• Clinical science

Vitiligo

Summary

Vitiligo is a common skin condition in which a patchy loss of epidermal melanocytes results in depigmentation. This loss is hypothesized to be a result of autoimmune destruction, oxidative stress, and/or intrinsic melanocyte defects in genetically predisposed individuals, and is commonly associated with other autoimmune diseases. The clinical course is highly variable, with unilateral or bilateral distribution of well demarcated, depigmented macules, which may progress during the course of disease. These lesions have a predilection for facial, acral, extensor, and sun-exposed areas of the body. Vitiligo is often a clinical diagnosis, but Wood's lamp examination, dermoscopy, and/or skin biopsy are useful in ambiguous cases. Limited disease may be controlled with topical corticosteroids or topical immunomodulators, while extensive or progressive disease may require systemic therapy, phototherapy, or surgery. Regardless of the treatment modality, patients continue to have episodes of skin depigmentation throughout their lives.

Epidemiology

  • Prevalence: 1–2% of the general population
  • Peak incidence: 20–30 years; can occur in any age group
  • Sex: =

References:[1][2]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

  • Vitiligo is characterized by an absence of melanocytes in the depigmented lesions.
  • The etiology is unknown, but is thought to be multifactorial.
    • Genetic predisposition
    • Autoimmune destruction of melanocytes
    • Oxidative stress (free radicals)
    • Intrinsic defects of melanocytes (early apoptosis, defective cell-to-basement membrane adherence)
  • May be triggered by stress or skin injury (e.g., sunburn)

References:[1]

Classification

  • According to location
    • Generalized (most common): widespread distribution of lesions, frequently with mucosal involvement
    • Localized: isolated area affected (e.g., dermatomal)
    • Universal: Almost the entire body is affected.

References:[1][2][3]

Clinical features

  • Well demarcated, depigmented (white) macules or patches , surrounded by normal skin
  • Unilateral or bilateral distribution, with stable or slowly progressive lesions
  • Commonly on the face (e.g., perioral and periocular regions), neck, scalp, acral surfaces (e.g., hands), extensor surfaces, or genitalia
  • Leukotrichia: depigmented hair
  • Coexisting autoimmune diseases (∼ 20% of patients)

References:[1][2][4]

Diagnostics

  • Usually a clinical diagnosis
  • If diagnosis is uncertain:
    • Wood's lamp examination: The vitiligo lesions appear as well defined blue-white areas.
    • Dermoscopy: Vitiligo lesions have a characteristic perilesional hyperpigmentation and telangiectasia.
    • Skin biopsy and histology: Melanocytes are absent, perilesional lymphocytes may be observed.
  • Serological markers of autoimmune disease (e.g., thyroid function tests and antithyroid antibodies) once vitiligo is confirmed

References:[1][2]

Differential diagnoses

  • Pityriasis alba: A common hypopigmented scaly patch seen in sun-exposed areas, esp. in children (resolves spontaneously or with topical steroids).
  • Pityriasis versicolor: a fungal infection characterized by scaly hypopigmented macules on the trunk

References:[1]

The differential diagnoses listed here are not exhaustive.

Treatment

References:[2][5]