Vitiligo

Introduction
Background
Vitiligo is an acquired pigmentary disorder of the skin and mucous membranes, and it is
characterized by circumscribed depigmented macules and patches. It is a progressive
disorder in which some or all of the melanocytes in the affected skin are selectively
destroyed. Vitiligo affects 0.5-2% of the world population, and the average age of onset is 20
years.
Pathophysiology
Vitiligo is a multifactorial polygenic disorder with a complex pathogenesis. It is related to
both genetic and nongenetic factors. Although several theories have been proposed about
the pathogenesis of vitiligo, the precise cause remains unknown. Generally agreed upon
principles are an absence of functional melanocytes in vitiligo skin and a loss of
histochemically recognized melanocytes, owing to their destruction. However, the
destruction is most likely a slow process resulting in a progressive decrease of melanocytes.
Theories regarding destruction of melanocytes include autoimmune mechanisms, 1 cytotoxic
mechanisms, an intrinsic defect of melanocytes, oxidant-antioxidant mechanisms, and
neural mechanisms.
Autoimmune destruction of melanocytes
The autoimmune theory proposes alteration in humoral and cellular immunity in the
destruction of melanocytes of vitiligo. Thyroid disorders, particularly Hashimoto thyroiditis
and Graves disease; other endocrinopathies, such as Addison disease and diabetes mellitus;
and alopecia areata; pernicious anemia; inflammatory bowel disease; psoriasis; and
autoimmune polyglandular syndrome are all associated with vitiligo. The most convincing
evidence of an autoimmune pathogenesis is the presence of circulating antibodies in
patients with vitiligo.2 The role of humoral immunity is further supported by the observation
that melanocytes are destroyed in healthy skin engrafted onto nude mice injected with
vitiligo patient sera.3
In addition to the involvement of humoral immune mechanisms in the pathogenesis of
vitiligo, strong evidence indicates involvement of cellular immunity in vitiligo. Destruction of
melanocytes may be directly mediated by autoreactive CD8+ T cells. Activated CD8+ T cells
have been demonstrated in perilesional vitiligo skin. In addition, melanocyte-specific T cells
have been detected in peripheral blood of patients with autoimmune vitiligo. 4
The following related eMedicine articles may be of interest:
 Hashimoto Thyroiditis
 Graves Disease
 Addison Disease
 Diabetes Mellitus, Type 1
 Diabetes Mellitus, Type 2
 Alopecia Areata
 Pernicious Anemia
 Inflammatory Bowel Disease
 Psoriasis
 Autoimmune Polyglandular Syndrome, Type 1
Additionally, for a Medscape CME course related to autoimmunity and medications, see
Drug Insight: Autoimmune Effects of Medications: What's New?.
Intrinsic defect of melanocytes
Vitiligo melanocytes may have an intrinsic defect leading to melanocyte death. These
melanocytes demonstrate various abnormalities, including abnormal, rough endoplasmic
reticulum and incompetent synthesis and processing of melanocytes. In addition, homing-
receptor dysregulation has also been detected. Early apoptosis of melanocytes has also
been suggested as a cause of reduced melanocyte survival; however, subsequent
investigation found that the relative apoptosis susceptibility of vitiligo melanocytes was
comparable with that of normal control pigment cells.5

Disturbance in oxidant-antioxidant system in vitiligo

Oxidant stress may also play an essential role in the pathogenesis of vitiligo. Studies suggest
that accumulation of free radicals toxic to melanocytes leads to their destruction. Because
patients with vitiligo exhibit a characteristic yellow/green or bluish fluorescence in clinically
affected skin, this led to the discovery that the fluorescence is due to accumulation of 2
different oxidized pteridines. The overproduction of pteridines led to the discovery of a
metabolic defect in tetrahydrobiopterin homeostasis in patients with vitiligo, which results
in the accumulation of melanocytotoxic hydrogen peroxide.6

Neural theory

Case reports describe patients afflicted with a nerve injury who also have vitiligo have
hypopigmentation or depigmentation in denervated areas. Additionally, segmental vitiligo
frequently occurs in a dermatomal pattern, which suggests that certain chemical mediators
are released from nerve endings that affect melanin production. Further, sweating and
vasoconstriction are increased in depigmented patches of vitiligo, implying an increase in
adrenergic activity. Finally, increased urinary excretion of homovanillic acid and
vanilmandelic acid (neurometabolites) has been documented in patients with vitiligo. This
may be a secondary or primary phenomenon.7

In summary, although the ultimate cause of vitiligo is not completely known, this condition
does not reflect simple melanocyte loss, but possible immunologic alterations and other
molecular defects leading to pigment cell destruction; however, melanocytes may be
present in depigmented skin after years of onset and may still respond to medical therapy
under appropriate stimulation.

