Dermatologic Therapy, Vol. 25, 2012, S10S16 2012 Wiley Periodicals, Inc.

Printed in the United States All rights reserved

DERMATOLOGIC THERAPY
ISSN 1396-0296

INVITED ARTICLE

Classification of vitiligo:
a challenging endeavor
Jana Hercogov*, Robert A. Schwartz & Torello M. Lotti
*Department of Dermatology and Venereology, 2nd Medical School, Charles
University of Prague, Prague Czech Republic, Dermatology and Pathology,
New Jersey Medical School, Newark, New Jersey, University of Rome
G. Marconi, Rome, Italy and Vitiligo Research Foundation, New York,
New York

ABSTRACT: The classification of vitiligo is mandatory for clinical and research purposes. Although the
etiology and pathobiology of vitiligo remain unknown, a working classification of vitiligo is imperative
for the scientific community to communicate. The authors delineate herein their efforts for vitiligo
classification utilizing clinical, genetic, pathobiological, epidemiological, and molecular characteristics
of vitiligo. These different classification approaches may aid clinicians to identify the most suitable
treatment for each individual vitiligo subject.

KEYWORDS: classification, treatment, vitiligo

Presently, there is no unanimously agreed classifi-
cation of vitiligo (1). This fact represents a major
limit to the design of clinical trials for vitiligo and
personalized treatment(s) (13).
Vitiligo is a complex and multisystem disease
that causes a selective, often progressive, loss of
functioning melanocytes, leaving white patches on
the skin and occasionally mucose. Hair may be
devoid of pigment. Internal organs containing
melanocytes may be affected.
The etiology underlying vitiligo remains to be
elucidated. The pathobiology of vitiligo is still
enigmatic. According to well-known models, one
or more environmental, physiological, or other
triggers might induce localized inactivation or
death of melanocytes and eventually sometimes
Address correspondence and reprint requests to: Torello Lotti,
MD, Chair of Dermatology and Venereology, University of
Rome G. Marconi, Via Vittoria Colonna 11, 00193 Rome, Italy,
or email: professor@torellolotti.it.
instigate an autoimmune response that then could
cause melanocytes destruction in areas more or
less distant from the site of initiation (13).
As the etiology and pathogenesis of vitiligo are
still unknown or uncertain, and considering that
several hypotheses, sometimes supported by
intriguing but not always proven data, are circu-
lated in the scientific community, the question if
vitiligo should be classified as a disease or a spec-
trum of disorders is central to its classification (1).
It has been suggested that, although the clinical
picture of vitiligo is similar, the etiology and
pathogenetic mechanism could vary individual by
individual. This could bring to the suggestive
hypothesis that classification of vitiligo is pres-
ently an impossible mission. Basic research has not
yet been translated into clinical benefit for patients
with vitiligo, and molecular classification of viti-
ligo is still impossible. This latter concept inhibits
movement toward personalized medicine in viti-
ligo patients and highlights an imperative corol-
lary: we must draft the classification of vitiligo.

