Abstract

Leukoderma may circumscribe melanocytic nevi. While the leukoderma is most commonly due to vitiligo, guanofuracin (1) and monoben-zone (2) may also produce a similar perinevic depigmentation at a distant site from local application. Vitiliginous depigmentation may begin about a lesion of seborrheic keratoses (3), fibroma, or a nevus (5). None of these lesions undergo involution and disappear following the physiologic effects of these various forms of leukoderma. A nevus may be surrounded by leukoderma for fifteen years and still produce melanin (4). Non-pigmented nevi may occur in albinos. However, certain other pigmented melanocytic nevi during their spontaneous involution exhibit an area of perinevic leucoderma. These nevi, originally called “Halo nevi” by Weber (6), are, in my opinion, a distinct lesion from a nevus haphazardly surrounded by vitiliginous depigmentation and the former manifest a specific clinical and histological picture. Clinically, they are most frequently found in the second or third decades, usually in women, and occur most frequently on the back and shoulders. These central brown nevi surrounded by a coin or oval area of leukoderma, after an undetermined period of time, disappear without scarring. Concommit-tant with the color change from brown to red to white, the nevus papule involutes to a macule and eventually blends in with the surrounding leukoderma. The characteristic microscopic picture has been described by Findley (7), and Lupton and Lund (8). Initially, the nevus cells actively proliferate at the junctional zone. These active cells intermingle with and are encompassed by a dense lymphocytic inflammatory infiltrate. In the later stages of this development, the nevus cells may completely disintegrate, leaving only pyknotic fibrillar tissue. Quite frequently in older lesions, a biopsy of the central lesion fails to show any nevus cells.

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