Genetics of vitiligo8
Vitiligo is characterized by incomplete penetrance, multiple susceptibility loci, and genetic
heterogeneity. The inheritance of vitiligo may involve genes associated with the
biosynthesis of melanin, a response to oxidative stress, and regulation of autoimmunity. 9
Human leukocyte antigens (HLAs) may be associated, but not in a consistent manner. For
example, HLA-DR4 is increased in blacks, HLA-B13 is increased in Moroccan Jews, and HLA-
B35 is increased in Yemenite Jews. An association with HLA-B13 is described in the presence
of antithyroid antibodies.
Frequency
United States
In the United States, the relative rate is 1%.
International
Vitiligo is relatively common, with a rate of 1-2%. Approximately 30% of cases occur with a
familial clustering of cases.
Sex
A female preponderance has been reported, but it is not statistically significant and the
discrepancy has been attributed to an increase in reporting of cosmetic concerns by female
patients.
Age
Vitiligo may appear at any time from birth to senescence, although the onset is most
commonly observed in persons aged 10-30 years.
 It rarely is seen in infancy or old age. Nearly all cases of vitiligo are acquired relatively early
in life.
 The average age of onset is approximately 20 years. The age of onset is unlikely to vary
between the sexes.
 Heightened concern about the appearance of the skin may contribute to an early awareness
of the condition among females.
Clinical
History
The most common form of vitiligo is an amelanotic macule or patch surrounded by healthy
skin. The  macules are chalk or milk-white in color, and lesions are well demarcated.
The lesions are not readily apparent in lightly pigmented individuals; however,  they are
easily distinguishable with a Wood lamp examination.
Physical
Vitiligo manifests as acquired white or hypopigmented macules or patches. The lesions are
usually well demarcated, and they are round, oval, or linear in shape. The borders may be
convex.6 Lesions enlarge centrifugally over time at an unpredictable rate. Lesions range from
millimeters to centimeters in size. Initial lesions occur most frequently on the hands,
forearms, feet, and face, favoring a perioral and periocular distribution.
Vitiligo lesions may be localized or generalized, with the latter being more common than the
former. Localized vitiligo is restricted to one general area with a segmental or
quasidermatomal distribution. Generalized vitiligo implies more than one general area of
involvement. In this situation, the macules are usually found on both sides of the trunk,
either symmetrically or asymmetrically arrayed.
The most common sites of involvement are the face, neck, and scalp. Many of the most
common sites of occurrence are areas subjected to repeated trauma, including the
following:
 Bony prominences
 Extensor forearm
 Ventral wrists
 Dorsal hands
 Digital phalanges
Involvement of the mucous membranes is frequently observed in the setting of generalized
vitiligo. Vitiligo often occurs around body orifices such as the lips, genitals, gingiva, areolas,
and nipples.
Body hair (leukotrichia) in vitiliginous macules may be depigmented. Vitiligo of the scalp
usually appears as a localized patch of white or gray hair, but total depigmentation of all
scalp hair may occur. Scalp involvement is the most frequent, followed by involvement of
the eyebrows, pubic hair, and axillary hair, respectively. Leukotrichia may indicate a poor
prognosis in regard to repigmentation. Spontaneous repigmentation of depigmented hair in
vitiligo does not occur.
Clinical variants
Trichrome vitiligo has an intermediate zone of hypochromia located between the achromic
center and the peripheral unaffected skin. The natural evolution of the hypopigmented
areas is progression to full depigmentation. This results in 3 shades of color—brown, tan,
and white—in the same patient (see Media File 1).
Marginal inflammatory vitiligo results in a red, raised border, which is present from the
onset of vitiligo (in rare cases) or which may appear several months or years after the initial
onset. A mild pruritus may be present (see Media File 2). 
Quadrichrome vitiligo is another variant of vitiligo, which reflects the presence of a fourth
color (ie, dark brown) at sites of perifollicular repigmentation. A case of pentachrome vitiligo
with 5 shades of color has also been described.7
Blue vitiligo results in blue coloration of vitiligo macules. This type has been observed in a
patient with postinflammatory hyperpigmentation who then developed vitiligo.
Koebner phenomenon is defined as the development of vitiligo in sites of specific trauma,
such as a cut, burn, or abrasion. Minimum injury is required for Koebner phenomenon to
occur.
Clinical classifications of vitiligo
The classification system is important because of the special significance assigned by some
authorities to each type of vitiligo. The most widely used classification of vitiligo is localized,
generalized, and universal types and is based on the distribution, as follows: 
 Localized
o Focal: This type is characterized by one or more macules in one area, most
commonly in the distribution of the trigeminal nerve.
o Segmental: This type manifests as one or more macules in a dermatomal or
quasidermatomal pattern. It occurs most commonly in children. More than half the
patients with segmental vitiligo have patches of white hair or poliosis. This type of
vitiligo is not associated with thyroid or other autoimmune disorders.
o Mucosal: Mucous membranes alone are affected.
 Generalized
o Acrofacial: Depigmentation occurs on the distal fingers and periorificial areas.
o Vulgaris: This is characterized by scattered patches that are widely distributed.
o Mixed: Acrofacial and vulgaris vitiligo occur in combination, or segmental and
acrofacial vitiligo and/or vulgaris involvement are noted in combination.
 Universal: This is complete or nearly complete depigmentation. It is often associated with
multiple endocrinopathy syndrome.
Classification by progression, prognosis, and treatment
When progression, prognosis, and treatment are considered, vitiligo can be classified into 2
major clinical types: segmental and nonsegmental.

