Vitiligo is an acquired type of leukoderma characterized by well-circumscribed chalk-white depigmented macules or patches. Vitiligo is usually asymptomatic, and lesions can range in size from millimeters to centimeters. While any part of the body can be affected, vitiligo often demonstrates distinct patterns including symmetric involvement of the face, upper chest, hands, ankles, axillae, groin, and around orifices (eyes, nose, mouth, urethra, and anus), often favoring sites of frequent friction or trauma. Distribution can be either localized, as in segmental vitiligo, generalized as in vitiligo vulgaris, or universal. Generalized forms include vulgaris (widely distributed, scattered macules and patches) and acrofacial (distal extremities and face). Mucous membrane involvement is not uncommon in generalized cases. In the universal form, nearly 100% of the body surface area is depigmented.

Vitiligo may accompany halo nevi. New-onset vitiligo may be seen in patients with metastatic melanoma. It can occur spontaneously and may herald metastatic disease, or it can be triggered by immunotherapy such as with BRAF inhibitors or PD-1 inhibitors. In the latter setting, it is considered a good prognostic sign. Rarely, vitiligo may be associated with uveitis.

Vitiligo occurs in equal proportions regardless of age, sex, or race and ethnicity. The natural progression of the disease is unpredictable, ranging from insidious to rapid in onset. Years of stable, nonprogressive disease can be observed with the disease subsequently taking an unexpected rapid trajectory.

While the precise etiology of vitiligo remains debated, two leading hypotheses include the following: 1) a host attack on normal melanocytes; and 2) intrinsic melanocyte defects. Genetic predisposition and trauma are other risk factors for vitiligo development. Exposure to depigmenting agents causes a vitiligo-like leukoderma in susceptible individuals. While the majority of vitiligo patients are otherwise healthy, an association with autoimmune thyroid dysfunction (hyperthyroidism or hypothyroidism) has been demonstrated. In new onset vitiligo patients with systemic symptoms, thyroid screening with antithyroid peroxidase (TPO) antibody and a serum thyrotropin is recommended. Additional associations include endocrinopathies, such as diabetes mellitus and Addison disease, along with other autoimmune processes. Rarely, it may exist as part of polyglandular autoimmune syndrome, particularly a type III syndrome (eg, Hashimoto thyroiditis, vitiligo, or alopecia areata and/or another organ-specific autoimmune disease).