Vitiligo

Vitiligo is an acquired, chronic autoimmune skin disease in which the body's own CD8+ cytotoxic T cells progressively destroy epidermal melanocytes, producing well-demarcated, chalk- or milk-white depigmented macules and patches — not simply lighter skin, but skin with essentially no functioning melanocytes left in the affected area at all.^[1] Global prevalence is estimated at roughly 0.5-2.0% of the population, though this likely underrepresents the true burden given substantial underrecognition and undertreatment, particularly where access to dermatologic care is limited.^[2] Two clinically important subtypes exist, and telling them apart is central to this chapter: non-segmental (generalized) vitiligo — roughly 85-90% of cases, bilateral and symmetric, with an unpredictable relapsing-progressing course — and segmental vitiligo, unilateral and typically following a dermatomal or blaschkoid distribution, with early, rapid spread that usually stabilizes within its first year or two and then remains fixed.^[1] Vitiligo is genuinely more than a cosmetic concern: it carries a real, substantial psychosocial and mental-health burden — measurably higher rates of anxiety, depression, and suicidal ideation than the general population and than patients with many other skin diseases — a burden that is disproportionately greater in patients with darker skin tones, where the contrast between depigmented and normally pigmented skin is visually far more prominent.^[2] It is also a marker of broader autoimmune susceptibility: patients with vitiligo carry a meaningfully increased risk of other autoimmune disease, thyroid disease foremost among them, which is why deliberate screening — not just treatment of the skin itself — is part of comprehensive vitiligo care.^[2][3] This chapter covers subtype recognition and its prognostic implications, the autoimmune-comorbidity and mental-health screening this diagnosis should trigger, site-based topical first-line therapy (corticosteroids and calcineurin inhibitors), narrowband UVB phototherapy for more extensive disease, ruxolitinib cream — a genuinely new, specifically approved topical JAK-inhibitor treatment advance — and the camouflage, sun-protection, and psychosocial-support measures that are a legitimate, guideline-endorsed part of management rather than an afterthought.

What vitiligo actually looks like

The hallmark lesion is a sharply demarcated, chalk- or milk-white macule or patch, often oval or irregularly shaped, that enlarges over time and can coalesce with adjacent lesions into larger areas of depigmentation.^[1] A thin rim of intermediate, blended pigmentation — trichrome vitiligo — is sometimes visible at the advancing edge, most easily seen in patients with darker native skin tone, and small, punctate or "confetti-like" depigmented macules scattered around an established patch are a recognized marker of currently active, spreading disease rather than stable disease.^[1] Hair within a vitiligo patch can itself lose pigment — poliosis (a localized patch of white hair) or leukotrichia — and its presence is a marker of deeper, more difficult-to-reverse follicular melanocyte loss.^[1] A halo nevus (a mole with a surrounding ring of depigmentation) is a recognized associated finding and can be an early clue in a patient who will go on to develop more typical vitiligo.

Vitiligo of the hands in a person with dark skin — the depigmented patches are sharply demarcated, and the contrast against the surrounding normal skin tone is visually far more prominent than the same extent of disease would appear in lighter skin. (James Heilman, MD, CC BY-SA 3.0, Wikimedia Commons)

Poliosis — a localized patch of white hair overlying a vitiligo patch — reflects melanocyte loss within the hair follicle itself and is a common associated finding. (Culinary123, CC BY-SA 3.0, Wikimedia Commons)

The 2 clinical subtypes — a genuinely important distinction

Distribution and Koebnerization

Classic sites include periorificial skin (around the eyes, mouth, and nose), the hands and fingers, the genitals, and bony prominences subject to repeated friction or pressure (elbows, knees, ankles, and the dorsal hands/feet).^[1] New lesions frequently appear at sites of physical trauma, friction, or sunburn — the Koebner phenomenon — which is why counseling on trauma avoidance and diligent sun protection is a genuine part of preventing new lesions, not just a generic skin-health tip.^[2]

