http://www.bio.davidson.

edu/Courses/Immunology/Students/Spring2003/Leese/Vi
tiligo.htm
Peter Leese Immunology at Davidson College 2003
This page is part of an undergraduate course at Davidson College.
Human Immune Leukoderma: Vitiligo
Overview:
There are several diseases marked by a lack of pigment in the skin that are
grossly referred to as leukoderma; some are caused by an inability of
melancocytes to produce melanin, while others are caused by melanocytes
either not being present or being destroyed. The latter are the pathology of the
phenotypically similar traits piebaldism and the disease vitiligo. Piebaldism,
which is present from birth, is a lack of melanocytes in the skin, while vitiligo is a
progressive disease in which the melanocytes are gradually destroyed causing
unpigmented areas on the skin. The exact etiology of vitiligo is unknown, but
four main theories exist to explain it: the autoimmune hypothesis, the neural
hypothesis, the self-destruct hypothesis, and the growth factor defect
hypothesis. It is believed that vitiligo is a polygenic trait and that a convergence
theory, combining elements of different theories across a spectrum of expression
is the most accurate etiology (Njoo & Westerhof 2001). Vitiligo is not a physically
damaging disease; other than an increased sensitivity to UV radiation most of
the diseases effects are social and psychological, especially for dark-skinned
races. There are both surgical and non-surgical treatments for vitiligo (Taneja
2002).
Picture 1. An African child exhibiting the piebald universalis phenotype-albinism.
Notice children with wildtype phenotype in background. Picture from The
appearance of ancient Israelites website.
Picture 2. Two people exhibiting the vitiligo phenotype; notice wildtype pigmentproducing skin is present in both pictures. Top panel is a white patient with
vitiligo; the lower panel is a black patient with vitiligo. Picture from The
appearance of ancient Israelites website.
Overview of Melanogenesis and Melanocytes:
The color in human hair, skin and irises is produced by the pigment melanin,
which is produced by the dermal melanoycte cells. The melanocyte cells
transform the peptide tyrosinase into two different forms of melanin, which then
is spread throughout the dermal cells and the keratinocytes via melanosomes to
darken tissue. Figure 1 shows the chemical metabolism that occurs intra-cellulary
to produce melanin from the precursors phenylalanine and tyrosine; this figure is
somewhat inaccurate as the end product of melanogenesis should be two
different types of melanin, eumelanin and pheomelanin. Eumelanin is
metabollized from DHICA and produces a brown color in hair in its intact form;
pheomelanin is metabolized from 5,6-indolequione, which produces a red color in

hair in its intact form. From these two slightly different forms of pigment in
various degrees of structural integrity come all the differing shades of Caucasian
hair (Prota 2000). In addition to coloration, melanin pigmentation in the skin also
provides photoprotection from UV radiation to the skin. However, the
melanocytes themselves are not immune from radiation damage: melanomas
are tumors of the melanocytes, which often present themselves as discolorations
owing to the pigment-producing nature of the cells (Janeway 2001).
Figure 1. Intracellular transformation of tyrosinase into pre-melanin metabolites,
and finally into melanin; several of the metabolites between tyrosinase and
melanin are toxic to melanocytes according to the self-destruct theory. Figure
from personal website of Dr. Rodolfo Nicolaus; permission pending.
Theories for the etiology of Vitiligo
Autoimmune Theory:
There is great anecdotal evidence that an autoimmune disorder causes the
destruction of melanocytes, and this theory is now generally accepted as the
common cause of vitiligo. It is known vitiligo appears in conjunction with several
other autoimmune disorders, such as juvenile diabetes mellitus, Addison's
disease, and pernicious anemia, and additionally organ-specific antibodies can
often be seen in patients with vitiligo. If the immune system raises antibodies or
cytotoxic T cells to damage melanocytes, the mode of action the cells take
against the melanocytes could be apoptosis induction directly against
melanocytes or Ig induced complement-both are demonstrated in figure 3.
Proving this theory, there is histological evidence in vitiligo patients that
apoptosis is occurring in the unpigmented skin lesions: there is damage to the
melanocytes and keratinocytes in these areas, and the melanocytes exhibit
nuclear shrinking, vacuolization, loss of dendrites, and detachment. If antibodies
do cause vitiligo, some research suggests the Igs may bind to tyrosinase related
proteins 1 and 2, which are important for melanogenesis, instead of Ig's
targeting the melanocytes directly (Huang et al. 2002).
Figure 3. Autoimmue theory of vitiligo showing both cell-mediated and humoral
autoimmune responses. Figure from Expert Reviews on Molecular Medicine
online; permission pending.
Neural Theory:
There is also evidence that peripheral nerve endings may secrete a substance
that is cytotoxic to melanocytes and causes their destruction. This is supported
by the segmental variety of vitiligo, which occurs in specific dermatomes,
indicating the skin is possibly only being affected by the nerves of that specific
dermatome. Additionally, vitiligo appears with certain neurological disorders such
as encephalitis, and trauma that causes peripheral nerve damage. Nerve endings
in depigmented areas were seen to produce abnormal neuropeptides and nerve
growth factors, and displayed axonal degeneration-these abnormal chemicals
may be toxic to melanocytes. Additionally, depigmented areas showed some

