Background

Lichen simplex chronicus (LSC) is thickening of the skin with variable scaling that arises secondary to
repetitive scratching or rubbing. Lichen simplex chronicus is not a primary process. Rather, a person
senses pruritus in a specific area of skin (with or without underlying pathology) and causes
mechanical trauma to the point of lichenification.
A proposed variant of lichen simplex chronicus is lichen amyloidosis. Lichen amyloidosis is described
as lichen simplex chronicus in which the keratinocytes have necrosed and formed keratinocyticderived amyloid in the dermis. The initial insult is pruritus with resultant amyloid formation, rather than
the reverse.[1, 2]

Pathophysiology
Lichen simplex chronicus is found on the skin in regions accessible to scratching. Pruritus provokes
rubbing that produces clinical lesions, but the underlying pathophysiology is unknown. Some skin
types are more prone to lichenification, such as skin that tends toward eczematous conditions (ie,
atopic dermatitis, atopic diathesis). A relationship likely exists between central and peripheral neural
tissue and inflammatory cell products in the perception of itch and ensuing changes in lichen simplex
chronicus. Emotional tensions in predisposed subjects may play a key role in inducing a pruritic
sensation, leading to scratching that can become self-perpetuating.[3] The possible interplay among
primary lesions, psychic factors, and the intensity of pruritus additively influence the extent and
severity of lichen simplex chronicus.
A small study looking at lichen simplex chronicus and the use of P-phenylenediamine (PPD)
containing hair dye showed clinically relevant improvement in symptoms after discontinuation of PPD
exposure, thus providing a basis for the role of sensitization and contact dermatitis in the etiology of
lichen simplex chronicus.

Epidemiology
Frequency
International
Exact frequency in the general population is unknown. In one study, 12% of aging patients with
pruritic skin had lichen simplex chronicus.

Mortality/Morbidity
No mortality occurs as a result of lichen simplex chronicus. Overall, pruritus of lichen simplex
chronicus is mild to moderate, but paroxysms may occur that are relieved by moderate-to-severe
rubbing and scratching. Pruritus is usually described as much worse during periods of inactivity,
usually at bedtime and during the night. Touch and emotional stress also may provoke pruritus, which
is relieved by moderate-to-severe rubbing and scratching.
Lesions cause little direct morbidity; however, occasionally patients report decreased or interrupted
sleep, which affects motor and mental functioning.
Lichen simplex chronicus may become secondarily infected after excoriation.
Lichen simplex chronicus is often visible enough to cause patients to seek treatment.

Race
No differences are reported in frequency among races, although prior authors claimed lichen simplex
chronicus was more common in Asians and African Americans. The appearance of lesions on darker
skin sometimes shows follicular prominence. Secondary pigmentary alterations are also more severe
in individuals with darker skin.

Sex
Lichen simplex chronicus is observed more commonly in females than in males. Lichen nuchae is a
form of lichen simplex that occurs on the midposterior neck and is observed almost exclusively in
women.

Age
Lichen simplex chronicus occurs mostly in mid-to-late adulthood, with highest prevalence in persons
aged 30-50 years.

History
Patients with lichen simplex chronicus usually describe stable pruritic plaques on one or more areas;
however, thickening of the skin occurs on any location that the patient can reach, including the
following:

Scalp
Nape of neck
Extensor forearms and elbows
Vulva and scrotum[4, 5]
Upper medial thighs, knees, lower legs, and ankles
Erythema is noted most in early lesions.
Pruritus is described as worse when patients are still or quiet and as much less or nonexistent when
patients are active.
Pruritus is usually intermittent; the resultant scratching provides temporary relief.
Patients may have a past medical history of a chronic skin condition or acute trauma. Patients with
atopic dermatitis may have lichen simplex chronicus in areas of former atopic outbreaks. Sites of
irritant or allergic contact dermatitis, insect bites, or other past minor skin trauma sometimes
demonstrate pruritus and, subsequently, lichen simplex chronicus.

