LAUSR

Dear Editor Topical imiquimod therapy has proven to be effective for a variety of infectious, neoplastic, and inflammatory dermatologic diseases; in this regard, Metcalf, Crowson, Naylor, Haque, and Cornelison (2007) showed reparative changes to the epidermis and the dermal collagen bundles in chronically sun-damaged skin, indicating also its potential use as an antiaging treatment. Besides, Smith, Hamza, Germain, and Skelton (2007) found that after imiquimod therapy, on sun-damaged skin, there was a less compact hyperkeratosis, a more uniform rete ridge pattern with a more ordered proliferation of the epidermis, and a decrease in sun-damaged melanocytes. However, until now there is no evidence in literature about the use of imiquimod 3.75% for chronically sun-damage pigmented lesions. The patient was a 75-year-old Caucasian female, with a clinical and dermoscopic prominent solar lentigo (SL) in her left cheek (Figure 1a). A chronic sun-damage was present, however, in absence of evident nonmelanoma skin cancers (NMSCs). The patient refused treatment with cryotherapy and fractional CO2 laser. With her consent, we decided to try imiquimod 3.75% cream, as off-label treatment. The patient was instructed to apply imiquimod 3.75% cream once daily (2-week treatment cycles separated by a 2-week no-treatment interval), with a follow-up period of 8 weeks. The patient applied a thin layer of cream to the treatment area avoiding the periocular areas, lips, and nares. The cream was applied prior to normal sleeping hours and removed ~8 hr later with mild soap and water. The patient was reevaluated 8 weeks after the final treatment cycle. A clear reduction of the SL was observed, with good cosmetic outcome (Figure 1b). She referred the onset of a severe local skin reaction during the 10th day of treatment, completed healed after 2 weeks. SL is a benign cutaneous lesion that arises in response to exposure to ultraviolet (UV) radiation. UV radiation can cause local proliferation of melanocytes and thus an accumulation of melanin in the skin cells (keratinocytes) (Scarcella, Dethlefsen, & Nielsen, 2018). SL can be treated with cryoterapy, lightening peelings, or with lasers, as Q-switched Nd:YAG lasers, fractional CO2 laser and picosecond laser (Scarcella et al., 2018). However, when these treatments are contraindicated, not available or refused by the patients, other therapeutic options may be taken into consideration. Although imiquimod cream is a validate and well-known treatment for actinic keratosis and NMSCs, literature lacks of reports about the use of imiquimod for also benign sun-damaged diseases. Imiquimod is an immune response modifier which induces the secretion of cytokines as interferon-alpha, tumor necrosis factor-alpha and interleukins 1, 6, 8, 10, and 12, inducing apoptosis, as well as increasing the expression of genes activating natural killer cells, macrophages, and dendritic cells (Stockfleth, 2015). Finally, topical imiquimod 3.75% cream has an acceptable tolerability profile, with an easy treatment regimen and elderly patients may find the once-daily treatment regimen easier to adhere than more frequent regimens (Stockfleth, 2015). In conclusion, in our patient imiquimod 3.75% cream showed an acceptable tolerability profile with the advantage of being self-applied by the patient (Stockfleth, 2015), showing an efficacy not only at the level of actinic keratosis and NMSCs, but also in case SL. Further studies are necessary to validate the use of imiquimod also for benign skin lesions, associated with chronic skin photodamage.