abnormal autonomic function, such as increased adrenergic tone, increased

norepinephrine, and an increased concentration of catecholamines. These data
then suggest that neurotransmitter release could, directly or indirectly, have an
affect on melanocyte destruction and depigmentation.
Self-Destruct Theory:
It is known that some of the intracellular pre-melanogenesis metabolites are
toxic to melanocytes, such as dopa and dopachrome. Normally melanocytes
possess cellular measures to counteract these toxic substances, but it is believed
that cells may lose the ability to counteract these toxic metabolites and are
destroyed by leakage of metabolites into the cytoplasm and eventually cell lysis.
There is evidence that points to this in that certain hydroquinone derivatives that
are similar to these intra-cellular metabolites cause leukoderma experimentally.
Growth Factor Defect Hypothesis:
A study in the 1980's found that melanocytes in lesions from vitiligo patients
contained melanocytes, but that these cells exhibited "defective growth and
passage capacities." The researchers then noted that the growth defects of the
melanocytes were partially corrected by adding a growth factor to their culture,
additionally suggesting that growth defects may be part of the pathology of
vitiligo. In depigmented areas, cellular analysis showed that there were
melanocytes but that they grew poorly. These data suggest that, whether a
primary or secondary cause, growth defects appear to play a role in leukoderma
and vitiligo (Njoo & Westerhof 2001).
Genetic Influences:
There does appear to be a strong genetic influence in vitiligo: a positive family
history has been reported in about 20% of patients and it has been found in
monozygotic twins. Studies have shown that vitiligo does not progress via a
simple Mendelian pattern, but more likely is coded polygenically and can be
expressed across a spectrum. There has been some evidence both proving and
disproving the involvement of the HLA system in the occurrence of vitiligo. So, it
is believed that genetic factors probably play a key role in the pathogenesis of
vitiligo, but the exact cause is unknown.
A team of researchers used the family histories kept by the American Vitiligo
Foundation to examine the Mendelian inheritance of vitiligo, and found that most
instances of the disease were clustered in families. They found that for patients
of vitiligo, offspring have the highest chance of developing the disease, followed
by siblings, parents and grandparents (Majumder et al. 1988). Before this work
Majumder's team published a report in 1988 suggesting a multiple recessive
homozygous model for the disease. In 1994 a seperate team of researchers
validated Majumder's proposition of multiple homozygous recessive alleles,
causing non-Mendelian inheritance of the disease; this team found that 3
"epistatically interacting autosomal diallelic loci" are involved in the

pathogenesis of the disease and affected individuals exhibit homozygous

recessive genotypes for all 3 loci (Nath et al. 1994).
Convergence Theory:
Following genetic studies, researchers have begun to lean towards a multifaceted etiology for vitiligo, that combines components of the aforementioned
theories and genetics. This theory states that genetic influences have a role in
causing vitiligo in addition to other elements, such as stress, accumulation of
toxic compounds, infection, autoimmunity, mutations, and impaired melanocyte
proliferation (Njoo & Westerhof 2001).
Treatment:
No person has brought more attention to vitiligo and its treatment possibilities
than the erratic performer Michael Jackson; Jackson was born black but claims to
suffer from vitiligo, causing his skin to become extremely pale. Despite many
repigmenting therapies, Jackson assumedly chose a bleaching treatment to rid
his skin of remaining pigment. Both re-pigmenting and bleaching treatments will
be discussed.
Picture 3. Patient in 1972 and 1979. Pre-vitiligo universalis. Photos taken from
BBC News online.
Picture 4. Patient in 1993 and 1996. Post-vitiligo universalis, and subsequent
bleaching treatment. Photos taken from BBC News online.

Immuno Suppressive Treatments:

As vitiligo is believed to be an autoimmune disorder, supressing the immune
system would then be an effective treatment at halting the spread of vitiligo and
even inducing repigmentation. Corticosteroids are the main choice for this
treatment and they effectively halt the progressive spread of vitiligo and also
lead to repigmentation of lesioned areas. For small, localized lesions, topical and
intralesional corticosteroids are used once a day. For rapidly spreading vitiligo or
vitiligo universalis, systemic corticosteroids are employed; however, the role of
systemic corticosteroids is controversial due to the serious adverse side effects.
Non-surgical Treatment: phototherapy and photochemotherapy
Currently, the most popular treatments for vitiligo are forms of phototherapy; it is
known that various sources of UV light can be successfully used to stimulate
repigmentation. Phototherapy can either be used by itself or in conjunction with
light-sensitizing drugs.
PUVA treatment is the most popular treatment for vitiligo currently; the concept
for the treatment dates back thousands of years, when the plants Psoralea
coryifolia Linnaues and Ammi majus Linnaeus where eaten or used topically in
Egypt and India to treat vitiligo. Today, isolates of the plants are used topically or

orally in conjunction with a synthetic compound to chemically increase sensitivity

