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warts may also manifest as dome-shaped, usually flesh- • Podophyllotoxin 0.5% solution or gel;
coloured papules; flat warts are flat-topped papules which • Cryotherapy withtrichloroacetic
Bichloroacetic or acid 35–85%;
may vary in colour from pink-red to reddish-brown [1,3]. • liquid nitrogen;
Lesions are frequently multifocal. Areas with increased • Electrofulguration;
friction are most commonly affected by condylomas; the • CO 2laser;
commonest location of primary infection in uncircum- • Imiquimod 5% cream.
cised men is the subpreputial region. Other sites of predi- Treatment is not confirmed to reduce transmission to
lection are the glans penis, coronal sulcus, frenulum, sexual partners nor to prevent progression to dysplasia or
prepuce, shaft and the scrotum (Fig. 1). They may also cancer. Treatments with antiviral or immunomodulatory
occur on the urethral meatus and can be intraurethral agents are associated with much lower rates of recurrence
(Fig. 2). The urethra is involved in 10–28% of patients [5]. It is estimated that 10–30% of genital warts resolve
[1,8]; condom users often have suprapubic warts. spontaneously within 3 months as a result of cell-
Subclinical lesions are detected by applying 3–5% acetic mediated immunity [6].
acid to the genital area for up to 5 min [6]. The acetic acid
produces white changes in HPV infected areas. However,
aceto-whitening is not a specific method for diagnosis,
Genital herpes
with false-positive results in up to 25% [6]. Subclinical
involvement is especially common in uncircumcised men. Herpes simplex virus (HSV) is the most common cause of
Treatment options for genital warts are [3,9]: genital ulceration [10]. Genital herpes simplex is predom-
inantly caused by HSV type 2, although HSV-1 is respon-
sible for 5–30% of cases of first-episode genital herpes
[10,11]. After infection, the viral genome remains in a
latent state in the nuclei of sensory neurones for the life of
the host [11]. Genital HSV-1 infections are usually less
severe and less prone to recur than those caused by HSV-
2. Genital herpes caused by HSV-1 is characterized by
lower rates of asymptomatic shedding and transmission.
From seroprevalence studies, genital herpes has increased
by ≈ 30% during the last two decades [10]. Transmission
of HSV occurs through both symptomatic lesions and
asymptomatic viral shedding. In 50–90% of transmis-
sions the infected partner is unaware of the herpes infec-
tion [10]. A recent study showed that condom use offers
significant protection against HSV-2 infection in suscep-
tible women [12].
Fig. 1. Multiple papular pigmented condylomata acuminata on the
Clinically, true primary genital herpes appears as mac-
penile shaft.
ules and papules, followed by vesicles, pustules and ulcers
[7]. Systemic complaints including fever, myalgias and
lethargy may be present, but are rare in men. Patients will
often have accompanying tender lymphadenitis. Recur-
rent episodes of genital herpes are characteristically less
severe and undergo rapid involution, healing within 5–
10 days [10,11]. Recurrent male genital infection may
present as three to five vesicles on the shaft of the penis.
Of those with a symptomatic first episode of HSV-2 genital
infection will recur in 80–90% within the following year,
but many patients will have unrecognized recurrent infec-
tions with asymptomatic viral shedding [13]. Asymptom-
atic shedding occurs most commonly in the first year after
the primary episode. The diagnosis of ulceration caused by
herpes may be highly suggestive when the usually
grouped blisters rupture and form coalescent grouped
Fig. 2. Numerous whitish condylomata acuminata on the tip of the erosions (Fig. 3). However, atypical clinical manifestations
penis. including deep, persistent ulcerations may occur in
Infestations
Scabies
Scabies is an infestation with a mite, Sarcoptes scabiei var
hominis. The mites burrow tunnels into the horny layer of
the epidermis. The female lays 2–3 eggs in the tunnels
each day; within 3–5 days the eggs hatch into larvae Fig. 4. Scabies; multiple erythematous papules.
which transform into nymphs, and these in turn meta-
morphose into adults [6]. Classic areas of infestation
include the web spaces of the hands, axillae, and the flexor
surfaces of the wrists [16]. Burrows are small, crooked lesions may be few or many, but it is very rare not to have
lines 4–6 mm long most frequently found in the web penile lesions in scabies (Fig. 4). The chief clinical symp-
spaces of the fingers, sides of the hands and flexor surfaces tom is pruritus, that is usually worse at night or after hot
of the wrist. With the development of the immune baths. Patients with very good hygiene have fewer specific
response to scabies, the patient develops erythematous lesions, making the diagnosis of scabies more difficult [6].
