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01 —What it is

Vitiligo is an autoimmune condition in which the body's own immune system attacks and destroys the melanocytes — the cells in the skin that make pigment (melanin). Where the melanocytes are destroyed, the skin loses its pigment and appears white. It affects around 0.5–2% of the world's population.^¹ Onset is most often in childhood or young adulthood. Around half of people with vitiligo develop their first patches before the age of 20.

It is not contagious. It is not caused by anything you did. It is not a 'stress disease' (though stress can worsen flares, it does not cause it). It is, increasingly, treatable.

02 —The biology

The current understanding is that vitiligo is driven by CD8+ T cells — specific immune cells — recognising melanocyte proteins as foreign and attacking them.^² The cytokine pathway most heavily involved is interferon-gamma (IFN-γ), signalling through the JAK1/JAK2 pathway, which then drives the recruitment of more T cells via the chemokine CXCL10.

This is why the recent JAK inhibitors — drugs that block this signalling pathway — have transformed treatment. It is a precise mechanistic match between drug and disease.

03 —What works

Topical therapy

• —Topical corticosteroids — first-line for limited disease. Effective, especially in early/active phases. Side-effect profile limits long-term continuous use.
• —Topical calcineurin inhibitors (tacrolimus, pimecrolimus) — preferred for the face and skin folds. Steroid-sparing.
• —Ruxolitinib 1.5% cream — the first FDA-approved (2022) and now EMA/MHRA-approved topical JAK inhibitor for non-segmental vitiligo. TRuE-V1 and TRuE-V2 were the pivotal phase 3 trials (Rosmarin et al., NEJM 2022): roughly 30% of patients achieved ≥75% improvement in facial VASI at week 24, versus <5% on vehicle.^³ Approved down to age 12.

Phototherapy

• —Narrowband UVB — the most established treatment for widespread vitiligo. 2–3 sessions per week for 6–12 months. Effective but practically demanding.
• —Excimer laser — targeted phototherapy for limited disease. Useful for small areas.

Systemic therapy

• —Oral mini-pulse corticosteroids — used in rapidly progressive disease to halt activity.
• —Oral JAK inhibitors (upadacitinib, ritlecitinib, povorcitinib) — currently in advanced trials for vitiligo. The pipeline here is unusually active; expect approvals in the next two to three years.

Surgical

For stable, refractory segmental vitiligo: melanocyte transplantation procedures (suction blister grafting, non-cultured epidermal cell suspension). Specialist centres only.

Camouflage and cosmetic adjuncts

Skin camouflage products are not a treatment, but they are a legitimate and well-evidenced psychosocial intervention. Changing Faces and similar services offer free skin camouflage clinics in the UK.

The era of 'there is nothing we can do' for vitiligo is over. Topical JAK inhibitors changed the conversation in 2022. The oral JAK pipeline will change it again.

04 —The psychosocial side

Vitiligo is one of the most psychologically loaded skin conditions in adolescence because it is highly visible, often progressive, and culturally stigmatised in many parts of the world. Quality-of-life studies consistently show impairment comparable to severe psoriasis or moderate eczema, despite the absence of pain or itch.^⁴

Psychosocial intervention is an active research area in vitiligo, with several published trials of cognitive-behavioural and acceptance-based approaches reporting improvements in disease-specific quality of life. Psychosocial intervention is not a substitute for medical treatment, but it is increasingly recognised as a parallel necessity rather than an optional adjunct.

05 —Sun and vitiligo

Vitiligo-affected skin has no melanin and is therefore highly vulnerable to UV damage. Daily broad-spectrum SPF 30+ is essential — both to protect the unpigmented skin and to reduce the contrast with surrounding pigmented skin. Sun-protective clothing helps. Tanning the surrounding skin to 'match' makes the contrast worse, not better.

06 —What to ask your doctor

• —Is my vitiligo currently active or stable? (This affects which treatments are likely to work.)
• —Am I a candidate for ruxolitinib cream? (Especially for facial vitiligo.)
• —Should I be considered for narrowband UVB phototherapy?
• —Are there oral options or clinical trials I should know about?
• —Is there a psychologist or counsellor familiar with skin conditions I can speak to?
• —Should my thyroid function be checked? (Vitiligo can be associated with autoimmune thyroid disease.)

1. 01
   Krüger C, Schallreuter KU. A review of the worldwide prevalence of vitiligo in children/adolescents and adults. Int J Dermatol 2012;51(10):1206-1212. PMID 22458952
2. 02
   Rashighi M, Harris JE. Vitiligo Pathogenesis and Emerging Treatments. Dermatol Clin 2017;35(2):257-265. PMID 28317534
3. 03
   Rosmarin D, Passeron T, Pandya AG, et al. Two Phase 3, Randomized, Controlled Trials of Ruxolitinib Cream for Vitiligo. N Engl J Med 2022;387(16):1445-1455. PMID 36260792
4. 04
   Linthorst Homan MW, Spuls PI, de Korte J, Bos JD, Sprangers MA, van der Veen JP. The burden of vitiligo: patient characteristics associated with quality of life. J Am Acad Dermatol 2009;61(3):411-420. PMID 19577331