- • Common viral infection characterized by flesh-colored,
pearly papules with central umbilication.
- • Self-limited in immunocompetent hosts.
Molluscum contagiosum is caused by the molluscum contagiosum
virus, a member of the DNA poxvirus group, and is common in children
and young adults. It is usually transmitted through sexual and other
The infection is characterized by firm, dome-shaped, flesh-colored, “pearly” papules
with central umbilication (see Figure 30–3). Although the
classic central umbilication may not be present on all lesions,
usually there are several on which this depression may be found.
If the lesion of molluscum contagiosum is incised, a central core,
usually waxy, can be expressed. The central umbilication and waxy
core help differentiate molluscum contagiosum from other diseases.
Lesions are most often asymptomatic but may be described as pruritic.
They are most often located in the pubic area, proximal and medial
thighs, and penile shaft. Lesions are larger and more numerous in immunosuppressed
Pearly papular lesions of molluscum contagiosum. Central
umbilication is present on some, but not all, of the lesions. (Courtesy
of Jay Sizemore, MD.)
Biopsy is rarely required to diagnose molluscum contagiosum.
If performed, histologic examination will reveal large eosinophilic
inclusion bodies within epidermal cells.
Molluscum contagiosum may be confused with condylomata acuminata,
and molluscum lesions that are more vesicular in appearance may
be confused with herpes simplex virus. Sebaceous gland hyperplasia,
basal cell carcinoma, and, in immunosuppressed individuals, fungal
infections such as cryptococcosis and histoplasmosis should also
be considered. If the patient presents with molluscum-like lesions
in the setting of systemic symptoms, evaluation should proceed quickly
to rule out disseminated fungal infection.
Although the course of infection in the immunocompetent host
is usually self-limited, generally resolving over months, patients
may desire treatment for cosmetic purposes. In contrast, molluscum
contagiosum in the immunocompromised host is often persistent, larger,
and more distressing to the patient in terms of appearance and often
Treatment requires either destructive or immunomodulatory modalities.
Molluscum contagiosum can be effectively treated with curettage
or incision followed by expression of the central white core of
the lesion, also known as the “molluscum body.” Other
therapeutic modalities include electrosurgery and cryotherapy. Cantharidin
may be used for lesions found outside the genital region but, because
of painful blisters and erythema that result from therapy, should
be avoided in sensitive areas of the body. Recent studies have found
variable success with imiquimod, applied three times a week overnight
for up to 16 weeks; clearance rates have ranged from 33% to
100%, depending on the population studied. Finally, podophyllin,
podofilox 0.5%, laser therapy, and trichloroacetic acid
may be used.
Molluscum contagiosum is usually not eliminated in one treatment
and lesions may continue to occur for a time after treatment. Relapse
is particularly frequent in immunocompromised hosts.
Barba AR, Kapoor S, Berman B. An open label safety
study of topical imiquimod
5% cream in the treatment of
Molluscum contagiosum in children. Dermatol Online J
small study [n = 12] found
5% cream nightly for 4 weeks to be a safe treatment
in children with molluscum contagiosum.)
Liota E, Smith KJ, Buckley R, et al. Imiquimod
therapy for molluscum
contagiosum. J Cutan Med Surg
(In this study, molluscum contagiosum lesions
in 14 of 19 immunocompetent adults, 4 of 4 adults with HIV type
1 disease, and 6 of 13 children resolved in less than 16 weeks with
Ting PT, Dytoc MT. Therapy of external anogenital warts and
molluscum contagiosum: A literature review. Dermatol Ther
(Recent comprehensive review of wart and molluscum
contagiosum treatments, including physical and chemical destruction,
surgical removal, and biologic response modifiers to enhance the
natural immune response.)
Squamous Intraepithelial Neoplasia & Squamous Cell Carcinoma
- • Lesions are characterized by skin-colored, pink
or white, flat-topped papules or plaques that may ulcerate over
- • Lesions typically are present for a year or longer.