to light. The patient is then exposed to a measured amount of natural sunlight
(PUVASOL) or artificial UV radiation (PUVA) to induce re-pigmentation.
The amino phenylalanine is also used to treat vitiligo, although it is not a photosensitizing chemical. It is known that phenylalanine is a precursor for melanin via
L-tyrosine, and it appears that there is a problem with L-phenylalanine
metabolism in vitiligo. A combination of topical application and oral ingestion of
phenylalanine with natural sunlight exposure resulted in repigmentation for 83%
of patients.
In addition to photochemotherapy, there are several forms of phototherapy,
without the light-sensitizing chemicals.
UV light in the wavelengths from 290-320 nm are often used to treat vitiligo.
There are few studies reporting the efficacy of this treatment, but anecdotally
the treatment appears effective, though not as good as other forms of
phototherapy. In addition to broad band UV (BUVB), there is also narrow band UV
treatment (NBUVB). This is a more recent form of UV phototherapy and was
initially used to treat psoriasis. This UV treatment operates between 305 and 311
nm, and is highly effective for treating psoriasis and moderately effective at
treating vitiligo. When used as monotherapy, NBUVB is slightly but not
significantly more effective at stimulating repigmentation than PUVA treatment.
In addition to UV treatment, the excimer laser has now been implemented as
phototherapy for vitiligo. The 308 nm laser produces light similar to the narrow
band UVB treatment, and has shown good results in stimulating repigmentation
of about 90% of patients. The excimer laser also allows more focused treatment
on specific lesions, or hard to reach areas of the body.
There is little scientific evidence examining why phototherapies are effective at
stimulating repigmentation; however, it is very strongly believed that if there are
stores of unaffected but immature melanyocytes in the lesioned area, these
melanocytes can be induced to produce melanin in the lesioned areas. Likewise,
there are often functional, but not melanin producing melanocytes at lesion
boundaries that can produce melanin that spreads into the lesions causing
repigmentation.
Surgical Treatment:
In addition to phototherapy, there is also surgical treament for vitiligo that
mainly consists of grafting patches of skin with healthy melanocytes to lesioned
sites. In both minigrafting and suction blister grafting, superficial layers of skin
are removed from normally-pigmented skin and these patches then grafted onto
the lesioned areas. These techniques are believed to work by healthy
melanocytes from the grafts proliferating into the lesioned areas and
repopulating them. Success rates for these techniques are between 80% and
90%. Full thickness grafts of skin are implanted in minigrafting, using 1-2 mm

healthy skin punches from areas such as the buttocks and followed by exposure
to sunlight or PUVA treatment. Success of minigrafting is around 67% in patients.
The future of surgical treatment for vitiligo is actually extracting melanocytes
from a donor area of the patient's healthy skin, culturing these melanocytes into
a large population, then grafting them as sheets onto the lesioned areas.
Preleminary trials with this technique have been highly successful; however
there is some concern about controlling malignancy in the cultured melanocytes.
Bleaching Treatment:
In addition to treatments to repigment skin, in extremely progressive, full-body
vitiligo called vitiligo universalis, the patient can opt to bleach the remaining
pigment off healthy skin. This treatment does have profound psychosocial
implications, especially for naturally dark-skinned individuals who become light
or white-skinned. This is the proposed medical scenario with performer Michael
Jackson, who claims to have been afflicted with vitiligo universalis. As opposed to
seeking repigmentation, Jackson opted instead for depigmentation of remaining,
naturally dark areas. This is a feasible scenario, although there is great debate as
to the authenticity of Jackson's claim (Taneja 2002).
References
Janeway, C. A. Jr., Travers, P., Walport, M., and Shlomchik, M. J. Immunobiology 5.
New York: Garland Publishing, 2001.
Huang, C.L., Nordlund, J.J., & Boissy, R. 2002. "Vitiligo: A manifestation of
apoptosis?" American Journal of Clinical Dermatology 3(5): 301-308.
Majumder, P.P., Das, S.K., Li, C.C. 1988. "A genetical model for vitiligo." American
Journal Human Genetics 43: 119-125.
Majumder, P.P., Nordlund, J.J., Nath, S.K. 1993. "Pattern of familial aggregation of
vitiligo." Archives of Dermatology 129: 994-998.
Nath, S.K., Majumder, P.P., Nordlund, J.J. 1994. "Genetic epidemiology of vitiligo:
multilocus recessivity cross-validated." American Journal of Human Genetics 55:
981-990.
Njoo, M.D., & Westerhof, W. 2001. "Vitiligo: Pathogenesis and Treatment."
American Journal of Clnical Dermatology 2(3): 167-181.
Prota, G. 2000. "Melanins, Melanogenesis and Melanocytes: Looking at Their
functional significance from the chemist's viewpoint." Pigment Cell Research 13:
283-293.
Taneja, A. 2002. "Treatment of Vitiligo." Journal of Dermatological Treatment 13:
19-258.
Davidson College Biology Bio 307
Spring Semester 2003

Contact Peter Leese or View Immunology at Davidson College

http://www.kalbe.co.id/files/cdk/files/11Vitiligo117.pdf/11Vitiligo117.html
Djunaedi Hidayat
Rumah Sakit Kusta Sitanala, Tangerang 1997
Vitiligo adalah kelainan pigmentasi kulit, seringkali bersifat progresif dan familial yang
ditandai oleh makula hipopigmentasi pada kulit yang asimtomatik(1,2,3). Selain kelainan
pigmentasi, tidak dijumpai kelainan lain pada kulit tersebut(1,4,5).