• Family history of vitiligo or of another autoimmune disease — vitiligo has a polygenic genetic architecture that substantially overlaps with genes implicated in other autoimmune conditions, which is the biological basis for its clustering with thyroid disease, type 1 diabetes, alopecia areata, and other autoimmune disorders within families.^[1][2]
• Personal history of another autoimmune disease, most importantly autoimmune thyroid disease — patients with vitiligo carry a roughly 2.5-fold increased risk of autoimmune thyroid disease and a more than 5-fold increased risk of positive thyroid autoantibodies compared with the general population.^[3]
• Koebner-prone triggers: physical trauma, friction, pressure, and sunburn at a given site can each precipitate a new lesion there.^[2]
• A halo nevus, which can precede or accompany more typical vitiligo.
• Patient-reported emotional or physical stress preceding onset or a flare is commonly described, though the evidence base for stress as a true precipitant — rather than a coincidentally timed association — is weaker than for the associations above.
• Occupational or product exposure to certain phenolic/catecholic chemicals (found in some rubber, adhesive, and industrial cleaning products) can produce a clinically similar but mechanistically distinct chemical/occupational leukoderma — worth asking about specifically when the distribution follows a plausible contact pattern rather than the classic sites above.

History

• Onset, duration, and progression pattern — has it spread recently, or been stable for a defined period? This distinction (active vs. stable disease) drives the entire treatment approach.
• Distribution pattern — unilateral/dermatomal versus bilateral/symmetric — and any association with a specific site of prior trauma, friction, or sunburn (Koebner).
• Family history of vitiligo or other autoimmune disease, and a personal review of systems for thyroid, glycemic, hematologic, and other autoimmune symptoms.^[2]
• Psychosocial impact — ask directly rather than assuming; validate the burden rather than treating it as something patients should simply accept, and screen for depression/anxiety using a standard tool when indicated.^[2]
• Skin type/Fitzpatrick phototype and cultural context, both of which meaningfully shape the visual and psychosocial impact of a given extent of disease and should shape the management conversation.^[2]

Examination

A Wood's lamp examination (365 nm UVA) is a simple, high-yield office tool: it makes fully depigmented vitiligo fluoresce a bright blue-white and sharpens border definition, which is especially useful in lighter skin types where the contrast with surrounding normal skin can otherwise be subtle, and helps confirm the true extent of disease before starting treatment.^[1] Baseline clinical photography (standard lighting/positioning, repeated at follow-up) is a genuinely valuable, low-cost way to track a process that changes too slowly for the patient — or the clinician — to reliably judge from memory alone.^[2] Examine for poliosis/leukotrichia, halo nevi, and, on general exam, for signs of an associated autoimmune condition (thyroid goiter, pallor).

Differential diagnosis

Screening for autoimmune comorbidity

Vitiligo itself is a clinical diagnosis and does not require laboratory confirmation, but the well-documented autoimmune clustering means baseline screening is a genuine, actionable part of a complete assessment rather than a routine reflex panel: TSH, generally paired with thyroid peroxidase (anti-TPO) antibodies given the specifically increased risk of autoimmune thyroid disease, is the single most useful test to obtain.^[3] Consider additional targeted testing (fasting glucose/HbA1c, CBC) when the history or review of systems points toward type 1 diabetes, pernicious anemia, or another specific associated condition, rather than ordering a broad autoimmune panel reflexively in every patient.^[2]

• Arrest progression in active/unstable disease before, or alongside, pursuing repigmentation.
• Achieve and, where treatment is pursued, maintain repigmentation, with realistic, explicitly set expectations about how slowly this process actually happens.
• Identify and appropriately refer coexisting autoimmune disease uncovered on screening, particularly thyroid disease.
• Recognize, screen for, and address the substantial psychosocial and mental-health burden of vitiligo as a core management target, not a secondary concern.
• Protect the skin — both to reduce sunburn risk in fully unprotected depigmented areas and to limit new-lesion formation via Koebnerization.
• Support fully informed patient choice among medical repigmentation therapy, camouflage, and, rarely, depigmentation, respecting that a patient's own priorities — not only objective disease extent — should drive the plan.
• Minimize relapse through appropriate maintenance therapy once repigmentation is achieved.

