Melanocytes are present in the basal layer of the epidermis and are responsible for skin pigmentation. In vitiligo, there is autoimmune destruction of melanocytes leading to localized loss of skin pigmentation.
Vitiligo causes localized loss of skin pigmentation, which presents as hypopigmented areas of skin. The areas of hypopigmented skin are typically chalk or milk- white in color and the lesions are well circumscribed.
Vitiligo can affect any part of the body, but it is common in peripheral body parts known as acral areas such as fingers, toes, and ears. It also is seen around orifices and body folds like the armpits, groin, and genitalia.
Vitiligo is normally a clinical diagnosis and no tests are needed to make the diagnosis. However, sometimes a Wood’s lamp (black light) is necessary to detect the white patches in lighter skinned individuals.
Increased frequencies of other autoimmune disorders, such as autoimmune thyroid disease, pernicious anemia, Addison’s disease and systemic lupus erythematosus have been identified in patients with vitiligo.
Topical corticosteroids are typically the first treatment of choice for patients with disease covering less than 10% of the body. Corticosteroids are avoided in thin skinned areas such as the face because of the potential for skin atrophy.
Topical calcineurin inhibitors including tacrolimus are second-line medications for vitiligo. Unlike topical corticosteroids, tacrolimus does not cause skin atrophy, and may be used for thin skinned areas such as the face. However, these agents are used with caution due to a possible link between tacrolimus and lymphoma.
Ultraviolet radiation therapy is used in patients with more extensive vitiligo. Examples of therapy include narrowband UVB and PUVA.
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