Multiple keratoacanthomas as an untoward response to imiquimod therapy for actinic keratoses.

Imiquimod treatment of actinic keratoses (AK), usually highly effective, may yield squamous cell carcinoma of the keratoacanthoma type (SCC-KA), histopathologi-cally reminiscent of the multiple self-healing squamous carcinomas of Ferguson-Smith. In this regard, dermatosis locus minoris resistentiae (DLMR), meaning dermatosis in " place of less resistance " , connotes the formation of a primary dermato-logical condition in a site of altered or compromised skin, and, although SCC-KA may occasionally be abortive and " reactive " , with a tendency towards spontaneous regression, it may progress to frank invasive SCC even with metastasis (1, 2). The " reactive " subset of SCC-KA may appear in areas of scar formation, psoriasis, discoid lupus erythematosus, laser resurfacing, radiation therapy, donor skin graft sites and Mohs' surgical site scars, as an unusual event representing DLMR (3–6). Herein, we report a case of secondary reactive and multiple (> 17) SCC-KA that occurred during an exuberant inflammatory response to imiquimod therapy utilized for extensive and confluent AK of the left forearm. A 60-year-old man with extensive photodamage and confluent AK of the forearms, worse on the left, was prescribed imi-quimod 5% cream thrice weekly for 6 weeks, but returned 8 weeks later with a generalized eruption and a peculiar markedly well-localized, exuberant, exudative reaction affecting the left forearm treatment site. He had used imiquimod nightly and was experiencing systemic symptoms including fever, chills, arthralgias and myalgias. A diffuse erythematous maculo-papular eruption was noted across the chest, back, and abdomen with excoriations, consistent with autosensitization (id). On the left forearm was an extensively eroded markedly indurated plaque on an erythematous base containing greater than 17 foci of well-delineated crusted inspissated discoid and exudative nodules, dome-shaped and hyperkeratotic, up to 1–1.5 cm in size (Fig. 1). The right forearm showed the typical imiquimod treatment response with eczematization and crusting. Treatment with 60 mg triamcinolone acetonide intramuscular and topical triamcinolone 0.1% ointment for the id reaction was instituted, and cephalexin for possible clinical infection of the forearm was begun after an incisional shave biopsy was performed of the largest dome-shaped hyperkeratotic nodule. Imiquimod was discontinued and local wound care to the forearm with petrolatum and loose bandages was instituted. On histopathological examination the first biopsy revealed absence of the typical crateriform morphology usually associated with solitary SCC-KA, but a nodular proliferation of cytologically malignant keratinocytes was seen invading the dermis with mitotic figures present, consistent with SCC-KA reminiscent of the …