Clinics in Dermatology (2014) 32, 6672

Pigmentation disorders: hyperpigmentation

and hypopigmentation
Electra Nicolaidou, MD, PhD, Andreas D. Katsambas, MD, PhD
1st Department of Dermatology, University of Athens School of Medicine, Andreas Sygros Hospital,
5 I. Dragoumi str, GR-16121, Athens, Greece

Abstract Pigmentation disorders include a large number of heterogeneous conditions that are usually
characterized by altered melanocyte density, melanin concentration, or both, and result in altered
pigmentation of the skin. Some of these disorders are extremely common (melasma, vitiligo), whereas
others are rare. In this contribution, we review the most common pigmentation disorders that appear
on the face. These lesions, even though mostly asymptomatic, have a great impact on a patients
quality of life.
2014 Elsevier Inc. All rights reserved.

Disorders of hyperpigmentation
Melasma
Melasma (a term derived from the Greek word melas,
meaning black) is a common acquired hypermelanosis that
occurs exclusively on sun-exposed areas, mostly on the face
and occasionally on the neck and forearms.
Epidemiology and etiology
Melasma is more common in women. Men have been
reported to represent 10% of cases.1 Melasma is more
apparent during and after periods of sun exposure.
The exact cause of melasma remains elusive, but the two
most important factors implicated in its etiopathogenesis are
sunlight and genetic predisposition. Other factors incriminated in the pathogenesis of melasma include pregnancy and
exogenous hormones (ie, oral contraceptives and hormone
replacement therapy), thyroid dysfunction, cosmetics, and
phototoxic and antiseizure drugs.2

Corresponding author. Tel.: + 30 210 3619542; fax: + 30 210 3600196.

E-mail address: katsabas1@ath.forthnet.gr (A.D. Katsambas).
0738-081X/$ see front matter 2014 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.clindermatol.2013.05.026

Clinical features and classification

The number of hyperpigmented patches may range from
one single lesion to multiple patches located usually
symmetrically on the face and occasionally the V-neck area.
The lesions have serrated, irregular, and geographic borders
(Figure 1). According to the distribution of lesions, the
following three clinical patterns of melasma are recognized2,3:
1. The centrofacial pattern. This is the most common
pattern. It involves the forehead, cheeks, upper lip,
nose, and chin.
2. The malar pattern. This involves the cheeks and nose.
3. The mandibular pattern. This involves the ramus of
the mandible.
Melasma can be classified into four histologic types using
Woods light examination2,3:
1. Epidermal type. The pigmentation is intensified under
Woods light examination. It is the most common type
of melasma. Melanin is increased in all epidermal
layers. Only a few scattered melanophages can be
observed in the papillary dermis.
2. Dermal type. The pigmentation is not increased under
Wood light examination. Many melanophages are
throughout the entire dermis.

Pigmentation disorders

67

3. Mixed type. Under Woods light examination, the

pigmentation becomes more apparent only in some
areas, whereas in others there is no change. Melanin is
increased in the epidermis, and there are many dermal
melanophages.
4. Indeterminate type. Woods light examination is of no
benefit in individuals with skin type VI.
In a recent study,4 however, Woods light examination
did not accurately determine the depth of pigment
deposition in patients with melasma. Dermal melanin
deposition is common and it may be underestimated with
Woods light examination.
Histopathology
Light microscopic findings of melasma4,5 include increased deposits of melanin in the epidermis or dermis, or
both, compared with adjacent normal skin and a mild
perivascular lymphohistiocytic infiltrate. The number of
epidermal melanocytes in lesional skin has been assessed by
immunohistochemistry and has been reported to be both
increased and similar to the number of melanocytes in normal
skin. The melanocytes are enlarged, intensely stained, and
with very prominent dendrites. The number of dermal
melanophages in the dermis and their melanin deposition is
increased in the dermal and mixed type of the disease.
Electron microscopy studies show increased melanosomes in
both melanocytes and keratinocytes in involved skin.
Treatment and prognosis
Sun protection is of pivotal importance in the treatment of
melasma. Without strict adherence, any treatment regimen
will fail. Recurrence during the summer is very common in
patients with melasma.
The treatment of melasma6 includes topical formulations, chemical peels, lasers, and light sources. Combinations of treatments are often used to maximize results in
difficult cases.
Topical treatment with a combination of hydroquinone,
tretinoin, and a steroid appears to be the most effective
initial therapy. Glycolic acid peels may be a useful
adjunct to topical treatment, especially after a patients
pretreatment with hydroquinone for 2 weeks to minimize
the risk for postprocedure hyperpigmentation. Fractional
laser therapy is the only laser treatment for melasma that
has been approved by the U.S. Food and Drug
Administration, and it could be used as a third-line
treatment in severe cases who have not responded to
other treatments and who are willing to accept the risk
for postprocedure hyperpigmentation.

