Annular atrophic plaques of the skin (Christianson's disease).

A 69-year-old Caucasian man presented to the Gainesville Veterans Administration Medical Center for evaluation of several asymptomatic enlarging lesions on the face and forearms that had been present for 10 to 15 years. They were initially small but had progressively enlarged, especially during the previous 5 years. He reported having sustained a concussive grenade blast injury of the left temple and right forearm during the Korean Conflict in 1951. The injured areas healed uneventfully in 2–3 weeks. The patient was otherwise healthy, and the review of systems was noncontributory. Laboratory work-up (complete blood count, chemical profile, erythrocyte sedimentation rate, rheumatoid factor, hepatitis profile, antinuclear antibodies, urinalysis, and chest X-ray) was within normal limits. Lyme antibody titers were negative. Physical examination revealed similar-appearing lesions located variously on both temples, left preauricular and infraauricular areas, and the right forearm (Fig. 1). The lesions were large (ranging from 4 to 12 cm in diameter), centrally atrophic patches with ivory-colored thickened edges, and had the distinct appearance of healed skin grafts. Blood vessels were easily seen through the atrophic skin. All lesions were located on sun-exposed areas (predominantly on the patient's left side). No similar lesions elsewhere on the body or skin graft donor sites were found. The patient was treated with doxycycline 100 mg by mouth twice a day for 21 days to no avail, Intralesional steroids and clobetasol propionate ointment under occlusion were used without any change in the lesions. At the submission of this paper, the lesions remain stable. Skin biopsies were taken from the edge and center of the lesions, Histologic examination (Fig. 2) of the center of a lesion showed a flattened epidermis without interface changes. Sclerosis of superficial and mid, but not deep, dermal collagen was present, particularly within the specialized connective tissue surrounding eccrine structures. A focus of lymphocytic inflammation with rare plasma cells and edema was present at the dermal-subcutaneous interface. Histologic examination of the edge of the lesion showed a flattened epidermis overlying a perivascular and periadnexal lymphohistiocytic inflammatory infiltrate. The papillary dermis was sclerotic centrally, and sclerosis was present around one eccrine unit. Increased interstitial mucin was noted. Direct immunofluorescence using antibodies to IgG, IgM, IgA, and C3 was negative, A silver stain for borrelia organisms was negative. Electron microscopy of a biopsy from the advancing border of a lesion revealed foci of complete cytoiysis of the basilar epidermis above an interrupted basal lamina (Fig, 3a). Cellular debris was evident even within the subajacent papillary dermis (Fig. 3b). Abundant colloid-like material associated with occasional 8–10-nm straight tubules was also present within the upper papillary dermis. A solitary lymphocyte lay closely apposed to a basilar keratinocyte having large cytoplasmic vacuoles. Electron microscopy of a biopsy from the center of the same lesion revealed a flattened basilar epidermis and focal reduplication and interruption of the basal lamina (Fig. 3c). Abundantly interspersed among the collagen bundles of the upper and lower papillary dermis were aggregates that appeared amorphous at low magnification. Upon higher magnification, however, the aggregates could be seen to be comprised of straight and wavy tubules embedded in a finely granular matrix (Fig. 3d). A dermal blood vessel was surrounded by several basal laminae, just outside of which were presumptive lymphocytes with cerebritorm nuclei and histiocytes. No dermal elastic fibers could be identified. Collagen fibrils appeared normal.