• Camouflage — color-matched, water-resistant camouflage cosmetics and dihydroxyacetone-based self-tanners, which temporarily stain depigmented skin to reduce visual contrast, are explicitly endorsed as appropriate management, usable either as monotherapy for patients who prioritize immediate cosmetic coverage over a months-long medical trial, or as an adjunct alongside medical treatment; counsel realistically that these methods can be genuinely effective but also time-consuming and costly for some patients.^[2]
• Sunscreen — genuinely essential counseling, not a routine afterthought: depigmented skin has no functioning melanocytes and therefore no natural UV protection at all, so affected areas both sunburn far more readily than surrounding normal skin and stand out in starker contrast whenever unaffected skin tans while depigmented skin cannot. Daily broad-spectrum SPF 30+ sunscreen, generously reapplied, plus sun-protective clothing and hats for patients with more extensive involvement, should be part of every management plan regardless of which medical therapy is chosen.^[2]
• Trauma/Koebner avoidance — minimize friction, tight clothing, and repeated pressure at affected or vulnerable sites, and treat any skin injury (including sunburn) promptly, since new lesions frequently arise exactly where the skin was recently traumatized.^[2]
• Psychosocial support — proactively discuss the real emotional burden of vitiligo, screen for depression and anxiety, and refer to counseling or a peer/patient support organization when appropriate; for pediatric and adolescent patients, involve caregivers and, where relevant, the school in supporting the child rather than leaving the burden solely on the patient.^[2]
• Patient education on the underlying biology and the genuinely slow pace of repigmentation — this single conversation does more to prevent a patient from abandoning an actually-working regimen too early than almost anything else in the visit.^[2]
• Localized micropigmentation (medical tattooing) can be considered for small, cosmetically sensitive, stable areas such as the lips in appropriately selected patients.
• Complementary and alternative therapies are commonly asked about but currently lack sufficient evidence to recommend; counsel patients accurately and non-dismissively rather than either endorsing or ridiculing their use.^[2]

Pregnancy

Breastfeeding

Topical corticosteroids and topical calcineurin inhibitors at recommended doses are compatible with breastfeeding; wash the area before the next feed if applying near the breast or nipple. Data on ruxolitinib cream during breastfeeding are limited; discuss with the prescriber. Narrowband UVB phototherapy is compatible with breastfeeding. Methotrexate is contraindicated during breastfeeding; other systemic agents require specialist input.

Pediatrics

Vitiligo very often begins in childhood or adolescence, and the psychosocial stakes are genuinely higher at this age given the documented risk of teasing, bullying, and self-consciousness — proactive screening and family/school-level support matter as much as the medical plan itself.^[2] Ruxolitinib cream is approved in Canada down to age 12, matching its pivotal trial population; it is not approved for younger children. Topical calcineurin inhibitors are commonly used off-label in younger children by dermatology at a lower concentration (tacrolimus 0.03%); favour the lowest effective topical corticosteroid potency and the shortest effective course given children's higher body-surface-area-to-weight ratio and thinner skin.

Older adults

The general approach does not otherwise change with age, but new-onset vitiligo — or a new flare of previously stable disease — in an older adult is still a reasonable prompt to screen for newly emerging autoimmune disease, and polypharmacy should be considered before starting any systemic option.

Darker skin tones

This deserves genuine, specific attention rather than a passing mention. Patients with Fitzpatrick IV-VI skin report a measurably greater psychosocial and quality-of-life burden from vitiligo than patients with lighter skin, driven directly by the far greater visual contrast between depigmented and normally pigmented skin at every extent of disease.^[2] Sun protection is proportionately more important for these patients specifically, since any tanning of unaffected skin further widens that contrast, in addition to the baseline sunburn risk depigmented skin carries regardless of skin tone. When potent or ultra-potent topical corticosteroids are used, the resulting risk of treatment-induced hypopigmentation is also more visually consequential and should be monitored for more vigilantly. Camouflage products historically had a narrower range of well-matched shades for deeper skin tones — an access and equity issue worth acknowledging directly with patients rather than assuming an off-the-shelf recommendation will serve them equally well, though the range of available shade-matched options has continued to expand. Above all, affirming, non-minimizing counseling — treating the visible impact of this disease as the genuinely significant issue it is for the patient in front of you, not as something to be talked out of caring about — is itself a meaningful part of care.^[2]

Set the follow-up interval around vitiligo's actual biology, not habit: repigmentation is inherently slow, and meaningful judgment of response — for any topical agent, ruxolitinib cream, or phototherapy — should wait until at least 3 months of adequate use, and often longer (ruxolitinib cream's own trial data show continued gains all the way through 52 weeks of continuous use).^[4][2] Baseline and serial standardized photography is a genuinely valuable, low-cost tool for tracking a process too gradual to reliably judge from memory or a single office visit.^[2]