Pigmented contact dermatitis (Riehl melanosis)

Riehl melanosis is a pigmentary dermatosis characterized by brownish gray facial pigmentation that is more

Fig. 1

Melasma of the forehead.

marked on the temples and the forehead. Today, Riehl

melanosis is almost synonymous with pigmented contact
dermatitis, the most common cause of which are sensitizing
chemicals in cosmetics.
Epidemiology and etiology
Riehl melanosis has mainly been reported in young and
middle-aged women.
Riehl first described in 1917 a reticular black to brownviolet pigmentation of the face and attributed it to exposure
to noxious substances.7 The disease was common in
Vienna between 1916 and 1920. It was again frequently
encountered in Europe during the Second World War, when
exposure to tar was thought to be responsible for the
eruption, and in Japan, several decades later, where it was
found to be due to allergic contact dermatitis from cosmetics.
The causative allergens were coal tar dyes, particularly
brilliant lake red R and other 1-phenylazo-2-naphthol
derivatives.8,9 Based on these findings, the terms pigmented contact dermatitis and pigmented cosmetic dermatitis
have been proposed for Riehl melanosis. The number of new
cases since 1978 has declined, probably due to allergen
avoidance in cosmetics. Reports of sporadic outbreaks and
cases still continue. Chemicals that have been more recently
implicated with Riehl melanosis include geraniol in a face
powder,10 topical minoxidil 5%,11 and diphenylcyclopropenone.12 Ultraviolet (UV) irradiation may also play a role in
the pathogenesis of Riehl melanosis, through the induction of
photocontact dermatitis.10
Clinical features
The pigmentary changes with Riehl melanosis occur
mainly on the face, but the neck, dorsal hands, and forearms
can also be affected. The patches usually have a reticular
pattern and a black to brown-violet hue. Occasionally,
erythematous macules or papules are present, suggesting a
mild contact dermatitis. Patch tests are used for the
identification of the offending substances.811
Histopathology
Histopathologic studies10 have shown liquefactive basal
cell degeneration, a dermal lymphohistiocytic infiltrate, a
thickened basal lamina, and a large number of melanophages

68
in the dermis. Spongiosis is absent. Direct immunofluorescence studies are negative.
Treatment
Removal of the causative agent, sun protection, and
topical treatment with hydroquinone usually improve the
appearance of lesions.

Erythromelanosis follicularis faciei

Erythromelanosis follicularis faciei (EFF) is a rare disease
characterized by hyperpigmentation, erythema, and follicular
papules localized on the face and neck.
Epidemiology and etiology
EFF was initially described in Asian men and later in white
men.13 There are also a few reports of EFF in women.14 The
cause of the disorder is unknown. An autosomal recessive
pattern of transmission has been reported in one family.15
Clinical features
The eruption usually begins as a red-brown telangiectatic
pigmentation in the preauricular regions that gradually
expands and covers the cheeks in an irregular pattern. Pale
follicular papules are present within the patches and there is
loss of vellus hairs. Keratosis pilaris of the upper extremities
and trunk is often observed in patients with EFF. No
photosensitivity is reported by patients.
Histopathology
Hyperkeratosis and dilatation of superficial dermal blood
vessels are observed in EFF lesions.16 Basal layer pigmentation reflects the clinical severity of hyperpigmentation.16
Enlargement of hair follicles from horny masses retained in
the infundibular region has also been reported.14
Treatment
Apart from sun avoidance and topical hydroquinone, topical
keratolytics (10% urea, ammonium lactate 12%) can be used
for the treatment of follicular papules. Laser treatment of the
background erythema and hyperpigmentation can be tried.

