Vitiligo
Clinical Snapshot
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.
Recognize the Condition
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.
The 2 clinical subtypes — a genuinely important distinction
Non-segmental vs. segmental vitiligo
Non-segmental (generalized) vitiligo
The most common form, accounting for roughly 85-90% of cases. Distribution is bilateral and often symmetric, involving acrofacial sites, larger body regions (generalized/vulgaris), or, rarely, nearly the entire body surface (universal). The course is genuinely unpredictable — periods of activity and spread alternate with periods of relative stability, and disease can continue to evolve for years.[1] This is the subtype studied in essentially every major clinical trial, including the ruxolitinib cream program, and it is the only subtype ruxolitinib cream is specifically approved for.[4] It also carries the stronger, better-documented association with other autoimmune comorbidity.[2]
Segmental vitiligo
Unilateral, typically following a dermatomal or blaschkoid distribution rather than crossing the midline. Onset is often earlier in life than non-segmental disease, spread is usually rapid at first, and the disease then characteristically stabilizes — often within about 1-2 years — and remains fixed thereafter.[1] Poliosis is disproportionately common in segmental disease. Evidence for medical (topical/light-based) treatment response is more limited than for non-segmental disease, and segmental vitiligo is often comparatively resistant to these therapies — but precisely because it is clinically stable, it may respond particularly well to surgical melanocyte-transplantation techniques once the disease has been stable long enough to be a surgical candidate.[2]
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]
Risk Factors
- 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.
Red Flags & Refer
Most vitiligo is appropriate for outpatient, primary-care-initiated topical management with dermatology involvement as needed, but escalate assessment for any of the following:
- Rapidly progressive or actively spreading disease (new lesions, enlarging existing patches, confetti-like punctate lesions) — this needs prompt attention to arrest progression rather than a "wait and see" approach, since active disease responds to disease-modifying treatment in a way that already-stable depigmentation does not.[2]
- Extensive body-surface-area involvement, or involvement of highly visible or functionally/psychologically sensitive sites (face, hands, genitals) with a significant reported quality-of-life impact — refer earlier rather than exhausting a slow stepwise topical trial alone.
- Symptoms suggesting an associated autoimmune condition: unexplained fatigue, weight change, heat or cold intolerance, palpitations, or neck swelling (thyroid disease); polyuria, polydipsia, or unexplained weight loss (type 1 diabetes); patchy hair loss (alopecia areata); or unexplained fatigue, glossitis, or neurologic symptoms (pernicious anemia) — screen and refer as indicated rather than treating the skin in isolation.[2][3]
- Any indication of significant depression, anxiety, or suicidal ideation — the documented mental-health burden of vitiligo is real and substantial, and this warrants the same urgency it would for any other cause.[2]
- Diagnostic uncertainty, particularly a presentation that does not fit the classic distribution or that raises concern for an alternative diagnosis (see Assessment & Diagnosis).
- A new, solitary, irregular, or rapidly changing depigmented/hypopigmented lesion in an older adult, especially with an atypical or asymmetric border — while most halo phenomena around a pigmented lesion are benign halo nevi, a halo or regression-like pattern around an atypical pigmented lesion warrants dermatologic evaluation to exclude a regressing melanoma before it is assumed to be routine vitiligo.
- Pediatric or adolescent onset — coordinate care proactively given the documented risk of teasing, bullying, and self-consciousness in this age group, and involve caregivers in psychosocial support planning from the outset.[2]
Assessment & Diagnosis
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
| Condition | Features that point away from vitiligo |
|---|---|
| Pityriasis versicolor (tinea versicolor) | Fine, often subtle scale on close inspection; coral-orange fluorescence on Wood's lamp (vitiligo fluoresces blue-white); confirm with KOH microscopy if uncertain. |
| Pityriasis alba | Ill-defined (not sharply demarcated) hypopigmentation, not true depigmentation; fine scale; most common on the face in children and adolescents; typically self-limited. |
| Postinflammatory hypopigmentation | A preceding inflammatory skin condition (eczema, psoriasis) at the same site; incomplete pigment loss (hypo-, not depigmentation); gradually repigments on its own. |
| Idiopathic guttate hypomelanosis | Small (2-5 mm), stable, sharply defined macules on chronically sun-exposed extremities in older adults; does not enlarge or spread the way active vitiligo does. |
| Chemical/occupational leukoderma | Distribution follows a plausible contactant/occupational exposure pattern (gloves, chemical handling) rather than the classic vitiligo-prone sites; history of phenolic/catecholic compound exposure. |
| Piebaldism | Congenital (present since birth), stable, non-progressive; classically includes a white forelock; family history of the same pattern. |
| Tuberous sclerosis (ash-leaf macules) | Hypopigmented (not fully depigmented), ash-leaf- or confetti-shaped macules present from infancy; look for other stigmata (facial angiofibromas, developmental history) and a family history. |
| Halo nevus alone | A single pigmented nevus with a surrounding ring of depigmentation and no other lesions elsewhere; can precede or accompany true vitiligo but is not itself vitiligo. |
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]
Treatment Targets
- 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.
