, 40, 43].
Para-aminobenzoate (Potaba) has been found to be
bene®cial in patients with noncalci®ed plaques. It is effective in a dose of 12 g per day (twenty four 500 mg
tablets or six 2 gram packets). In a retrospective review of
32 patients treated for at least 3 months, Carson reported
improvement in penile discomfort in eight, decreased
plaque size in 18, and improvement in penile angulation
in 18 [6]. However, this agent is very expensive, unpleasant to take and the recommended dose may be associated with signi®cant gastrointestinal side e€ects [26].
Potaba is to be taken for 12 months, which allows time
for the disease to stabilize and patients with persisting
symptoms may then be candidates for surgical treatment.
When the disease reaches the mature stage with curvature of the penis resulting in erectile dysfunction, surgical correction is indicated after a preliminary evaluation
for impotence with duplex Doppler study, dynamic infusion pharmacocavernosometry and cavernosography
(DICC) with/without nocturnal penile tumescence (NPT)
testing.
Early stage disease is more likely to respond to
medical therapy compared to long-standing Peyronie's
plaques. Most authorities currently recommend a trial
of medical therapy with a safe, inexpensive and welltolerated agent [17].
Other forms of treatment
These include radiation therapy, diathermy, laser treatment, ultrasound therapy, local injection of interferon
a-2b, dexamethasone, calcium channel blockers (verapamil), superoxide dismutase and collagenase into the
plaque, and iontophoresis ± rubbing of agents such as
steroids/histamine on the penis, the drug gets absorbed
through the skin and subcutaneous tissue [34, 35]. Recently iontophoresis with a combination of dexamethasone, lidocaine and verapamil has been reported to yield
pain relief in 96% of patients and improvement in penile
deviation in 37% in patients with a short history of
disease [39].
Intralesional injection of verapamil: 10 mg of verapamil is diluted in 10 cc of normal saline and injected
throughout the plaque every 2±4 weeks for a total of 6±
12 injections. A decrease in penile curvature has been
reported in 61% of the patients (range, 10±40°), an increase in penile curvature in 8.3%, and no change
in 31%. Improved sexual performance has been reported
in 91% of treated men. There were no recurrences over a
follow-up period of 6 years. [23]. None of the intralesional agents has been shown to have a long-term e€ect
in a controlled trial till date [8].
Current medical therapy (including vitamin E and
p-aminobenzoate) for PD results in symptomatic relief
only in some patients with painful and prolonged early
stage of the disease with active in¯ammation. Local radiation may sometimes be e€ective in relieving penile
pain and discomfort.
Recently, extracorporeal shock waves (ESWT) were
used to noninvasively target the plaque of PD [19, 30].
The mechanism of action of ESWT in PD is twofold:
direct damage to the plaque and increased vascularity of
the plaque (by local heat generation), which results in
local in¯ammatory reaction, lysis of the plaque, and
removal by phagocytic cells (macrophages).
Each patient is treated with a minimum of three
sessions of ESWT (3000 shock waves at an energy
density of 0.11±0.17 mJ/sq mm) at 3-week intervals.
Over a mean follow-up of 7.5 months (range, 5±11
months), 47% of the patients have reported an improvement in penile angulation (mean reduction, 29.3°)
(range, 10±60°). Sixty percent of patients with pain on
erection report immediate relief (mean reduction on the
visual analog scale, 2.3) (range, 1±4). No adverse e€ects
are reported except minimal bruising at treatment site.
In those with disease duration <12 months, ESWT
results in signi®cant improvement in both pain and angulation. However, the treatment is more e€ective in
reducing penile angulation in those with long standing
disease (>12 months) [19, 30].
Surgical treatment
The surgical management of PD consists of either correction of the penile deformity (once the disease is fully
stable) or the insertion of a penile prosthesis in those
with a concomitant erectile dysfunction. The various
operations are discussed below, but the choice rests between a Nesbit-type procedure and the implantation of a
penile prosthesis. The mere presence of a lump or a
minor erectile deformity is not an indication for surgery.