papules and nodules. Non-specific secondary, eczematous Generalized crusted scabies is found in immunocompro-
lesions are very common [16]. Multiple typical scabetic mised or physically incapacitated individuals; it has been
burrows and papules are often present on the glans penis, reported in patients with HIV infection and in organ-
scrotum and penis shaft [7]. Elsewhere on the skin the transplant recipients. These patients present with wide-
Fig. 6. Lichen planus; numerous annular violaceous papules on the Fig. 7. Lichen sclerosus; a typical white sclerotic ring at the tip of
glans penis. foreskin.
other sites. However, it may occur as the initial or sole Uncommonly, lichen sclerosus involves only the shaft of
manifestation. Rarely, lesions may become eroded similar the penis. If the glans is involved, haemorrhage is com-
to the erosive lichen planus of the oral mucosa. The diag- mon. In addition, haemorrhagic bullae, erosions and fis-
nosis is helped by the finding of typical lichen planus sures may also be present [7,20]. A very typical finding
papules, particularly on the wrists, hands, forearms, is the presence of a sclerotic white ring at the tip of the
shins, ankles and lumbosacral region. Oral lesions are prepuce (Fig. 7). With disease progression, the sclerotic
common and occur either as white reticulate streaks or lesions lead to contraction of the genital mucosa with sub-
as erosive lesions. In atypical cases biopsy may be neces- sequent paraphimosis or phimosis with inability to retract
sary to confirm the diagnosis. Most cases of genital the prepuce. Gradual narrowing of the external meatus
lichen planus respond to short courses of mild topical results in varying degrees of stricture and urinary flow
glucocorticoids [7]. may be obstructed [1,24]. Presenting symptoms are
pruritus, burning, painful erections, difficulty in retract-
ing the foreskin, dysuria, and a poor urinary stream. The
Penile lichen sclerosus
aetiopathology of lichen sclerosus is still unknown but
Lichen sclerosus of the male genitalia is a chronic inflam- genetic factors, an association with auto-immunity,
matory disorder presenting as a chronic, sclerosing atro- several infective agents such as borrelia, and local factors
phic process of the glans and foreskin, leading to meatal are postulated. The course of penile lichen sclerosus is
stenosis and acquired phimosis. Most authors consider chronic. The association between lichen sclerosus and
lichen sclerosus of the penis synonymous with balanitis squamous cell carcinoma (SCC) is a well-known phenom-
xerotica obliterans [20]. However, the latter can be a con- enon in women, and it has been observed in 3–6% of
sequence of other scarring dermatoses such as lichen pla- patients with vulvar involvement. There are anecdotal
nus and bullous disorders. The incidence of genital lichen reports of men developing penile SCC in association with
sclerosus in young boys with phimosis has been estimated lichen sclerosus. In a retrospective study of 86 uncircum-
at ≈ 15%, but the exact frequency in men is unknown cised patients with lichen sclerosus, five (6%) developed
[20,21]. Of 357 patients referred for diagnosis of genital malignant changes [25]. Three patients had SCC, one had
skin disease, 52 had lichen sclerosus [22]. Penile lichen in situ carcinoma and one had verrucous carcinoma. The
sclerosus is most common in middle-aged uncircumcised presence of HPV 16 was shown by PCR in four of the five
men. In a prospective study of 43 men with narrowing of cases. In a recent study of 20 patients with penile SCC, half
the prepuce referred for circumcision, lichen sclerosus had histological evidence of lichen sclerosus [26]. Periodic
was present in 32% [23]. Only 21% of the men had been follow-up of patients with lichen sclerosus is advisable,
clinically diagnosed as having lichen sclerosus. The initial including biopsy of any clinically suspicious lesions. A
lesions of lichen sclerosus are white, polygonal and flat- potent or ultra-potent topical steroid is the treatment of
topped papules or plaques. The lesions progress to ivory- choice for adults and children [21,27]. Topical clobetasol
coloured atrophic and sclerotic white plaques. In men, the proprionate 0.05% was helpful in ameliorating the symp-
glans and foreskin are usually affected, but not the peria- toms and lesions of lichen sclerosus. In men and young
nal region. However, the frenulum, urethral meatus and boys the most frequent surgical procedure required is
the anterior urethra may also be involved [7,20,21]. circumcision for a phimosis.
