Disseminated Superficial Actinic Porokeratosis on the Face Treated with Imiquimod 5% Cream
A 19-year-old, single, unemployed, Caucasian female (skin type III) presented with multiple facial lesions. She had been suffering from multiple pigmented annular papules and plaques on her face for 7 years. The lesions were slowly progressive with no signs of self-healing. She had been a normal, healthy, full-term baby and had normal physical milestones of development as a child. She appeared to be immunocompetent with no history of recurrent infections or any other skin lesions. Her parents and siblings (3 brothers and 2 sisters) were all normal and healthy. She had no family history of a similar condition or other skin problems. Her medical history was unremarkable with no other obvious complaints, and she was not overexposed to sunlight as she spent most of her time indoors. Upon examination, the central part of the face, i.e. the malar area and nose including the ala nasi, showed scattered annular papules and plaques of different sizes ranging from 0.3 to 2 cm. The lesions were asymptomatic and symmetrically distributed on both sides of the face (figs. , ). Routine laboratory tests were done and the results were within normal ranges. Multiple biopsies were taken from different lesions. The diagnosis was confirmed as DSAP, with a classic and very illustrative pathological picture (figs. –). Treatment options were multiple, though none was considered an obvious first choice. All physical modalities were excluded to avoid the possibility of side effects like scarring and disfigurement, as the lesions were located in the central part of the face and involved the skin overlying the nasal cartilage. We first prescribed a topical retinoic acid 0.1% cream that has keratolytic and antineoplastic effects, and it was assumed that this might rectify the faulty clonal epidermopoiesis. The patient applied the cream twice daily for 3 months without a significant response. Six months later, the patient presented again and the picture was almost unchanged except for a few small new lesions in the malar area and on the nose. We decided to give her imiquimod 5% cream to be used once a day (3 times per week) for 24 weeks. She came for a follow-up every 2 weeks. Her skin started to respond after 1 month. Side effects like erythema, crustations and pruritus were experienced and were controlled by topical emollient cream; we avoided corticosteroids and calcineurin inhibitors because they can counter the effects of imiquimod. On completion of the therapy, the response was very satisfactory for both the patient and the therapist. There were some lesions with only a partial response. Central scarring and the scars across the nose improved in their color, thickness and texture, constituting an added benefit of imiquimod in this indication. The patient maintained a once-weekly application of imiquimod. There has been no relapse after follow-up for 2 years now.