Kata vitiligo berasa dan bahasa lain vitellus yang berarti anak sapi, karena kulit penderita
berwarna putih seperti kulit anak sapi yang berbercak putih(3). Istilah vitiligo mulai diperkenalkan oleh Celsus, seorang dokter Romawi pada abad ke-2 Di seluruh dunia insidensnya
rata-rata 1% (0,148,8%)(2,7).
Penyakit ini dapat mengenai semua ras dan kedua jenis kelamin dengan perbedaan yang tidak
bermakna(3). Sedangkan menurut Domonkos (1982), penyakit ini lebih sering diderita oleh
orang kulit berwarna dan biasanya dengan derajat yang lebih berat(5).
Penyakit dapat terjadi sejak lahir sampai usia lanjut dengan frekuensi tertinggi pada usia 1030
tahun(1,2,3,5). Menurut statistik di Amerika Serikat 50% dan penderita vitiligo mulai timbul
pada usia sebelum 20 tahun dan 25% pada usia di bawah 8 tahun(3).
Penyebab vitiligo yang pasti belum diketahui, diduga suatu penyakit herediter yang
diturunkan secara autosomal domi-nan(1,2,3,5). Dari penyelidikannya, Lerner (1959)
melaporkan 38% penderita vitiligo mempunyai keluarga yang menderita vitiligo, sedangkan
Eli -Mofty (1968) menyebut angka 35%(6).
Beberapa faktor pencetus terjadinya vitiligo antara lain(2,3):
1) Faktor mekanis
Pada 1070% penderita vitiligo timbul lesi setelah trauma fisik, misalnya setelah tindakan
bedah atau pada tempat bekas trauma fisik dan kimiawi.
2) Faktor sinar matahari atau penyinaran ultra violet A
Pada 715% penderita vitiligo timbul lesi setelah terpajan sinar matahari atau UV A dan
ternyata 70% lesi pertama kali timbul pada bagian kulit yang terpajan.
3) Faktor emosi/psikis
Dikatakan bahwa kira-kira 20% penderita vitiligo berkembang setelah mendapat gangguan
emosi, trauma atau stres psikis yang berat.
4) Faktor hormonal
Diduga vitiligo memburuk selama kehamilan atau pada penggunaan kontrasepsi oral. Tetapi
pendapat tersebut masih diragukan.
PATOGENESIS
Masih sedikit yang diketahui tentang patogenesis vitiligo, sehingga patofisiologi penyakit ini
masih menjadi teka-teki Sampai saat ini terdapat 3 hipotesis klasik patofisiologi vitiligo
yang dianut, yang masing-masing mempunyai kekuatan dan kelemahan yaitu(1-5):
1) Hipotesis autositoksik
Hipotesis ini berdasarkan biokimiawi melanin dan prekursornya. Dikemukakan bahwa
terdapat produk antara dari biosintesis melanin yaitu monofenol atau polifenol. Sintesis
produk antara yang berlebihan tersebut akan bersifat toksik terhadap melanosit. Lerner (1959)
mengemukakan bahwa melanosit normal mempunyai proteksi terhadap proses tersebut,
sedangkan pada penderita vitiligo mekanisme proteksi ini labil, sehingga bila ada gangguan,
produk antara tersebut akan merusak melanosit dan akibatnya terjadi vitiligo(1,3). Hal ini
secara klinis dapat terlihat lesi banyak dijumpai pada daerah kulit yang mengandung pigmen
lebih banyak (berwarna lebih gelap). Juga hal ini dapat terjadi pada pekerja-pekerja industri
karet, plastik dan bahan perekat karena banyak berkontak dengan bahan fenol dan katekol(3).
2) Hipotesis neurohumoral
Hipotesis ini mengatakan bahwa mediator neurokimiawi seperti asetilkolin, epinefrin dan
norepinefrin yang dilepaskan oleh ujung-ujung saraf perifer merupakan bahan neurotoksik
yang dapat merusak melanosit ataupun menghambat produksi melanin. Bila zat-zat tersebut
diproduksi berlebihan, maka sel melanosit di dekatnya akan rusak. Secara klinis dapat terlihat
pada vitiligo segmental satu atau dua dermatom, dan seringkali timbul pada daerah dengan
gangguan saraf seperti pada daerah paraplegia, penderita polineuritis berat(3).