Segmental: This usually has an onset early in life and rapidly spreads in the affected area.
The course of segmental vitiligo can arrest, and depigmented patches can persist unchanged
for the life of the patient (see Media File 3).

Nonsegmental: This type includes all types of vitiligo, except segmental vitiligo (see Media
File 4).10
Causes
Theories regarding destruction of melanocytes include autoimmune mechanisms, cytotoxic
mechanisms, intrinsic melanocyte defects, oxidant-antioxidant mechanisms, and neural
mechanisms.
 Autoimmune and cytotoxic hypotheses: Aberration of immune surveillance results in
melanocyte dysfunction or destruction.
 Neural hypothesis: A neurochemical mediator destroys melanocytes or inhibits melanin
production.
 Oxidant-antioxidant mechanisms: An intermediate or metabolic product of melanin
synthesis causes melanocyte destruction.
 Intrinsic defect of melanocytes: Melanocytes have an inherent abnormality that impedes
their growth and differentiation in conditions that support normal melanocytes.
Because none of these theories alone is entirely satisfactory, some have suggested a
composite hypothesis.
Differential Diagnoses
Addison Disease Postinflammatory depigmentation
Alezzandrini Syndrome Prior treatment with corticosteroids
Chemical leukoderma Scleroderma
Halo Nevus Tinea Versicolor
Idiopathic Guttate HypomelanosisTreponematosis
Leprosy Tuberous Sclerosis
Malignant Melanoma Vogt-Koyanagi-Harada Syndrome
Nevus Anemicus Waardenburg Syndrome
Onchocerciasis (River Blindness)
Piebaldism
Pityriasis Alba
Other Problems to Be Considered
Vitiligo and ocular disease
The uveal tract and retinal pigment epithelium contain pigment cells. Choroidal
abnormalities have been reported in up to 30% of patients, and iritis has been reported in
approximately 5% of patients. Exophthalmos may occur in the setting of concomitant Graves
disease. Uveitis is the most significant ocular abnormality associated with vitiligo. The most
severe form of uveitis is seen in the Vogt-Koyanagi-Harada syndrome. This syndrome is
characterized by vitiligo, uveitis, aseptic meningitis, dysacusis, tinnitus, poliosis, and
alopecia.

Alezzandrini syndrome includes facial vitiligo, poliosis, deafness, and unilateral visual
changes. The affected eye has decreased visual acuity and an atrophic iris. 6
Although the color of the irides does not change in patients with vitiligo, depigmented areas
in pigment epithelium and choroid occur in up to 40% of patients.

