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

2. 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.

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

4. 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

5. 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).

6. 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)

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

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