VITILIGO

Hervina*

*Departement Of Dermatology and venereolgy

Faculty of Medicine Muhammadiyah University of North Sumatera
** Departement Farmacology Faculty of Medicine Muhammadiyah University of
North Sumatera

ABSTRAK

Vitiligo merupakan penyakit kulit dan membran mukosa kronis akibat destruksi
melanosit, dengan karakteristik makula depigmentasi, mempunyai faktor predisposisi
multifaktorial dan faktor pencetus seperti trauma, terbakar matahari, stres, dan penyakit sistemik.
Penyebab pasti penyakit ini belum diketahui. Teori patofisiologi vitiligo yang paling berperan
antara lain mekanisme autoimun, sitotoksik, biokimia, oksidan –antioksidan, neural dan virus.
Manifestasi klinis berupa makula amilanotik berwarna putih susu atau kapur, biasanya berbatas
tegas dan tepi dapat berlekuk. Klasifikasi vitiligo antara lain segemental, akrofasial, generalisata
dan universal atau berdasarkan pola daerah yang terkena yaitu jenis fokal, campuran dan
mukosa. Penyakit endokrinopati yang sering ditemukan pada pasien vitiligo antara lain disfungsi
tiroid, penyakit hipertiroid lain (penyakit grave) atau hipotiroid (tiroiditis hashimoto).
Pemeriksaan laboratorik yang membantu dalam membangun diagnosis vitiligo, antara lain kadar
thyroid stimulating hormone, dan darah lengkap. Pada pemeriksaan histologi tidak ditemukan
melanosit pada lesi kulit. Pengobatan berupa tabir surya, kortikosteroid topikal, imunomodulator
topikal, kalsipotriol topikal, pseudokatalase, kortikosteroid sistemik, PUVA, NBUVB, laser
helium neon, khellin, suction blister graft dan imunosupresan sitemik.
Kata kunci : Vitiligo, etiologi, penatalaksanaan
ABSTRACK