Physical
One or more slightly erythematous, scaly, well-demarcated, lichenified, firm, rough plaques with
exaggerated skin lines are noted.
Each palm-sized plaque may have 3 zones. A 2- to 3-cm wide peripheral zone that is barely thickened
may have isolated papules. The middle zone has lenticular and hemispheric prurigo papules that may
be excoriated. The central zone has the greatest thickening and pigmentary alteration.
Pigmentary changes (especially hyperpigmentation) are seen variably as in any dermatitic lesion.
Rubbing plays a key role in lesion formation and is visualized variably by white scratch marks, erosion,
and ulceration from deeper scratching.
Lichen simplex chronicus is one of the hyperkeratotic processes from which a cutaneous horn may
grow.[6]
Patients may scratch lesions de novo when observed. Some patients may start scratching while
discussing the itch or describing the lesions.
Note the images below.

Plaque of lichen simplex chronicus demonstrating accentuated skin markings.

Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.

Area of lichen simplex chronicus originally believed to be chronic contact

dermatitis. The true nature was revealed when the patient admitted to rubbing this area while watching television.
Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.

Causes
Atopic dermatitis results in a higher probability of developing lichen simplex chronicus.
Insect bites, scars (eg, traumatic, postherpetic/zoster[7] ), acne keloidalis nuchae,[8]xerosis, venous
insufficiency, and asteatotic eczema are common factors.
Psychological factors appear to play a role in the development or exacerbation of lichen simplex
chronicus.[9] Anxiety has been reported to be more prevalent in patients with lichen simplex chronicus.
Neurodermatitis is a term formerly used interchangeably with lichen simplex chronicus, suggesting a
role of anxiety or obsession as part of the pathological process of developing lesions.
Lithium has been linked to lichen simplex chronicus in one reported case. Lichen simplex chronicus
was dependent on the administration of lithium as evidenced by the observation that the lichen
simplex chronicus remitted when the medication was discontinued and recurred when it was
restarted.[10]
A small study looking at lichen simplex chronicus and the use of PPD-containing hair dye showed
clinically relevant improvement in symptoms after discontinuation of PPD exposure, thus providing a
basis for the role of sensitization and contact dermatitis in the etiology of lichen simplex chronicus.[11] .
Several of the patients who cleared after avoiding paraphenylenediamine had widespread, not
localized, dermatitis.
Long-term exposure to street traffic exhaust has been associated with an increase in the frequency of
childhood skin diseases, including lichen simplex chronicus.[12]
Some reserve the diagnosis of lichen simplex for patients who have no known predisposing skin
disorder. The term secondary lichenification has been used if the eruption is initiated by a primary
dermatosis.

Laboratory Studies
An elevated serum immunoglobulin E level occasionally supports the diagnosis of an underlying
atopic diathesis. Perform potassium hydroxide examination and fungal cultures to exclude tinea cruris
or candidiasis in patients with genital lichen simplex chronicus.

Other Tests
Patch testing helps exclude allergic contact dermatitis as an underlying primary dermatosis (eg,
allergic contact dermatitis to nickel with secondary lichen simplex chronicus) or as a factor in
chronicity (eg, allergic contact dermatitis to topical corticosteroids used to treat lichen simplex
chronicus).

Procedures
Frequently, skin biopsy is performed to exclude other disorders, particularly psoriasis or mycosis
fungoides (cutaneous T-cell lymphoma) in elderly patients.[13]

Histologic Findings
Histologic examination demonstrates hyperkeratosis, acanthosis, spongiosis, and patches of
parakeratosis in the epidermis. Epidermal thickening of all layers is noted, with elongation of rete

ridges and with pseudoepitheliomatous hyperplasia. Papillary dermal fibrosis with vertical streaking of
collagen bundles is characteristic.
A characteristic finding of LSC that is noted on electron microscopy is frequent collagen fibers
attached to and just above the lamina basalis.

Medical Care
Treatment is aimed at reducing pruritus and minimizing existing lesions because rubbing and
scratching cause lichen simplex chronicus. Location, lesion morphology, and extent of the lesions
influence treatment. For example, a thick psoriasiform plaque of lichen simplex chronicus on a limb is
commonly treated with a highly potent topical corticosteroid or intralesional corticosteroids, whereas
vulvar lesions are more commonly treated with a mild topical corticosteroid or a topical calcineurin
inhibitor. Widespread lesions are more likely to require systemic treatment or total body phototherapy.
Note the following treatments:

