A case of paradoxical fibrosis and development of morphea in a patient on dupilumab

Recent observations of improvement in keloids with the administration of dupilumab have led to research that has implicated interleukin (IL) 4 and IL-13 signaling as potential mediators of sclerosing and fibrotic skin diseases, particularly with increased expression of transforming growth factor β downstream of IL-13.1, 2, 3 As such, dupilumab, an IL-4 receptor α antagonist, inhibits IL-4 and IL-13 signaling and has been suggested as a potential treatment for sclerosing disorders, with an active phase 2 interventional randomized placebo-controlled trial currently underway investigating its efficacy in morphea. Here, we present the case of a patient developing morphea while being treated with dupilumab. This potential paradoxical reaction, where a postulated therapy appears to contribute to the pathogenesis of the disease, has been reported in psoriasis, in which the inhibition of tumor necrosis factor α through its inhibitors leads to increased activity of interferon α, postulated to induce disease development.4