Vitiligo and autoimmune disorders

Vitiligo is frequently associated with disorders of autoimmune origin, with thyroid
abnormalities being the most common. Vitiligo usually precedes the onset of thyroid
dysfunction. Patients with autoimmune polyendocrinopathy candidiasis-ectodermal
dystrophy have an increased prevalence of vitiligo. In this genetic syndrome, autoantibodies
cause destruction of endocrine cells.11
Moreover, studies suggest that an association exists between a positive family history of
vitiligo, autoimmune/endocrine diseases, leukotrichia, and an increased incidence of vitiligo
in children. In addition, pediatric patients with a positive family history of vitiligo show an
earlier age of disease onset.12

Vitiligo and auditory abnormalities13

Melanin may play a significant role in the establishment and/or maintenance of the
structure and function of the auditory system and may modulate the transduction of the
auditory stimuli by the inner ear.14 The membranous labyrinth of the inner ear contains
melanocytes, and the heaviest pigmentation is present in the scala vestibuli. Because vitiligo
affects all melanocytes, auditory disturbances may result. Several studies have described
familial vitiligo associated with hearing abnormalities and hypoacusis in 16% of patients
younger than 40 years who have vitiligo.14

Vitiligo and melanoma15,16

Vitiligolike depigmentation can occur in patients with malignant melanoma and is believed
to result from a T-cell–mediated reaction to antigenic melanoma cells and cross-reactivity to
healthy melanocytes. Most patients with melanoma or with vitiligo develop antibodies to
similar antigens that are present both on melanocytes and on melanoma cells. These
findings support the hypothesis that the clinical link between the 2 diseases results from
immune responses to antigens shared by normal and malignant pigment cells. Studies have
demonstrated that a halo nevus, hypopigmentation, or depigmentation may occur in
patients with melanoma. The depigmentation or hypopigmentation spreads centrifugally
from the trunk to other parts of the body. The sites of depigmentation may be remote from
the original site of melanoma. Although metastasis has most likely occurred in the majority
of patients, active vitiligo in these patients may signal a longer survival time than expected.
Workup
Laboratory Studies
Although the diagnosis of vitiligo generally is made on the basis of clinical findings, biopsy is
occasionally helpful for differentiating vitiligo from other hypopigmentary disorders.
Vitiligo may be associated with other autoimmune diseases, especially thyroid disease and
diabetes mellitus. Other associated autoimmune diseases include pernicious anemia,
Addison disease, and alopecia areata. Patients should be made aware of signs and
symptoms that suggest the onset of hypothyroidism, diabetes, or other autoimmune
disease. If signs or symptoms occur, appropriate tests should be performed. 16  
 Thyrotropin testing is the most cost-effective screening test for thyroid disease.
Antinuclear antibody screening is also helpful. A CBC count with indices helps rule
out anemia.
 Clinicians should also consider investigating for serum antithyroglobulin and
antithyroid peroxidase antibodies, particularly if thyroid involvement is suspected.
Antithyroid peroxidase antibodies are regarded as a sensitive and specific marker of
autoimmune thyroid antibodies. Screening for diabetes can be accomplished with
fasting blood glucose or glycosylated hemoglobin testing.
Other Tests
Vitiligo is diagnosed by means of inspection with a Wood lamp.
Histologic Findings
Microscopic examination of involved skin shows a complete absence of melanocytes in
association with a total loss of epidermal pigmentation. Superficial perivascular and
perifollicular lymphocytic infiltrates may be observed at the margin of vitiliginous lesions,
consistent with a cell-mediated process destroying melanocytes. Degenerative changes have
been documented in keratinocytes and melanocytes in both the border lesions and adjacent
skin. Other documented changes include increased numbers of Langerhans cells, epidermal
vacuolization, and thickening of the basement membrane. Loss of pigment and melanocytes
in the epidermis is highlighted by Fontana-Masson staining and immunohistochemistry
testing.17,18
Treatment
Medical Care
No single therapy for vitiligo produces predictably good results in all patients; the response
to therapy is highly variable. Treatment must be individualized, and patients should be
made aware of the risks associated with therapy. During medical therapy, pigment cells
arise and proliferate from the following 3 sources:

The pilosebaceous unit, which provides the highest number of cells, migrating from the
external root sheath toward the epidermis

Spared epidermal melanocytes not affected during depigmentation 19

The border of lesions, migrating up to 2-4 mm from the edge
Systemic phototherapy
Systemic phototherapy induces cosmetically satisfactory repigmentation in up to 70% of
patients with early or localized disease.16

