Vitiligo
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%.
Keep reading — start your free trial
You've read your 2 free diagnosis previews. Create your free account to unlock the full Vitiligo outline — plus all 514 diagnoses, 5,500+ board-style questions, flashcards, and an AI tutor. Your 7-day free trial includes everything, and there's no credit card required.
Risk factors
- Polygenic inheritance (NLRP1, PTPN22, TYR, HLA, FOXP3 loci)
- 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
Signs / physical exam
- Well-demarcated milky-white (chalk-white) macules and patches — completely depigmented (vs hypopigmented)
- Distribution patterns:
- • Non-segmental (most common, 85-90%): symmetric, on periorificial face (around eyes, mouth), dorsal hands, axillae, genitalia, elbows, knees; progressive course
- • Segmental: unilateral, dermatomal or quasi-dermatomal distribution; younger patients; rapid early progression then stable
- • Acrofacial: face, dorsal hands and feet; common variant
- • Universal: >80% BSA depigmentation
- Wood's lamp examination: bright milky-white fluorescence highlights subclinical lesions
- Leukotrichia (white hairs) within patches — poor prognostic sign for repigmentation
- Confetti-like depigmentation = active rapid progression
Classic findings
Symmetric, well-demarcated, completely depigmented macules around eyes, mouth, hands, and genitalia — accentuated under Wood's lamp.
Differential diagnosis
- Tinea versicolor — Hypopigmented finely scaling macules on trunk; KOH 'spaghetti and meatballs'; Wood's lamp pale yellow
- Pityriasis alba — Ill-defined hypopigmented patches on face of children with atopy; mild scale; partial pigment loss
- Post-inflammatory hypopigmentation — History of preceding dermatitis/inflammation; not completely depigmented
- Tuberous sclerosis — Ash-leaf macules present at birth; epilepsy, intellectual disability, facial angiofibromas, shagreen patch
- Halo nevus — Pigmented nevus with surrounding depigmented ring; benign
- Idiopathic guttate hypomelanosis — Multiple small (2-5 mm) hypopigmented macules on sun-exposed extremities in older adults
- Lichen sclerosus — Porcelain-white atrophic plaques, especially genital and figure-of-eight perianal
- Hypopigmented mycosis fungoides — Adult-onset hypopigmented patches refractory to therapy; biopsy
Diagnostic workup
Diagnostic criteria
Clinical: characteristic acquired depigmented macules ± Wood's lamp confirmation.
Labs
- Clinical diagnosis — Wood's lamp confirms depigmentation
- TSH and TPO antibodies (screen autoimmune thyroid disease) at diagnosis and periodically (every 1-2 years)
- Consider CBC, B12, vitamin D, ANA based on symptoms/risk
- Skin biopsy rarely needed: absence of melanocytes on H&E and S-100/MART-1 stains
Imaging
- Not indicated
Diagnostic algorithm
| Pattern | Distribution | Course / Therapy Notes |
|---|---|---|
| Non-segmental (85-90%) | Symmetric — periorificial, hands, axillae, genitalia | Progressive; NBUVB + topical ruxolitinib / TCI / steroid |
| Segmental | Unilateral, dermatomal | 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 |
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
- Cosmetic camouflage: self-tanners (dihydroxyacetone), tinted concealers, micropigmentation
Rapidly progressive / active vitiligo
- Short courses of oral minipulse corticosteroids (dexamethasone 2.5 mg on 2 consecutive days/week × 3-6 months) to halt progression
- Combine with NBUVB phototherapy
Stable segmental or localized
- Surgical melanocyte transplantation: punch grafting, suction blister grafting, melanocyte-keratinocyte transplantation
- 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
- Associated autoimmune diseases — particularly autoimmune thyroid disease
- Ocular: uveitis, iritis, retinal pigmentary abnormalities (Vogt-Koyanagi-Harada syndrome)
- 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)
Practice Dermatology questions on FirstPassPA
Turn this outline into retention. 5,500+ board-style questions with an AI tutor that explains every answer — free to start, no card required.
Start studying free → Browse all 514 diagnosesEducational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA or PAEA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants; End of Rotation™ is a program of the Physician Assistant Education Association.