E. Nicolaidou, A.D. Katsambas

pathogenesis of the disease.19 A variety of possible causative
agents have been reported,17,18 including ingestion of
ammonium nitrate, orally administered X-ray contrast media,
exposure to chlorothalonil, chronic hepatitis C infection, and
exposure to environmental contaminants.
Clinical features
EDP is characterized by oval or round-shaped blue-gray
patches over the face, trunk, and extremities (Figure 2). Early
lesions may have a raised, erythematous border that
disappears later, and usually it is not evident upon initial
consultation. The lesions are occasionally pruritic, and their
diameter may vary from a few millimeters to several
centimeters. The trunk and proximal extremities are more
usually affected, followed by the face and neck. There seems
to be no predilection for exposed or unexposed areas.
Histopathology
The histologic features of EDP are relatively nonspecific.18 The inflammatory border of the lesions may show
vacuolization of the basal cell layer and occasional colloid
bodies. There is also mononuclear infiltrate of the mid and
upper dermis, and pigment incontinence with many melanophages. In the inactive lesions, the incontinence of pigment
prevails, whereas the vacuolization of the basal cell layer and
the cellular infiltrate show different degrees of intensity.
Treatment
There is no consistently effective therapy for EDP. In
children, a high rate of spontaneous remission has been
observed.18 Dapsone, clofazimine, and narrow-band UVB
phototherapy have been used with good results in small
series.19,20

Poikiloderma of Civatte
Poikiloderma is a combination of linear telangiectasia,
mottled hyperpigmentation/depigmentation, and superficial

Erythema dyschromicum perstans

Erythema dyschromicum perstans (EDP) or ashy dermatosis is an idiopathic, acquired, and chronic skin disorder
characterized by hyperpigmented patches on the trunk, face,
and extremities.
Epidemiology and etiology
Most adult patients with EPD are of Hispanic origin,17 but
white adult patients have also been reported. As far as
children are concerned, there are more reports with white
children than with Hispanic children.18 There appears to be
no sexual predilection for EDP.
The cause of EDP remains unknown. There is considerable
evidence that an immunologic mechanism is involved in the

Fig. 2 Erythema dyschromicum perstans. The patient had similar

lesions on the face.

Pigmentation disorders

69

atrophy in a reticular pattern. Poikiloderma of Civatte (PC) is

a rather common, benign, acquired poikiloderma of the face
and neck.

Epidemiology and etiology

PC occurs most frequently in fair-skinned, middle-aged,
or elderly women; however, the disease has been seen in
other age groups, as well as in men.21
The cause of PC remains obscure. The predilection for
sun-exposed areas suggests a fundamental role for chronic
sun exposure. Hormonal factors in combination with the
normal aging process may also be involved, as is suggested
by the age and sex distribution of the patients.
Photosensitizing chemicals in perfumes or cosmetics
have been implicated in the pathogenesis of the disorder,
and a statistically significant difference of positive patch
test reactions to fragrances has been reported in patients
with PC compared with control subjects. 22 Genetic
predisposition, possibly expressed as an increased susceptibility to sun radiation, has also been implicated in the
pathogenesis of the disorder.23
Clinical features
Symmetrical patches with reddish brown, reticulate
pigmentation, telangiectasia, and atrophy develop on the
lateral cheeks and the sides of the neck (Figure 3). The
area shaded by the chin is not affected. Lesions usually
are asymptomatic, but occasionally patients report rosacealike flushing. 21 PC runs a chronic, benign, but
irreversible course.
Histopathology
The epidermis is atrophic and there is hydropic
degeneration of the basal layer. Numerous melanophages
are present in the dermis along with a perivascular or
bandlike lymphocytic infiltrate. In late stages, dilated blood
vessels are demonstrated.
Treatment
Pulse dye laser and ablative fractional laser resurfacing
have been used with variable results.24

Phototoxic dermatitis
Phototoxic dermatitis is initiated by a photochemical
reaction between UV radiation and a phototoxic substance.
Phototoxic substances can be applied topically (psoralens),
ingested (several drugs), or contacted accidentally (phototoxic plants). After exposure to the sun, erythema and blisters
usually develop. Prominent postinflammatory hyperpigmentation is a typical characteristic.
Berloque dermatitis is the result of the topical application
of the phototoxic oil of bergamot or related substances
found in perfumes and other cosmetics. If sun exposure is

Fig. 3 Poikiloderma of Civatte. (Courtesy of Alexander C.

