A 24-year-old woman presents with a 6-month history of progressive loss of skin pigmentation. Examination reveals well-demarcated milky-white macules and patches distributed symmetrically over the face (perioral and periorbital regions), hands, and elbows. The lesions are asymptomatic. Under Wood lamp examination (365 nm), the affected areas show bright blue-white fluorescence. The structure marked **A** in the diagram represents the characteristic appearance of these lesions. Which of the following best describes the PRIMARY PATHOGENIC MECHANISM underlying the development of the lesions marked **A**?
A. Autoimmune destruction of melanocytes mediated by CD8+ cytotoxic T cells targeting melanocyte antigens (tyrosinase, MART-1, gp100)
B. Vasoconstriction of dermal capillaries leading to transient blanching without true loss of melanocytes
C. Post-inflammatory hypopigmentation following resolution of a preceding inflammatory dermatosis
D. Fungal infection causing disruption of melanin synthesis with characteristic scale on KOH mount
Explanation
Why "Autoimmune destruction of melanocytes mediated by CD8+ cytotoxic T cells targeting melanocyte antigens (tyrosinase, MART-1, gp100)" is right
The symmetric depigmented patches marked A in the diagram are pathognomonic for vitiligo, a chronic autoimmune depigmenting disorder. The British Association of Dermatologists Vitiligo Guidelines 2024 establish that vitiligo results from progressive loss of melanocytes in the epidermis, with the PRIMARY PATHOGENIC MECHANISM being complex autoimmune destruction mediated by CD8+ cytotoxic T cells that target melanocyte-specific antigens including tyrosinase, MART-1, and gp100. The IFN-γ-CXCL10 axis is central to this immune-mediated destruction. This is the definitive mechanism distinguishing vitiligo from other causes of depigmentation and is essential for understanding why immunosuppressive and JAK inhibitor therapies are effective.
Why each distractor is wrong
Fungal infection causing disruption of melanin synthesis with characteristic scale on KOH mount: This describes tinea versicolor, which presents with fine scale and "spaghetti and meatballs" appearance on KOH mount. Vitiligo is asymptomatic, has sharp borders, and shows no scale or fungal elements. The clinical presentation and Wood lamp findings are distinctly different.
Vasoconstriction of dermal capillaries leading to transient blanching without true loss of melanocytes: This describes nevus anemicus, which is a benign vascular lesion that does NOT accentuate under Wood lamp examination. Vitiligo shows bright blue-white fluorescence on Wood lamp due to actual melanocyte loss, not vasoconstriction.
Post-inflammatory hypopigmentation following resolution of a preceding inflammatory dermatosis: Post-inflammatory hypopigmentation is typically ill-defined, transient, and resolves spontaneously over months to years. The symmetric, progressive, well-demarcated milky-white macules with sharp borders and accentuation on Wood lamp are characteristic of true vitiligo, not post-inflammatory changes. Additionally, the patient's presentation does not indicate preceding inflammation.
High-YieldNEET PG
Vitiligo = CD8+ T cell-mediated autoimmune destruction of melanocytes; Wood lamp accentuation confirms true depigmentation (absent melanocytes), not hypopigmentation or vascular phenomena.
British Association of Dermatologists Vitiligo Guidelines 2024
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