Definition
Vitiligo is a chronic acquired skin disorder characterised by well-defined depigmented (white) patches due to selective destruction or loss of functional melanocytes, resulting in reduced or absent melanin production. It can occur at any age but often appears before age 30.
Types
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Non-segmental vitiligo (NSV) – most common
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Symmetrical distribution
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Includes subtypes:
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Generalised
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Acrofacial (affecting face and extremities)
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Universal (extensive, affecting >80% of body surface)
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Mixed patterns
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Segmental vitiligo (SV)
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Unilateral, follows a dermatomal distribution
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Earlier onset, more stable after rapid initial progression
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Focal vitiligo
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Localised depigmentation in one or few small areas
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Causes and Pathogenesis
Exact cause is unknown, but multiple mechanisms are implicated:
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Autoimmune theory – immune-mediated destruction of melanocytes (strongest evidence)
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Neurogenic factors – interaction between melanocytes and nerve endings causing damage
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Oxidative stress – increased free radical damage to melanocytes
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Genetic predisposition – family history in ~20–30% of cases; associated with certain HLA types
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Often associated with other autoimmune disorders (thyroid disease, type 1 diabetes, pernicious anaemia, alopecia areata)
Risk Factors
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Family history of vitiligo or autoimmune disease
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Autoimmune disorders
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Physical or emotional stress
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Skin trauma (Koebner phenomenon)
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Sunburn
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Certain chemicals (phenolic compounds)
Symptoms and Signs
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White (depigmented) macules or patches with sharp borders
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Common sites: face, hands, arms, feet, and around body openings (eyes, mouth, genitalia)
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Hair over affected areas may turn white (leukotrichia)
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No scaling or inflammation, skin texture is normal
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May be associated with psychosocial distress due to cosmetic impact
Diagnosis
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Clinical examination – distribution and pattern of lesions
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Wood’s lamp examination – accentuates depigmented patches
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Skin biopsy – shows absence of melanocytes (used if diagnosis uncertain)
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Blood tests – to screen for associated autoimmune diseases (thyroid function, blood glucose, vitamin B12, ANA)
Treatment
No cure exists, but therapies can restore pigmentation and control progression. Choice depends on extent, location, and activity of disease.
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General measures
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Sun protection to reduce contrast between affected and normal skin and prevent sunburn
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Cosmetic camouflage (makeup, self-tanning products)
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Psychological support or counselling
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Medical therapies
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Topical corticosteroids (e.g., clobetasol propionate) – effective in localised disease; risk of skin atrophy with prolonged use
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Topical calcineurin inhibitors (tacrolimus 0.1% ointment, pimecrolimus) – particularly for face and intertriginous areas; safer for long-term use
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Topical vitamin D analogues (calcipotriol) – sometimes used in combination with steroids
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Phototherapy
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Narrowband UVB (NB-UVB) – first-line for widespread disease; 2–3 times per week for several months
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PUVA (psoralen + UVA) – less commonly used due to side effects; effective in some cases
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Excimer laser (308 nm) – for small localised lesions
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Systemic therapies (for rapidly progressive disease)
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Short courses of oral corticosteroids to halt progression
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Immunomodulators (under specialist supervision)
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Surgical options (for stable vitiligo >1 year, unresponsive to medical therapy)
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Autologous melanocyte or skin graft transplantation
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Punch grafting, blister grafting, or cellular grafting techniques
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Depigmentation therapy (for extensive disease >50% BSA)
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Monobenzyl ether of hydroquinone to depigment remaining normal skin for uniform appearance
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Prognosis
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Unpredictable course – some experience spontaneous repigmentation, others progressive spread
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Segmental vitiligo is more stable than non-segmental
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Early treatment improves chance of repigmentation
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Psychosocial impact can be significant, requiring supportive care
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