Multiple Eruptive Dermatofibromas in a Patient Receiving Efalizumab

Comment Although dermatofibromas (DFs) are very common, their pathogenesis is poorly understood. It has recently been proposed that this should be regarded as an immunoreactive process, mediated by dermal antigen-presenting cells that trigger an abortive immune response to as yet unidentified antigenic stimuli. According to this hypothesis, the development of MED in immunodeficient states could be facilitated by the inhibition of downregulatory T cells; alternatively, multiple DFs could develop as an exaggerated response to a putative pathogen that could not be cleared by the suppressed immune system [4–6] . Efalizumab (anti-CD11a) is a humanized monoclonal antibody, which blocks multiple T-cell-dependent functions involved in the pathogenesis of psoriasis, including T cell activation and migration to the skin provoking a partial immunosuppressed state [7] . We believe that this combination is not just coincidental and that the development of DF can be attributed to the medication. In a review of the literature we found only 1 patient with psoriasis receiving prednisolone and ultraviolet B phototherapy who developed MED, but the authors attributed the eruption of DF to the HIV infection which the patient suffered [8] . Moreover, the development of new DFs stopped after immunosuppressive therapy had been discontinued in our patient. As dermatologists prescribing new biological drug therapies we should be alert to the appearance of new side effects not found in clinical trials.