The terminology describing squamous intraepithelial neoplasia
has proved to be confusing at times to the nondermatologist. The
histology of intraepithelial neoplasia is described using terminology
similar to that used to describe Papanicolaou (Pap) smears and represents
a spectrum from mild dysplasia of the epithelium to severe dysplasia
(carcinoma in situ). The final step in this pathway is frankly invasive
squamous cell carcinoma, which has metastatic capability. Vulvar involvement
with intraepithelial neoplasia is referred to as vulvar intraepithelial
neoplasia, and penile involvement as penile intraepithelial neoplasia.
There is currently a move to use this more general terminology and
steer away from the terms used to describe various types of intraepithelial
neoplasia that were used in the past that included, but were not
limited to, Bowen’s disease, bowenoid papulosis, keratotic
balanitis, and erythroplasia of Queyrat.
Multifocal intraepithelial neoplasia has been documented to occur
in a slightly younger age group (20–40 years) than unifocal
disease (typically >50 years) and is more likely
to be linked to high-risk HPV types, primarily 16 and 18. Multifocal intraepithelial
neoplasia is less likely to progress to frankly invasive squamous
cell carcinoma, as compared with single lesion intraepithelial neoplasia.
Risk factors for the development of intraepithelial neoplasia
include advanced age, smoking, and compromised immune status. The
presence of a long-standing inflammatory dermatologic condition
such as lichen sclerosis is a risk factor for the development of
squamous cell carcinoma.
The appearance of intraepithelial neoplasia is variable, and
lesions may be flesh-colored, red, or white. Multifocal intraepithelial
neoplasia (formerly known as bowenoid papulosis) usually appears
as multiple discrete flat-topped papules or plaques on the glans,
prepuce, and penile shaft in men or the vestibule and outer labia
minora in women. Single lesion intraepithelial neoplasia is usually
a larger, well-defined patch or plaque with scale that may ulcerate
over time. Some forms of intraepithelial neoplasia, especially after
progression to squamous cell carcinoma, may appear more verrucous,
become friable, and bleed easily (see Figure 30–4). Long-standing
squamous cell carcinoma may result in destruction of the genitalia
(see Figure 30–5).
Squamous cell carcinoma in situ (vulva). (Courtesy of
Lauren Hughey, MD.)
Squamous cell carcinoma resulting in destruction of the
penis. (Courtesy of Jay Sizemore, MD.)
The history is the key to the correct evaluation and diagnosis
of patients with intraepithelial neoplasia and squamous cell carcinoma.
The time course of the lesion is long, often on order of years. The
lesions are usually asymptomatic, although some patients may complain
of pruritus, with growth so slow as to often be imperceptible.
The diagnosis of intraepithelial neoplasia and squamous cell
carcinoma should be confirmed by biopsy.
Vulvar intraepithelial neoplasia and penile intraepithelial neoplasia
may be confused with condylomata acuminata. Some forms of squamous
cell carcinoma may be confused with granuloma inguinale (donovanosis).
Biopsy can distinguish between these etiologies.
Treatment of vulvar intraepithelial neoplasia, penile intraepithelial
neoplasia, and squamous cell carcinoma involves local destruction
or removal of lesions. Patients should be referred to a dermatologist
and may require referral to a gynecologist or urologist if the disease
process is advanced.
Inflammatory Papules & Plaques
- • Characterized by often widespread papulosquamous,
hyperpigmented, scaling lesions that develop a “Christmas
tree” pattern on the back.
- • Widespread rash is often preceded by a “herald
A common rash affecting children and young adults, pityriasis
rosea is often asymptomatic but distressing due to its generalized
nature. The etiology is unclear but is thought to be a postviral exanthema,
a hypothesis supported by the self-limited nature of the rash and
the fact that cases often appear in clusters.
