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Dermatology & Immunology & Family Medicine

Vitiligo | Clinique Omicron Québec

Vitiligo is an inflammatory, autoimmune skin disease - the most common cause of acquired depigmentation worldwide - characterized by the selective destruction of cutaneous and follicular melanocytes by activated cytotoxic CD8+ T lymphocytes + leading to the appearance of achromic macules and plaques (milky white + then pure white) + with well-defined contours + on a background of normal-colored skin. With a worldwide prevalence of 0.5 to 2 % of the population + an even distribution between genders and ethnic groups + and onset often in the second or third decade of life (50 % of cases start before the age of 20) + vitiligo is one of the most psychosocially impacting dermatoses - particularly in dark-skinned people, where the contrast with healthy skin is maximal. The pathophysiology is now well established as autoimmune: activation of melanocyte-specific cytotoxic CD8+ T lymphocytes → destruction of melanocytes via the perforin-granzyme + pathway and by IFN-γ → JAK1/JAK2 → CXCL9/CXCL10 signaling → recruitment of new T lymphocytes → maintenance of the autoimmune loop + with a strong genetic component (heritability estimated at 75-80 %) and significant associations with other autoimmune diseases (Hashimoto's thyroiditis + Graves' disease + type 1 diabetes + rheumatoid arthritis + lupus + alopecia areata + psoriasis). Understanding the JAK-STAT pathway in the pathogenesis of vitiligo has paved the way for JAK inhibitors - ruxolitinib (Opzelura®) + FDA 2022 approval - which are the first targeted therapy approved specifically for non-segmental vitiligo + representing a major advance in the management of a disease long lacking effective treatments.

Clinical classification

  • Non-segmental vitiligo (VNS - most frequent form: 85-90 %): bilateral + symmetrical distribution + progressive extension + lesions on any body area + predilection for areas of friction and trauma (Koebner phenomenon - appearance of new macules at sites of cutaneous trauma) + periorificial areas (mouth + eyes + nostrils) + extremities + genitals + frequent association with other autoimmune diseases
  • Segmental vitiligo (VS - 10-15 %) : unilateral distribution + limited to one or more dermatomes + often early onset (child) + rapid evolution then stabilization + not as frequently associated with systemic autoimmune diseases + early involvement of hair follicles (leukotrichia = white hairs in the affected area - poor prognosis for repigmentation) + more resistant to treatments
  • Universal vitiligo : depigmentation of more than 80 % of the body surface + extreme form of VNS
  • Active (expanding) vitiligo : appearance of new lesions + extension of existing plaques + Koebner's phenomenon present → stage requiring systemic immunosuppressive treatment to halt extension
  • Wood lamp : examination under ultraviolet light (UVA 365 nm) in a darkened room → achromic macules turn a brilliant fluorescent white → allows precise delineation of lesions + detection of subclinical lesions + and distinction of vitiligo from other causes of depigmentation