Topical steroids are the current treatment of choice because they decrease inflammation and itch
while concurrently softening the hyperkeratosis.[14, 15, 16] Because lesions are by nature chronic,
treatment most likely is lifelong. On larger and more active lesions, a midpotency steroid may be
used to treat acute inflammation. Occasionally, occlusion is used to increase potency and enhance
delivery of the agent. Occlusion also provides a physical barrier to the scratching. Midpotency
topical steroids are not recommended for thin skin (eg, vulva, scrotum, axilla, face). Direct long-term
therapy more at daily use of low-potency nontrophogenic topical corticosteroids. High-potency
topical corticosteroids may be used for 3-week courses on thicker-skinned areas.
Oral antianxiety medications and sedation may be considered in certain patients. According to
individual need, treatment can be scheduled throughout the day, at bedtime, or both. Antihistamines
such as diphenhydramine (Benadryl) and hydroxyzine (Atarax) are common. Doxepin (Sinequan)
and clonazepam (Klonopin) may be considered in appropriate cases.
For infected lesions, a topical or oral antibiotic can be considered.
Other topical medications reported to decrease pruritus include doxepin cream [17] and capsaicin
cream.[18]
One study suggests that topical aspirin/dichloromethane is effective in patients with lichen simplex
chronicus who have not responded to topical corticosteroids.[19]
For topical corticosteroid unresponsive patients or those with lesions on thin skin, a few case reports
and small studies have shown efficacy of topical immunomodulators tacrolimus and pimecrolimus. [20]
A more investigational treatment for patients who fail conventional therapy is local botulinum toxin
injections.[21, 22]
Transcutaneous electrical nerve stimulation (TENS) has been reported as a possible effective
treatment in a small, open trial of cases of lichen simplex chronicus resistant to topical corticosteroid
treatment.[23]
A clinical guideline summary from the American College of Obstetricians and
Gynecologists, Diagnosis and management of vulvar skin disorders, may be helpful.[24]

Consultations

Consultation with a dermatologist may be considered for severe cases requiring more than topical
treatments or to facilitate patch testing.
Consultation with an allergist may be considered in individuals with multisystemic atopic symptoms.
Consultation with a psychiatrist may be necessary for patients with severe stress or compulsive
scratching.

Practice Essentials
Pityriasis alba, a common skin disorder in children and young adults. It is characterized by the
presence of ill-defined, scaly, faintly erythematous patches. These lesions eventually subside, leaving
hypopigmented areas that then slowly return to normal pigmentation. The term is derived from the
words pityriasis (scaly) and alba (white).

Signs and symptoms

Pityriasis alba lesions often occur on the face, with the cheek being a particularly common
site.[1] Initially, erythema may be conspicuous, and minimal serous crusting of some lesions may occur.
The individual lesions are characterized as follows:

Rounded, oval, or irregular plaques that are red, pink, or skin colored and have fine lamellar or
branny scaling with indistinct margins
Usually 1-4 cm in diameter
Most commonly range in number from 4 or 5 to 20 or more
Found on the face, upper arms, neck, or shoulders; the legs and trunk are less commonly involved;
in approximately one half of all patients, the lesions are limited to the face
Uncommon variants of pityriasis alba are as follows:

Pigmenting pityriasis: Typical lesion has a central zone of bluish hyperpigmentation surrounded by a
hypopigmented, slightly scaly halo of variable width; the lesions are usually confined to the face and
are often associated with dermatophyte infection[2]
Extensive pityriasis alba (see Differentials): Differentiated from the classic form by the widespread
and symmetrical involvement of the skin, the absence of a preceding inflammatory phase, a higher
female-to-male ratio, and, histologically, the absence of spongiosis [3]
In the extensive variant, lesions are less erythematous, less scaly, more persistent, asymptomatic,
and more frequently seen on the trunk and less often on the face.[4]
See Clinical Presentation for more detail.

Diagnosis
A workup, as follows, may be undertaken to exclude other causes of hypopigmentation:

Wood's light examination: May help in determining the presence of vitiligo, which will glow more
brightly and have edges with sharper demarcation
Potassium hydroxide (KOH) stain of a skin scraping: Will be positive if the patient has tinea
versicolor (also called pityriasis versicolor), tinea faciei, or tinea corporis
Skin biopsy: Not usually necessary or particularly helpful in establishing a diagnosis of pityriasis alba
but may be indicated if a diagnosis of mycosis fungoides (cutaneous T-cell lymphoma) is a
significant possibility
See Workup for more detail.

