Funding sources: none. Conflicts of interest: none declared. Madam, Atopic dermatitis (AD) is an intractable inflammatory skin disease characterized by an intensely pruritic skin rash with a typical morphology and distribution in accordance with an impaired skin barrier. Pruritus in AD affects quality of life and is sometimes difficult to control. There is a wide variety of mediators of pruritus, including histamine, neuropeptides, prostaglandins, serotonin and bradykinin. It has recently been reported that interleukin (IL)‐31, a 4‐helix‐bundle cytokine, is a new candidate of itch mediator, preferentially produced by T cells skewed toward Th2.1 Transgenic mice overexpressing IL‐31 spontaneously developed severe pruritus, resulting in eczematous skin lesions with hyperkeratosis, acanthosis and inflammatory cell infiltration, which closely resembled those of AD.1 Leucocytes in patients with AD expressed significantly higher IL‐31 levels compared with those of control subjects.2 In addition, IL‐31 levels correlate with disease activity in AD.3 Epinastine is an H1‐histamine receptor antagonist that is widely used throughout the world (18 countries). As epinastine is known to inhibit the development of Th2 immune responses,4 it is of interest to evaluate the effect of epinastine on IL‐31 expression. In this study, we have evaluated the effect of epinastine on serum IL‐31 levels in patients with AD in line with pruritus.