Transcript
Dr. Neal Bhatia (00:07):
Hi. I'm Dr. Neal Bhatia. I'm Chief Medical Editor of Practical Dermatology and Director of Clinical Dermatology at Therapeutics Clinical Research, in San Diego, California.
(00:16):
When we think about the chronic cases and the chronicity timeline of atopic dermatitis, especially in adults, there, again, are many different cytokines at play, many different pathways at play. Many of them start in the acute phases with more of the Th2 side, interleukin-4, 13, a little bit of 5 perhaps, maybe a little bit more of some of the other cytokines. Of course, TSLP and OX40 tend to be a little bit more on the neurogenic side, and you see more upregulation of those as the cascade continues.
(00:43):
But then as lichenification continues, you see more lichen simplex chronicus, a little bit more of the chronicity of old smoldered eczema, where the itch is out of proportion to the rash. And you see more thickening of the skin, that tends to be a function of interleukin-22, especially when it creates more epidermal hyperplasia.
(00:59):
Overall, the Th17 pathway has a lot of influence on all phases of atopic dermatitis, but especially in the later phases where you tend to see that more psoriasiform type change, a little bit more thickening of the skin, and obviously that epidermal hyperplasia that goes with lichen simplex. So the whole cascade, especially in adults, especially with itching getting out of proportion to the amount of rash, that tends to show all the different phases of the immune system kind of working together.
