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Received May 29, 2017; Accepted Oct 23, 2017
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
Atopic dermatitis (AD) is a chronic pruritic inflammatory skin disease caused by abnormal skin barrier function and aberrant immune responses along with cutaneous hyperreactivity to environmental triggers [1]. AD has a complex etiology that involves activation of multiple immunological and inflammatory pathways along with disruption of epidermal barriers, elevated IgE levels, peripheral eosinophilia, and a predominance of Th2 cells expressing IL-4, IL-5, and IL-13 [2]. The main treatment for AD is skin hydration with emollients and suppression of cutaneous inflammation using topical steroids to reduce the number and severity of flares [1]. However, the use of steroids should be limited to the most severe cases due to their side effects, which include adrenal suppression, osteoporosis, hypertension, diabetes, obesity, and striae [3]. Recently, new treatments for AD, such as Th2 antagonists, cytokine antagonists, phosphodiesterase inhibitors, barrier repair therapies, and allergen-directed immunotherapy, have emerged. Although these therapeutic agents have greatly improved patient outcomes, the current treatments for AD are still not ideal and novel therapeutic strategies are required in the search for better drugs with safety and efficacy.
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