Management
Pityriasis alba resolves spontaneously; treatment consists primarily of good general skin care and
education of a young patients parents about the benign nature of this self-limited disorder. Therapy
may also include the following:

Low-potency topical steroids (eg, hydrocortisone 1%, desonide 0.05%): May help with erythema and
pruritus associated with the initial lesions and may accelerate repigmentation of existing lesions; use
should be limited, however, to avoid long-term skin atrophy and steroid changes
Tar paste: May be helpful for chronic lesions on the trunk
Bland emollient cream: Used to reduce the scaling of lesions, especially on the face
Psoralen plus ultraviolet light A (PUVA) photochemotherapy: May be used to help with
repigmentation in extensive cases; recurrence rate is high after treatment is stopped[5]
Tacrolimus ointment 0.1% and pimecrolimus cream 1%: Have been reported to be beneficial in the
treatment of pityriasis alba[6, 7, 8]
Laser therapy: Treatment with a 308-nm excimer laser twice a week for 12 weeks has been shown
to be effective against pityriasis alba[9]
See Treatment and Medication for more detail.

Image library

Note the characteristic, ill-defined, hypopigmented macules in this 6-year-old child with
pityriasis alba.

Background
Pityriasis alba, a relatively common skin disorder in children and young adults, is characterized by the
presence of ill-defined, scaly, faintly erythematous patches. These lesions eventually subside, leaving
hypopigmented areas that then slowly return to normal pigmentation (see the images
below).[10] Lesions may progress through the following 3 clinical stages (see Clinical Presentation):

Papular (scaling) erythematous

Papular (scaling) hypochromic

Smooth hypochromic

in this 6-year-old child with pityriasis alba.

Note the characteristic, ill-defined, hypopigmented macules

Pityriasis alba.

The duration of pityriasis alba varies from 1 month to 10 years, with most cases resolving over a
period of several months to a year.[1] Diagnosis is made clinically, and treatment consists of skin care
and education of a young patients parents about the benign nature of the disorder. Hydrocortisone
may decrease erythema, scaling, and pruritus, if present. (See Prognosis, Workup, and Treatment.)
Pityriasis alba, although a nonspecific finding, is commonly associated with atopic dermatitis. The
etiology of pityriasis alba is unknown, but xerosis that presents in individuals with atopic diathesis is
an important element in the development of the disease. (See Pathophysiology and Etiology.)

Extensive pityriasis alba

Extensive pityriasis alba is believed to be a primary, acquired hypopigmentation observed in females

aged 18-25 years of mixed ethnic origin; it is characterized by hypochromic, nonscaly macules
developing on the back and abdomen, increasing in number and progressively coalescing over the
whole trunk into larger patches surrounded by smaller, well-defined macules. Although the single skin
lesions of extensive pityriasis alba do not differ substantially from those of pityriasis alba, consistent
differences are as follows[11] :

A widespread and symmetrical involvement of the trunk by numerous round, nonscaly,

hypomelanotic patches without a preceding inflammatory phase and chronic in duration (this is as
opposed to face predominance, as found in pityriasis alba)
A decrease in epidermal melanin, as found on histologic examination; spongiosis is absent
Ultrastructural studies suggest a reduced number of active melanocytes and a decrease in number
and size of melanosomes
No reported atopy, associated pathologies, or familial occurrences
The age of occurrence and the sex ratio (female preponderance) differ from those of pityriasis alba
Widespread lesions of classical pityriasis alba can be observed in atopic dermatitis, but they should
not be confused with those of extensive pityriasis alba
Debate exists as to the validity of the term extensive pityriasis alba, which some believe to be a
confusing misnomer applied to a pathoetiologically different entity. Some authors believe that
extensive pityriasis alba overlaps with another condition, described as "progressive and extensive
hypomelanosis" in persons of mixed racial background and also reported as "progressive and
confluent hypomelanosis of the melanodermic metis" or "creole dyschromia. The alternate name of
"progressive extensive hypomelanosis" has been proposed.[11]

Patient education
Educate the parents about the benign, self-limited nature of pityriasis alba.

