Acquired autoimmune depigmenting disorder with discrete milky-white macules and patches due to melanocyte loss.
Also known as: vitiligo, leukoderma, depigmentation
Overview
An acquired chronic depigmenting disorder of the skin and mucous membranes characterized by well-demarcated milky-white macules and patches resulting from progressive loss of functional epidermal melanocytes.
Epidemiology
Worldwide prevalence ~0.5-2%. Onset before age 20 in 50%. No sex or racial predilection, but psychosocial impact greater in skin of color. Family history in ~20%.
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Personal or family history of autoimmune disease: thyroid (most common — Hashimoto, Graves), pernicious anemia, Addison disease, type 1 diabetes, alopecia areata, rheumatoid arthritis
Koebner phenomenon — trauma, friction, sunburn at sites of skin injury
Stress (anecdotal)
Chemical exposure (phenol derivatives, monobenzone — chemical leukoderma)
Pathophysiology
Autoimmune destruction of melanocytes by CD8+ cytotoxic T-cells targeting melanocyte antigens (tyrosinase, MART-1, gp100). Interferon-γ-driven CXCL9/CXCL10 chemokines recruit autoreactive T-cells. Oxidative stress (impaired antioxidant defenses in melanocytes) and intrinsic melanocyte fragility contribute. JAK-STAT pathway central — basis for new topical JAK inhibitor therapy.
Clinical presentation
Symptoms
Most often asymptomatic; mild pruritus at active edges in some patients
Psychosocial distress, depression, anxiety, decreased quality of life — especially in skin of color and visible areas
Younger; early rapid then stable; good surgical candidate
Acrofacial
Face + dorsal hands/feet
Common variant; similar to non-segmental
Universal
>80% BSA depigmented
Consider depigmentation therapy (MBEH)
Mucosal
Lips, genitalia
Often refractory to topicals; JAK inhibitor, NBUVB targeted
Vitiligo clinical patterns and management considerations.
Treatment
First-line
Topical corticosteroids: high-potency (clobetasol 0.05%, betamethasone dipropionate 0.05%) BID × 2-4 months for limited disease — pulse therapy (e.g., 2 weeks on / 2 weeks off) to limit atrophy
Topical calcineurin inhibitors: tacrolimus 0.1% ointment BID — preferred for face/intertriginous (no atrophy); equally effective as topical steroids in many trials
Topical JAK inhibitor: ruxolitinib 1.5% cream BID (FDA-approved 2022 for nonsegmental vitiligo ages ≥12) — significant repigmentation in 50% by 6-12 months
Narrowband UVB phototherapy (311-313 nm) 2-3x/week — first-line for widespread disease; combine with topicals for additive effect
Excimer laser (308 nm) for localized lesions
Sunscreen daily — protect depigmented areas (no melanin protection) and reduce contrast with surrounding skin
Best results in stable disease >1 year, segmental disease, and areas with intact hair pigment
Extensive (>50% BSA)
Depigmentation therapy: monobenzyl ether of hydroquinone (MBEH) 20% cream — permanent depigmentation of remaining pigmented skin for cosmetic uniformity
Irreversible — counsel extensively
Second-line / adjunct
Afamelanotide (α-MSH analog) + NBUVB — promising in trials
Oral JAK inhibitors (ritlecitinib, upadacitinib) — emerging evidence
Antioxidants (ginkgo biloba, vitamin E, polypodium leucotomos) — limited evidence
Mental health support, vitiligo support groups; address quality of life as actively as the skin disease
Complications
Sunburn and increased risk of skin cancer in depigmented areas (though epidemiologic studies surprisingly show LOWER skin cancer rates in vitiligo patients, possibly from increased sun-protective behavior and altered immunity)
Psychosocial: depression, anxiety, social isolation, low self-esteem, sexual dysfunction
Hearing: sensorineural hearing loss (rare; melanocyte loss in inner ear)
PANCE pearls
Wood's lamp examination is the bedside test — depigmented vitiligo glows milky-white; hypopigmented conditions (versicolor, post-inflammatory) do not.
Screen all vitiligo patients for autoimmune thyroid disease at diagnosis and periodically.
Topical ruxolitinib (JAK inhibitor) is now first-line for nonsegmental vitiligo — significant cultural shift in vitiligo therapy since 2022 FDA approval.
Leukotrichia (white hairs in patch) predicts poor repigmentation response because hair follicle melanocyte reservoir is depleted.
Vitiligo is not 'just cosmetic' — its psychosocial impact often exceeds objective severity; address mental health proactively.
References
AAD 2023 — Joint AAD-NPF-Vitiligo Working Group Updated Recommendations for the Management of Vitiligo (Rosmarin et al., J Am Acad Dermatol)
VGICC 2023 — Vitiligo Global Issues Consensus Conference Guidelines (Taïeb et al., Br J Dermatol; updated)
FDA Ruxolitinib — FDA Approval of Topical Ruxolitinib 1.5% Cream for Nonsegmental Vitiligo (2022)
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