Katoulis, MD, Athens, Greece.)

minimal, then hyperpigmentation of the face and neck,

usually in a streaked pattern, may appear with little or no
erythema. Histopathology shows increased melanin in the
basal layer and, in later stages, accumulation of melanin in
dermal melanophages.
Drug-induced facial hyperpigmentation
Numerous medications have been implicated in the
appearance of dark lesions on the skin. Drugs can cause
hyperproduction of melanin by stimulating epidermal
melanocytes, either directly or indirectly, through a
nonspecific cutaneous inflammation. They may also
impair melanin clearance from dermal macrophages by
binding to melanin and creating a stable complex. The
accumulated melanin is found either free in the dermis or
within dermal macrophages. Apart from the accumulation
of melanin, other mechanisms responsible for druginduced dark lesions include the accumulation of the
triggering medication itself, the synthesis of special
pigments under the influence of the drug, and the
deposition of iron from drug-induced damage to dermal
vessels.25 More than one of the above mechanisms are
sometimes implicated in a drug-induced lesion, and to
distinguish these lesions from true hypermelanosis, we use
for them the term hyperpigmentation.
Drugs that can cause hyperpigmentation of the face
include antimalarials, amiodarone, cytotoxic drugs, minocycline, phenothiazines (mainly chlorpromazine), tricyclic
antidepressants (particularly imipramine and desipramine),
and anticonvulsants.
Drug-induced hyperpigmentation usually has a slow
onset and progresses very gradually over months or even
years after the initiation of the drug. Apart from the usual
brownish coloration that we observe in most facial
hypermelanoses, drug-induced hyperpigmentation may
also have a blue-gray hue (Figure 4). Sun-exposed
areas, as well as mucous membranes (mouth, conjunctivae), are favorite sites for the lesions, and sun exposure
usually aggravates them. Other lesions, such as

70
inflammatory or lichenoid rashes, may accompany the
drug-induced hyperpigmentation, which usually fades,
although not always completely, when the responsible
medication is discontinued.
Histologic findings of drug-induced hyperpigmentation
are quite variable and depend on the causative factor.
Usually, melanin, another pigment, or both can be found
either free in the dermis or within dermal macrophages.

Facial hypermelanosis secondary to

systemic disorders
Addison disease
Addison disease is caused by a primary adrenocortical
insufficiency. It is characterized by hypermelanosis, weakness, nausea, vomiting, and diarrhea. Laboratory findings
include low serum sodium level, high serum potassium level,
and elevated blood urea nitrogen. The diagnosis is confirmed
by specific tests for adrenal insufficiency.
The hypermelanosis in Addison disease occurs as a
change in the intensity of normal skin pigmentation or as the
development of new areas of pigmentation, for example,
gingival or buccal mucous membrane. It results from the
melanogenic action of increased blood levels of certain
pituitary peptides. There is increased melanin in melanocytes
and there may be melanophages in the dermis.
Hemochromatosis
In hemochromatosis, one of the most common genetic
disorders, iron is deposited in a variety of tissues, leading to a
whole spectrum of systemic findings. Serum ferritin and
serum iron are elevated.
The skin acquires a slate gray or gray-brown discoloration. Light exposed areas, such as the face and the back of
the hands, are more prominently involved. Other cutaneous
signs include ichthyosislike changes, alopecia, koilonychia,
and spotty intraoral pigmentation.
Histopathologically, there is increased basal layer melanin and deposition of hemosiderin in the dermis. Sometimes,

E. Nicolaidou, A.D. Katsambas

the pigment is concentrated around sweat glands and
endothelial cells.
Porphyria cutanea tarda
Many patients with porphyria cutanea tarda have facial
hyperpigmentation resembling melasma. Other associated
features include bullae, atrophic scars, milia, and facial
hirsutism. There is a massive increase in all urine porphyrins.

Disorders of hypopigmentation
Vitiligo
Vitiligo is an acquired disease characterized by destruction of functional melanocytes mainly in the skin, resulting
in the appearance of well-circumscribed white macules
and patches.
Epidemiology and etiology
Vitiligo is a common disease, affecting 0.5% to 2% of the
general population. Age of onset during childhood has been
reported in 25% to 30% of patients.26 There is no clear sex
predilection for the disease.
Vitiligo is a multifactorial disease related to both genetic
and environmental factors.27 The absence of functional
melanocytes in vitiligo skin is probably the result of their
destruction.
Several pathogenic hypotheses for the destruction of
melanocytes have been proposed:

The
The
The
The
The

autoimmune hypothesis
intrinsic defect of melanocytes hypothesis
defective free radical defense hypothesis
reduced melanocyte survival hypothesis
transepidermal melanocytorrhagy hypothesis

It is possible that vitiligo is not a single disorder but rather

a common phenotype of several different pathophysiologically disorders.
Clinical features and classification
Vitiligo is characterized by milk-white macules and
patches with discrete margins. Lesions are usually symmetrically distributed on the face (Figure 5), neck, axillae,
elbows, knees, shins, and dorsal aspect of the hands and feet.
The following classification divides vitiligo into three
general types: localized, generalized, and universal.

