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Vitiligo - Anogenital in
See also in: Overview,External and Internal Eye
Other Resources UpToDate PubMed

Vitiligo - Anogenital in

See also in: Overview,External and Internal Eye
Contributors: Vivian Wong MD, PhD, Susan Burgin MD
Other Resources UpToDate PubMed

Synopsis

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 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).

Codes

ICD10CM:
L80 – Vitiligo

SNOMEDCT:
56727007 – Vitiligo

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Diagnostic Pearls

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Differential Diagnosis & Pitfalls

Best Tests

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Management Pearls

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Therapy

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Drug Reaction Data

Below is a list of drugs with literature evidence indicating an adverse association with this diagnosis. The list is continually updated through ongoing research and new medication approvals. Click on Citations to sort by number of citations or click on Medication to sort the medications alphabetically.

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References

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Last Reviewed:07/27/2017
Last Updated:02/08/2021
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Vitiligo - Anogenital in
See also in: Overview,External and Internal Eye
Vitiligo : Dorsum of hand, Face, Fingers, Hair color change, Symmetric extremities distribution, Depigmented macules/patches
Clinical image of Vitiligo
A white macule and a similar patch on the forearm.
Copyright © 2021 VisualDx®. All rights reserved.