The first symptoms of pityriasis rosea frequently include nonspecific
viral respiratory tract symptoms followed by the development of
the herald patch, usually located on the trunk. The herald patch
is usually 2–10 cm in diameter, ovoid, erythematous, and
slightly raised with a collarette of scale at the margin.
Several days to weeks after the appearance of the herald patch,
a widespread rash appears, with lesions typically concentrated on
the trunk. The extremities may become involved and, rarely, the palms
and soles. Genital involvement may also occur, leading the patient
to present to an STD clinician for care. The generalized rash is
salmon-colored and, like the herald patch, ovoid with a collarette
of scale (see Figure 30–6). Lesions follow Langer lines
(cleavage lines) and, when they occur on the back, result in a “Christmas
tree” pattern. Pityriasis rosea may occur in an inverse form,
in which the rash is concentrated on the extremities and the trunk
is spared. The rash also may be localized.
Pityriasis rosea. (Courtesy of Lauren Hughey, MD.)
Although classic pityriasis rosea is readily recognized, less
typical patterns of rash distributions often present diagnostic
challenges. The most common symptom reported in patients with pityriasis
is pruritus. Otherwise, no systemic symptoms occur at the time the
rash is present.
The diagnosis of pityriasis rosea is usually based on the clinical
appearance of the rash. Biopsy is rarely necessary to make the diagnosis.
The herald lesion may be confused with tinea corporis, especially
in the absence of the generalized rash. Secondary syphilis is an
important consideration in the differential diagnosis, and a nontreponemal
serologic test (eg, rapid plasma reagin [RPR] or
Venereal Disease Research Laboratories [VDRL])
should be performed to rule out this etiology in sexually active
individuals. (See Chapter 19 for discussion of the presentation
of secondary syphilis.)
The rash usually lasts 5–8 weeks, and the control of
pruritus is the primary goal of therapy. Topical or systemic corticosteroids
and a commonly used antihistamine such as hydroxyzine, 25 mg orally
up to four times daily, may be used to provide symptom relief.
Stulberg DL, Wolfrey J. Pityriasis rosea. Am Fam
review of the diagnosis and management of this common condition.)
- • Superficial dermatophyte infection most commonly
caused by Trichophyton rubrum, Trichophyton mentagrophytes, and
- • Rash often has a leading edge and scale.
Tinea cruris is a common dermatologic condition encountered by
primary care providers and STD clinicians. The condition is most
commonly caused by the dermatophytes T rubrum, T mentagrophytes,
and M canis and is transmitted by transfer of arthroconidia-laden
scales through direct contact with an infected individual or through
contact with objects that carry the infected scales. Autoinfection
may also play a role.
Once infection occurs, the organism invades the stratum corneum
and the terminal hair of the affected area, resulting in a rash
that frequently extends from the groin to the inner thighs and perineal
or perianal areas. The rash often has a leading edge and scale with
central clearing, giving it an annular appearance. The primary symptom
The diagnosis may be confirmed by scraping the leading edge of
the affected skin and adding 10–15% potassium
hydroxide to the specimen. Examination under a microscope often
reveals septate hyphae coursing through the squamous cells. A culture
of skin scrapings, plated on Sabouraud agar media and incubated
at room temperature, typically yields an organism within 2 weeks.
Seborrheic dermatitis, psoriasis, candidiasis, eczema, and lichen
simplex chronicus are the primary dermatoses to be differentiated
from tinea cruris. Eczema, unlike tinea cruris, more commonly involves
the labia majora and scrotum. Psoriasis can usually be differentiated
based on the presence of typical psoriatic lesions elsewhere on
Treatment of tinea cruris most often involves topical therapy
with an antifungal agent such as an azole (miconazole, clotrimazole,
etc), an allylamine (naftifine, terbinafine), benzylamine derivatives
(butenafine), and hydroxypyridones (ciclopirox olamine). Occasionally,
oral therapy may be required. Possible oral therapeutic agents include
fluconazole, 150–300 mg weekly for 2–4 weeks;
itraconazole, 200 mg/day for 1 week; terbinafine, 250 mg/day
for 2–4 weeks; ketoconazole, 200 mg/day for 4–8
weeks; and griseofulvin, 250 mg twice daily until cured.