Treatment

Treatment Indication Efficiency and protocol Remarks
Topical dermocorticoids (1st line - localized lesions) VNS localized + active + trunk and limb lesions Clobetasol 0.05 % (Dermovate®) or betamethasone 0.1 % pulsed (5 d/wk × 3 months) → 40-60 % repigmentation of treated lesions + characteristic perifollicular repigmentation (islets of pigment around follicles) Risk of skin atrophy + telangiectasias + stretch marks if used for a long time → avoid the face + folds → use less potent formulations on the face (mometasone 0.1 %)
Topical calcineurin inhibitors (TCIs) Face + neck + folds + sensitive areas + children Tacrolimus 0.1 % (Protopic®) + or pimecrolimus 1 % (Elidel®) × 2/d → repigmentation 50-75 % on the face + better tolerance profile than corticoids on sensitive areas + no skin atrophy Treatment of choice for face and folds + may sting on application → fades over time + no atrophy + less effective on extremities
Ruxolitinib cream 1.5 % (Opzelura®) - JAK1/JAK2 inhibitor Non-segmental vitiligo >10 % surface + adult ≥12 years old 2 applications/d + FDA 2022 approval + Health Canada in progress → repigmentation 30 % of facial surface (primary TRuE-V endpoint) at 24 weeks vs 8 % placebo + better efficacy on face + modest results on extremities First topical JAK inhibitor approved for vitiligo + mechanism: blockade of IFN-γ → JAK-STAT pathway → reduced cytotoxic signal against melanocytes + high cost + local adverse effects (acne + nasopharyngitis)
Narrow-spectrum UVB phototherapy (NB-UVB - 311 nm) Extensive VNS (>5-10 % surface) + active + or localized VNS refractory to topical therapy 2-3 sessions/week × 6-24 months + significant repigmentation in 50-75 % of cases + best repigmentation on face + trunk + worse on extremities and lips + can be combined with tacrolimus (synergy) Reference treatment for extensive forms + can be done in a phototherapy center or at home (equipment available) + risk of photoaging + photocarcinogenesis with prolonged use.
Systemic corticosteroid minipulse (stop extension) VNS rapidly expanding + active + Koebner phenomenon present Dexamethasone 2.5 mg × 2/week (non-consecutive) × 3-6 months + or methylprednisolone 8 mg/d × 2 d/month → effective in stopping extension + less effective in inducing repigmentation Short-term treatment to stabilize active disease + phototherapy relay + adverse effects of systemic corticoids
Melanocyte transplants (stable forms) Stable vitiligo for ≥ 2 years + segmental + lesions resistant to medical treatment Non-cultured epidermal graft (NCES) + or melanocyte cultures → repigmentation 80-95 % on stable forms + long-lasting results Reserved for specialized centers + only if vitiligo is stable (otherwise inevitable recurrence on graft).

Screening for associated autoimmune diseases

  • Systematic check-up recommended: TSH + anti-TPO (Hashimoto's thyroiditis - the most frequent association: 15-30 % of patients with vitiligo) + fasting blood glucose + HbA1c (type 1 diabetes) + CBC (Biermer anemia + frequent association) + vitamin B12 + intrinsic factor if anemia
  • Other associations to look for if clinical symptoatology : ANA + anti-dsDNA (lupus) + antiadrenal antibodies (Addison's disease - rare but serious association) + anti-CCP antibodies + RF (rheumatoid arthritis)
ℙ️ Segmental vitiligo differs from non-segmental vitiligo in several important respects: it is unilateral + limited to one or a few dermatomes + spreads rapidly, then stabilizes + reaches the hair follicles early (leukotrichia - white hairs in the area - a poor prognostic sign for repigmentation, as follicular melanocytes are the source of repigmentation under treatment) + and responds less well to phototherapy and topicals. Leukotrichia (white hairs in a vitiligo macule) is a poor prognostic sign: if all follicular melanocytes are destroyed, spontaneous repigmentation or repigmentation under treatment is highly unlikely.
Medical consultation recommended

Consult a physician or dermatologist if white macules appear and spread rapidly over the skin + particularly if they appear in the context of stress or skin trauma (Koebner's phenomenon) + or if they are accompanied by fatigue + weight gain + or thyroid symptoms (frequent association with Hashimoto's thyroiditis). For diagnosis of vitiligo (Wood's lamp) + autoimmune assessment + and initiation of topical treatment or referral to phototherapy, Clinique Omicron offers medical consultations at its points of service in Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.

Consult at Clinique Omicron

Clinique Omicron's specialized physicians and nurse practitioners (IPS) diagnose vitiligo by clinical examination and Wood's lamp, distinguishing it from other causes of depigmentation (pityriasis versicolor + piébaldism + scleroderma), prescribe the appropriate initial topical treatment (dermocorticoids + tacrolimus, depending on location), check for associated autoimmune diseases (TSH + anti-TPO + glycemia), refer extensive forms to dermatology for NB-UVB phototherapy, and provide psychological follow-up if necessary. Consultations are available at several points of service in Quebec, and via telemedicine. To book an appointment, visit cliniqueomicron.ca.

The content of this page is provided for information purposes only and does not replace the advice of a physician or dermatologist. Leukotrichia (white hairs in a vitiligo macule) is a poor prognostic sign for repigmentation under treatment, as follicular melanocytes - the source of repigmentation - are destroyed. Segmental vitiligo responds less well to treatment than non-segmental vitiligo.

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