3) Hipotesis imunologik
Vitiligo merupakan suatu penyakit autoimun; pada penderita dapat ditemukan autoantibodi
terhadap antigen sistem melanogenik, yaitu autoantibodi anti melanosit yang bersifat
toksik terhadap melanosit. Dari hasil-hasil penelitian terakhir, tampaknya hipotesis
imunologik yang banyak dianut oleh banyak ahli(2,8). Hal ini disokong dengan kenyataan
bahwa insidens vitiligo meningkat pada penderita penyakit autoimun(2,3,6), yaitu antara lain:
penyakit kelenjar tiroid, alopesia areata, anemia pernisiosa, anemia hemolitik
autoimun,skleroderma, artritis rheumatoid(1,2,4,5).
KLASIFIKASI
Bermacam-macam klasifikasi dikemukakan oleh beberapa ahli. Koga (1977) membagi
vitiligo dalam 2 golongan yaitu(3):
1) Vitiligo dengan distribusi sesuai dermatom.
2) Vitiligo dengan distribusi tidak sesuai dermatom.
Berdasarkan lokalisasi dan distribusinya, Mosher (1987) membagi menjadi(2,3):
1) Tipe lokalisata, yang terdiri atas:
a) Bentuk fokal : terdapat satu atau lebih makula pada satu daerah dan tidak segmental.
b) Bentuk segmental : terdapat satu atau lebih makula dalam satu atau lebih daerah dermatom
dan selalu unilateral.
c) Bentuk mukosal : lesi hanya terdapat pada selaput lendir (genital dan mulut).
2) Tipe generalisata, yang terdiri atas:
a) Bentuk akrofasial : lesi terdpat pada bagian distal ekstremitas dan muka.
b) Bentuk vulgaris : lesi tersebar tanpa pola khusus.
c) Bentuk universalis : lesi yang luas meliputi seluruh atau hampir seluruh tubuh.
Dapat pula terjadi bentuk-bentuk campuran atau bentuk-bentuk peralihan, misalnya dari
bentuk lokalisata menjadi bentuk generalisata.
MANIFESTASI/GAMBARAN KLINIS
Makula hipopigmentasi yang khas pada vitiligo berupa bercak putih seperti susu, berdiameter
beberapa milimeter sampai sentimeter, berbentuk bulat, lonjong, ataupun tak beraturan, dan
berbatas tegas. Selain hipopigmentasi tidak dijumpai kelainan lain pada kulit(1-4). Kadangkadang rambut pada kulit yang terkena ikut menjadi putih. Pada lesi awal kehilangan pigmen
tersebut hanya sebagian, tetapi makin lama seluruh pigmen melanin hilang(1).
Lesi vitiligo umumnya mempunyai distribusi yang khas. Lesi terutama terdapat pada daerah
terpajan (muka, dada, bagian atas, punggung tangan), daerah intertriginosa (aksila, lipat
paha), daerah sekitar orifisium (sekitan mulut, hidung, mata dan anus), pada bagian ekstensor
permukaan tulang yang menonjol (jari-jari, lutut, siku), daerah tibia anterior, daerah sekitar
puting susu dan umbilikus(1,2,3,4). Daerah mukosa yang sering terkena terutama genital,
bibir dan gusi(2).
Di samping itu dapatpula ditemukan bentuk-bentuk lain dari lesi vitiligo, antara lain(3):
1) Trichome vitiligo : vitiligo yang terdiri atas lesi berwarna coklat, coklat muda dan putih.
2) Vitiligo inflamatoar: lesi dengan tepi yang meninggi eritematosa dan gatal.
3) Lesi linear. Diagnosis ditegakkan terutama berdasarkan anamnesis dan pemeriksaan klinis,
dan ditunjang oleh pemeriksaan histopatologik serta pemeriksaan dengan lampu Wood(3).
Pemeriksaan histopatologi lesi vitiligo menunjukkan tidak dijumpainya melanosit dan granul
melanin di epidermis; pewarnaan perak atau reaksi dopa, memberi hasil negatif. Pada
pemeriksaan dengan mikroskop elektron terlihat hilangnya melanosit(9), sedangkan pada tepi
lesi sering dijumpai melanosit yang besar dengan prosesus dendritikus yang panjang;
beberapa penulis menjumpai infiltrat limfositik di dermis(10). Pada lesi awal atau tepi lesi