Gupta AK, Chaudhry M, Elewski B. Tinea corporis,
tinea cruris, tinea nigra, and piedra. Dermatol Clin
(Review of the diagnosis,
management, and prevention of tinea infections with special attention
to differential diagnosis.)
- • May be caused by allergic response to an agent
or the direct irritant effect of an agent.
- • Acute inflammation manifests as erythema, edema,
vesicles, bullae, or superficial erosions with exudation.
- • Chronic inflammation is characterized by lichenification,
scaling, fissures, and hypo- or hyperpigmentation.
Contact dermatitis is one of the most common non-STD genital
dermatoses encountered in a patient presenting for STD evaluation.
It is characterized by an inflammatory response mediated by a specific
immunologic response (type IV) to an allergen (allergic contact
dermatitis), or occurring as the result of a direct irritant effect
of an agent on the skin (irritant contact dermatitis).
The inflammatory process may be acute or chronic at the time
the patient presents for care. The acute phase of a contact reaction
is often characterized by erythema, edema, vesicles, and bullae, with
progression to erosions and exudation in some cases (see Figure
30–7). The patient may complain about irritation, itching,
and burning at this time. The onset of symptoms may provide a clue
to the pathophysiology of the response, because allergic contact
dermatitis classically presents within 12–48 hours of antigen
exposure and persists for 3–4 weeks, whereas irritant contactants
may elicit symptoms within minutes to hours. However, this is not
a hard and fast rule, and the differentiation between potential
pathophysiologies (allergic versus irritant) involved in the process
is not important in terms of determining the treatment regimen.
Contact dermatitis secondary to neomycin cream. (Courtesy
of Lauren Hughey, MD.)
Although the distribution and location of a contact dermatitis
rash can give important clues as to the offending agent when located
in other areas of the body, the warmth and dampness that is inherently
present in the genital area often lead to the contactant being spread
around and the subsequent loss of any defined pattern. If the etiology
of the allergic or irritative response is not elicited and the response
becomes chronic, the skin often becomes lichenified and scaly, and
fissures may develop. In addition, postinflammatory hyper- or hypopigmentation
may result, leading to additional cosmetic concerns. Table 30–2
lists some common causes of contact dermatitis affecting the genital
Table 30–2. Common Causes of Contact Dermatitis Affecting the Genital Area. ||Download (.pdf)
Table 30–2. Common Causes of Contact Dermatitis Affecting the Genital Area.
|Topical medications (eg, benzocaine, nupercaine, diphenhydramine, neomycin)|
|Latex (condoms, diaphragms, elastic bands)|
|Personal hygiene products|
|Wart medications (eg, trichloroacetic acid, podophyllin, liquid nitrogen, fluorouracil, cantharidin)|
|Feces or urine|
The diagnosis of contact dermatitis is dependent on a thorough
history and examination of the patient. It is important to ask about
sexual and grooming habits of both the patient and his or her sex
partners, because the patient’s dermatologic condition
may be a manifestation of a response to something the partner is
using (ie, condoms or spermicide). Examining the skin outside the
genital area may yield important clues as well.
Patients in whom a specific contactant cannot be implicated or
who fail to respond to appropriate treatment may require referral
to a dermatologist for patch testing. Patch testing is not a useful diagnostic
test for irritant contact dermatitis, which is not an immunologically
The differential diagnosis of contact dermatitis is broad. For
chronic contact dermatitis it includes atopic dermatitis, seborrheic
dermatitis, psoriasis, and fungal infections such as tinea cruris. Acute
contact dermatitis may be confused with herpes simplex virus infection,
pemphigus vulgaris, candidiasis, and other blistering or erosive
diseases. The differentiation between these diseases may be made
on the basis of history and the distribution of lesions, especially
when other areas of the body are involved.