Choose Initial Treatment
Step 1 — match first-line topical therapy to body site
Topical corticosteroids, topical calcineurin inhibitors, and ruxolitinib cream are all considered appropriate first-line monotherapy for any form of vitiligo, and the choice between them is driven mainly by body site and by the fact that effective vitiligo treatment requires months, not days, of continued application.[2]
Face, eyelids, neck, and genital/flexural skin a topical calcineurin inhibitor — tacrolimus 0.1% ointment (0.03% in children) or pimecrolimus 1% cream, applied twice daily — is preferred at these sites specifically because it carries no atrophy risk even with the prolonged courses vitiligo treatment demands, unlike a topical corticosteroid used continuously for months at the same site.[2] A low-potency topical corticosteroid (e.g., hydrocortisone) is a reasonable alternative where a calcineurin inhibitor is unavailable or not tolerated.
Trunk and limbs a potent topical corticosteroid (e.g., betamethasone dipropionate 0.05%) applied on an intermittent schedule — commonly 2 weeks on, 2 weeks off — which meaningfully mitigates the atrophy and striae risk that continuous use over the many months vitiligo treatment requires would otherwise carry.[2] A topical calcineurin inhibitor or ruxolitinib cream are equally reasonable first-line alternatives here.
Resistant, thicker, or localized trunk/limb lesions not responding to a potent-corticosteroid trial an ultra-high-potency agent (e.g., clobetasol propionate 0.05%) for a limited course, stepping back down once response begins.
Step 2 — ruxolitinib cream as a genuinely current first-line option
Ruxolitinib cream 1.5% is a topical Janus kinase 1/2 (JAK1/JAK2) inhibitor and is the only topical agent specifically approved by Health Canada for repigmentation of nonsegmental vitiligo, in patients 12 years of age and older, for both facial and non-facial disease — approved in October 2024 on the strength of the TRuE-V1/TRuE-V2 phase 3 trial program.[4] It directly interrupts the interferon-γ-CXCL9/CXCL10-JAK-STAT signaling loop that autoreactive T cells use to recruit and amplify the attack on melanocytes — the specific immune pathway now understood to drive vitiligo — rather than simply suppressing inflammation nonspecifically, and its approval represents the first mechanistically targeted, vitiligo-specific medical therapy.[4][2] In the two pivotal trials, facial repigmentation (F-VASI75, at least 75% improvement in the facial Vitiligo Area Scoring Index) at 24 weeks was achieved by 29.8% and 30.9% of ruxolitinib-treated patients versus 7.4% and 11.4% on vehicle cream (P<0.001 in both trials), and with continued twice-daily use this rose to 52.6% and 48.0% by week 52 — response genuinely builds slowly and keeps building well past the first few months.[4] Apply a thin layer to affected areas (up to about 10% of body surface area, matching the population studied) twice daily; the most common adverse effects are application-site acne (about 6%), application-site pruritus (about 5%), and nasopharyngitis (about 5-6%), generally mild to moderate.[4]
Step 3 — phototherapy for more extensive disease
Narrowband UVB (NB-UVB, 311-313 nm) is the current evidence-preferred phototherapy modality for vitiligo — safer and more effective than broadband UVB, PUVA, or UVA1 — and is appropriate alone or combined with topical therapy for more extensive or generalized disease.[2] Vitiligo phototherapy is a genuinely protracted commitment: sessions 2-3 times weekly for a minimum of 6-12 months before response is fully assessed, then stepped down to 1-2 times weekly maintenance once repigmentation is achieved, or discontinued if response is adequate.[2] Excimer laser/lamp (308 nm) delivers the same targeted UVB wavelength to a smaller field and is a reasonable option for more localized disease. Do not combine a topical calcineurin inhibitor with intentional/therapeutic UV exposure without discussing the product's specific warning against this combination with the patient — the theoretical concern is a possible interference with the skin's own UV-damage response — even though off-label combination under specialist supervision is a described practice.[2]
Step 4 — systemic therapy specifically to arrest rapidly progressive disease
For unstable, rapidly spreading disease, an off-label systemic agent can be used specifically to halt progression — not as a routine repigmentation strategy — since no systemic therapy is currently approved for vitiligo in Canada.[2] A low-dose weekend oral corticosteroid "mini-pulse" — the best-described regimen uses betamethasone or dexamethasone 5 mg as a single oral dose on 2 consecutive days each week, typically continued for 3-6 months — arrested progression within 1-3 months in about 89% of patients with active disease in the original published series, with weight gain as the most frequent adverse effect.[5] Cyclosporine, methotrexate, azathioprine, and minocycline are alternative off-label options described for the same indication and should be reserved for dermatology-directed use given their respective toxicity and monitoring requirements.[2]