Pathophysiology
Pityriasis alba
Ultrastructural studies in patients with pityriasis alba have noted that despite reduced pigment in
lesional skin, there is no difference in melanocytes between lesional and nonlesional skin in the same
patient, although this finding is still under debate. Degenerative changes in melanocytes and reduced
keratonocyte melanosomes have also been noted.[12]

Extensive pityriasis alba

Hypopigmentation in extensive pityriasis alba may be primarily caused by the reduced numbers of
active melanocytes and the decrease in the number and size of melanosomes in the affected skin.
In a study by Zaynoun et al of 9 patients with extensive pityriasis alba, the density of functional
melanocytes was found to be reduced in affected areas, although cytoplasmic activity and the transfer
of melanosomes to keratinocytes were generally normal. While the number and size of melanosomes
tended to be reduced, they demonstrated a normal distribution pattern in the keratinocytes. [13]
In the same study, the presence of hyperkeratosis and parakeratosis was inconsistent, and these
conditions were thought unlikely to contribute significantly to the pathogenesis of the hypomelanosis.
Various amounts of intercellular edema were found.

Etiology
No known cause of pityriasis alba has been reported. The condition is not contagious, and no
infectious agent has been identified.
Leading theories as to the origin of the lesions in pityriasis alba involve atopy and postinflammatory
changes, with a large number of patients with pityriasis alba having a history of atopic disease, and
atopic patients are being more prone to developing the condition.[14, 1]
Theories of origin also include hypopigmentation secondary to pityriacitrin, a substance produced
by Malassezia yeasts that acts as a natural sunscreen.

In one study, atrophic sebaceous glands were noted in almost half the cases of pityriasis alba. In
another study, iron deficiency anemia was reported in 16.5% of patients[1] ; this may be a coincidental
finding, however, and the clinical relevance of anemia is not yet known. Excessively dry skin, which is
frequently exacerbated by cold, dry environments, also appears to be a common factor in pityriasis
alba.
Reported contributory factors related to the development of pityriasis alba are excessive and
unprotected sun exposure, poor hygienic habits, and environmental influences such as temperature,
humidity, and altitude.[15]

Epidemiology
Sex
Pityriasis alba is most often seen in individuals younger than 16 years. However, it can be noted at
any age.

Epidemiology
Occurrence in the United States
Although the exact incidence has not been described, up to 5% of children may have pityriasis
alba.[16] The disorder is not seasonal, but the dry, slightly scaly appearance tends to worsen during
cold months, when the air is relatively dry inside the home. In addition, sun exposure may make the
lesions more obvious during spring and summer. The condition is more common in patients with a
history of atopy.

International occurrence
In a study of 9955 schoolchildren aged 6-16 years who lived in a tropical region, the prevalence of
pityriasis alba was 9.9%.[17, 18] Another study, in Nepal, showed that the prevalence of pityriasis alba
within a wide range of dermatoses was 5.2%.[19]

Race-, sex-, and age-related demographics

Pityriasis alba occurs in people of all races. One study found the incidence to be slightly higher in
light-skinned people. However, the condition is frequently more apparent and cosmetically
bothersome in patients with darker complexions.[14] Both sexes are equally susceptible to the disease,
but a slight male predominance has been noted.[1, 15]
Pityriasis alba is most common in children aged 3-16 years, with 90% of cases occurring in children
younger than 12 years. The disease occasionally is found in adults.[14]

Prognosis
Pityriasis alba is generally self-limited, and the prognosis is good, with eventual complete
repigmentation. No long-term residual effects are expected.
Cosmetic appearance while the lesions are present may be an issue with some pediatric patients but
is more likely to be of concern to their parents. Risk of sunburn is slightly increased in areas of
hypopigmentation.
The duration of symptoms is different for each patient. Recurrent crops of new lesions may develop at
intervals, with the duration of pityriasis alba varying from 1 month to 10 years. Usually, however,
cases resolve over a period of several months to a year.[1] Treatment may shorten the duration of the
lesions to several weeks in certain cases. (See the image below.)

The hypopigmentation produced by pityriasis alba may take a year or longer to

return to normal.

History

Pityriasis alba (PA) is generally asymptomatic but may be mildly pruritic. Patients may describe any of
the following 3 clinical stages:

Papular erythematous lesions

Papular hypochromic lesions
Smooth hypochromic lesions
Pityriasis alba lesions often occur on the face, with the cheek being a particularly common
site.[1] Initially, erythema may be conspicuous, and minimal serous crusting of some lesions may occur.
However, because the erythema is usually very mild, most parents of young patients do not recall the
erythematous stage. Erythema later subsides completely to leave areas of hypopigmentation with or
without fine scaling.
Recurrent crops of new lesions may develop at intervals, with the duration of pityriasis alba varying
from 1 month to 10 years. Most cases, however, resolve over a period of several months to 1 year.

