Vitiligo
Acquired depigmentation; non-segmental / segmental / focal vitiligo; leucoderma
Vitiligo is an acquired autoimmune depigmentation affecting approximately 1% of the global population. It results from autoimmune destruction of melanocytes, producing well-demarcated patches of complete depigmentation. UK practice classifies vitiligo into non-segmental (the commonest, often progressive), segmental (localised, often unilateral) and focal patterns. The skin-oncology relevance is twofold — depigmented skin lacks melanin photoprotection and is at increased risk of UV-induced damage and skin cancer (though paradoxically melanoma incidence is reduced in vitiligo patients overall), and vitiligo developing during ICI therapy for melanoma is a strong predictor of improved progression-free and overall survival — see irAE-induced vitiligo.
Clinical features
- Well-demarcated milk-white patches of complete depigmentation.
- Non-segmental vitiligo — bilateral, often symmetrical; periorificial, acral, flexural and friction sites; tends to progress. 90% of cases.
- Segmental vitiligo — unilateral, dermatomal distribution; usually limited extent; childhood onset; rarely progressive.
- Focal vitiligo — isolated small patch; intermediate.
- Universal vitiligo — > 80% body surface; rare.
- Onset bimodal — 10–20 years and 40–50 years.
- Wood's lamp confirms depigmentation (bright milk-white fluorescence).
- Leukotrichia (white hair) within patches predicts poor repigmentation response.
Autoimmune associations
- Autoimmune thyroid disease — Hashimoto / Graves in 15–20%.
- Type 1 diabetes mellitus.
- Pernicious anaemia.
- Addison disease.
- Alopecia areata.
- Inflammatory bowel disease.
- Psoriasis.
- Reduced melanoma and BCC incidence overall in vitiligo cohorts (paradoxical immunosurveillance hypothesis).
- Baseline screen — TSH, FBC, vitamin B12, autoimmune screen if clinically indicated.
Skin-cancer context
- Depigmented skin is at increased local risk of sun damage, AK and squamous lesions due to absent melanin photoprotection.
- Photoprotection is essential — SPF 50+ broad-spectrum, UV-protective clothing.
- Overall melanoma and BCC incidence is reduced in vitiligo populations in case-control studies — suggesting active immunosurveillance.
- ICI-induced vitiligo in melanoma patients is a strong biomarker of clinical response — see irAE-induced vitiligo. Do not treat or suppress this; counsel about prognostic implications.
- Vitiligo halo around naevi — Sutton naevus / halo naevus; usually benign.
Management
- Topical corticosteroids — superpotent (clobetasol) for limited disease; rotate to avoid atrophy.
- Topical calcineurin inhibitors — tacrolimus 0.1%, pimecrolimus 1%; first-line for face / eyelid / genital.
- Phototherapy — narrowband UVB 311 nm twice weekly; targeted PUVA for limited disease.
- Topical ruxolitinib 1.5% cream — first JAK inhibitor approved for non-segmental vitiligo (FDA 2022; UK access via specialist).
- Oral mini-pulse betamethasone / dexamethasone — for rapidly progressive disease.
- Excimer laser 308 nm — for localised resistant patches.
- Melanocyte transplantation — autologous; for stable segmental vitiligo.
- Depigmentation therapy — monobenzone for universal / extensive disease where repigmentation impractical.
- Cosmetic camouflage — make-up, tanning lotions.
- Photoprotection of depigmented skin — strict SPF 50+.
- Psychological support — substantial psychosocial morbidity.
References
- Ezzedine K et al. Vitiligo. Lancet; 2015.
- Eleftheriadou V et al. British Association of Dermatologists guidelines for the management of people with vitiligo 2021. Br J Dermatol. 2022;186(1):18-29.
- Rosmarin D et al. Two phase 3, randomized, controlled trials of ruxolitinib cream for vitiligo. N Engl J Med; 2022.
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