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 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 ketoconazole
BSystemic corticosteroids
COral methotrexate
DTopical tacrolimus
ENarrowband UVB phototherapy
Reveal answer & full explanation
Correct answer: D — Topical tacrolimus
ATopical ketoconazole
BSystemic corticosteroids
COral methotrexate
DTopical tacrolimus✓
ENarrowband UVB phototherapy
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)
Topical ketoconazole — tempting because tinea versicolor also causes asymptomatic light patches in young adults, but its macules are hypopigmented rather than depigmented, carry a fine scale, and favor the trunk and shoulders rather than periorificial and acral skin; an antifungal does nothing for the autoimmune melanocyte loss of vitiligo (confused-with tinea versicolor)
Additional high-yield points
Face and neck vitiligo respond best to treatment; acral and lip/tip areas respond least — set expectations early
Question 2DermatologyMedium
A 24-year-old woman presents with progressively enlarging white patches on her skin over the past 8 months. The lesions began around her eyes and mouth and have since appeared symmetrically on the dorsal hands and elbows. They are asymptomatic. Her history includes Hashimoto thyroiditis. On exam, there are several well-demarcated, completely chalk-white macules and patches without scale; under Wood's lamp examination the lesions fluoresce a bright milky-white. Which of the following is the most likely diagnosis?
AVitiligo
BTinea versicolor
CPityriasis alba
DPiebaldism
ETuberous sclerosis
Reveal answer & full explanation
Correct answer: A — Vitiligo
AVitiligo✓
BTinea versicolor
CPityriasis alba
DPiebaldism
ETuberous sclerosis
Why Vitiligo is correct
Acquired, progressive, completely depigmented (chalk/milky-white, not merely hypopigmented) macules in a symmetric periorificial and acral distribution (eyes, mouth, dorsal hands, elbows) is the classic non-segmental pattern.
Wood's lamp accentuation to a bright milky-white confirms true depigmentation (loss of functional melanocytes), distinguishing it from hypopigmented mimics.
The personal history of autoimmune thyroid disease (Hashimoto) fits the well-established association; guidelines recommend screening all vitiligo patients with TSH and TPO antibodies at diagnosis and periodically.
Why the others are wrong
Tinea versicolor — Malassezia overgrowth causing finely scaling hypopigmented (not depigmented) macules on the trunk; KOH shows "spaghetti and meatballs" and Wood's lamp gives a pale yellow, not milky-white, fluorescence.
Pityriasis alba — ill-defined hypopigmented patches with fine scale on the face of atopic children with only partial pigment loss; lacks the sharp, complete depigmentation and Wood's lamp accentuation seen here.
Tuberous sclerosis — produces hypopigmented ash-leaf macules that are present at birth rather than acquired and progressive, and is accompanied by epilepsy, intellectual disability, facial angiofibromas, and a shagreen patch, none of which are present in this otherwise well young woman.
Piebaldism — it also causes true depigmentation that accentuates under Wood's lamp, but it is an autosomal dominant congenital disorder with a white forelock and stable ventral and midline patches present from birth, not acquired, progressively enlarging periorificial and acral patches in a young adult.
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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) — ≥75% facial repigmentation (F-VASI75) in ~30% at 24 weeks and ~50% by 52 weeks; use limited to ≤10% BSA
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 of depigmented skin; skin cancer risk is NOT increased (epidemiologic studies surprisingly show equal or 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
IVTF 2023 — Seneschal J, et al. Worldwide expert recommendations for the diagnosis and management of vitiligo: Position statement from the International Vitiligo Task Force. Part 2: Specific treatment recommendations. J Eur Acad Dermatol Venereol 2023;37:2185-2195
VGICC 2012 — Ezzedine K, et al. Revised classification/nomenclature of vitiligo and related issues: the Vitiligo Global Issues Consensus Conference. Pigment Cell Melanoma Res 2012;25(3):E1-E13
FDA Ruxolitinib — FDA Approval of Topical Ruxolitinib 1.5% Cream for Nonsegmental Vitiligo (2022)
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