Vitiligo

Specialty: Skin.

• achromic plates
• delimited white spots
• acquired leukoderma

Why it occurs

• Selective autoimmune destruction of melanocytes mediated by active CD8+ cytotoxic T lymphocytes
• Theory of intracellular oxidative stress (accumulation of reactive oxygen species that induce melanocyte apoptosis)
• Neural theory (release of toxic neurochemical mediators in epidermal nerve endings)
• Polygenic genetic predisposition associated with histocompatibility genes (HLA)
• Koebner phenomenon induced by friction or constant physical trauma to the skin.

Initial workup

Clinical evaluation with Wood's light (which reveals bright chalk-white fluorescence and precisely delineates subclinical lesions). Immunological and endocrine laboratory study: thyroid profile (TSH), anti-thyroid peroxidase antibodies (anti-TPO), antithyroglobulin antibodies, morning serum cortisol, fasting blood glucose and complete blood count.

Standard management

• Clobetasol propionate 0.05% cream — very high potency corticosteroid applied to localized lesions to stop the autoimmune inflammatory attack; limited to 1-2 months monitoring atrophy
• Tacrolimus 0.1% ointment — preferred topical immunomodulator for lesions on the face, neck and intertriginous areas for its long-term safety
• Methylprednisolone in oral minipulses — indicated to stop the active and rapid progression of generalized vitiligo, under strict medical control
• Narrow band UVB phototherapy (complementary physical therapy that stimulates the proliferation and migration of melanocytes of the hair follicle sheath).