Step 5 — maintenance therapy once repigmentation is achieved
Relapse is common — disease often recurs within about 2 years of stopping therapy — so a deliberate maintenance plan (for example, continuing a topical agent at a reduced frequency) meaningfully reduces relapse risk and should be discussed before treatment is simply stopped once the patient is satisfied with the result.[2]
Step 6 — surgical referral for stable, localized, recalcitrant disease
For disease that has been clinically stable for at least about 12 months and has not responded to an adequate trial of topical/phototherapy, surgical melanocyte-transplantation techniques (cellular suspension or punch grafting, suction blister grafting, or needling) can achieve repigmentation that medical therapy cannot, and may be a particularly good option for segmental vitiligo specifically, since this subtype is both classically stable and often resistant to non-surgical therapy.[2] These techniques are not widely accessible in Canada, so referral to a centre with this expertise is appropriate rather than an assumption that it is broadly available.[2]
Non-Pharmacologic Treatment
- 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]
Special Populations
Pregnancy
Low-to-mid-potency topical corticosteroids and topical calcineurin inhibitors are reasonable choices in pregnancy given their minimal systemic absorption at recommended use; reserve high- and ultra-high-potency corticosteroids, and any prolonged large-surface-area use, for genuine need. Data specifically on ruxolitinib cream in human pregnancy are limited; given minimal systemic absorption at recommended topical use it is not expected to pose a major risk, but its use in pregnancy should be a shared decision with the prescriber rather than a default choice. Narrowband UVB phototherapy is generally considered compatible with pregnancy. Methotrexate is contraindicated in pregnancy (teratogenic); cyclosporine and azathioprine may be continued when the maternal benefit clearly outweighs the risk, but only under specialist direction. For most patients, actively treating vitiligo is reasonably deprioritized during pregnancy in favour of other clinical priorities, and this is a legitimate, not a neglectful, choice.
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]
Monitoring & Follow-Up
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]
Common Errors to Avoid
- 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.
Clinical Decision Algorithm
Drug Tables
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.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Tacrolimus, topical ointment 0.03%/0.1% | Dosing: Apply BID | Local burning/stinging, especially early in treatment; rare, unconfirmed theoretical malignancy signal noted on product labeling | None clinically significant given minimal systemic absorption at recommended use | 0.1% for adults, 0.03% for children. No atrophy risk even with prolonged use — the preferred agent for face/eyelids/genitals. |
| Pimecrolimus, topical cream 1% | Dosing: Apply BID | Local burning/stinging, generally milder than tacrolimus | None clinically significant given minimal systemic absorption at recommended use | Alternative to tacrolimus for sensitive sites; may be better tolerated in some patients. |
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.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Hydrocortisone 1-2.5%, topical | Dosing: Apply once or twice daily | Local burning/stinging; atrophy uncommon at this potency | None clinically significant given minimal systemic absorption | Low potency. Reasonable alternative to a calcineurin inhibitor for the face/eyelids/genitals where one is unavailable or not tolerated. |
| Desonide, topical 0.05% | Dosing: Apply once or twice daily | Local burning/stinging; atrophy and striae uncommon at this potency | None clinically significant given minimal systemic absorption | Low-mid potency. A reasonable sensitive-site alternative, including in young children. |
| Betamethasone dipropionate 0.05%, topical | Dosing: Apply BID during "on" weeks of a 2-weeks-on/2-weeks-off schedule | Striae, telangiectasia, atrophy with prolonged continuous use | None clinically significant given minimal systemic absorption | Potent topical corticosteroid; 1st-line agent for trunk/limb lesions used on an intermittent schedule. |
| Clobetasol propionate 0.05%, topical | Dosing: Apply once or twice daily for a limited course, then step down | Skin atrophy, striae, telangiectasia; higher risk given the prolonged courses vitiligo treatment needs | None clinically significant with topical use at recommended doses | Ultra-high potency. Reserve for resistant or thicker localized trunk/limb lesions not responding to a potent-agent trial; avoid the face and flexures. |
