LAUSR

ficial lymphocytic infiltrates in the dermis (Fig. 1c). The diagnosis of inflammatory DSP was made. The large irregular plaques and pruritus subsided gradually after systemic etretinate at 20 mg/day, and a topical corticosteroid was started; however, large numbers of small, non-inflammatory pigmented annular lesions persisted. Vitamin D analogue cream, imiquimod cream, adapalene gel and keratolytic treatments were also ineffective. Topical diclofenac 1% gel twice daily for 1 month reduced the colour and scaling of the brownish, non-inflammatory annular lesions, resulting in the satisfaction of the patient (Fig. 2a,b). There have been no promising or standard treatments for DSP. Topical diclofenac gel is a treatment option for the management of actinic keratosis owing to its anti-inflammatory effect that works by blocking cyclooxygenase-2, which inhibits cell proliferation and angiogenesis. The efficacy of topical diclofenac gel for disseminated superficial actinic porokeratosis was confirmed in two of eight cases in a study by Vlachou and seven of 13 cases in a study by Marks. In the present case, the topical diclofenac gel largely resolved the recalcitrant annular lesions for which no other therapy had been effective. Although the efficacy was limited to the applied area, and the lesion reappeared after discontinuance of the diclofenac gel, this treatment was quite helpful in the absence of desirable alternatives. The clinical presentation of the present case was unique, as hundreds of pruritic inflammatory annular lesions had spread over the entire body without apparent triggers. An atypical variant of porokeratosis that accompanies intense pruritus and affects the entire body has been reported under several descriptive terms, such as inflammatory DSP and eruptive disseminated porokeratosis. This entity often accompanies internal malignancy or immunosuppression, and 30% of the patients developed inflammatory DSP after pre-existing classical porokeratosis lesions, without apparent triggers. Porokeratosis is believed to develop due to the peripheral expansion of clones of mutant epidermal keratinocytes, which would normally be suppressed by immune mechanisms. Immunological reactions against clones of mutant keratinocytes may also play a role in inflammatory DSP. This case is of interest because topical diclofenac gel combined with systemic etretinate was effective in treating the recalcitrant inflammatory DSP. The further accumulation of similar cases is needed to clarify the best treatment option for inflammatory DSP.