The cornerstone of treatment of contact dermatitis is identification
and removal of the offending agent. Unfortunately, the longer the
process continues, the more difficult it can be to determine the
etiology of the initial insult, especially as patients often self-treat
and thereby may confuse the picture. If the specific contactant
cannot be identified, the patient should be instructed to avoid
all topical agents in the genital area except clear water and petrolatum.
Unscented, mild soaps may be used in moderation if the patient feels
the need to cleanse the area with something besides water.
Acute contact dermatitis may be improved through the use of cool
soaks and sitz baths. Oral prednisone may speed recovery of acute
allergic dermatitis at doses of 40–60 mg/day and
should be tapered rapidly over 5–10 days. Topical low-
and mid-potency corticosteroids, such as 1% hydrocortisone
ointment twice daily or triamcinolone 0.1% twice daily,
respectively, may be used as well, especially if inflammation is
not severe. Topical corticosteroid creams and ointments may be used
for chronic contact dermatitis, although long-term use of these
products may lead to steroid atrophy. Finally, nighttime sedation
(eg, with an antihistamine) should be employed to prevent symptoms
of irritation and itching that are often noticed more at night.
McKenna JK, Leiferman KM. Dermatologic drug reactions.
Immunol Allergy Clin North Am
(This review focuses on the most common or severe cutaneous
drug reaction patterns. Knowledge of the clinical morphology and
the most commonly associated medication aids in rapid diagnosis
and institution of the appropriate therapy.)
- • Common dermatologic condition that frequently
affects the genitalia.
- • Skin findings outside the genital region are often
the key to the diagnosis.
Psoriasis is a relatively common dermatologic disorder caused
by an unusually rapid proliferation of the epidermis. Although the
cause is unknown, there is a strong hereditary component to the disease,
and approximately one third of patients report a family history.
Psoriasis also is seen more frequently in HIV-infected individuals.
For example, preexisting psoriasis may worsen in an individual who
becomes HIV-infected or, conversely, an HIV-infected individual
with a genetic predisposition may present with psoriasis for the
first time. Therefore, psoriasis may be one of the first signs of
HIV infection and should lead the clinician to consider HIV testing
of the individual, especially when the onset of disease is rapid
and the case is severe.
Psoriasis is classically manifested as red, sharply demarcated
plaques with silvery scale and frequently involves the scalp, elbows,
knees, gluteal cleft, and umbilicus. Approximately 50% of patients
with psoriasis have typical nail findings including, but not limited,
to nail pitting. Genital lesions, when present, are often not as
thick as those found on other areas of the body and typically have
less scale. Pruritus may or may not be present.
Inverse psoriasis, a variant with prominent genital involvement,
may predominantly involve the skinfolds such as the axilla, gluteal
fold, inframammary skin, umbilicus, and crural creases. The lesions
of inverse psoriasis may not be as thick and well marginated, and
the classic silvery scale is often less apparent. Although inverse
psoriasis may be seen in immunocompetent hosts, immunodeficient
individuals, particularly those who are HIV-infected, are more likely
to present with this form of psoriasis.
Psoriasis often has nail manifestations, including nail pitting, “oil-drop
spots” (brownish-red discoloration of the nail bed), and
onycholysis. Nail findings should be sought during the clinical evaluation
of the patient, because they may provide helpful diagnostic clues,
especially given the often less characteristic qualities of the
The diagnosis is often made on the basis of a consistent genital
rash in the setting of characteristic lesions present elsewhere
on the body. Biopsy may be necessary to confirm the diagnosis in
the absence of extragenital involvement or when the genital lesions
are not characteristic.
The differential diagnosis of genital psoriasis includes lichen
simplex chronicus, vulvar intraepithelial neoplasia or penile intraepithelial
neoplasia, tinea cruris, and seborrheic dermatitis. Inverse psoriasis,
in particular, may be confused with a fungal infection and should
be considered in the differential diagnosis when a patient has a
refractory yeast infection.
