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Dear Editor,A 73‐year‐old man presented with an asymptomatic, well‐demarcated, infiltrated, erythematous plaque on the left cheek (Figure 1A). Five months earlier, he had been treated for actinic keratosis in this location with imiquimod 5% cream three times a week for 4 weeks. The patient had no personal or family history of autoimmune disease. Skin biopsy revealed a dense superficial and deep perivascular and periadnexal lymphoid infiltrate reaching the dermo‐hypodermal junction (Figure 1B). There was a well‐developed interface lesion with dyskeratotic keratinocytes predominantly affecting the follicular epithelium, and infundibular hyperkeratosis (Figure 1C). Immunohistochemistry showed a clear predominance of T over B cells and similar proportions of CD4 and CD8. No mucin deposits were demonstrated. A complete blood test with immunological profile showed negative antinuclear, anti‐double stranded DNA, anti‐extractable nuclear antigen, and anti‐histone antibodies. Based on these findings, a diagnosis of discoid lupus‐like reaction to imiquimod was established. The lesion resolved after a 4‐week treatment with clobetasol propionate cream.1FIGUREClinical presentation and histological findings. (A) A well‐demarcated, infiltrated, erythematous plaque on the left cheek. (B) A dense perivascular and periadnexal lymphoid infiltrate formed by lymphocytes without atypical features extending deep down to the vessels of the dermal‐hypodermal junction (hematoxylin and eosin, original magnification 40×). (C) A
Dermatologic Therapy – Wiley
Published: Sep 1, 2022
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