Hematoxylin-eosin staining showed an unremarkable epidermis and a mild superficial dermal perivascular lymphocytic infiltrate. No thrombotic phenomena were observed. Verhoeff–van Gieson staining revealed an absence of elastic fibers in the dermis.
Anetoderma, also known as macular atrophy, was first described by Jadassohn in 1892. It is an unusual disease of unknown etiology. It is clinically characterized by small, atrophic papules that herniate inward at palpation1 and is classified as primary or secondary. Primary anetoderma develops on clinically normal skin without any preceding dermatoses and may be associated with several systemic diseases. It is broadly categorized into 2 clinical types: Schweninger-Buzzi anetoderma (no preceding erythema) and Jadassohn-Pellizari anetoderma (preceded by macular erythema or papular urticaria). Secondary anetoderma develops over other dermatoses such as acne, pilomatricoma, syphilis, and varicella.1 Anetoderma may present as multiple round, nonfollicular, finely wrinkled patches of skin that appear sunken, atrophic, or flaccid and demonstrate inward herniation. Lesions typically appear on the upper part of the trunk and the proximal portions of the extremities. The primary histopathologic feature is elastic tissue loss in the dermis. Elastophagocytosis may be present.2
Atrophic Macules and Soft Papules in a 24-Year-Old Woman. Arch Dermatol. 2007;143(1):109-114. doi:10.1001/archderm.143.1.109-f