Vitiligo

VITILIGO
UNIVERSITY OF ADEN
FACULITY OF MEDICINE

1. Vitiligo Prepared By :- Dr Monther Fadel Nagi Dermatology Resident

2. Vitiligo

3. Definition • Vitiligo is the acquired loss of epidermal pigmentation and is characterized histologically by the absence of epidermal melanocytes . There are six types based on the extent and distribution of the involved areas: localized (single or few macules in one anatomic area); segmental; generalized; universal (entire body surface is depigmented ); acrofacial (fingers, lips); and mucosal.

4. Etiology • Three pathophysiologic theories suggest possible etiologies: • Autoimmune theory (autoantibodies against melanocytes ) • Neural theory (neurochemical mediator selectively destroys melanocytes) • Self-destructive process whereby melanocytes fail to protect themselves against cytotoxic melanin precursors • Although vitiligo is considered to be an acquired disease, 25% to 30% is familial; the mode of transmission is unknown (polygenic or autosomal dominant with incomplete penetrance and variable expression).

5. Clinical Manifestation(s) • Initially the disease is limited, but the lesions tend to become more extensive over the years . Physical Examination • Hypopigmented and depigmented lesions favor sun-exposed regions, intertriginous areas , genitalia, and sites over bony prominences (type A vitiligo ) . • Areas around body orifices are also commonly involved .

6. Clinical Manifestation(s) • The lesions tend to be symmetric. • Occasionally, the lesions are linear o pseudodermatomal (type B vitiligo ). • Vitiligo lesions may occur at trauma sites ( Koebner’s phenomenon ). • The hair in affected areas may be white. • The margins of the lesions are usually well demarcated, and when a ring of hyperpigmentation is seen, the term trichrome vitiligo is used. • The term marginal inflammatory vitiligo is used to describe lesions with raised borders .

7. Diagnostic Tests • Physical examination • Wood’s light examination may enhance lesions in light-skinned individuals .

8. DIFFERENTIAL DIAGNOSIS Acquired • Chemical induced • Halo nevus • Idiopathic guttate hypomelanosis • Leprosy • Leukoderma associated with melanoma • Pityriasis alba • Postinflammatory hypopigmentation • Tinea versicolor • Vogt- Koyanagi syndrome ( vitiligo , uveitis, and deafness)

9. DIFFERENTIAL DIAGNOSIS Congenital • Albinism, partial ( piebaldism ) • Albinism, total • Nevus anemicus • Nevus depigmentosus • Tuberous sclerosis

10. TREATMENT First Line • Treatment is indicated primarily for cosmetic purposes when depigmentation causes emotional or social distress. Depigmentation is more noticeable in darker complexions . • Cosmetic masking agents ( Dermablend , Covermark ) or stains ( Dy -O- Derm , Vita-Dye ) or sunless tanning lotions ( dihydroxyacetone ) • Topical midpotency steroids (e.g., triamcinolone 0.1% or desonide 0.05% cream QD for 3–4 months)

11. TREATMENT Second Line • PUVA ( psoralen phototherapy): oral or topical psoralen administration followed by phototherapy with UVA (150–200 treatments required over 1–2 years) or narrowband UVB phototherapy • Excimer laser (best for small or localized areas of vitiligo ) • Total depigmentation (in cases of extensive vitiligo ) with 20% monobenzyl ether or hydroquinone. This is a permanent procedure, and patients will require lifelong protection from sun exposure. • Intralesional steroid injection • Systemic prednisone (5 mg QD on 2 consecutive days per week for 2–4 months)

12. TREATMENT Third Line • Topical immunomodulators ( tacrolimus , pimecrolimus ) can also induce repigmentation of vitiliginous skin lesions. Their potential for systemic immunosuppression or increased risk of skin or other malignancies remains to be defined. • Calcipotriol , a synthetic analogue of vitamin D3, has also been used in combination with UV light or clobetasol , with limited results