A full discussion of the treatment of psoriasis is outside the
scope of this chapter. Although topical corticosteroids are first-line
therapy, potent and ultrapotent formulations usually are necessary, and
long-term corticosteroid use is likely. Patients should be referred
to a dermatologist for management.
- • Disease of cell-mediated immunity characterized
by many different morphologic appearances.
- • Lesion characteristics depend on the type of epithelium
Lichen planus is a disease of cell-mediated immunity characterized
by well-circumscribed violaceous or brown flat-topped papules with
white striae (Wickham striae) and scale, when keratinized epithelium
is involved. The glans penis or keratinized surfaces of the vulva
may be involved, and lesions may have a polyhedral or an annular
configuration. Mucous membrane involvement with lichen planus is
marked by the presence of a fernlike or lacy reticular pattern on the
vulvar vestibule, vagina, or, in instances when the mouth is involved,
the buccal mucosa. Severe mucous membrane involvement, known as
erosive lichen planus, may result in denudation of the epithelium
and a malodorous, profuse vaginal discharge. The papular and mucous
membrane variants of lichen planus may coexist in one patient.
Severe itching may be present, especially with the papular variant,
whereas burning, irritation, and dyspareunia are more common with
erosive lichen planus, particularly when the vaginal area is involved.
Characteristic areas of involvement in lichen planus that may yield
diagnostic clues during the examination include the ventral aspect
of the wrist (papular lichen planus) and the buccal mucosa (fernlike
The clinical diagnosis of lichen planus is made by finding typical
fernlike white papules on the mucous membranes or modified mucous
membranes of the buccal mucosa or vagina. A biopsy may be necessary
to confirm the diagnosis.
The differential diagnosis of papular genital lichen planus includes
a host of dermatologic conditions, including Bowen disease (vulvar
intraepithelial neoplasia or penile intraepithelial neoplasia),
psoriasis, and candidiasis. Erosive lichen planus may be mistaken
for lichen sclerosus, cicatricial or bullous pemphigoid, or pemphigus.
Papular lichen planus usually resolves over the course of years.
Erosive lichen planus, especially severe forms, may lead to genital
scarring, obliteration of the vaginal vault, or resorption of the genitalia.
Topical, and occasionally oral, corticosteroids are often necessary
to control disease. The patient should be referred to a dermatologist
or gynecologist for optimal management.
Vesicles, Bullae, & Erosions
Erythema Multiforme, Stevens-Johnson Syndrome, & Toxic Epidermal Necrolysis
- • Rash characterized by targetoid lesions, with
or without blisters, and frequent mucous membrane involvement.
- • Often associated with specific medications and
Erythema multiforme is a dermatologic disease frequently encountered
during the practice of medicine. It is characterized by targetoid
lesions, with or without blisters, that tend to be in an acral distribution.
Oral lesions and mucosal involvement may also be present, and it
is possible for the rash to be confined to the palms, soles, and
mucous membranes alone. Blisters located on mucosal surfaces erode
quickly to form ulcers. Although lesions heal relatively quickly,
scarring may result, especially when involvement is severe, as in
Stevens-Johnson syndrome and toxic epidermal necrolysis.
Erythema multiforme may be associated with various medications
and infectious processes. Recurrent erythema multiforme, for instance,
is commonly associated with herpes simplex virus infections. Many
experts think that erythema multiforme is on one end of a clinical
spectrum, followed by Stevens-Johnson syndrome and toxic epidermal
necrolysis, but this idea is controversial. Stevens-Johnson syndrome
and toxic epidermal necrolysis are characterized by progressively increased
mucosal involvement, widespread full-thickness epidermal necrosis
and detachment (<10% for Stevens-Johnson
syndrome and >30% for toxic epidermal
necrolysis), and increasing mortality rates ranging from 5% for
Stevens-Johnson syndrome to 40% for toxic epidermal necrolysis.
