Until recently, the pathogenesis of atopic dermatitis (AD) has been attributed to primary abnormalities of the immune system [–]. Intensive study revealed the key roles played by TH1/TH2 cell dysregulation, IgE production, mast cell hyperactivity, and dendritic cell signaling in the evolution of the chronic, pruritic, inflammatory dermatosis that characterizes AD (op. cit). Hence, current therapy has been largely directed towards ameliorating TH2-mediated inflammation and pruritus (e.g.[]). In this brief review, we will assess emerging evidence that inflammation in AD results from inherited and acquired insults to the barrier, and describe the features of certain barrier-repair alternatives as therapeutic products for the treatment of AD. A recently-developed approach, based upon lipid replacement with a ceramide-dominant, triple-lipid formulation that corrects the underlying lipid biochemical abnormality, potentially represents a new paradigm for therapy of AD.
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