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.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Ruxolitinib, topical cream 1.5% | Dosing: Apply a thin layer BID to affected areas, up to about 10% BSA | Application-site acne (~6%), application-site pruritus (~5%), nasopharyngitis (~5-6%); generally mild-moderate; no major cardiovascular events or deaths seen through 2 years of pooled trial follow-up | None clinically significant given minimal systemic absorption at recommended topical use | JAK1/JAK2 inhibitor interrupting the interferon-γ-CXCL9/CXCL10-JAK-STAT signaling loop central to vitiligo pathogenesis. F-VASI75 at week 24: 29.8%/30.9% (TRuE-V1/V2) vs. 7.4%/11.4% vehicle, P<0.001; rising to 52.6%/48.0% by week 52 with continued use. |
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.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Betamethasone or dexamethasone, oral mini-pulse | Regimen: 5 mg PO single dose after breakfast on 2 consecutive days/week, typically for 3-6 months | Weight gain (most common); insomnia, mood change, hyperglycemia with longer courses | Numerous — review the full interaction profile even for an intermittent regimen | The best-described regimen for arresting rapidly spreading disease. No oral tablet monograph matching this specific low-dose weekly regimen currently exists in the Pharmasist Drug Database, so named as text only. |
| Cyclosporine | Dosing: Per dermatology-directed protocol | Nephrotoxicity, hypertension, increased infection risk | Numerous — CYP3A4 substrate with many clinically significant interactions | Alternative when an oral corticosteroid pulse is contraindicated or ineffective; requires renal-function/blood-pressure monitoring. |
| Methotrexate | Dosing: Weekly, per dermatology-directed protocol | Hepatotoxicity, myelosuppression; teratogenic | NSAIDs, trimethoprim-sulfamethoxazole, and other folate-antagonist or nephrotoxic drugs increase toxicity risk | Requires folic acid supplementation and baseline/periodic CBC and LFT monitoring; contraindicated in pregnancy. |
| Azathioprine | Dosing: Per dermatology-directed protocol | Myelosuppression, hepatotoxicity, GI upset | Allopurinol markedly increases toxicity; interacts with other myelosuppressive agents | Check TPMT/NUDT15 status before starting where available; slower onset of effect than other options here. |
| Minocycline | Dosing: 100 mg PO BID, typically for up to 3-6 months | Photosensitivity; rare drug-induced lupus-like reaction, hepatotoxicity, or DRESS with prolonged use; can itself rarely cause a distinct blue-gray skin/mucosal pigmentation | Reduced absorption with divalent/trivalent cation products (antacids, iron, calcium); may reduce oral contraceptive efficacy | A comparatively better-tolerated systemic option specifically studied for halting rapidly progressive nonsegmental vitiligo, though still off-label. |
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.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Broad-spectrum sunscreen, SPF 30+ | Use: Apply daily to affected areas and reapply per product directions; pair with sun-protective clothing/hats for extensive disease | Occasional local irritation/allergic contact dermatitis to a specific formulation | None significant | Genuinely essential, not optional: depigmented skin has no natural UV protection at all. No Pharmasist Drug Database monograph exists for sunscreen as a product category; named as text only. |
| Camouflage cosmetics / DHA-based self-tanner | Use: Apply per product directions; self-tanners typically need reapplication every few days as they fade | Occasional local irritation; uneven staining with self-tanners if applied incorrectly | None significant | Endorsed as appropriate monotherapy or adjunct management; counsel on realistic cost/time expectations. No Pharmasist Drug Database monograph exists for these OTC cosmetic products; named as text only. |
| Monobenzone (depigmentation) | Use: Per dermatology-directed protocol only | Permanent, irreversible depigmentation of remaining normally pigmented skin; contact dermatitis; depigmentation at sites of contact beyond where applied | None significant | Reserved for exceptional cases of extensive, treatment-resistant disease where the patient prefers uniform depigmentation over further repigmentation attempts; should only be prescribed by a dermatologist experienced with this therapy. No Pharmasist Drug Database monograph exists; named as text only. |
References
- Vitiligo — The Lancet (Ezzedine K, Eleftheriadou V, Whitton M, van Geel N). Lancet 2015;386(9988):74-84
- Canadian Consensus Guidelines for the Management of Vitiligo — Dermatology and Therapy (Prajapati VH, Lui H, Miller-Monthrope Y, Ringuet J, Turchin I, Hong HC-h, Lynde C, Papp KA, Yeung J, Gooderham MJ). Dermatol Ther (Heidelb) 2025;15(6):1351-1369
- The Prevalence of Thyroid Disease in Patients With Vitiligo: A Systematic Review — British Journal of Dermatology (Vrijman C, Kroon MW, Limpens J, Leeflang MMG, Luiten RM, van der Veen JPW, Wolkerstorfer A, Spuls PI). Br J Dermatol 2012;167(6):1224-1235
- Two Phase 3, Randomized, Controlled Trials of Ruxolitinib Cream for Vitiligo — New England Journal of Medicine (Rosmarin D, Passeron T, Pandya AG, et al.). N Engl J Med 2022;387:1445-1455
- Oral Mini-Pulse Therapy With Betamethasone in Vitiligo Patients Having Extensive or Fast-Spreading Disease — International Journal of Dermatology (Pasricha JS, Khaitan BK). Int J Dermatol 1993;32(10):753-757
Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.