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Working classification of vitiligo
The scientific community is aware that there is no
reliable classification of vitiligo. Vitiligo profiling
is mandatory for designing clinical trials with
possible meta-analysis outcomes. The not-yet-
universally agreed upon treatment of vitiligo
patients will improve according to a more precise
vitiligo profiling.
These concepts have prompted the present
authors to enumerate their working classification
of vitiligo, hoping that it will be widely adopted by
the international scientific community until a
consistent genetic etiologic, pathobiological, or
molecular classification of vitiligo becomes avail-
able for the patients benefit.
Working sections of classification
of vitiligo
The present authors propose the following
classifications:
1. Clinical classification of vitiligo
2. Genetic classification of vitiligo
3. Pathobiological classification of vitiligo
4. Epidemiological classification of vitiligo
5. Multisystem organ dysfunction-based classifi-
cation of vitiligo
6. Trigger-based classification of vitiligo and other
leukodermas
7. Molecular classification of vitiligo
Working clinical classification of vitiligo
The hereunder clinical classification seems most
appropriate for the clinician.
1. Localized
Focal: one or more macules in one area, but
not clearly in a segmental distribution
Unilateral/segmental: one or more macules
involving a unilateral segment of the body
lesions stop abruptly at the midline
Mucosal: mucous membranes alone
2. Generalized
Vulgaris scattered patches that are widely
distributed
Acrofacialis distal extremities and face
Mixed acrofacialis and vulgaris
3. Universalis
Complete or nearly complete depigmentation
Special forms
1. Trichrome vitiligo
2. Quadrichrome vitiligo
3. Inflammatory vitiligo
Vitiligo classification
More simply, vitiligo can be divided into three
types (2): localized, generalized, and universal
(when vitiligo involves more than 80% of the skin
surface) (2,3).
Practical implication of the working clinical classi-
fication. The localized forms typically begin in
childhood. Among those, the most common is the
form affecting the trigeminal dermatome. It tends
to be stable or regressive (4,5) and accompanied by
poliosis. Associated systemic autoimmune disor-
ders are unusual. This has a relevant impact on the
follow-up and on the treatment of the affected
subjects.
The generalized vitiligo may begin later on in
life, in both sexes, at sites sensitive to confrication,
trauma, or pressure. This form is typically progres-
sive, with flares that may involve hair in the later
stages.
Autoimmune disorders are often associated with
this form both in the affected subjects and in the
family members, stressing the concept of a consis-
tent follow-up and need of systemic treatments for
those subjects (6).
Universal vitiligo is often associated with mul-
tiple comorbidities both in the affected subjects
and in the family members. Melanocytes can be
affected in the inner ear and in the eye, requiring a
multidisciplinary diagnostic approach and follow-
up of these patients (1).
Genetic classification of vitiligo
Considering vitiligo as a single disease and not as a
spectrum of possibly different disorders leading to
the selective loss/inactivation of melanocytes, epi-
demiological studies indicate that this disorder is
inherited in a non-Mendelian, multifactorial, and
polygenic pattern (79).
The penetrance is variably incomplete (7,9).
Environmental exposure and recessive alleles at
multiple unlinked loci act synergically and epistati-
cally in the development of vitiligo. The impor-
tance of environmental exposure over the genetics
has been recently shown (7).
According to one study (7), monozygotic twins
with identical DNA have only a 23% concordance
in developing vitiligo. This accounts for a predo-
minant nongenetic direct component in vitiligo
patients.
Genetic association studies may soon facilitate
structuring of a clinically relevant regional classi-
fication according to:
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Hercogov et al.
Human leukocyte antigen (HLA) haplotypes:
1. Different ethnicities have different HLA-
associated susceptibility
2. Particular HLA haplotypes are strongly asso-
ciated in patients (and in their family
members) with vitiligo and autoimmune
disorders (10)
3. Susceptibility loci similar to HLA, i.e., the
CTLA4 (cytotoxic T lymphocyte antigen 4)
could identify the cases in which vitiligo
is regularly associated with concomitant
autoimmune diseases (11)
4. Similarly single nucleotide polymorphisms
(PTPN22, mannose-binding lectin, NALP-1
(12)) seem epidemiologically significantly
linked to autoimmune diseases like lupus
erythematosus, Addisons disease, autoim-
mune thyroiditis, autoimmune gastritis, and
pernicious anemia (11,13)
Genome-wide association studies are presently
being carried out by two main groups: one led by
Xuejun Zhang in China and another headed by
Richard Spritz (14) in the United States.
These studies have clarified the fact that differ-
ent populations may have varied susceptibility for
vitiligo, that different roles are played by genes
involved in vitiligo susceptibility versus vitiligo age
of onset, and that HLA haplotypes and similar sus-
ceptibility loci may account for a weak or strong
association with autoimmune disorders in the viti-
ligo patient and in her or his family members.
Practical implication of the working genetic classi-
fication of vitiligo. The evaluation of these studies
will identify the genetic differences in the different
populations regarding susceptibility for vitiligo
and age of onset. These studies will delineate
the vitiligo patient subgroups that are prone to
develop selected comorbidities, mainly autoim-
mune disorders.
Hopefully, these studies will, in the future,
indicate to the clinician which follow-up is
required for the different vitiligo subjects and
which systemic and/or topical approaches may
be beneficial in the single case. Personalized treat-
ments will follow.
Pathobiological classification of vitiligo
Presently, several hypotheses are considered as at
least partially documented in vitiligo.
Autoimmune hypothesis. Auto-antibodies in the
sera of some vitiligo subjects have been shown.
They are directed against melanocyte antigens
S12
expressed on the cell surface, against intracellular
pigment, and even against nonpigment cell anti-
gens (common tissue antigens) (15).
There is evidence of direct correlation between
levels of some of these antibodies and disease
activity (16,17).
Cellular immunity is present in vitiligo in
selected groups of subjects. Melan-A-specific
CD8+T cells are highly represented in the blood of
the vitiligo patients. Their number correlates with
disease extent.
Neurohumoral hypothesis. Increased levels of neu-
ropeptide Y have been shown intralesionally and
perilesionally in vitiligo skin (18). Vitiligo patients
with progressive disease have increased urine levels
of homovanillic acid and vanillylmandelic acid (19).
Autocytotoxic hypothesis. A defect in the melanin
receptor may result in concomitant increase in
melanin synthesis, leading to cellular death or apo-
ptosis (20).
Clinical implications: possible identification of
vitiligo subjects with cell receptor alterations.
Biochemical hypothesis. In some cases of vitiligo,
melanocytes could autonomously undergo death
or apoptosis because of intracellular accumulation
of (6R) and (7R)-L-erythro-5,6,7,8-tetrahydro-
biopterin (6BH4 and 7BH4).
These substances could inhibit melanocyte phe-
nylalanine hydroxylase, the enzyme that converts
dietary phenylalanine to tyrosine, and the levels
of hydrogen peroxide-inducing cell damage or
apoptosis (20,21).
Clinical implications: if proved, this should
bring to targeted biochemical treatments.
Oxidative stress hypothesis. High hydrogen perox-
ide levels in vitiligo epidermis have been reported.
This could be the consequence of:
1. Single nucleotide polymorphism in the catalase
gene (22)
2. Increased levels of 6BH4 and 7BH4 (23)
3. Reduced glutathione peroxidase activity (24)
4. Increase in norepinephrine levels (25)
5. Defective calcium uptake (20)
Clinical implications: high levels of H2O2 corre-
late with low levels of the catalase enzyme. Thus,
adequate supplementation of cutaneous and sys-
temic catalase enzyme could treat or possibly cure
vitiligo.
Melanocytorrhagy hypothesis. Melanocytes are not
anchored to keratinocytes by desmosomes. They
 Vitiligo classification