Narrow-band UV-B phototherapy is widely used and produces good clinical results. Narrow-
band fluorescent tubes (Philips TL-01/100W) with an emission spectrum of 310-315 nm and
a maximum wavelength of 311 nm are used. Treatment frequency is 2-3 times weekly, but
never on consecutive days. This treatment can be safely used in children, pregnant women,
and lactating women. Short-term adverse effects include pruritus and xerosis. Several
studies have demonstrated the effectiveness of narrow-band UV-B therapy as monotherapy.
UV-B narrow-band microphototherapy20 is therapy targeting the specific small lesions.
Selective narrow-band UV-B (311 nm) is used with a fiber optic system to direct radiation to
specific areas of skin. Narrow-band UV-B has become the first choice of therapy for adults
and children with generalized vitiligo.
Psoralen photochemotherapy involves the use of psoralens combined with UV-A light.
Treatment with 8-methoxypsoralen, 5-methoxypsoralen, and trimethylpsoralen plus UV-A
(PUVA) has often been the most practical choice for treatment, especially in patients with
skin types IV-VI who have widespread vitiligo. Psoralens can be applied either topically or
orally, followed by exposure to artificial UV light or natural sunlight. Vitiligo on the back of
the hands and feet is highly resistant to therapy. 
The best results from PUVA can be obtained on the face, trunk, and proximal parts of the
extremities. However, 2-3 treatments per week for many months are required before
repigmentation from perifollicular openings merges to produce confluent repigmentation.
The total number of PUVA treatments required is 50-300. Repigmentation occurs in a
perifollicular pattern.
The advantages of narrow-band UV-B over PUVA include shorter treatment times, no drug
costs, no adverse GI effects (eg, nausea), and no need for subsequent photoprotection.
Laser therapy
Another innovation is therapy with an excimer laser, which produces monochromatic rays at
308 nm to treat limited, stable patches of vitiligo. This new treatment is an efficacious, safe,
and well-tolerated treatment for vitiligo when limited to less than 30% of the body surface.
However, therapy is expensive. Localized lesions of vitiligo are treated twice weekly for an
average of 24-48 sessions.
According to studies from 2004 and 2007, combination treatment with 0.1% tacrolimus
ointment plus the 308-nm excimer laser is superior to 308-nm excimer laser monotherapy
for the treatment of UV-resistant vitiliginous lesions.21,22
Steroid therapy
Systemic steroids (prednisone) have been used, although prolonged use and their toxicity
are undesirable.23 Steroids have been reported anecdotally to achieve success when given in
pulse doses or low doses to minimize adverse effects. The benefits versus the toxicity of this
therapy must be weighed carefully. More research is necessary to establish the safety and
effectiveness of this therapy for vitiligo.
A topical steroid preparation is often chosen first to treat localized vitiligo because it is easy
and convenient for both doctors and patients to maintain the treatment. The results of
therapy have been reported as moderately successful, particularly in patients with localized
vitiligo and/or an inflammatory component to their vitiligo, even if the inflammation is
subclinical.
In general, intralesional corticosteroids should be avoided because of the pain associated
with injection and the risk of cutaneous atrophy.
Topical therapies
Topical tacrolimus ointment (0.03% or 0.1%) is an effective alternative therapy for vitiligo,
particularly when the disease involves the head and neck. Combination treatment with topical
tacrolimus 0.1% plus the 308-nm excimer laser is superior to monotherapy with the 308-nm excimer
laser monotherapy for UV-resistant vitiliginous lesions. On the face, narrow-band UV-B works better
if combined with pimecrolimus 1% cream rather than used alone. 24,25
The combination of topical calcipotriene and narrow-band UV-B or PUVA results in
improvement appreciably better than that achieved with monotherapy.
Depigmentation therapy
If vitiligo is widespread and attempts at repigmentation do not produce satisfactory results,
depigmentation may be attempted in selected patients.
The long-term social and emotional consequences of depigmentation must be considered.
Depigmentation should not be attempted unless the patient fully understands that the
procedure generally results in permanent depigmentation. Some authorities have
recommended consultation with a mental health professional to discuss potential social
consequences of depigmentation.
A 20% cream of monobenzylether of hydroquinone is applied twice daily for 3-12 months.
Burning or itching may occur. Allergic contact dermatitis may be seen. 26
Topical PUVA is of benefit in some patients with localized lesions. Cream and solution of 8-
methoxypsoralen (0.1-0.3% concentration) are available for this treatment. 6 It is applied 30
minutes prior to UV-A radiation (usually 0.1-0.3 J/cm2 UV-A) exposure. It should be applied
once or twice a week. Physicians who prescribe PUVA therapy should be thoroughly familiar
with the risks associated with the treatment. Additional UV-A exposure should be avoided
while skin is sensitized because severe burns may occur if patients receive additional UV-A
exposure. Sunscreens should be given to all patients with vitiligo to minimize risk of sunburn
or repeated solar damage to depigmented skin. Patients must understand that most
sunblocks have a limited ability to screen UV-A light.
Of general concern, tanning of surrounding normal skin exaggerates the appearance of
vitiligo, and this is prevented by sun protection. Sunscreens with a sun protection factor of
15 or higher are best.
Surgical Care
Surgical alternatives exist for the treatment of vitiligo; however, because of the time-
consuming nature of surgical therapies, these treatment regimens are limited to segmental
or localized vitiligo. Unilateral (segmental) vitiligo has been shown as the most stable form,
responding well to surgical interventions in numerous studies. Such areas as dorsal fingers,
ankles, forehead, and hairline tend to not repigment well. Patients who have small areas of
vitiligo with stable activity are candidates for surgical transplants. The most important
factors indicating stability are as follows:
 No progression of lesions for at least 2 years
 Spontaneous repigmentation indicates vitiligo inactivity
 A positive minigrafting test disclosing repigmentation at 4-5 minigrafts, which, to date, is the
most accurate evidence of vitiligo stability
 Absence of new koebnerization, including the donor site for the minigrafting test
 Unilateral vitiligo most stable form of vitiligo 27  
Five basic methods for repigmentation surgery have been described, as follows 28,29 :

