VİTİLİGO Vitiligo is characterized clinically by development of totally white macules, microscopically by complete absence of melanocytes.

Epidemiology Sex: Equal in both sexes. Age of onset: At any age, but in 50% between the ages of 10 and 30 yeras. A few cases at birth. Race:All races. Inheritance: Polygenic. > 30% have reported vitiligo in a parent, sibling or a child.

Pathogenesis The autoimmune theory The neurogenic hypothesis The self-destruct hypotesis

History After a -physical trauma ( Koebner), illness or emotional stress. After the death of a relative or after severe physical injury After a sunburn reaction

Physical examination “Chalk” or pale white, sharply marginated macules, 5 mm to 5 cm or more in diameter Focal type, segmental type, generalized Around the eyes, mouth, digits, elbows, knees, low back, genital areas Associated cutaneous findings: White hair (poliosis), prematurely gray hair, alopecia areata, halo nevi. General examination: Up to 30% of cases associated with thyroid disease (Hashimoto thyroiditis, Graves’ disease); diabeytes mellitus (< 5%); pernicious anemia; Addison’disease( uncommon), MEN (rare).

Differential diagnosis Pityriasis alba Pityriasis versicolor Chemical leukoderma (phenolic germicides) Leprosy Nevus depigmentosus Nevus anemicus Tuberous sclerosis Post-inflammatory leukoderma Hypopigmented Mycosis Fungoides Vogt-Koyanagi-Harada Syndrome ( vision problems, photophobia, bilateral dysacusia) Waardenburg’s syndrome (commonest cause of congenital deafness, white macules and white forlock, iris heterochromia)

Course and prognosis Chronic disease The course is highly variable. Up to 30%, spontaneous repigmentation in a few areas.

Therapy Sunscreens Cosmetic coverup Repigmentation: Topical glucocorticoids, topical photochemotherapy, systemic photochemotherapy, narrow-band UVB, tacrolimus, pimecrolimus Minigrafting Depigmentation