Vitiligo - Anogenital in
While the precise etiology of vitiligo remains debated, two leading hypotheses include: 1) host attack on normal melanocytes; and 2) intrinsic melanocyte defects. Genetic predisposition and trauma are other risk factors for vitiligo development. 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 anti-thyroid 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 type III (Hashimoto thyroiditis, vitiligo, and alopecia areata and/or another organ-specific autoimmune disease).
Variants of vitiligo include:
- Inflammatory vitiligo – Margins of vitiligo with raised erythematous inflammatory borders.
- Trichrome vitiligo – Three distinct zones including a depigmented zone, a uniformly hypopigmented intermediate band, and a zone of normal skin. More common in individuals of African descent.
- Vitiligo ponctué (aka confetti type) – Tiny, punctate-like depigmented macules on a hyperpigmented macule or on normal skin.
- Blue vitiligo – When vitiligo develops on a postinflammatory hyperpigmented lesion, giving it a bluish tint.
Related topic: Segmental vitiligo
L80 – Vitiligo
56727007 – Vitiligo
- A history of prior trauma or skin inflammation can usually be elicited in cases of post-inflammatory hypopigmentation.
- Albinism, piebaldism, and other genetic disorders – Begin in infancy.
- Morphea – Look for sclerotic plaques.
- Lichen sclerosus – Look for sclerotic plaques, often in the genital area; can be severely pruritic.
- Chemical leukoderma or drug-induced hypopigmentation – Look for history of chemical use and/or topical corticosteroids.
Last Updated: 09/24/2019