are mainly attached to the extracellular matrix vitiligo mainly based on psychological and envi-
molecule fibronectin. High levels of tenascin are ronmental factors, with obvious impact on the
present in the vitiligo epidermis, facilitating a loss potential treatments.
of melanocytes (26,27).
Clinical implications: according to this hypoth-
Multisystem organ dysfunction-based
esis, a continuous Koebner phenomenon could
classification of vitiligo
represent the cause of vitiligo, and therapies
should focus on anchoring melanocytes properly Many disorders and syndromes are variably asso-
in the epidermis. ciated with vitiligo. Selected vitiligo subjects can be
affected by multisystem organ dysfunction, the
Decreased melanocyte lifespan hypothesis. vitiligo systemic syndromes. Most of those cases
Several cytokines, such as interleukin-1 and are discovered at birth or during infancy.
interferon-gamma, mainly produced and released
by keratinocytes, may induce apoptosis of melano- Disorders and syndromes possibly associated with
cytes because of a deficiency in survival signals vitiligo (in alphabetical order)
by interfering with the melanocyte membrane Less common associations:
tyrosine kinase receptor C-KIT (28). Reduced levels Acrokeratosis paraneoplastica of Bazex
of C-KIT receptors in vitiligo melanocytes or of Alezzandrini syndrome
growth factors could induce premature apoptosis APECED* syndrome
and decreased melanocytes survival. (*Autoimmune polyendocrinopathy candidiasis
Clinical implications: inactivating exceedingly ectodermal dysplasia)
apoptotic cytokines in the vitiligo skin and/or nor- Asthma
malizing the C-KIT melanocytes receptors may Ataxia-telangiectasia
prove beneficial. Deafness
DOPA-responsive dystonia
Overview Dysgammaglobulinemia
Hemolytic anemia (autoimmune)
All the previously mentioned hypotheses have
Hepatitis C
produced theories that could explain the onset
HIV
of vitiligo. Unfortunately, all vitiligo subjects are
Inflammatory bowel disease
included in one or more of the previously men-
Kabuki syndrome
tioned data and theories.
Kaposi sarcoma
Accordingly, vitiligo could instead represent a
More common associations:
spectrum of many different disorders with different
Addisons disease
etiologies and pathogeneses manifesting as a
Alopecia areata
common phenotype: the loss of melanocytes
Atopic dermatitis
and/or their products.
Autoimmune thyroid disease
Chronic urticaria
Epidemiological classification of vitiligo
Diabetes mellitus
The prevalence of vitiligo in the general population Halo nevi
ranges from 0.3 to 8.8 cases per 100 in different Hypoacusis
regions of the world. Genetic studies are non- Hypoparathyroidism
contributory (1,7,8). Ichthyosis
According to analytical epidemiology studies, Lymphoma
associating HLA antigens with vitiligo in the differ- Melanoma
ent ethnic groups is not explanatory; thus, assess- Mitochondrial myopathy, encephalopathy, lactic
ing the potential role of unknown environmental acidosis, and stroke (MELAS) syndrome
factors in the development of vitiligo may be Morphea
valuable. Multiple sclerosis
Clinical epidemiology also confirms patients Myasthenia gravis
quality of life and life stress events may contribute Non-melanoma skin cancer
to explain the onset and long-term outcome of Nail dystrophy
vitiligo. Ocular abnormalities
Clinical implications: epidemiological research Pemphigus vulgaris
may contribute to a working classification of Pernicious anemia

