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- W2100181803 endingPage "245" @default.
- W2100181803 startingPage "245" @default.
- W2100181803 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." @default.
- W2100181803 created "2016-06-24" @default.
- W2100181803 creator A5050608918 @default.
- W2100181803 date "2010-01-01" @default.
- W2100181803 modified "2023-10-16" @default.
- W2100181803 title "Therapeutic Implications of a Barrier-based Pathogenesis of Atopic Dermatitis" @default.
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- W2100181803 doi "https://doi.org/10.5021/ad.2010.22.3.245" @default.
- W2100181803 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2917676" @default.
- W2100181803 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20711259" @default.
- W2100181803 hasPublicationYear "2010" @default.
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