1. Confirm the diagnosis first — reconsider the differential (pityriasis versicolor, postinflammatory hypopigmentation, chemical leukoderma, piebaldism, and the other mimics) if the distribution or course does not fit typical vitiligo.
2. Confirm an adequate trial was actually completed before concluding failure — "adequate" for vitiligo means months of correct, adherent use, not weeks; premature judgment of failure is a genuinely common and avoidable error given how slowly repigmentation happens.
3. Reassess disease activity specifically — if the disease is still actively spreading despite the current plan, address that activity directly (phototherapy, or a systemic mini-pulse/agent) before expecting the same regimen to also produce repigmentation.
4. Consider combining modalities — off-label combination of topical therapy with phototherapy, or with ruxolitinib cream, is supported over simply substituting one monotherapy for another.^[2]
5. Refer to dermatology for treatment-resistant, extensive, rapidly progressive, or diagnostically uncertain disease, and specifically to discuss surgical melanocyte-transplantation options for stable, localized, recalcitrant disease (particularly segmental vitiligo).
6. Revisit psychosocial and camouflage support regardless of medical treatment trajectory — quality-of-life support is not contingent on repigmentation succeeding, and should continue even if the medical plan needs to change.

• Judging a topical or light-based therapy a failure before an adequate multi-month trial has actually been completed — vitiligo's repigmentation biology is inherently slow, and premature discontinuation is one of the single most common reasons a genuinely effective plan appears not to work.
• Using a potent or ultra-potent topical corticosteroid continuously, without an intermittent schedule, over the many months vitiligo treatment typically requires, meaningfully raising the risk of atrophy and striae.
• Treating the face with a potent topical corticosteroid rather than a calcineurin inhibitor or ruxolitinib cream, given the combination of high absorption at this site and the length of therapy needed.
• Never screening for the well-documented autoimmune association — thyroid disease above all — or dismissing a patient's reported symptoms as unrelated.
• Treating vitiligo as "purely cosmetic" and failing to screen for or acknowledge its genuine, substantial psychosocial and mental-health burden, particularly in patients with darker skin tones and in pediatric/adolescent patients, for whom this burden is well documented to be greater.
• Omitting sunscreen counseling — depigmented skin has no natural UV protection whatsoever, and this is one of the most practical, easily overlooked points in the entire management plan.
• Assuming ruxolitinib cream, a topical calcineurin inhibitor, or a topical corticosteroid must be used strictly sequentially rather than considering earlier combination with phototherapy when disease is extensive.
• Missing active, still-spreading disease and treating only for repigmentation, rather than first addressing ongoing disease activity with a therapy actually aimed at arresting it.
• Treating a patient's interest in camouflage makeup or a self-tanner as a sign of poor psychological adjustment rather than the legitimate, guideline-endorsed management option it actually is.
• Overlooking surgical referral as an option for stable, localized, recalcitrant disease — particularly segmental vitiligo, which is often resistant to medical therapy alone but can respond well to grafting techniques.

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Topical Calcineurin Inhibitors

First-line for the face, eyelids, neck, and genital/flexural sites, and a reasonable choice anywhere a prolonged, atrophy-free course is preferred. Can be combined with phototherapy off-label, though product labeling specifically warns against concomitant intentional UV exposure.

Topical Corticosteroids

Use the lowest potency that controls the condition and an intermittent (e.g., 2-weeks-on/2-weeks-off) schedule for potent/ultra-potent agents, since vitiligo treatment courses typically run months rather than weeks.

Topical JAK Inhibitor

The only agent specifically approved by Health Canada for vitiligo repigmentation (October 2024), for nonsegmental vitiligo in patients 12 years and older, facial and non-facial disease.

Systemic Options for Unstable/Progressive Disease

All off-label; no systemic therapy is currently approved for vitiligo in Canada. Reserve for active, rapidly spreading disease specifically to arrest progression, not as a routine repigmentation strategy, and prefer dermatology-directed initiation and monitoring.

Camouflage, Sun Protection, and Depigmentation (Non-Drug/OTC)

Legitimate, guideline-endorsed parts of comprehensive management — appropriate as monotherapy or as an adjunct to medical treatment, not merely a cosmetic afterthought.