Associated factors
Patient or family history may include asthma and hay fever. It may also include eczema in the
characteristic areas of atopic dermatitis, with pityriasis alba being a nonspecific finding commonly
associated with this condition.[20]
The patient may have a prior history of rash or eczema at the sites of hypopigmentation; skin irritation
produced by any of a variety of causes may heal with postinflammatory hypopigmentation.
The patient should be asked about prior therapy; potent topical steroids may produce
hypopigmentation. Moreover, patients may develop irritant or allergic contact dermatitis from the use
of various topical creams, lotions, or medications; when these are discontinued and the area recovers
from the contact dermatitis, an area of postinflammatory hypopigmentation may occur.
The clinician should look for seasonal variations in appearance; the scaling areas of
hypopigmentation frequently develop during winter but become more apparent following sun exposure
during the spring and summer.

Physical Examination
The correct diagnosis of pityriasis alba (PA) is usually suggested by the age of the patient, fine
scaling, hypopigmentation, and the distribution of lesions.

Characteristic lesions
Pityriasis alba is often diagnosed following an incidental finding on clinical examination. The individual
lesions are rounded, oval, or irregular plaques that are red, pink, or skin colored and have fine
lamellar or branny scaling with indistinct margins. (See the image below.)

Pityriasis alba.

{{mediacaption:2202615_5}} .
Usually 1-4 cm in diameter, the lesions most commonly number from 4 or 5 to 20 or more. They are
visible primarily in contrast to dark skin; increasing sunlight in spring and summer also makes them
more apparent.

Affected areas

The lesions appear on the face, upper arms, neck, or shoulders; the legs and trunk are less
commonly involved. In approximately one half of all patients, the lesions are limited to the face. The
areas around the mouth, chin, and cheeks are the most commonly affected. (See the image below.)

Lesions of pityriasis alba are usually bilateral and located on the face, arms, and neck.

In 20% of affected children, the neck, arms, and shoulders are involved in addition to the face. Less
commonly, the face is spared and scattered lesions are present on the trunk and limbs.

Variants
Uncommon variants of pityriasis alba are the pigmenting variety and the extensive type. In pigmenting
pityriasis alba, the typical lesion has a central zone of bluish hyperpigmentation surrounded by a
hypopigmented, slightly scaly halo of variable width. The lesions are usually confined to the face and
are often associated with dermatophyte infection.[2]
Extensive pityriasis alba is differentiated from the classic form by the widespread and symmetrical
involvement of the skin, the absence of a preceding inflammatory phase, a higher female-to-male
ratio, and, histologically, the absence of spongiosis.[3] In the extensive variant, lesions are less
erythematous, less scaly, more persistent, asymptomatic, and more frequently seen on the trunk and
less often on the face.[4]

Important aspects of examination

Examine patients for keratotic lesions on the elbows and knees and for small pits in the nails, which
may suggest a diagnosis of psoriasis.
Examine for the following potential signs of atopic dermatitis:

Eczema in the popliteal or antecubital fossa

Nipple eczema
Cheilitis
Dennie-Morgan infraorbital fold
Anterior neck folds
Wool intolerance
White dermographism
Infra-auricular fissuring

Approach Considerations
Hypopigmentation may occur in other disorders, such as those caused by fungi (eg, tinea versicolor),
previous inflammatory conditions (eg, postinflammatory hypopigmentation), idiopathic disorders
(eg, vitiligo), or malignancy (mycosis fungoides), or it may occur secondary to medications such as
retinoic acid, benzoyl peroxide, and topical steroids. Clinicians should rule out these other disorders
when evaluating a patient who may have pityriasis alba.
A workup may be undertaken to exclude other causes of hypopigmentation; however, most of this
would be accomplished through a dermatology referral.
A Wood's light examination may help in determining whether a patients rash is due to vitiligo, which
will glow more brightly and have edges with sharper demarcation.

