Vitiligo differential diagnosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Differentiating Vitiligo from other Diseases

  • Annular lichenoid dermatitis of youth
  • Chemical leukoderma
  • Certain chemicals, particularly aromatic derivatives of phenols and catechols, can destroy melanocytes, resulting in chemical leukoderma that may be differentiated from vitiligo by the history of toxin exposure, lesions with bizarre borders and scale, a “confetti-like” distribution, and symptomatic pruritus.
  • Discoid lupus erythematosus
  • Guttate hypomelanosis
  • Presents with hypopig- mented macules in a photodistribution on a background of actinic damage primarily on the arms and legs; unlike vitiligo, the macules are usually 5 mm in diameter or less.
  • Halo nevus
  • Hypopigmented mycosis fungoides
  • Idiopathic guttate hypomelanosis
  • Ito’s hypomelanosis
  • Linear distribution, unilateral or bilateral pattern of hypopigmented streaks; sporadic; chromosomal or genetic mosaicism (involving blood or skin cells)
  • Leprosy
  • Lichen sclerosus
  • Mycosis fungoides
  • Nevus anemicus
  • Nevus depigmentosus
  • Nevoid hypomelanosis
  • Onchocerciasis
  • Photodistributed vitiligo-like drug reaction in HIV patients
  • Piebaldism
  • White forelock, midline depigmentation of anterior body, bilateral shin depigmentation; autosomal dominance.
  • Pinta
  • Pityriasis alba
  • Common in children with atopy; also may have fine scale, but lesions retain some pigment and are less sharply demarcated.
  • Postinflammatory depigmentation
  • Postinflammatory hypopigmentation
  • A history of trauma or inflammation of the affected area will precede the loss of pigment.
  • Sarcoidosis
  • Scleroderma-related leukoderma
  • Tinea versicolor
  • May be differentiated by the presence of fine scale, positive potassium hydroxide preparation, and distribution primarily on the trunk and neck.
  • Topical steroid leukoderma
  • Tuberous sclerosis
  • Ash-leaf white spots, typically later appearance of other cutaneous symptoms (e.g., shagreen patches, angiofibromas, periungual fibromas, or connective tissue nevi) and possibly neurological sequelae; autosomal dominance.
  • Vogt–Koyanagi–Harada syndrome
  • Waardenburg’s syndrome
  • White forelock, hypertelorism, deafness (varies according to genotype); possible association with con- genital megacolon (Hirschsprung’s disease)

References