Noncultured epidermal suspensions: After the achromic epidermis is removed, an epidermal
suspension with melanocytes and keratinocytes previously prepared by trypsinization of
normally pigmented donor skin is spread onto the denuded area and immediately covered
with nonadherent dressings.

Thin dermoepidermal grafts: The depigmented epidermis is removed by superficial
dermabrasion, including the papillary dermis, and very thin dermoepidermal sheets
harvested with dermatome are grafted onto the denuded skin.

Suction epidermal grafting: Epidermal grafts can be obtained by vacuum suction, usually
with 150 mm Hg. The recipient site can be prepared by suction, freezing, or dermabrasion of
the sites 24 hours before grafting. The depigmented blister roof is discarded, and the
epidermal donor graft is placed on the vitiliginous areas.

Punch minigrafting: Small donor grafts are inserted into the incision of recipient sites and
held in place by a pressure dressing. The graft heals readily and begins to show
repigmentation within 4-6 weeks. Some pebbling persists but is minimal, and the cosmetic
result is excellent.

Cultured epidermis with melanocytes or cultured melanocyte suspensions: Depigmented
skin is removed using liquid nitrogen, superficial dermabrasion, thermosurgery, or carbon
dioxide lasers; very thin sheets of cultured epidermis are grafted or suspensions are spread
onto the denuded surface.27
Micropigmentation30 is another option. Tattooing can be used to repigment depigmented
skin in dark-skinned individuals. Color matching is difficult, and the color tends to fade. Skin
can be dyed with dihydroxyacetone preparations, although the color match is often poor.
Consultations
Consultation with an ophthalmologist is warranted. Additionally, psychological needs must
be addressed on a continual basis with appropriate referrals to mental health specialists. 7
Medication
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Corticosteroids
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic
effects. In addition, these agents modify the body's immune response to diverse stimuli.
These drugs are used to stop spread of vitiligo and accomplish repigmentation. Data
supporting the efficacy of such treatment is largely anecdotal. More study is needed to
establish the safety and efficacy of systemic agents.

