Vitiligo: Clinical Features, Pathogenesis, and Management Overview

Definition

Vitiligo is a chronic autoimmune depigmentation disorder causing well-defined white macules due to melanocyte destruction. Prevalence: 0.5–2% globally; onset often before age 30.

Clinical Hallmarks

• Chalk-white macules with sharp margins.
• Symmetrical distribution (non-segmental) or dermatomal (segmental).
• Koebner phenomenon: New lesions at trauma sites.
• Leukotrichia: White hair within patches (poor repigmentation prognosticator).
• Halo nevi: Perinevoid depigmentation.
• No symptoms: Typically asymptomatic; no scale, atrophy, or induration.

Pathogenesis (Multifactorial)

• Autoimmune: CD8+ T-cell mediated melanocyte killing (IFN-γ/CXCL10 axis).
• Genetic: >50 loci (NLRP1, PTPN22, MHC, TYR); 20% familial.
• Oxidative stress: Melanocyte redox imbalance (low catalase, high H₂O₂).
• Neural: Segmental pattern; neuropeptide dysregulation.

Associated Conditions

• Autoimmune thyroid disease (Hashimoto's, Graves') – 15–30%.
• Type 1 diabetes, pernicious anemia, Addison's, alopecia areata, psoriasis.
• Screen: TSH, anti-TPO, CBC, metabolic panel at diagnosis.

Management Algorithm

1. Confirm diagnosis: Clinical ± Wood's lamp (chalk-white fluorescence) ± biopsy if atypical.
2. Assess: Subtype, extent (BSA), activity (progressive vs. stable), impact (DLQI/VitiQoL).
3. Stabilize (if active): Topical TCI ± short-course oral steroid pulse; NB-UVB.
4. Repigment: Combine topical + phototherapy; excimer for localized; JAK inhibitors emerging.
5. Maintain: Taper to 1–2×/week topical or monthly NB-UVB.
6. Protect: Broad-spectrum SPF 50+ daily; avoid trauma.
7. Support: Psychosocial screening; refer to support organizations.