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Hercogov et al.

Psoriasis Table 1. Differential diagnosis in vitiligo: the

Rheumatoid arthritis leukodermas
Sarcoidosis
Chemically induced leukoderma (often occupational)
Schmidt syndrome
Arsenic
Systemic lupus erythematosus Phenols and other derivatives, catechols
Turner syndrome Infections
Twenty-nail dystrophy Leishmaniasis (post-kala-azar)
VogtKoyanagiHarada syndrome Leprosy
(From (1), adapted from Alikhan et al. (29).) Onchocerciasis
Clinical implications: a classification based on Secondary syphilis
the disorders and syndromes associated with viti- Tinea versicolor
ligo would be of great help for pediatricians and the Treponematoses (pinta and syphilis)
geneticists. This classification could probably lead Genetic syndromes
to the discovery of relevant and as yet unidentified ChdiakHigashi syndrome
Hypomelanosis of Ito
causes of vitiligo and to their specific treatments.
Oculocutaneous albinism
Piebaldism
Trigger-based classification of vitiligo and Tuberous sclerosis
other leukodermas VogtKoyanagiHarada syndrome
Waardenburg syndrome
Vitiligo is not always characterized by uniformly Post-inflammatory hypopigmentation
and well-circumscribed totally depigmented Atopic dermatitis/allergic contact dermatitis
macules and patches. Trichrome vitiligo has an Nummular dermatitis
intermediate variable in size than zone between Phototherapy and radiotherapy-induced
normal and depigmented skin (1,30). Quad- hypopigmentation
richrome vitiligo is a form of trichrome vitiligo with Pityriasis alba
Post-traumatic hypopigmentation (scar)
additional marginal or perifollicular hypopigmen-
Psoriasis
tation (31). Inflammatory vitiligo presents with Sarcoidosis
raised inflammatory erythematous borders at the Systemic lupus erythematosus
margins of the white macules or patches (1). Topical or systemic drug-induced depigmentation
Dermatologists separate vitiligo, depigmented Neoplastic
patches of unknown origin, from leukodermas, Amelanotic melanoma
which are totally depigmented or hypopigmented Halo nevus
patches caused by a definite etiologic agents. Melanoma-associated leukoderma
Vitiligo and leukodermas may sometimes need Mycosis fungoides
special attention to be differentiated (see Table 1). Idiopathic
Clinical implications: considering that tri- Idiopathic guttate hypomelanosis
Lichen sclerosus et atrophicus
chrome, quadrichrome, and inflammatory vitiligo
Lichen striatus-like leukoderma
exist, the present authors think that both scientists Morphea
and dermatologists should not ignore the classifi- Melasma (caused by contrast between lighter and
cation of leukodermas and should use this classifi- darker skin)
cation to identify common pathways leading to Progressive (or acquired) macular hypomelanosis
trichrome and quadrichrome vitiligo and leuko- Malformations
dermas of known or unknown origin(s). This Nevus anemicus
classification may facilitate understanding and Nevus depigmentosus/hypopigmentosus
treating the individual vitiligo patient. Nutritional
Kwashiorkor
Selenium deficiency
Molecular classification of vitiligo
From (1), adapted from Alikhan et al. (29).
By genome-wide linkage and genome-wide asso-
ciation studies of generalized vitiligo, geneticists could represent the basis for a molecular classifica-
have identified multiple loci that contribute not tion of vitiligo based on simultaneous interactive
only to vitiligo susceptibility, but also to other actions of molecules provoking autoimmune
autoimmune disease susceptibility (911). destruction of melanocytes, development of
Most of those genes encode molecules, the most autoimmune disorders, and immune surveillance
studied being immunoregulatory proteins, which of malignant melanoma (9,10).

