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From Skin Therapy Letter Posted: 08/10/2012; Skin Therapy Letter. 2012;17(7) © 2012 SkinCareGuide.com
A Look at Epidermal Barrier Function in Atopic Dermatitis
Physiologic Lipid Replacement and the Role of Ceramides
- Abstract and Introduction
- Epidermal Barrier Dysfunction
- Morphological Changes in Epidermal Lipids in AD
- Filaggrin Mutations and Exogenous Factors in AD Contribute to Epidermal Barrier Dysfunction
- Lipid Replacement Therapy in AD
- Natural Vs. Synthetic Ceramides
- Other Non-steroidal Barrier Repair Products
- Conclusion
Abstract and Introduction
Abstract
This review summarizes and discusses the role and efficacy of moisturizers, particularly the more recently introduced ceramide-based formulations, in the skin care regimen of patients with both active and quiescent atopic dermatitis (AD). It is now well established that a complex interplay of environmental and genetic factors are responsible for disease onset and chronicity. Indeed, several novel genetic mechanisms have been recently discovered to be associated with AD pathogenesis. Moreover, it is increasingly recognized that the epidermal barrier plays a critical role in the initiation, perpetuation, and exacerbation of AD. The skin of patients with AD harbors several defects in epidermal barrier function, including filaggrin and ceramides. An improved understanding of these etiopathogenic factors has led to the development of topical ceramide-dominant moisturizers to replace the deficient molecules and re-establish the integrity of barrier defenses. Some of these products have demonstrated efficacy in the treatment of adult and childhood AD that are similar to mid-potency topical steroids. More importantly, they have been shown to be safe with very few associated side-effects. We recommend the addition of such new agents as both the first step of treatment and in the maintenance of clinically quiescent skin of patients with AD.
Introduction
Atopic dermatitis (AD) is a chronic, inflammatory, pruritic skin disease of increasing prevalence (affecting 15-30% of children and 2–10% of adults).[1] AD is considered by many to be the first step in the "atopic march" that can progress to include asthma and allergic rhinitis, as well as be a precursor to, rather than a consequence of, food allergies.[1] The precise sequence of biochemical events leading to the development of AD has still not been fully elucidated, but most experts agree that it involves a complex interplay of environmental and genetic factors that induce derangements in the structure and function of the epidermal barrier and immune system. Diagnosis can be challenging, as the variability of clinical presentation can be confounding. Morphology alone cannot reliably confirm the diagnosis and the spectrum of features associated with AD must be considered. While several sets of diagnostic criteria for AD have been proposed and validated, the traditionally used being that of Hanifin and Rajka, full agreement amongst clinicians and uniformity of criteria are still lacking.[2]
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