Fig. 9. Balanitis circumscripta plasmacellularis Zoon; a well- Fig. 10. Balanitis circinata; well-demarcated, erythematous plaque
circumscribed, shiny red plaque. with a ragged border on the glans penis.
Fig. 11. Bowenoid papulosis; multiple flat pigmented papules. Fig. 12. Penile SCC presenting as an erythematous, nodular, erosive
lesion on the glans penis.
Erythroplasia of Queyrat
and superficial basal cell carcinoma. Lesions may some-
Erythroplasia of the glans penis, described in 1911 by times be heavily pigmented and thus may resemble mela-
Queyrat [36], is a carcinoma in situ presenting as a noma in these cases. Biopsy is required to confirm the
sharply demarcated, slightly raised erythematous plaque diagnosis. If untreated, invasive SCC may arise in ≈ 5% of
on the glans penis or the inner side of the foreskin [1]. An cases. Surgical excision is the best treatment option for
individual lesion may be 10–15 mm in diameter, and sol- small lesions [9], preferably by cryosurgery or CO2 laser;
itary or multiple lesions occur; they are usually bright both methods have been used for many years with excel-
red, glistening and not tender. Their surface may be some- lent results.
what smooth, scaly to frankly warty. Patients usually
complain of pruritus, pain, bleeding and difficulty in
Penile SCC
retracting the foreskin. With time clinical ulceration may
occur and tends to correlate with histological evidence of Of all cancers affecting the penis 95% are SCC; the disease
invasive SCC. Most patients are in their fifth decade or is rare, with age-standardized incidence rates of 0.3–1.0/
older. In one series of 100 patients, 90% of cases occurred 100 000 men. However, the incidence rates are 10–20%
in men with a median age of 51 years. Erythroplasia is in some countries of Africa and South America [37]. The
usually seen in uncircumcised men, who account for 80– age at the onset of penile SCC has a wide range (20–
90% of reported cases. A definite diagnosis is made by a 90 years) with a peak around the fifth decade. Risk factors
biopsy showing the typical histological picture of intra- are phimosis, lack of circumcision, chronic inflammatory
epidermal carcinoma in situ. Early invasion should be conditions, multiple sexual partners and HPV infection
excluded by obtaining several biopsies. Transformation of [33,38]. Penile SCC is extraordinarily rare in circumcised
erythroplasia into SCC has been reported to occur in 10– males; the relative risk for developing penile cancer in
33% of cases [37]. Surgical excision is the treatment of uncircumcised compared with those circumcised at birth
choice, but topical 5-fluorouracil and the CO2 laser may is 3.2. Phimosis has been reported to be present in 44–
also be used. 85% of men with penile SCC [38]. In a series of studies,
HPV DNA was identified in 40–50% of cases with penile
cancer, most being of high-risk HPV 16 [2,38]. Prevention
Bowen’s disease
of SCC includes early detection and treatment of pre-
Bowen’s disease refers to SCC in situ and may arise any- cancerous lesions. The clinical appearance of penile SCC
where on the skin. Bowens’ disease of the glans penis is varies from erythematous plaque, induration to more
termed erythroplasia of Queyrat [1] and is usually found verrucous and exophytic lesions that may coalesce into an
on the shaft of the penis as a solitary, sharply defined irregularly shaped mass (Fig. 12). As it increases in size,
plaque of scaly erythema. Clinical variants include superficial ulceration, necrosis and bleeding may become
crusted and ulcerated plaques, keratotic plaques and ele- evident; it may become large, developing into a locally
vated flesh-coloured plaques. The skin of the inguinal and destructive mass [37]. The primary lesion may occur on
suprapubic areas may also be involved. Patients may have the glans or may be hidden under the foreskin. Primary
more than one lesion. Bowen’s disease may be confused tumour pathological staging and grading, and the
with bowenoid papulosis, nummular eczema, psoriasis involvement of pelvic and inguinal lymph nodes, are the
main factors used to predict the prognosis of patients with 20 English I, Laws R, Keough G, Wilde J, Foley J, Elston D. Der-
penile SCC. The treatment of penile SCC depends on matoses of the glans penis and prepuce. J Am Acad Dermatol
tumour staging and includes surgery, radiotherapy, laser 1997; 37: 1–24
surgery and chemotherapy [39]. Moh’s micrographic 21 Powell J, Wojnarowska F. Lichen sclerosus. Lancet 1999;
353: 1777–83
surgery has been used to advantage.
22 Mallon E, Hawkins D, Dinneen M et al. Circumcision and
genital dermatoses. Arch Dermatol 2000; 136: 350–4
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