S14

Accordingly, the psycho-neuro-immune-
endocrinology (PNIE) axis could offer to the
present authors consideration other molecules
generated by the interaction of the internal and
external environments with the different PNIE
sections (1).
Most probably, some of these vitilogenic mol-
ecules will be specific for the individual and the
vast majority of those molecules will be shared
with many other individuals clustered in the differ-
ent subtypes of vitiligo or, more probably, in the
different disorders belonging to that spectrum that
manifests with the common phenotype nowadays
described as vitiligo.
The present authors have hypothesized different
approaches to vitiligo classification, stressing the
concept that molecular classification is mandatory.
One can hypothesize that this personalized
molecular approach to the classification of vitiligo
is not practical, and thus, conclude that there is no
realistic possibility of classifying vitiligo and no
realistic hope to identify the cure(s) for vitiligo(s).
This idea is invalid, not only because a working
molecular classification of vitiligo(s) is already at
the horizon, but also mainly because it is conceiv-
able that a limited number of molecules play a
major role in depigmentation and repigmentation
of the skin, which is shared by the majority of the
subjects that manifest with the same (or very
similar) phenotype.
Conclusion
Classification of a disease with many different
clinical presentations, with unknown etiology,
modest genetic data, multiple, and fragmented
pathogenetical hypotheses is in general terms a
mission impossible. The classification of vitiligo
should thus be considered an impossible event,
but this is not entirely true.
In fact, we can benefit from different working
classifications to aid the clinical dermatologist in
discovering the different clinical presentations and
comorbidities and in designing the most rational
therapeutic approach in the different cases.
The multiple working classifications of vitili-
go(s) drafted by the present authors in this paper
not only will help the dermatologist and the vitiligo
subject in their everyday fight against vitiligo, but
also these working classifications will probably
represent common fertile ground for the scientific
community involved to solve the melanocyte
enigma and its major phenotypic manifestation
vitiligo.
Vitiligo classification
Acknowledgements
The present authors thank Alessandra Fabbri
Palmieri for her secretarial help in writing this
paper. The present authors are grateful to Dr. Igor
Korobko and Dr. Yan Valle for their continuous sci-
entific discussion with the authors on the scientific
content of this paper.
Conflict of interest
None.
References
1. Lotti T, Hercogov J, eds. Vitiligo problems and solutions.
New York, NY: Marcel Dekker Inc., 2004: 1866.
2. Shajil EM, Chatterjee S, Agrawal D, Bagchi T, Begum R. Viti-
ligo: pathomechanisms and genetic polymorphism of sus-
ceptible genes. Indian J Exp Biol 2006: 44: 546539.
3. Nordlund JJ, Lerner AB. Vitiligo. It is important. Arch Der-
matol 1982: 118: 58.
4. Onunu AN, Kubeyinje EP. Vitiligo in the Nigerian African: a
study on 351 patients in Benin City in Nigeria. Int J Derma-
tol 2003: 42: 800802.
5. Hann SK, Lee HJ. Segmental vitiligo: clinical findings in 208
patients. J Am Acad Dermatol 1996: 35: 671674.
6. Barona MI, Arrunategui A, Falabella R, Alzate A. An epide-
miologic case-control study in a population with vitiligo.
J Am Acad Dermatol 1995: 33: 621625.
7. Alkhateeb A, Fain PR, Thody A, Bennet DC, Spritz RA. Epi-
demiology of vitiligo and associated autoimmune diseases
in Caucasian probands and their families. Pigment Cell Res
2003: 16: 208214.
8. Majumder PA. Genetics and prevalence of vitiligo vulgaris.
In: Hann SK, Nordlund JJ, eds. Vitiligo: a monograph on the
basic and clinical science. Oxford: Blackwell Science Ltd,
2000: 1820.
9. Sun X, Xu A, Wei X, et al. Genetic epidemiology of vitiligo: a
study of 815 probands and their families from South China.