Indications for surgery in PD with
and without erectile dysfunction
Currently, there is no clear-cut evidence as to when (i.e.,
at which stage of the disease) semi-invasive and surgical
procedures are indicated, although it is believed that
conservative therapy is indicated in the earlier in¯ammatory and painful stage [8]. The role of conservative
therapy in nonresponders to drug therapy and for those
with calci®ed plaques who do not want surgery, remains
unanswered. In contrast to this, surgery (e.g., penile
straightening with or without plaque excision) can be
performed in patients with severe penile angulation
without loss of erection [24]. In those with PD and
erectile dysfunction, insertion of penile prosthesis is the
®rst-line therapy [24]. Many such patients, in fact, ask
249
for other treatments following failure of drug and intralesional therapy.
Dorsal penile curvature with preservation of penile
erection and optimal rigidity is treated by plaque incision/excision, grafting, and penile plication. Jean, Wessells and associates recently reported on partial penile
disassembly and corporal resection in a PD patient with
distal corporal narrowing with poor glans support [21].
On the other hand, severe erectile dysfunction due to
dorsal penile deviation combined with distal ¯accidity of
the penis in late stage of the disease may necessitate the
insertion of a penile prosthesis.
Surgery can only create a penis that is adequately
straightened to the extent that any residual curvature
does not impede sexual intercourse and erectile function
can be preserved at preoperative levels. Three surgical
procedures are commonly used in the treatment ofPD:
1. Penile plication (Nesbit's procedure) [45]
2. Plaque excision or incision with grafting (tunica
vaginalis/saphenous vein/dermal grafts/cadaveric
pericardium/dermabraded preputial patch) [4, 9, 13,
18, 28, 32]
3. Penile prosthesis implantation with or without corporoplasty [32]
The ®rst two procedures should only be used in men
who have no diculty in obtaining or maintaining
erections, and these procedures should not be employed
until it is reasonably certain that the PD is stable. Plication results in penile shortening, erectile dysfunction,
and diminished sexual satisfaction.
Penile prosthesis implantation is usually the procedure of choice when there is coexisting diculty obtaining or maintaining erections. Prosthesis should be
inserted only after resolution of the acute painful, in¯ammatory stage, which may take approximately
6 months.
Penile plication [24, 45]
Penile plication may be a reasonable option when there
is penile curvature without signi®cant narrowing or poor
distal rigidity. On the convex surface opposite the point
of maximal curvature, 1-cm longitudinal incisions are
made on the normal tunica. The incisions are then closed
transversely with running 3±0 PDS suture. Excellent
results with this procedure have been reported in 89% of
the patients and good results in 7%.
Plaque excision and grafting [4, 9, 13, 18, 28, 33, 46]
Large, thick, or calci®ed plaques are best excised. Access
to the plaque can be obtained through a degloving incision with circumcision or through a dorsal or ventral
longitudinal penile incision. Access to a dorsal plaque
requires re¯ection and preservation of the neurovascular
bundle, whereas access to a ventral plaque requires
elevation of the corpus spongiosum and urethra.
The defect in the tunica albuginea following plaque
excision is ®lled with a graft. Tissue used for grafting
includes: tunica vaginalis, temporalis fascia, saphenous
vein, lyophilized dura, dorsal penile skin and penile
dermal ¯ap. Synthetic graft materials (Dacron or GoreTex) have also been used but are not recommended
because of their inelasticity.
Plaque incision and saphenous vein graft has recently
been reported to yield good results (penile straightening
in 80% of the patients) during a follow-up period of
32 months.
Penile prosthesis implantation with
or without corporoplasty [32]
When men have both penile deformity and diculty in
obtaining or maintaining erections (due to vasculogenic
erectile dysfunction), penile prosthesis implantation is
preferred. Both semirigid and in¯atable (2-piece/3-piece)
penile prostheses are available. Semirigid prosthesis, is
however, often much more dicult to insert in patients
with corporal ®brosis. In most patients with PD an in¯atable prosthesis is utilized.
Conclusions
Peyronie's disease is an acquired condition probably
resulting from injury with a variable and sometimes selflimiting natural history. Patient and partner counseling
can be very helpful. Penile pain during erection is the
most common symptom in the early stage of the disease,
which can be treated by various agents. In patients who
develop a sexual disability because of signi®cant erectile
deformity, surgical treatment is indicated. No one surgical procedure is applicable to all patients with PD, and
the procedure should be selected based on the patient's
®ndings and wishes.
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