Reference Work Entry

Encyclopedia of Molecular Mechanisms of Disease

pp 2227-2228


  • Johannes BayerAffiliated withDepartment of Dermatology, University Hospital of Muenster
  • , Stefan BeissertAffiliated withDepartment of Dermatology, University Hospital of Muenster

Definition and Characteristics

Vitiligo is an acquired, idiopathic hypomelanotic disorder in which a progressive loss of melanocytes from the epidermis and hair follicles results in well-circumscribed cutaneous depigmented macules [1].


Vitiligo is the most common pigmentary disorder worldwide. The prevalence is 0.5–2% without a predilection for age, sex or race.


Several candidate genes have been proposed for vitiligo susceptibility, including genes important for melanin biosynthesis, response to oxidative stress and/or regulation of autoimmunity [2,3]. However, none of these vitiligo susceptibility genes has yet been identified. Case-control studies examining human leukocyte antigens (HLA) have shown a positive association with HLA DR4 and a negative association with HLA DR3 [4].

Molecular and Systemic Pathophysiology

The mechanisms leading to the loss of pigment cells are not yet fully understood. Melanocytes could be destroyed by necrosis, apoptosis or transepidermal elimination of melanocytes [5]. There are multiple hypotheses to explain the aetiology of vitiligo: autoimmune, autocytotoxic, neural, environmental and genetic factors.

Diagnostic Principles

An immunohistopathology of the skin should be drawn and associated autoimmune disease should be excluded (thyroid studies, antinuclear antibodies (ANA), other organ specific antibodies, fasting blood glucose levels and a complete blood count).

Therapeutic Principles

Vitiligo is a challenging disease to treat, but there are several options. First line treatments include topical corticosteroids, topical calcineurin inhibitors, or phototherapy (UVB UVA1, PUVA). Novel therapeutic approaches include pseudocatalase with UVB.

Copyright information

© Springer-Verlag GmbH Berlin Heidelberg 2009
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