The diagnosis of erythema multiforme, Stevens-Johnson syndrome,
or toxic epidermal necrolysis is made on the basis of the characteristic
skin lesions, the extent of cutaneous and mucous membrane involvement,
and the medication history. In the case of recurrent erythema multiforme,
a history of recurrent herpes simplex virus infection is helpful.
A biopsy may be necessary to confirm the diagnosis and rule out
Pemphigus vulgaris and bullous pemphigoid may be difficult to
differentiate from blistering forms of erythema multiforme. Fixed
drug eruption should also be considered in the differential diagnosis,
although the number of lesions seen in a fixed drug eruption is
usually far fewer than the number seen in erythema multiforme.
Evaluation of patients presenting with symptoms consistent with
these entities is urgent, because withdrawal of the offending drug
is the most important aspect of treatment of drug-induced disease.
In cases of recurrent erythema multiforme, suppression of herpes
simplex virus is helpful, although the acute treatment of the virus
is not as beneficial. Local care is important to prevent bacterial
superinfection. The use of intravenous immune globulin has been
reported to be helpful in more severe, blistering forms of erythema
multiforme whereas corticosteroid use continues to be controversial.
- • Skin and mucous membrane lesions may be present.
- • Lesions recur at the same sites following rechallenge
with the implicated drug.
Fixed drug eruption is a hypersensitivity reaction to a specific
medication. Commonly implicated medications are listed in Table
30–3. Lesions vary in appearance depending on the type
of epithelium involved. Lesions involving keratinized epithelium,
for instance, appear as a well-demarcated, round, erythematous plaque
whereas mucous membrane lesions blister and erode quickly. The glans
penis is the most commonly involved genital site. Patients may complain
of burning in the area of involvement. Rechallenge with the offending
medication results in a recurrence of the lesions in the same places.
The lesions frequently become more severe and result in more pronounced
postinflammatory hyperpigmentation with each rechallenge.
Table 30–3. Drugs Commonly Implicated in Fixed Drug Eruptions.
Diagnosis is usually based on the appropriate clinical appearance
in the setting of a consistent medication history. Biopsy is rarely
needed but the histologic findings are characteristic. Recurrent
herpes simplex virus, erosive lichen planus, and trauma are the
primary etiologies to be considered in the differential diagnosis.
Withdrawal of the offending agent is the primary treatment, and
lesions usually resolve within 7–10 days after removal
of the agent. Local care may be necessary.
- • The most common genital dermatosis characterized
by white or hypopigmented lesions.
- • Women are affected more often than men.
Lichen sclerosus is a relatively common, often asymptomatic disorder
that results in hypopigmentation, thinning of the skin, and increased
tissue fragility. It most commonly affects the genitalia although
other sites may be involved, including the trunk and arms. The etiology
is unknown, but it has been associated with autoimmune diseases.
Findings on physical examination include white papules and plaques
that are covered by atrophic skin having the consistency of cigarette
paper. The lesions may become confluent, and the periclitoral area,
labia minora, interlabial sulcus, perineum, and perianal area may
become involved (see Figure 30–8). When all of these areas
are involved, a classic figure-of-eight pattern may result. In men,
involvement of the prepuce and glans are most common. Pruritus is
the most common symptom. Due to tissue fragility, secondary changes
may occur, including ecchymoses, erosions, and excoriations—findings
that may be confused with sexual abuse, especially in children.
Long-standing, poorly controlled lichen sclerosus is associated
with genital scarring as well as an increased risk for squamous
Classic hypopigmented lesions of lichen sclerosis. (Courtesy
of Lauren Hughey, MD.)
The differential diagnosis of lichen sclerosus includes vitiligo,
postinflammatory hypopigmentation, and the end stage of other poorly
controlled genital dermatoses, including lichen planus and cicatricial
The diagnosis may be made on a clinical basis but should be confirmed
by biopsy. Patients should be referred to a dermatologist for management.