Vitiligo is a chronic skin disease and mucous membrane due to melanocyte destruction,
with characteristic depigmented macules, has multifactorial predisposing factors and
precipitating factors such as trauma, sunburn, stress, and systemic diseases. The exact cause of
this disease is not yet known, but there are several theories that explain the loss of
melanocytepidermal in vitiligo. The pathophysiology theory of vitiligo which has the most role is
the mechanism of autoimmune, cytotoxic, biochemical, oxidant, antioxidant, neural and viral.
Clinical manifestations in the form of amyotic antibiotics are milky white or limestone, usually
firmly defined and curved edges. The classification of vitiligo includes segemental, akrofasial,
generalized and universal or based on the pattern of the affected area namely focal, mixed and
mucous types. Endocrinopathies that are often found in vitiligo patients include thyroid
dysfunction, other hyperthyroid diseases (grave disease) or hypothyroidism (hashimoto
thyroiditis). Laboratory examinations that help in establishing a diagnosis of vitiligo include
levels of thyroid stimulating hormone and complete blood. On histology, melanocytes were not
found in skin lesions. Treatment in the form of sunscreen, topical corticosteroids, topical
immunomodulators, topical calcipotriol, pseudocatalase, systemic corticosteroids, PUVA,
NBUVB, neon helium laser, khellin, suction blister graft and immunosuppressant system.
Keywords: vitiligo, etiology, treatment
PRELIMINARY
Vitiligo is a chronic skin disease and
mucous membrane that results from the
destruction of melanocytes, with
characteristics of depigmented macules,
multifactorial predisposing factors, and
precipitating factors such as trauma,
sunburn, stress and systemic diseases. 1 The
prevalence of this disease is around 1% in
the world's population.2 Vitiligo often
occurs under the age of 20 years, but can
also occur in old age.2
Vitiligo has several predilections,
including periorifisial, facial, genital,
mucous membranes, extensor area, hands
and feet.3
DEFINITION
Vitiligo is a chronic skin disease and
mucous membrane caused by the destruction
of melanocytes, with characteristics of
depigmented macules, multifactorial
predisposing factors, and precipitating
factors such as trauma, sunburn, stress and
systemic diseases.1
EPIDEMIOLOGY
This disease is spread throughout the
world. The prevalence of this disease is
quite high at around 1% in the population in
the world.2 Vitiligo often occurs at the age
of under 20 years, but can also occur in old
age.3
Vitiligo is often found in newborns,
rarely in adults, the incidence in men and
women, not significantly different.8 His age
ranges from birth to 12 years, but most
(73%) are aged 4 years or younger.8 These
cancers are 6 % of all cancers in the world in
2002 or the fifth most cancer and an
estimated 45,000 cases were diagnosed in
2004.8
ETIOLOGY
The exact cause of Vitiligo is not
known for sure, but perhaps the virus is one
of the vitiligo etiologies.4 Convergent theory
states stress factors, accumulation of toxic
substances, autoimmune, mutations, changes
in cellular environment and migration of
disturbed melanocytes have pean in the
pathogenesis of vitiligo.4
DIAGNOSE
In vitiligo patients, there are some
clinical manifestations in the form of milky
white amelanotic macules or like chalk,
usually with firm boundaries and curved
edges. Lesions can be seen by examination
using Wood's lamp. Lesions expand
centrifugally and can occur in all areas of
the body, including mucous membranes.
Initial lesions often appear on the area of the
skin exposed to sunlight, located on the
elbow, knees, fingers, and flexor wrists.1
Vitiligo with childhood onset has a
predilection of early lesions that are
different from the onset of slow vitiligo.
Predilection of vitiligo lesions of childhood
childhood onset include the eyelids and
lower extremities, while the main areas of
slow onset vitiligo include the upper
extremities, especially the hands. Vitiligo
onset of childhood has a higher prevalence
of allergic disease and a lower prevalence of
thyroid disease. Vitiligo lesions can be
preceded by severe sunburn, pregnancy,
trauma to the skin, and /or emotional stress.2
DIFERENTIAL DIAGNOSE
1. Tinea Versikolor
a. Changed Skin Color
b. Pruritus
c. Makul Hipopigmentasi
d. Soft Skuamous
2. Ptiriasis Alba
a. Makula Hipopigmentasi
b. Soft Skuamous
PATOFISIOLOGY
The pathogenesis of vitiligo is still
unclear.1 It is estimated that there are
several possibilities, according to the theory
of cellular immune mechanisms, there is
melanocyte destruction in vitiligo which is
directly mediated by autoreactive T cell
reagents. Mart-1 (melanoma antigen
identified by T cells), Glycoprotein 100 and
tyrosinase. Activated CD8 + T cells can be
found in the skin of the vetiliginous lesions
The number of T-helper cells in vitiligo
lesions is reduced. Transforming growth
factor-β is known to function to inhibit
vitiligo activity, but autoimmune diseases
can cause a reduced T regulator, so that in
vitiligo patients can be found transforming
serum growth factor-β levels which are the
main products of regulator T are reduced.
This can cause cellular immunity to
increase, so that the maturation of regulator
T cells decreases and results in impaired
inflammatory inhibition. Production of
proinflammatory cytokines such as IL-1β,
IL-6, IL-8, and TNF-α increases in
vitiliginous patients.4
TREATMENT
Non-pharmacological treatment of
vitiligo is used Autologus skin graft / skin
layer of the dermis or epidermis by
transferring normal skin 2-4 mm to the
vitiligo rash.6
Pharmacological management of
vitiligo is topical topical phototherapy
(methoxalene 1% and 8-methoxypsoralen),
systemic phototherapy, psoralen 20-30 mg
or 0.6 mg / kgBW taken 2 hours before
irradiation (1/2 - 4). minutes) for 6 months.6
CONCLUSION
Vitiligo is a skin disease and
chronic mucous membranes with
distinctly delimited characteristics of
depigmented macules. The prevalence of
vitiligo in the world is 0.1-2% with peak
onset aged 10-30 years.8 The exact cause
is unknown, but there are several theories
that explain the loss of epidermal
melanocytes in vitiligo. The
pathophysiological theory of vitiligo
which is the most important is the
mechanism of autoimmune, cytotoxic,
biochemical, oxidant-antioxidant, neural,
and viral.9
Lesions can be seen using Wood's
lamp. Treatment varies including
sunscreen, topical corticosteroids, topical
immunumodulators, topical calcipotriol,
pseudokatalase, systemic corticosteroids,
PUVA, NBUVB, excimer laser, bioskin,
L-phenylalanine, antioxidants,
depigmentation, autologous thin split-
thickness grafting, suction blister grafts,
transplants autologous, camouflage histopathology, etiology, and work-up.
melanocyte culture, Tumor Necrosis J Am Acad Dermatol. 2011;
Factor-α inhibitors, and systemic 65(3):473-91.
9
immunosuppressants. 5. Birlea SA, Fain PR, Spritz RA. A
Romanian population isolate with high
REFERENCES frequency of vitiligo and associated
autoimmune diseases. Arch Dermatol.
1. Halder RM, Taliaferro SJ. Vitiligo. 2008; 144(3):310-6.
Dalam: Goldsmith L, Katz S, Gilchrest 6. Silverberg JI, Silverberg AI, Malka E,
B, Paller A, Leffell D, Wolff K, editor. Silverberg NB. A pilot study assesing
Fitzpatrick’s dermatology in general the role of 25 hydroxy vitamin d levels
medicine. Edisi ke- in patients with vitiligo vulgaris. J Am
7. New York: McGraw-Hill Inc; 2008. Acad Dermatol. 2010; 62(6):937-41.
2. Nicolaidou E, Antoniou C, Miniati A, 7. Anstey AV. Disorders of skin colour.
Lagogianni E, Matekovits A, Stratigos Dalam: Burns T, Breathnach S, Cox
A, et al. Childhood-and later-onset N, Griffiths C, editor. Rook’s textbook
vitiligo have diverse epidemiologic of dermatology. Edisi ke-8.
and clinical characteristics. J Am Acad Chichester: Blackwell Publishing Ltd.;
Dermatol. 2011; 66(6):954-8. 2010.
3. Rekam Medis Rumah Sakit Umum 8. Geel NV, Speeckaert R, Taieb A,
Pusat Moehammad Hoesin. Data Picardo M, Bohm M, Gawkrodger
rekam medis divisi dermato- DJ, et al. Koebner’s phenomenon in
kosmetologi poliklinik ilmu kesehatan vitiligo: European position paper.
kulit dan kelamin rumah sakit umum Pigment Cell Melanoma Res. 2011;
pusat Moehammad 24(3):564-73.
Hoesin/Fakultas Kedokteran 9. Ezzedine K, Gauthier Y, Leaute-
Universitas Sriwijaya. Palembang: Labreze C, Marquez S, Bouchtnei S,
RSUPMH/FK Unsri; 2011. Jouary T, et al. Segmental vitiligo
4. Alikhan A, Felsten LM, Daly M, associated with generalized vitiligo
Petronic- Rosic V. Vitiligo: a (mixed vitiligo): a retrospective case
comprehensive overview introduction, series of 19 patiens. J Am Acad
epidemilology, quality of life, Dermatol. 2011; 65(5):965-71.
diagnosis, associations,