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Hervina*
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 estimated 45,000 cases were diagnosed in
2004.8
Vitiligo is a chronic skin disease and
mucous membrane that results from the
destruction of melanocytes, with ETIOLOGY
characteristics of depigmented macules,
multifactorial predisposing factors, and The exact cause of Vitiligo is not
precipitating factors such as trauma, known for sure, but perhaps the virus is one
sunburn, stress and systemic diseases. 1 The of the vitiligo etiologies.4 Convergent theory
prevalence of this disease is around 1% in states stress factors, accumulation of toxic
the world's population.2 Vitiligo often substances, autoimmune, mutations, changes
occurs under the age of 20 years, but can in cellular environment and migration of
also occur in old age.2 disturbed melanocytes have pean in the
pathogenesis of vitiligo.4
Vitiligo has several predilections,
including periorifisial, facial, genital, DIAGNOSE
mucous membranes, extensor area, hands
and feet.3 In vitiligo patients, there are some
clinical manifestations in the form of milky
DEFINITION white amelanotic macules or like chalk,
usually with firm boundaries and curved
Vitiligo is a chronic skin disease and edges. Lesions can be seen by examination
mucous membrane caused by the destruction using Wood's lamp. Lesions expand
of melanocytes, with characteristics of centrifugally and can occur in all areas of
depigmented macules, multifactorial the body, including mucous membranes.
predisposing factors, and precipitating Initial lesions often appear on the area of the
factors such as trauma, sunburn, stress and skin exposed to sunlight, located on the
elbow, knees, fingers, and flexor wrists.1
systemic diseases.1
Vitiligo with childhood onset has a
EPIDEMIOLOGY predilection of early lesions that are
different from the onset of slow vitiligo.
This disease is spread throughout the
Predilection of vitiligo lesions of childhood
world. The prevalence of this disease is
childhood onset include the eyelids and
quite high at around 1% in the population in
lower extremities, while the main areas of
the world.2 Vitiligo often occurs at the age
slow onset vitiligo include the upper
of under 20 years, but can also occur in old
extremities, especially the hands. Vitiligo
age.3
onset of childhood has a higher prevalence
Vitiligo is often found in newborns,
of allergic disease and a lower prevalence of
rarely in adults, the incidence in men and
thyroid disease. Vitiligo lesions can be
women, not significantly different.8 His age
preceded by severe sunburn, pregnancy,
ranges from birth to 12 years, but most
trauma to the skin, and /or emotional stress.2
(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
DIFERENTIAL DIAGNOSE increase, so that the maturation of regulator
T cells decreases and results in impaired
1. Tinea Versikolor inflammatory inhibition. Production of
a. Changed Skin Color proinflammatory cytokines such as IL-1β,
b. Pruritus IL-6, IL-8, and TNF-α increases in
c. Makul Hipopigmentasi vitiliginous patients.4
d. Soft Skuamous
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
2. Ptiriasis Alba Pharmacological management of
a. Makula Hipopigmentasi vitiligo is topical topical phototherapy
b. Soft Skuamous (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