Mauro Picardo (Italy)


Sungbin Im (Korea), Seung Kyung Hann (Korea), Wiete Westerhof (Netherlands), Yutaka Mishima (Japan), Rafael Falabella (Columbia), Jean Bolognia (USA), Jean-Claude Bystryn (USA), Rebat Halder (USA), Stanley Bleehan (England), Giovanni Orecchia (Italy).

Additional information

IFPCS Vitiligo Research Group

Vitiligo European Task Force at the ESPCR web page


Consensus Definition and Description of Vitiligo vulgaris

Vitiligo is a specific type of leukoderma.

  • It is best defined as an acquired (post partum) disorder that selectively destroys (or that results in the selective disappearance) of some or all melanocytes residing in the interfollicular epidermis and occasionally in the follicle as well.
  • The mechanism(s) by which the melanocytes are lost (or by which melanocytes are made to disappear) may be multiple but are not yet identified unequivocally.
  • Vitiligo is characterized by white macules on the skin that can be few or many in number. The depigmentation can be wide spread, even a complete loss of all interfollicular melanocytes.
  • The cause(s) of vitiligo are unknown but it is considered likely that the melanocytes of the affected individual genetically are more susceptible to one or several environmental factors that initiate the processes resulting in the loss of melanocytes and appearance of white spots on the integument.
  • There are two types of vitiligo, bilateral and unilateral (also called segmental). The bilateral form is further subdivided into localized and generalized types. The unilateral form does not cross the midline and is not dermatomal in distribution.
  • The question whether vitiligo is a systemic disorder of all melanocytes in the skin, eyes and ears is not resolved.
  • There are other types of leukoderma characterized by absence of melanocytes in the interfollicular skin and follicles. Leukoderma can be classified as follows:

Classification of Leukoderma (depigmentation only)
Genetic, congenital depigmenation
  • Piebaldism
  • Waardenburg’s syndromes (types 1 – 4)
  • Albinism-deafness syndrome
  • others
Acquired Depigmentation
  • Primary (not known to be caused by another disease)
    • Vitiligo vulgaris
    • Rozycki syndrome
  • Secondary (caused by or associated with another disorder)
    • Chemical leukoderma
    • Depigmentation associated with melanoma
    • Depigmentation associated with halo nevi
    • Other halo phenomenon
    • Depigmentation associated with lymphomas
    • Vogt Koyanagi Harada syndrome
    • Allezendrini syndrome
    • Idiopathic guttate hypomelanosis
    • Lichen sclerosis et atrophicus
    • Scleroderma
    • Post traumatic (e.g. thermal and radiation burns)
    • Post inflammatory (e.g. lupus erythematosus)
    • Post infectious (e.g. herpes zoster, pinta)
    • White (not gray) hair (familial and sudden whitening)
    • others

There are forms of leukoderma that have persistance of melanocytes that have altered function such as albinism. These types of leukoderma are not classified here

Animal models

There are several animal models of acquired depigmentation. These are not forms of vitiligo but models of leukoderma. They are useful and important to study to learn about all forms of depigmentation and pigment cell biology.

  • Smyth chicken
  • mi<vit>/mi<vit> mouse
  • Sinclair and Duroc swine
  • Arabian and other breeds of horses
  • Belgian Terveran dogs
  • Persian cats
  • others