masih dapat dijumpai beberapa melanosit dan granul melanin(10). Pada pemeriksaan dengan
lampu Wood, lesi vitiligo tampak putih berkilau dan hal ini berbeda dengan kelainan
hipopigmentasi lainnya(3).
PENATALAKSANAAN
Karena penyebab dan patogenesisnya masih banyak yang belum diketahui, sampai sekarang
pengobatan vitiligo masih bersifat nonspesifik(8). Pernah pula dilaporkan regresi spontan,
tetapi persentasinya sangat kecil(7,8).
Beberapa cana dan usaha yang dilakukan untuk mengatasinya, yaitu(11):
1) Psoralen dan UVA
Fotokemoterapi dengan psoralen dan radiasi ultraviolet natural atau artifisial masih dianggap
sebagai pengobatan dengan hasil yang cukup baik(8). Psoralen untuk mengobati vitiligo
sudah dipakai sejak zaman Mesir kuno dan India(12).
Psoralen yang sering dipakai adalah 8-metoksipsoralen atau trimetil psoralen; hasilnya sangat
bervariasi. Hal ini disebabkan oleh variasi absorpsi obat yang besar pada tiap individu(13).
Psoralen dapat dipakai secara topikal atau sistemik. Bila lesi meliputi daerah yang luas (lebih
dari 2025% luas permukaan kulit tubuh), psoralen sistemik dapat dipakai(7); metode ini dianggap memberi harapan untuk timbulnya repigmentasi(14). Bila 8-metoksipsoralen yang
dipakai, dosisnya 0,3 mg per kilogram berat badan. Obat dimakan 2 jam sebelum dijemur
sinar mata hari. Pajanan sinar matahani dapat dimulai dengan lama 5 menit dan dapat
diperpanjang 5 menit tiap kali pengobatan. Sebaiknya jangan dijemur lebih dari 30 menit per
tempat. Umumnya repigmentasi dimulai setelah 30 sampai 50 kali pengobatan.
Repigmentasi dimulai sebagai bintik-bintik sekitar folikel rambut dan meluas secara perlahan
dan berkonfluensi(9). Pada pemakaian psoralen secara topikal, penderita harus diperingatkan
untuk mencuci obat setelah pemakaian dan selanjutnya melindungi kulit dan pajanan sinar
matahari(6). Mekanisme kerja obat ini masih belum diketahui dengan Pasti(7). Menurut
Ortonne (19769) psoralen dan sinar ultraviolet A akan merangsang mitosis melanosit pada
folikel rambut dan melanosit tersebut akan bermigrasi ke daerah lesi. Sedangkan Nordlund
(1982) mengatakan bahwa psoralen tidak secara langsung merangsang pertumbuhan sel-sel
melanosit, tetapi merusak beberapa bahan penghambat atau sel di epidermis yang
bertanggung jawab terhadap pemusnahan sel-sel melanosit(15).
Honigsmann (1987) mengatakan bahwa repigmentasi timbul karena stimulasi peningkatan
jumlah melanosit fungsional, hipertrofi melanosit, aktivitas tirosinase dan mempercepat
migrasi melanosit dan adneksa kulit(14).
Pengobatan tersebut digunakan secara terus menerus selama memberi hasil yang cukup baik,
yaitu timbulnya repigmentasi yang dimulai dan folikel rambut yang makin lama makin melebar dan berkonfluensi. Pada pengobatan dengan PUVA, penderita harus sanggup menjalani
100 sampai 300 kali pengobatan(2). Pengobatan sebaiknya dihentikan bila selama 3 bulan
tidak terjadi repigmentasi(7,9).
2) Kortikosteroid
Pemakaian kortikosteroid topikal pada vitiligo berdasarkan pada hipotesis autoimun. Kumani
(1984) menggunakan klobetasol propionat 0,05% dengan hasil yang cukup baik(16). Pernah
pula dilaporkan penggunaan triamsionolon asetonid 0,1% intralesi atau betametason 17
valerat 0,1% secara topikal(9). Pada kasus yang dini pemberian kortikosteroid intralesi efektif
pada 50% penderita dan penggunaan kortikosteroid topmkal dapat mencegah perkembangan
lebih lanjut. Biasanya diperlukan terapi yang lama dan adanya efek samping akibat
pemakaian steroid yang lama menyebabkan pemakaiannya terbatas(2,11).
3) Fluorourasil
Untuk menimbulkan pigmentasi pada lesi, dapat dipakai fluorourasil secana topikal.
Pemakaian fluorourasil tersebut di-lakukan secara tertutup di atas kulit yang telah

diepidermabrasi. Pada kulit yang erosif tersebut dioleskan krim fluorourasil 5% dan ditutup
dengan bahan polietilen untuk jangka waktu 24 jam. Cara pengobatan ini dihentikan setelah
aplikasi sebanyak 710 kali. Salah satu hipotesis mengatakan bahwa fluorourasil juga
mengakibatkan kolonisasi melanosit di epidermis yang kemudian bermigrasi ke daerah lesi
sewaktu proses epitelisasi(3).
4) Zat warna
Karena vitiligo mengganggu penampilan seseorang maka dapat dipakai zat wanna topikal
sebagai kamuflase(11). Beberapa kosmetik kamuflase dapat dipakai dan yang banyak
terdapat di Indonesia antara lain Dermablend Cover cream, Derma Color Cover Cream,
Covermark Cover Cream dan lain-lain(17).
5) Lain-lain
a) Tehnik bedah:
tandur kulit/epidermis(18).
invitro cultured epidermal auto graft bearing melanocytes(19)
b) Akupunktur
Diperkirakan akupunktur memberikan efek stimulasi terhadap melanosit, perbaikan
mikrosirkulasi, peningkatan respons imunitas dan efek regulasi fungsi organ(20).
c) Monobenzil hidrokuinon adalah bahan pemutih yang memberikan efek samping vitiligo.
Obat ini dapat menyebabkan kerusakan melanosit dan biasanya dipakai pada vitiligo yang
sangat luas, sehingga sisa kulit yang normal diputihkan seluruhnya. Biasanya dipakai dalam
bentuk krim dengan konsentrasi 2-4%(21). Cara pengobatan di atas memang memerlukan
waktu yang lama, pengobatan biasanya memerlukan waktu 18 bulan sampai 2 tahun(7).
Selain itu setiap penderita vitiligo perlu menggunakan tabir cahaya(22), karena dosis
eritematosa minimal (MED) kulit penderita vitiligo lebih rendah dari orang normal(23).
Biasanya dipakai tabir cahaya dengan sun protective factor (SPF) 15(22). Efek psikososial
vitiligo juga tidak boleh dilupakan. Tiap penderita memerlukan dukungan psikologis, lebihlebih bila terdapat hambatan sosial atau psikis(23,24).
Vitiligo bukan penyakit yang membahayakan kehidupan, tetapi prognosisnya masih
meragukan dan bergantung pula pada kesabaran dan kepatuhan pen derita terhadap
pengobatan yang diberikan.
KEPUSTAKAAN
1. Lorincz AL. Disturbances of melanin pigmentation. In Moschella SL & Hurley Hi (eds.):
Dermatology. Vol. II. 2nded. Philadelphia, WB. Saunders Co. 1985: 1292-6.
2. Mosher DB, Fitzpatrick TB, Ortonne JP, Hon Y. Disorders of pigmentation. In Fitzpatrick
TB et al. (eds.): Dermatology in general medicine. 3rded. New York, McGraw Hill Book Co.
1987: 81021.
3. Achyar RY. Kelainan-kelainan hipopigmentasi dan vitiligo. Dalani Sugito TL dick. (eds.) :
Kelainan pigmentasi kulit dan penanggulangannya (Simposium). Jakarta, PADVI Jaya. 1988 :
46-60.
4. Mosher DB, Pathak MA, Fitzpatrick TB. Vitiligo : etiology pathogenesis, diagnosis and
treatment. In Fitzpatrick TB et al. (eds.): Update: Demiatology in general medicine. New
York, McGraw Hill Book Co. 198320555.
5. Domonkos AN, Arnold HL, Odom RB. Andrews diseases of the skin. 7thed. Philadelphia,
WB. Saunders Co. 1982: 10579.
6. McBurney El. Vitiligo. Clinical picture and pathogenesis. Arch Dermatol 1979; 139:
12957.
7. Symposium. Management of vitiligo in children. Ped Dermatol 1986; 3/6: 498510.

