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Definition & Pathogenesis - Patchy Puzzle Pieces

  • Definition: Acquired, chronic depigmenting disorder characterized by the selective loss of functional melanocytes from the epidermis and, occasionally, hair follicles.
  • Melanocytes: Neural crest-derived cells responsible for melanin production; primarily in skin (epidermal, follicular reserves), but also eye (uvea) and inner ear.
  • Key Pathogenetic Theories:
    • Autoimmune: Most accepted; T-cell (CD8+) mediated destruction of melanocytes.
    • Neural: Neurochemical mediators (e.g., neuropeptides) damage melanocytes or inhibit melanin synthesis.
    • Oxidative Stress: Accumulation of Reactive Oxygen Species (ROS) and ↓antioxidant defenses (e.g., catalase) damage melanocytes.
    • Genetic: Polygenic; associations with HLA (e.g., HLA-DRB1*07) and immune-related genes.
    • Melanocytorrhaphy: Defective melanocyte adhesion and chronic detachment leading to transepidermal loss. Vitiligo on hands

⭐ Koebner phenomenon (isomorphic response), the development of new vitiligo lesions at sites of skin trauma, is a common indicator of active disease progression and is seen in about 20-60% of patients.

Clinical Features & Types - Spot the Signs

  • Types:
    • Non-segmental (NSV): Most common; often symmetrical.
      • Generalized: Widespread macules.
      • Acrofacial: Lips, distal fingers/toes.
      • Mucosal: Oral/genital mucosa.
      • Universal: Affects >80% of body surface area.
    • Segmental (SV): Unilateral, dermatomal; earlier onset, stable course.
    • Mixed: Features of both NSV and SV.
  • Morphology:
    • Chalky/milky white, depigmented macules or patches.
    • Well-demarcated borders.
    • Trichrome vitiligo: Intermediate zone of hypopigmentation between normal and depigmented skin.
    • Koebner phenomenon: Lesions at sites of trauma.
  • Common Sites: Extensor surfaces (elbows, knees), periorificial areas (eyes, mouth, nostrils), hands, feet, genitals.
  • Associated Autoimmune Conditions: Thyroid disease (Hashimoto’s, Graves’), alopecia areata, pernicious anemia, type 1 diabetes.

Vitiligo on hands showing depigmented patches

⭐ Wood's lamp examination (wavelength 365 nm) accentuates depigmented areas, appearing as bright blue-white fluorescence, especially useful in fair-skinned individuals where contrast is low under normal light.

Diagnosis & DDx - Confirming the Clues

  • Clinical Diagnosis: Based on characteristic depigmented macules/patches.
  • Wood's Lamp Examination:
    • Accentuation of depigmentation (chalky white fluorescence).
    • Helps identify subclinical/early lesions. Vitiligo under Wood's lamp
  • Skin Biopsy (Rarely needed):
    • Confirms absence of melanocytes.
    • May show marginal lymphocytic infiltrate.
  • Differential Diagnosis (DDx):
    • Pityriasis alba
    • Tinea versicolor (KOH: spaghetti & meatballs)
    • Idiopathic guttate hypomelanosis
    • Piebaldism (congenital, stable)
    • Chemical leukoderma
    • Leprosy (sensory loss)

⭐ Wood's lamp is crucial for detecting subtle lesions and assessing true extent, especially in fair-skinned individuals.

Vitiligo Management - Repigmenting Roadmap

Goals: Arrest progression, induce repigmentation.

Vitiligo on arms

  • Medical Therapies:
    • Topical: Corticosteroids (e.g., clobetasol propionate), calcineurin inhibitors (tacrolimus, pimecrolimus), JAK inhibitors (tofacitinib).
    • Phototherapy: NB-UVB (311-313 nm), PUVA.
    • Systemic: Corticosteroids (oral mini-pulse for active disease), JAK inhibitors.
  • Surgical Therapies (for stable vitiligo):
    • Autologous melanocyte transplant (MKTP), punch grafting, suction blister grafting.
  • Depigmentation (extensive vitiligo >80% BSA):
    • Monobenzyl ether of hydroquinone (MBEH).
  • Always: Sunscreen use.

⭐ For generalized vitiligo, NB-UVB phototherapy (311-313 nm) is a first-line treatment, offering good efficacy and safety.

High‑Yield Points - ⚡ Biggest Takeaways

  • Autoimmune destruction of melanocytes causes well-demarcated depigmented patches.
  • Koebner phenomenon (new lesions at trauma sites) is frequently observed.
  • Wood's lamp examination accentuates lesions, appearing as chalky white fluorescence.
  • Strong association with other autoimmune diseases (e.g., thyroiditis, pernicious anemia).
  • Segmental vitiligo follows dermatomes; non-segmental is more common and widespread.
  • Mainstay treatments include topical corticosteroids, calcineurin inhibitors, and NB-UVB phototherapy.
  • Surgical therapies like melanocyte transplantation are for stable, localized disease_

Practice Questions: Vitiligo

Test your understanding with these related questions

Match the following woods lamp findings: 1. Erythrasma, 2. Pityriasis versicolor, 3. Tinea capitis, 4. Vitiligo || a. Yellow b. Coral red fluorescence c. Pink d. Green e. Milky white

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Flashcards: Vitiligo

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_____dermal melasma -appears slightly grey or bluish on gross examination and shows less color contrast with Wood s lamp

TAP TO REVEAL ANSWER

_____dermal melasma -appears slightly grey or bluish on gross examination and shows less color contrast with Wood s lamp

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