Fig. 4 Drug-induced hyperpigmentation. The patient had similar

lesions on the body.

1. Localized
a. Focal: one or more lesions in one area, but not in
a segmental distribution
b. Segmental: one or more lesions involving a
unilateral segment of the body
2. Generalized

Pigmentation disorders

71
Psychological support can be helpful to many patients, as
it is a caring and sympathetic approach by the dermatologist.

Postinflammatory hypomelanosis
Cutaneous inflammation can alter several pathways that
regulate skin color, resulting in the appearance of residual
hypopigmented lesions. Many dermatoses, including psoriasis, seborrheic dermatitis, atopic dermatitis, sarcoidosis,
mycoses fungoides, and lupus can lead to postinflammatory
hypopigmentation.
Lesions of postinflammatory hypopigmentation usually
gradually resolve. In resistant cases, UVB phototherapy and
epidermal or melanocyte grafting may be helpful.

Fig. 5

Vitiligo on the face.

a. Vulgaris: scattered lesions widely distributed, universal (more than 80% of body surface area affected)
b. Acrofacial: several lesions on the extremities and
face
3. Universal: more than 80% of body surface area
affected
Histopathology
In classical vitiligo, no dihydroxyphenylalanine-positive
melanocytes can be detected. In early lesions, some melanocytes with decreased dihydroxyphenylalanine-positivity can
be detected.
Treatment and prognosis
The course of vitiligo is unpredictable. The disease may
stabilize for a long period or exacerbate rapidly. Spontaneous
repigmentation has also been reported, especially in the
summer. Some patients report development of new lesions in
stressful periods.
Several treatment modalities have been used for the
management of vitiligo.2831 Topical corticosteroids, topical
calcineurin inhibitors (tacrolimus and pimecrolimus), phototherapy (narrowband UVB, photochemotherapy), excimer
laser, and surgery (minigrafting, suction blister epidermal
grafting, grafting of cultured autologous melanocytes, and
grafting of non-cultured epidermal cell suspensions) have all
been used with variable results. Lesions on the face and
patients with darker skin phototype (III-V) respond better to
treatment. In widespread disease, depigmentation of islands
of normally pigmented skin with 20% monobenzyl ether of
hydroquinone is an option.

Pityriasis alba
Pityriasis alba is a very common condition that is formally
categorized as postinflammatory hypomelanosis, even
though its actual pathogenesis is not completely clear. It is
characterized by multiple ill-defined macules and patches
that are symmetrically distributed mainly on the face,
particularly the cheeks. The lesions are hypopigmented
with pityriasiform scaling and may persist for months or
years before resolving spontaneously. Histologically, there is
subacute spongiotic dermatitis with decreased melanin in the
epidermis. No treatment is more effective than emollients.

Piebaldism
Piebaldism is an autosomal dominant disorder characterized by poliosis and stable, circumscribed areas of
leukoderma.
Epidemiology and etiology
Piebaldism is quite uncommon. It is estimated to occur in
1 to 40,000 white individuals. It results from mutations in the
KIT proto-oncogene, which encodes a member of the
tyrosinase kinase family of transmembrane receptors that is
found on the surface of melanocytes.32 The KIT receptor is
required for the normal development of melanocytes.
Clinical features
The lesions are present at birth. Scalp poliosis (white
forelock) is present in 80% to 90% of patients. All the hairs
of the forelock are white, and the underlying skin is also
amelanotic. This white patch is midline in location and can
extend up to the root of the nose. Poliosis of the eyebrows
and eyelashes is common.
Apart from the face, amelanotic lesions appear also on the
trunk and extremities. They are irregular in shape, wellcircumscribed, and contain normally pigmented and hyperpigmented macules and patches. The presence of lesions
since birth, the stability of lesions, and the presence of
pigmented patches within lesions differentiate piebaldism
from vitiligo.

72
Histopathology
No melanocytes can be found in either the epidermis or
the hair follicles of lesional skin. Melanocytes and
keratinocytes of hyperpigmented macules have an abundance of melanosomes.
Treatment and prognosis
Lesions are stable. Surgical treatment with autologous
transplantation techniques (minigrafting, suction blister
epidermal grafting, grafting of cultured autologous melanocytes, and grafting of noncultured epidermal cell suspensions) can be used to improve the appearance of lesions.

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