Abstract |
In this review, I first provide relevant background information about normal epidermal barrier structure and function. I then update recent information about how inherited defects in either filaggrin and/or in the serine protease inhibitor, lymphoepithelial Kazal-type inhibitor 1, converge to stimulate the development of atopic dermatitis (AD). Next I explain the multiple mechanisms whereby a primary barrier abnormality in AD can lead to inflammation. Furthermore, I explore how certain acquired stressors, such as a reduced external humidity, high pH soaps/ surfactants, psychological stress, as well as secondary Staphylococcus aureus infections initiate or further aggravate AD. Finally, and most importantly, I compare various therapeutic paradigms for AD, highlighting the risks and benefits of glucocorticoids and immunomodulators vs. corrective, lipid replacement therapy.
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Authors | Peter M Elias |
Journal | Annals of dermatology
(Ann Dermatol)
Vol. 22
Issue 3
Pg. 245-54
(Aug 2010)
ISSN: 2005-3894 [Electronic] Korea (South) |
PMID | 20711259
(Publication Type: Journal Article)
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