Topical steroids: triamcinolone 0.1% ointment or cream (Aristocort), hydrocortisone 2.5 %

ointment, clobetasol ointment or cream (Clobex)
For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing
migration of polymorphonuclear leukocytes and reversing capillary permeability.
Intramuscular injection may be used for widespread skin disorder, or intralesional injections
may be used for localized skin disorder. Moderately high potency; available as ointment
(0.1%) or cream (0.5%).
Adult
Apply a thin film qd; more frequent applications may be required, especially in areas where
preparation tends to be removed before absorption is complete
Pediatric
Apply as in adults
Coadministration with barbiturates, phenytoin, and rifampin decreases effects of
triamcinolone
Documented hypersensitivity; fungal, viral, and bacterial skin infections
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans;
may use if benefits outweigh risk to fetus
Precautions
Do not use in decreased skin circulation; prolonged use, applications over large areas, and
use of potent steroids and occlusive dressings may result in systemic absorption; systemic
absorption may cause Cushing syndrome, reversible HPA axis suppression, hyperglycemia,
and glycosuria
Psoralens
These agents are used with UV-A exposure for the treatment of localized or generalized
vitiligo.

Methoxsalen (8-MOP, Oxsoralen)

Inhibits mitosis by covalently binding to pyrimidine bases in DNA when photoactivated by
UV-A. Effective in treating hyperkeratosis.
Adult
PO: 0.3-0.4 mg/kg PO with food 1.5 h before UV-A exposure once or twice weekly;
alternatively, 0.57 mg/kg 1.5-2 h before UV exposure; at least 48 h apart
Topically: 0.1% ointment; apply 30 min before controlled UV-A exposure once or twice
weekly
Pediatric
<12 years: Not recommended
>12 years: Administer as in adults
Toxicity increases with phenothiazines, griseofulvin, nalidixic acid, tetracyclines, thiazides,
and sulfanilamide
Documented hypersensitivity; squamous cell cancer; cataracts; light-sensitive diseases (eg,
lupus, porphyria); ingestion of photosensitizing drugs; hepatic disease; arsenic therapy;
noncompliance or unwillingness to use protective glasses after treatment
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans;
may use if benefits outweigh risk to fetus
Precautions
Prolonged use with UV-A causes photoaging of skin; phototoxic reactions possible; caution
with hepatic insufficiency; eye protection necessary during and after therapy; use only if
response to other therapy is inadequate; long-term use may increase risk of skin cancer

Trioxsalen (Trisoralen)
For treatment of hyperkeratosis. In UV-A radiation, inhibits mitosis by covalently binding to
pyrimidine bases in DNA.
Adult
0.6-0.8 mg/kg PO with food 1.5 h prior to UV-A exposure once or twice weekly;
alternatively, 10 mg/d once 2-4 h before controlled exposure to UV-A or sunlight; not to
exceed 14 d
Pediatric
<12 years: Not recommended
>12 years: Administer as in adults
None reported
Documented hypersensitivity; a history of melanoma, acute lupus erythematosus, or
porphyria; inability to comply with instructions regarding UV-A exposure and eye protection
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans;
may use if benefits outweigh risk to fetus
Precautions
Prolonged use with UV-A causes photoaging of skin; severe burns may occur from sunlight
or UV-A exposure if dose or frequency is exceeded; caution with hepatic insufficiency

Calcipotriene (Dovonex)
Adult
Apply to affected areas bid (qam, qhs, and after washing); apply thin film, avoiding eyes and
lips; do not cover with occlusive dressing.
Pediatric
Not recommended
Substances that stimulate absorption should not be administered concomitantly because of
potential effects on calcium metabolism
Systemic treatment of calcium deficiency; kidney or liver dysfunction; hypercalcemia or
calcium metabolism problems
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans;
may use if benefits outweigh risk to fetus
Precautions
Breastfeeding not advised during treatment; low incidence of temporary skin irritation
(reddening, itching); temporarily or permanently discontinue or decrease frequency if
sensitivity or severe irritation; in clinical studies, no hypercalcemia observed at maximal
dose of 30 g/d
Immunomodulator

Tacrolimus (Protopic) ointment 0.03% or 0.1%

Adult
Apply to the affected area twice daily; continue for 1 wk after signs and symptoms resolve.
Avoid occlusive dressings
Pediatric
Protopic 0.03% only: Apply as in adults
Miscellaneous
Medicolegal Pitfalls
 Physicians who prescribe PUVA therapy should be thoroughly familiar with the risks
of burns, cataract formation, and carcinogenesis associated with treatment.
 Patients should be made aware of signs and symptoms that suggest the onset of
hypothyroidism, diabetes, or other autoimmune diseases. If signs or symptoms
occur, appropriate tests should be performed.
 Treatment must be individualized, and patients should be made aware of the risks
associated with therapy.