8. Ortonne JP. Vitiligo. In Orfanos CE et al. (eds.) : Dermatology in fivecontinents.

Proceeding of the XVII World Congress of Dermatology. Berlin, Springer-Verlag. 1988 :
2107.
9. Kukita A. On vitiligo vulgaris. In Tham SN etal. (eds.) : Proceedings of the Dermatological
Society of Singapore. Singapore, Dermatological Society of Singapore. 1987: 169.
10. Lever WF, Schaumburg-Lever G. Histopathology of the skin. 6th ed Philadelphia, JB.
Lippincott Co. 1983 : 4412.
11. Nasution D. Penanggulangan kelainan hipopigmentasi dan vitiligo. DaIwa Sugito TL
dick. (eds) : Masalah pigmentasi kulit dan penanggulangannya (Simposiuni). Jakarta, PAD VI
Jaya. 1988 : 61-6.
12. Todes-Taylor N, Abel EA. Cox AJ. The occurence of vitiligo after psoralens and
ultraviolet A therapy. J Am Acad Dermatol 1983; 9/4: 52632.
13. Parrish JA, Fitzpatrick TB, Shea C, Pathak MA. Photochemotherapy of vitiligo. Arch
Dermatol 1976; 112: 15314.
14. Honigmann H, Wolff K Fitzpatrick TB, Pathak MA, Parrish JA. Oral photochemotherapy
with psoralens and UVA (PYVA): principles and practice. In Fitzpatrick TB. et al. (eds.):
Dermatology in general medicine. 3rd ed. New York, McGraw Hill Book Co. 1987: 153358.
15. Nordlund ii, Lerner AB. Vitiligo. It is important. Arch Dermatol 1982; 118:58
16. Kumari J. Vitiligo treated with topical clobetasoJ propionate. Arch Derniato] 1984; 120:
6315.
21. Handoko RP. Penanggulangan kelainan hiperpignientasi dan melasma. Dalam Sugito TL
dkk. (eds). Masalab pigmentasi kulit dan penanggulang annya (Simposium). Jakarta, PADVI
Jaya. 1988 : 405.
17. Kusumadewi. Kaniuflase estetik kelainan pigmentasi kulit. Dalam SugitoTL dkk. (eds.) :
Masalah pigmentasi kulit dan penanggulangannya (Simposium). Jakarta, PAD VI Jaya. 1988 :
809.
22. Widodo J. Tabirsurya dan aplikasi pada kelainanpigmentasi kulit. Dalam Sugito TL dkk.
(eds.). Masalah pigmentasi kulit dan penanggulangannya (Simposium). Jakarta, PADVI Jaya.
1988 : 98107.
18. Falabella R. Repigmentation of segmental vitiligo by autologous minigrafting. I Am Acad
Dennatol 1983; 9: 51421.
23. Westerhof W. Recent advances of pigmentary disorders and their management. Dalam
Sugito TL dkk. (eds.). Masalah pigmentasi kulit dan penanggulangannya (Simposium).
Jakarta, PADVI Jaya. 1988: 10819.
19. Falabella R, Escobar C, Borrero J. Treatment of refractory and stable vitiligo by
transplantation of In vitro cultured epidermal autografts bearing melanocytes. JAm Acad
Dermatol 1992; 26: 2306.
24. Mansjur S. Aspekpsikososial penderitakelainanpigmentasi. DalamSugito TL dkk. (eds.).
Masalah pigmentasi kulit dan penanggulangannya (Simposium). Jakarta, PADVI Jaya, 198 :
6779.
20. Widya DK. Akupunktur pada kelainan pigmentasi kulit. Dalam Sugito TL dkk. (eds.).
Masalah pigmentasi kulit dan penanggulangannya (Simposium). Jakarta, PADVI Java. 1988 :
907

