Vitiligo Treatment

Vitiligo — characteristic sharply demarcated depigmented patches on the dorsal hands and wrists

Vitiligo: acral depigmented macules/patches on bilateral hands — Harrison's, p. 1518

Vitiligo is an autoimmune disorder causing loss of melanocytes, resulting in well-demarcated depigmented patches. Treatment aims to halt progression and achieve repigmentation.

Goals of Treatment

Stop active disease progression
Repigment affected skin
Maintain achieved repigmentation

First-Line Therapies

Topical Agents

Agent	Details
Topical corticosteroids (TCS)	High-potency (e.g., clobetasol) for trunk/extremities; moderate-potency for face. First-line for localized disease. Monitor for skin atrophy with prolonged use.
Topical calcineurin inhibitors (TCIs)	Tacrolimus 0.1% or pimecrolimus 1%. Preferred for face and intertriginous areas (steroid-sparing). Safe for long-term use.
Ruxolitinib cream (JAK inhibitor)	FDA-approved (2022) for non-segmental vitiligo in adults/adolescents ≥12 years. JAK1/2 inhibitor targeting the IFN-γ/CXCL10 pathway. Most effective repigmentation agent to date for facial lesions.

Phototherapy

Narrow-band UVB (NB-UVB) is the mainstay of phototherapy for vitiligo (Harrison's, p. 1712):

Fluorescent bulbs emitting ~311 nm radiation
Superior efficacy over broad-band UVB
Suitable for widespread disease or lesions resistant to topicals
2–3 sessions/week for a minimum of 6–12 months
Can be combined with topical agents for enhanced effect

PUVA (Psoralen + UVA):

Oral or topical psoralen + UVA exposure
Effective but higher risk (nausea, phototoxicity, cataract risk with oral psoralen)
Less commonly used now that NB-UVB is available

Excimer laser (308 nm):

Targeted phototherapy for localized lesions
Allows high-dose UV delivery to affected patches while sparing normal skin
Faster response than whole-body NB-UVB

Surgical Options

Reserved for stable segmental or focal vitiligo (no new lesions for ≥12 months):

Procedure	Details
Suction blister epidermal grafting	Most widely used; good cosmetic outcomes
Split-thickness skin grafting	For larger areas
Punch grafting	Small, focal patches
Melanocyte-keratinocyte transplantation (MKTP)	Cultured cells; can cover large areas

Systemic Therapies

Oral mini-pulse corticosteroids (e.g., betamethasone 5 mg on 2 consecutive days/week): used to halt rapidly progressive disease
Oral JAK inhibitors (ruxolitinib, baricitinib — investigational/emerging): promising phase II/III trial data for widespread disease
Afamelanotide (MC1R agonist implant): used in combination with NB-UVB, accelerates repigmentation

Camouflage / Depigmentation

Cosmetic camouflage (waterproof concealers, self-tanners) for psychosocial impact
Depigmentation with monobenzone (monobenzyl ether of hydroquinone): considered only when >50% BSA is affected and repigmentation has failed — permanently depigments remaining normal skin

Special Considerations

Factor	Guidance
Segmental vitiligo	Less responsive to medical treatment; surgical options preferred
Active/inflammatory vitiligo	Treat inflammation first (TCIs, TCS, systemic steroids) before surgery
Children	Prefer TCIs and NB-UVB; avoid prolonged high-potency TCS
Face/eyelids	TCIs + NB-UVB or excimer laser; avoid TCS long-term
Koebner phenomenon	Minimize trauma; treat wounds promptly

Monitoring

Assess repigmentation at 3–6 months
Wood's lamp examination to detect early lesions and assess progress
Screen for associated autoimmune conditions: thyroid disease (most common), type 1 diabetes, Addison's disease, alopecia areata

Key takeaway: Mild/localized disease → topical TCS or TCIs ± excimer. Moderate/widespread → NB-UVB ± topicals. Rapidly progressive → systemic mini-pulse steroids. Stable localized → surgical grafting. Ruxolitinib cream is a significant recent advance for facial non-segmental vitiligo.

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