Vitiligo in Adult
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).
L80 – Vitiligo
56727007 – Vitiligo
- Discoid lupus erythematosus – Presents with atrophy, telangiectasia, and follicular plugging, which are absent in vitiligo.
- Scleroderma – Depigmented vitiligo-like macules or patches may occur in scleroderma; however, there is perifollicular retention of pigment, which is a differentiating clinical sign. Look for associated sclerotic skin. Check antinuclear antibodies (ANA) with nucleolar or speckled pattern, anti-centromere, anti-Scl-70 antibody. Associated with Raynaud phenomenon, arthralgias, mat telangiectasias, and CREST syndrome.
- Albinism, piebaldism, and other genetic disorders – Begin in infancy.
- Lichen sclerosus – Look for sclerotic plaques, often in the genital area; can be severely pruritic.
- Medication-induced or chemical-induced leukoderma – Look for history of certain medications or chemicals.
- Onchocerciasis – Shins are common site of involvement. Suspect if patient is coming from endemic area (Africa, Central or South America).
- Tinea versicolor – Potassium hydroxie (KOH) positive. Mild scale noted; often seen in the shoulders, upper trunk.
- Pityriasis alba – Typically affects the cheeks of atopic individuals; presents with hypopigmented, not depigmented, macules with ill-defined borders.
- A history of prior trauma or skin inflammation can usually be elicited in cases of post-inflammatory hypopigmentation.
- Leprosy – Lesions are usually hypopigmented, not depigmented. Some can have an erythematous border. Lesions are anesthetic. Patient must have recently lived in an endemic area.
- Nevus depigmentosus – Common on the trunk; usually present since birth. Despite its name, it is hypopigmented.
- Nevus anemicus – Not a true pigmentary disorder, but rather a localized area of relative vasoconstriction in the skin secondary to increased sympathetic supply.
- Idiopathic guttate hypomelanosis – Characteristic pattern and shape of lesions different from vitiligo, including well-demarcated, 0.4- to 0.7-mm macules that do not coalesce, are symmetric, and involve the extensor forearms and shins; the face is rarely involved.
- Cutaneous T-cell lymphoma (mycosis fungoides) – Can have an associated scale. Lesions are usually hypopigmented, not depigmented.
- Morphea – Look for sclerotic plaques.