http://www.medterms.com/script/main/art.asp?articlekey=9864 Melissa Conrad

Stppler, MD 2006

Pronounced vit-uh-LIE- go. A condition in which the skin turns white due to the
loss of melanocytes. These cells produce melanin, the pigment that gives the
skin its characteristic color. (Melanocytes also impart color to the retina of the
eye and the mucous membrane tissues lining the inside of the mouth, nose,
genital and rectal areas). In vitiligo, the melanocytes are mysteriously destroyed,
leaving de-pigmented patches of skin on different parts of the body. The hair that
grows in areas affected by vitiligo may also turn white.
Vitiligo is a common disorder. It occurs in 1-2% of people and affects both sexes
and all races equally. Vitiligo is never present at birth. It crops up between the
ages of 10 and 30 in about half of cases and before age 40 in 95% of cases. More
than 30% of people with vitiligo have a family history of the disorder, pointing to
the presence of genetic factors capable of contributing to the condition.
As the skin gradually loses its color, patch by patch, other people may treat
someone with vitiligo like a leper, thinking they have a contagious skin disease.
In fact, vitiligo is called "white leprosy" in India. Women with it are often
discriminated against in marriage. If they develop vitiligo after marriage, it can
be grounds for divorce.
In people with vitiligo, the melanocytes self-destruct, probably because of an
autoimmune reaction in which the body mistakenly attacks its own cells. The
resulting white patches of skin may enlarge and increase in number for a while,
and then the condition may stabilize, only to start up again later. Injury, illness, a
bad sunburn and severe stress have been known to provoke the onset or
progression of vitiligo.
Vitiligo is sometimes associated with more serious disorders that also have an
autoimmune cause, including: hyperthyroidism (overactivity of the thyroid
gland), adrenocortical insufficiency (the adrenal gland does not produce enough
cortisol), alopecia areata (patches of baldness), and pernicious anemia (a low
level of red blood cells caused by the failure of the body to absorb vitamin B12).
Vitiligo is also a feature of a number of genetic diseases.
People with vitiligo must protect their skin from exposure to the sun. Affected
areas of skin can become seriously sunburned while the surrounding skin tans.
Affected people must be vigilant about using sunscreen with a high sun
protection factor (an SPF of 30 or above) on exposed skin. During long periods
outdoors, they should wear long sleeves, pants and wide-brimmed hats.
If the affected area is small, application of creams containing corticosteroids may
help restore pigment. Chronic use of steroids, however, can result in thinning of
the skin and stretch marks in some areas.
Dermatologists most commonly today use a remedy called PUVA for those
seeking to darken white skin patches, especially when the condition is extensive.
PUVA involves taking a drug called psoralen, which makes the skin very sensitive
to light, followed by exposure of the affected skin to a special lamp that
generates only ultraviolet A radiation. Occasionally, when the vitiligo patches are

very limited, psoralen can be applied directly to the skin before ultraviolet A
treatment.
The downside of PUVA therapy is that it is time-consuming and care must be
taken to avoid side effects, which can sometimes be severe. At least a year of
twice-weekly treatments is usually needed to restore melanin production. The
treatments are 50 to 70% successful in restoring color on the face, trunk and
upper arms and legs. But hands and feet respond poorly to this approach. PUVA
should not be used in children under 12, in pregnant or nursing women, or in
people with certain medical conditions. Long-term use of PUVA can cause
freckling and, when used for years to treat psoriasis, PUVA increases the risk of
skin cancer. Risks aside, the most effective treatment available now is PUVA. The
goal of PUVA therapy in vitiligo is to reverse the effects of the disease and repigment the white patches.
What is vitiligo, and what causes it?
Vitiligo (vit-ill-EYE-go) is a pigmentation disorder in which melanocytes (the cells
that make pigment) in the skin are destroyed. As a result, white patches appear
on the skin in different parts of the body. Similar patches also appear on both the
mucous membranes (tissues that line the inside of the mouth and nose), and the
retina (inner layer of the eyeball). The hair that grows on areas affected by
vitiligo sometimes turns white.
The cause of vitiligo is not known, but doctors and researchers have several
different theories. There is strong evidence that people with vitiligo inherit a
group of three genes that make them susceptible to depigmentation. The most
widely accepted view is that the depigmentation occurs because vitiligo is an
autoimmune disease -- a disease in which a person's immune system reacts
against the body's own organs or tissues. As such, people's bodies produce
proteins called cytokines that alter their pigment-producing cells and cause
these cells to die. Another theory is that melanocytes destroy themselves.
Finally, some people have reported that a single event such as sunburn or
emotional distress triggered vitiligo; however, these events have not been
scientifically proven as causes of vitiligo.