Potassium hydroxide (KOH) stain of a skin scraping will be positive if the patient has tinea versicolor
(also called pityriasis versicolor), tinea faciei, or tinea corporis. This would likely be performed by a
dermatologist.
A biopsy would be required for atypical lesions noted in the differential. This would likely be performed
by a dermatologist.

Histologic Findings
Skin biopsy is not usually necessary or particularly helpful in establishing a diagnosis of pityriasis alba.
Biopsy may be indicated, however, if a diagnosis of mycosis fungoides is a significant possibility. The
biopsy should be performed by a skin disease specialist, considering the common location of the
cheek and the potential approximation of this area to the facial artery.
Only a few histologic studies of pityriasis alba have been reported, and most maintain that the
microscopic features of the disease are those of a mild, chronic, nonspecific dermatitis with
decreased melanin production.[12, 13, 14, 23] The following features have been seen on biopsy specimens,
although none are specific enough to make the diagnosis[1] :

Hyperkeratosis (33.33%)
Parakeratosis (40%)
Acanthosis (53.33%)
Spongiosis (80%)
Perivascular infiltrate (100%)
However, a histopathologic diagnosis of pityriasis alba may be proposed when the following features
are observed in a biopsy specimen taken from a characteristic skin lesion:
Irregular or markedly reduced pigment by melanin of the basal layer
No significant difference in melanocyte count between lesional and normal skin
Reduced number of active melanocytes and decreased number and size of melanosomes in
affected skin[9]

Approach Considerations
Pityriasis alba resolves spontaneously; treatment consists primarily of good general skin care
and education of the patients parents about the benign nature of this self-limited disorder.
Patients should use adequate sun protection to prevent darkening of the natural skin color.
Lesions of pityriasis alba do not repigment well upon sun exposure, and darkening of the
surrounding skin may worsen the cosmetic appearance.
Because pityriasis alba is usually self-limited and asymptomatic, pharmacologic treatment is
often unnecessary.

Pharmacologic therapy
Topical steroids (eg, hydrocortisone 1%, desonide 0.05%) may help with erythema and
pruritus associated with the initial lesions and may accelerate repigmentation of existing
lesions. Use should be limited, however, with frequent breaks from use, to avoid long-term
skin atrophy and steroid changes. Only low-potency (class 5, 6) topical steroids should be
prescribed.[24, 25, 26]
For chronic lesions on the trunk, a mild tar paste may be helpful. Bland emollient creams are
used to reduce the scaling of lesions, especially on the face.
Psoralen plus ultraviolet light A (PUVA) photochemotherapy may be used to help with
repigmentation in extensive cases, although the recurrence rate is high after treatment is
stopped.[5]

Tacrolimus ointment 0.1% and pimecrolimus cream 1% have also been reported to be
beneficial in the treatment of pityriasis alba.[6, 7, 8] Because of the high cost of tacrolimus,
however, it is seldom indicated. Pimecrolimus 1% has been proposed as a therapeutic option
over a 3-month period.[7]
In a double-blind, placebo-controlled trial, Patrizi and colleagues concluded that sorbityl
furfural palmitate (AR-GG27) cream was effective against mild to moderate atopic
dermatitis in patients with pityriasis alba. Patients in the study, who were aged 2 months to 15
years, were assessed after 15 and 30 days, with a statistically significant improvement seen in
the AR-GG27 patients compared with those on placebo.[27]
In another study, an open-label, noncontrolled, nonrandomized trial by Bhat et al involving
patients with eczema associated with pityriasis alba, as well as persons with various forms of
irritant dermatitis, RV 2427B cream was found to be effective in 84% of patients as evaluated
by an investigator, and in 76% of patients as evaluated through self-assessments. The cream
contained 4% zinc oxide, 2.5% dry colloidal oat extract, 0.5% oat oil, 0.2% copper sulfate,
and 0.1% zinc sulfate.[28]

Laser therapy
Treatment with a 308-nm excimer laser twice a week for 12 weeks has been shown to be
effective against pityriasis alba.[9]

Consultations
Consultation with a dermatologist is usually unnecessary; the patient is typically monitored by the
primary care provider.
Extensive pityriasis alba may warrant a referral to a dermatologist for possible oral psoralen plus
ultraviolet-A (PUVA) photochemotherapy. PUVA for extensive pityriasis alba may achieve a marked
degree of improvement; however, PUVA is not without risks and is seldom required.