Msk Dermatology · Year 2 · from Msk Dermatology

Case 2: Vitiligo - Melanocyte Destruction

Patient Presentation

Demographics: 28-year-old female

Chief Complaint: Expanding white patches on hands and face

History of Present Illness: The patient noticed depigmented patches on the dorsum of her hands 6 months ago. The patches have slowly expanded and new patches appeared on her face around her eyes and mouth. She has no symptoms (no itching, pain, or scaling). She has a history of hypothyroidism.

Family History:

  • Mother has vitiligo
  • Aunt has type 1 diabetes

Physical Examination:

  • Skin:
  • Sharply demarcated, depigmented (chalk-white) macules and patches
  • Distribution: Dorsal hands, periorbital, perioral
  • Bilateral and symmetric
  • No scale, no atrophy
  • Wood lamp: Enhanced depigmentation (bright white fluorescence)
  • Thyroid: Non-tender, no nodules

Workup and Results

Laboratory Studies:

  • TSH: 8.2 mU/L (elevated - known hypothyroidism)
  • Anti-TPO antibodies: Positive

Wood Lamp Examination:

  • Bright white fluorescence in affected areas
  • Helps delineate extent of involvement

Clinical Image

Clinical photograph showing characteristic depigmented patches of vitiligo with sharply demarcated borders, demonstrating the typical distribution around the periorbital and perioral areas.

Diagnosis

Vitiligo (Generalized/Common Type)

Features:

  • Acquired depigmentation
  • Autoimmune destruction of melanocytes
  • Associated autoimmune conditions (thyroid disease)
  • Family history of autoimmunity

Discussion

This case illustrates melanocyte biology and destruction:

  • Melanocyte Origin: The lecture describes how melanocytes originate from neural crest cells and reside in the stratum basale of the epidermis.
  • Autoimmune Destruction: The lecture identifies vitiligo as resulting from autoimmune destruction of melanocytes. T-cell mediated destruction leads to complete loss of melanin production in affected areas.
  • Melanin Function: The lecture explains that melanin produced by melanocytes (eumelanin = brown/black; pheomelanin = red/yellow) protects against UV radiation damage. Loss of melanocytes in vitiligo increases photosensitivity.
  • Tyrosinase: The lecture notes that tyrosinase is the rate-limiting enzyme in melanin synthesis. Antibodies against melanocyte antigens (including tyrosinase) may contribute to vitiligo pathogenesis.

Treatment Plan

  1. Sun Protection:
  • Sunscreen SPF 30+ (affected areas prone to sunburn)
  • Protective clothing
  1. Topical Therapy:
  • Topical corticosteroids (first-line for limited disease)
  • Topical calcineurin inhibitors (tacrolimus) - face-safe
  • Trial for 3-6 months
  1. Phototherapy:
  • Narrowband UVB for extensive disease
  • Stimulates melanocyte migration from hair follicles
  1. Cosmetic Options:
  • Cosmetic camouflage (cover-up makeup)
  • Self-tanners (temporary)
  1. Screening:
  • Annual thyroid function tests
  • Screen for other autoimmune conditions if symptoms develop

Teaching Points

  1. Melanocytes originate from neural crest and reside in stratum basale
  2. Vitiligo results from autoimmune destruction of melanocytes
  3. Tyrosinase is the rate-limiting enzyme in melanin synthesis
  4. Vitiligo is associated with other autoimmune conditions (thyroid, diabetes)
  5. Wood lamp examination enhances depigmented areas

All cases for this lecture as Markdown