Vitiligo

Acquired chronic depigmenting disorder characterized by well-defined depigmented macules and patches

Epidemiology

  • Global prevalence: ~0.5–2%
  • Affects all races and sexes equally
  • Typical onset: before 30 years of age
  • Positive family history in ~20–30%
  • Associated with autoimmune diseases

Aetiology

Vitiligo is multifactorial, with the following key mechanisms:

Autoimmune hypothesis (most accepted)

  • Autoantibodies and cytotoxic CD8+ T cells target melanocytes
  • Association with autoimmune thyroid disease, type 1 diabetes, alopecia areata

Oxidative stress

  • Accumulation of reactive oxygen species damages melanocytes

Genetic susceptibility

  • Polygenic inheritance (HLA-A2, NLRP1, PTPN22)

Neural & intrinsic melanocyte defects

  • Neurochemical mediators and melanocyte fragility

Pathophysiology

Loss of functional melanocytes → absence of melanin production → depigmented (chalk-white) skin.

Clinical presentation

Skin Lesions

  • Well-demarcated depigmented macules/patches
  • Chalk-white appearance
  • Symmetric distribution common
  • No scaling or inflammation
  • Lesions enlarge centrifugally
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Common Sites

  • Face (periorificial areas)
  • Hands and feet
  • Flexural areas
  • Genitalia
  • Sites of trauma (Koebner phenomenon)

Hair Involvement

  • Leukotrichia (white hair) may be present → poor prognostic sign

Investigations

Test
Finding
Wood’s lamp
Bright blue-white fluorescence
Skin biopsy (rare)
Absence of melanocytes
Autoimmune screening
Thyroid function tests
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Management

Therapy
Indication
Topical corticosteroids
Localized vitiligo
Topical calcineurin inhibitors
Face, intertriginous areas
Narrowband UVB (NB-UVB)
Generalized vitiligo
Excimer laser (308 nm)
Localized lesions
Systemic corticosteroids (mini-pulse)
Rapidly progressive disease