The Pathophysiology of Atopic Dermatitis
19
October

By Adem Lewis / in , , , , , , , /


This educational program has been developed
by Regeneron Pharmaceuticals and Sanofi Genzyme. The speaker has been compensated for his time
and effort. There’s increasing evidence that there’s the
cycle between barrier dysfunction and inflammation in the skin. If you have intrinsic dry skin and barrier
dysfunction, that allows your skin to get stimulated and sort of antigenized more easily. Then you get the cytokine milieu and inflammation. That percolates back up to the skin and there’s
actually a negative effect from these Th2 aspects on the skin barrier itself. When you have more open, inflamed skin, the
skin barrier itself is affected. Then you have this inflammatory milieu and it’s our
desire to try to tampen down that inflammation. L-4 and IL-13 will decrease your epidermal
function. It will impact on your antimicrobial functions
and your keratinocyte differentiation. They’ll decrease your liposomes and a variety
of things that are decreasing the performance of the epidermis. Then obviously there’s this impact on inflammation
and on allergy and an amplification effect with the TH2 cytokines. We also know that in kids, as well as adults,
when you have significant eczema, the inflammation and the abnormalities are not just physically
in the skin of inflamed skin. It also can be found in the skin of uninflamed
skin and it can be found circulating in the blood as well. There’s a degree of a systemic inflammatory
disorder associated with atopic dermatitis.


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