Int J Dermatol 2006: 45: 11761181.
10. Spritz RA. The genetics of generalized vitiligo. Curr Dir
Autoimmun 2008: 10: 244257.
11. Birlea SA, Laberge GS, Procopciuc LM, Fain PR, Spritz RA.
CTLA4 and generalized vitiligo: two genetic association
studies and a meta-analysis of published data. Pigment Cell
Melanoma Res 2009: 22: 230234.
12. Jin Y, Malloux CM, Gowan K, et al. NALP1 in vitiligo-
associated multiple autoimmune disease. N Engl J Med
2007: 356: 12161225.
13. Fain PR, Gowan K, LaBerge GS, et al. A genomewide screen
for generalized vitiligo: confirmation of AIS1 on chromo-
some 1p31 and evidence for additional susceptibility loci.
Am J Hum Genet 2003: 72: 15601564.
14. Spritz RA, Gowan K, Bennett DC, Fain PR. Novel vitiligo
susceptibility loci on chromosome 7 (AIS2) and 8 (AIS3)
confirmation of SLEV1 on chromosome 17, and their roles
in an autoimmune diathesis. Am J Hum Genet 2004: 74:
188191.
15. Bystryn JC. Serum antibodies in vitiligo patients. Clin Der-
matol 1989: 7: 136145.
S15
Hercogov et al.
16. Cu J, Arita Y, Bystryn JC. Cytolytic antibodies to melanocytes
in vitiligo. J Invest Dermatol 1993: 100: 812815.
17. Norris DA, Kissinger RM, Naughton GM, Bystryn JC.
Evidence for immunologic mechanisms in human
vitiligo: patients sera induce damage to human melano-
cytes in vitro by complement-mediated damage and
antibody-dependent cellular cytotoxicity. J Invest Dermatol
1988: 90: 783789.
18. AlAbadie MS, Senior HJ, Bleehen SS, Gawkrodger DJ. Neu-
ropeptide and neuronal marker studies in vitiligo. Br J Der-
matol 1994: 131: 160165.
19. Morrone A, Picardo M, de Luca C, Terminali O, Passi S,
Ippolito F. Catecholamines and vitiligo. Pigment Cell Res
1992: 5: 6569.
20. Schallreuter KU, Wood JM, Pittelkow MR, et al. Regulation
of melanin biosynthesis in the human epidermis by tetrahy-
drobiopterin. Science 1994: 263: 14441446.
21. Schallreuter KU, Buttner G, Pittelkow MR, Wood JM,
Swanson NN, Korner C. Cytotoxicity of 6-biopterin to
human melanocytes. Biochem Biophys Res Commun 1994:
204: 4348.
22. Schallreuter KU, Moore J, Wood JM, et al. In vivo and in vitro
evidence for hydrogen peroxide (H2O2) accumulation in
the epidermis of patients with vitiligo and its successful
removal by a UVB-activated pseudocatalase. J Investig Der-
matol Symp Proc 1999: 4: 9196.
23. Schallreuter KU, Wood JM, Ziegler I, et al. Defective tetrahy-
drobiopterin and catecholamine biosynthesis in the depig-
mentation disorder vitiligo. Biochim Biophys Acta 1994:
1226: 181192.
S16
24. Beazley WD, Gaze D, Panske A, Panzig E, Schallreuter KU.
Serum selenium levels and blood glutathione peroxidase
activities in vitiligo. Br J Dermatol 1999: 141: 301303.
25. Badri AM, Todd PM, Garioch JJ, Gudgeon JE, Stewart DG,
Goudie RB. An immunohistological study of cutaneous
lymphocytes in vitiligo. J Pathol 1993: 170: 149155.
26. Gauthier Y, Cario-Andre M, Lepreux S, Pain C, Taieb A. Mel-
anocyte detachment after skin friction in non lesional skin
of patients with generalized vitiligo. Br J Dermatol 2003:
148: 95101.
27. Le Poole IC, van den Wijngaard RM, Westerhof W, Das PK.
Tenascin is overexpressed in vitiligo lesional skin and
inhibits melanocytes adhesion. Br J Dermatol 1997: 137:
171178.
28. Kitamura R, Tsukamoto K, Harada K, et al. Mechanisms
underlying the dysfunction of melanocytes in vitiligo
epidermis: role of SCF/KIT protein interaction and the
downstream effector, MITF-M. J Pathol 2004: 202: 463
475.
29. Alikhan A, Felsten LM, Daly M, Petronic-Rosic V. Vitiligo: a
comprehensive overview Part I. Introduction, epidemiol-
ogy, quality of life, diagnosis, differential diagnosis, associa-
tions, histopathology, etiology, and work-up. J Am Acad
Dermatol 2011: 65: 473491.
30. Hann SK, Kim YS, Yoo JH, Chun YS. Clinical and histopatho-
logic characteristics of trichrome vitiligo. J Am Acad Derma-
tol 2004: 42: 589596.
31. Ortonne JP. Vitiligo and other disorders of hypopigmenta-
tion. In: Bolognia J, Jorizzo J, Rapini R, eds. Dermatology.
Philadelphia: Mosby Elsevier, 2008: 928.