Vitiligo: Clinical Overview, Impact, and Treatment Landscape

What Is Vitiligo?

An acquired, chronic autoimmune disorder causing patchy loss of skin pigment due to melanocyte destruction. Affects 0.5–2% of population; median onset 20s; equal sex distribution.

Clinical Features

• Well-circumscribed, chalk-white macules/patches.
• Common sites: face (periorificial), neck, hands, feet, genitalia, body folds.
• Symmetrical (non-segmental) or dermatomal (segmental).
• Leukotrichia (white hair) in patches = poorer repigmentation prognosis.
• Koebner phenomenon: trauma induces new lesions.
• Asymptomatic (no itch/pain); sun sensitivity in depigmented areas.

Psychosocial Impact

• Significant QoL impairment: stigma, anxiety, depression, social avoidance.
• VitiQoL and DLQI scores correlate with extent, visibility, cultural factors.
• Higher impact in darker skin tones due to contrast.

Treatment Landscape

Category	Examples	Role
Topical	TCIs (tacrolimus, pimecrolimus), steroids, calcipotriene, ruxolitinib 1.5% cream	First-line for limited disease; face/neck preferred
Phototherapy	NB-UVB (2–3×/wk), excimer laser (308 nm)	Gold standard for generalized; home units improve adherence
Systemic	Oral mini-pulse steroids, JAK inhibitors (tofacitinib, upadacitinib)	Rapidly progressive / extensive disease
Surgical	Grafting (suction blister, MKTP)	Stable disease only (no new lesions × 1 yr)
Depigmentation	Monobenzone 20%	>50% BSA, patient choice; irreversible
Camouflage	High-coverage makeup, self-tanners	Immediate cosmetic improvement

Key Principles

• Early treatment → better outcomes.
• Combination therapy > monotherapy.
• Sun protection is non-negotiable (SPF 50+ daily).
• Address psychosocial burden proactively.