LAUSR

hypertrichosis in this child. The treatment was stopped, and the patient was switched back to tacrolimus. No treatment was performed on our pediatric patients because safe treatment was a priority over cosmetic needs. Acquired local hypertrichosis is common with long-term topical use of certain drugs (such as minoxidil, glucocorticoids, and tacrolimus), endocrine dysfunction, local chronic irritation, and chronic inflammation. However, to our knowledge, there are no reports of crisaborole-induced localized hypertrichosis in pediatric patients with AD. In vitro studies have shown that PDE-4 inhibitors (apremilast) reduce the secretion of IFN-c, TNF-a, and IL-2. For example, in alopecia areata (AA), multiple loci have been associated with AA, including HLA, ULBP1, CTLA4, and IL-2/IL-21, although the exact cause and pathophysiology of alopecia areata have not been determined. Recent studies on immune activation in alopecia areata found that Th1/IFN-c, Th2, PDE4, IL-23, and IL-9 upregulation were present. By catalyzing the conversion of cyclic adenosine monophosphate (cAMP) to AMP, PDE upregulates the inflammatory pathway and leukocytic activity. According to Keren et al., increased PDE activity was observed in inflammatory states compared with that in the control group, which may contribute to hair loss. PDE-4 inhibitors effectively improve AA by counteracting inflammatory factors. We speculate that PDE-4 inhibition activity downregulated IL2 secretion, which may be related to localized hypertrichosis in this child. However, the exact underlying mechanism remains unknown. Further studies are needed to confirm this phenomenon, and practitioners should be familiar with the uncommon adverse effects of crisaborole.