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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Question 1DermatologyMedium
A 28-year-old male has a 4-year history of white patches on his bilateral dorsal hands and face that have expanded slowly over time. Vitiligo is confirmed on Wood lamp examination. He is distressed about his appearance. Which of the following is the most appropriate initial therapy?
ANarrowband UVB phototherapy
BTopical tacrolimus
CSystemic corticosteroids
DExcimer laser
Reveal answer & full explanation
Correct answer: B — Topical tacrolimus
ANarrowband UVB phototherapy
BTopical tacrolimus✓
CSystemic corticosteroids
DExcimer laser
Why Topical tacrolimus is correct
Vitiligo is caused by autoimmune destruction of melanocytes
For limited vitiligo (under 10% body surface area (BSA)), first-line options are topical corticosteroids or topical calcineurin inhibitors (tacrolimus, pimecrolimus)
Topical calcineurin inhibitors such as tacrolimus are preferred for the face and sensitive areas given their favorable side-effect profile compared to topical corticosteroids
This patient has bilateral dorsal hands and face involvement; the face component makes tacrolimus the preferred initial choice
Why the others are wrong
A) Narrowband UVB phototherapy — narrowband ultraviolet B (NB-UVB) phototherapy (311-313 nm) is most effective for widespread (extensive) vitiligo, stimulating melanocyte migration and proliferation; it is not the initial therapy for limited disease
C) Systemic corticosteroids — systemic corticosteroids carry significant side-effect risk and are not standard first-line therapy for limited vitiligo
D) Excimer laser — excimer laser is a targeted phototherapy option, generally used when topical agents and field phototherapy have been tried
Ruxolitinib cream 1.5%: first FDA-approved topical Janus kinase 1/2 (JAK1/2) inhibitor for non-segmental vitiligo (approved 2022)
Afamelanotide implant plus NB-UVB: used for darker skin types
Cosmetic options: camouflage makeup, self-tanners
Realistic expectations: repigmentation takes 3-12 months; face and neck respond best; hands and feet respond poorly
Question 2DermatologyMedium
A 31-year-old woman presents 8 weeks postpartum for evaluation of new patchy skin depigmentation involving the dorsa of her hands, periorbital skin, and perioral area. The patches are well-demarcated, asymptomatic, and milky-white; Wood lamp examination accentuates the depigmentation. She is not breastfeeding and uses condoms for contraception. She has no other medical problems. Which of the following is the most appropriate initial treatment?
ATopical tacrolimus
BNarrowband UVB phototherapy
COral methotrexate
DSystemic corticosteroids
Reveal answer & full explanation
Correct answer: A — Topical tacrolimus
ATopical tacrolimus✓
BNarrowband UVB phototherapy
COral methotrexate
DSystemic corticosteroids
Why Topical tacrolimus is correct
This patient has nonsegmental vitiligo involving the face and acral surfaces — an autoimmune destruction of melanocytes that can be triggered or exacerbated by the postpartum immunologic shift
For limited disease, especially on the face and other sensitive sites, topical calcineurin inhibitors (tacrolimus, pimecrolimus) are first-line
They are preferred over potent topical steroids because they avoid skin atrophy and telangiectasias with prolonged use
Topical tacrolimus is safe, effective, and well-tolerated for facial and limited vitiligo
Because she is not breastfeeding, the usual lactation cautions around systemic agents do not apply, but initial therapy is still topical for limited disease
Why the others are wrong
Narrowband UVB phototherapy — an excellent option for widespread or treatment-resistant vitiligo but not initial therapy for a few facial/acral patches, and logistically demanding (2-3 sessions/week) (right-concept-wrong-setting)
Oral methotrexate — reserved for rapidly progressive or extensive vitiligo refractory to first-line therapy; disproportionate for limited disease (overtreatment)
Systemic corticosteroids — sometimes used as oral mini-pulse therapy for rapidly progressive disease, but the adverse-effect profile makes them inappropriate as initial treatment of limited stable vitiligo (overtreatment)
Additional high-yield points
Face and neck vitiligo respond best to treatment; acral and lip/tip areas respond least — set expectations early
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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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