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Tinea versicolor
3%
1/34
Destruction of melanocytes
88%
30/34
Postinflammatory hypopigmentation
6%
2/34
Impaired wound healing
0%
0/34
Post-surgical scarring
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This teenage patient is presenting with signs of vitiligo. Vitiligo is believed to be a result of the autoimmune destruction of melanocytes. Vitiligo is a disorder of pigmentation that results in patches of white, depigmented skin. Although the exact pathogenesis of vitiligo is unknown, it is believed to be caused by a complex interaction between both genetic and environmental factors. The disorder is often associated with other autoimmune diseases and has an unpredictable course. Treatment attempts to facilitate repigmentation by inhibiting the immune response and may include the use of corticosteroids or ultraviolet therapy. Response to therapy is highly variable. Plensdorf et al. discuss the four types of vitiligo. Generalized vitiligo affects more than 10% of the body; acral/acrofacial vitiligo affects the face and distal extremities. Localized vitiligo affects a small body surface area; segmental vitiligo affects a single dermatome or body part. Colucci et al. review the options for treating vitiligo. They report that first line therapies include topical corticosteroids, calcineurin inhibitors, phototherapy and photochemotherapy, as they are safe and effective. Second line therapies involve vitamin D analogues, targeted phototherapy, oral corticosteroids and surgery. Figure A shows depigmented skin in the perioral region. Illustration A shows hypopigmented skin lesions seen in tinea versicolor. Incorrect answers: Answers 1 and 3: Tinea versicolor and postinflammatory hypopigmentation are associated with a decrease in pigment not the absence of pigment that is observed in vitiligo. Answers 4 and 5: Impaired wound healing and post-surgical scarring are not typically associated with complete loss of pigmentation.
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