Dr Robert Sidbury Explains Pathophysiology, Comorbidity Risk of Atopic Dermatitis

Although understanding on the pathophysiology of atopic dermatitis (AD) remains limited, the inflammatory mechanisms of the condition have been linked directly and indirectly with several comorbidities, said Robert Sidbury, MD, MPH, chief, Division of Dermatology, Seattle Children's Hospital.

Transcript

Can you explain the pathophysiology of AD and its association with other comorbidities?

To the extent that it's possible, there's a lot we do not know about AD and its pathophysiology. But at least in terms of how to link it to the comorbidities, which is the thrust of the recent publication in the Journal of the American Academy of Dermatology, the links can either be direct or indirect.

For example, filaggrin is a protein in the skin, which has been shown to be one of the biggest risk factors for patients with AD. Either a decrease or absence of filaggrin in the skin has been shown to be a susceptibility. Filaggrin is almost like caulk in the skin and so you can therefore reason that diminution of filaggrin in the skin might lead to increased dryness, increased itch from the inflammation that stems from that dryness, increased risk of infections and allergies, all because that skin barrier is not as intact.

There's also a condition called ichthyosis vulgaris, which shares that same mutation and filaggrin as a contributing factor to the cause of the disease and ichthyosis vulgarities is one of the minor diagnostic criteria of AD or eczema. So there's some direct ways to to link and then there's some indirect ways to link.

If you think about the symptoms of AD or eczema like itch. What does that mean? It means potentially sleep loss. What does that mean? It means potentially decreased quality of life, it means possibly inattention at work, could mean potential confusion with things like [attention-deficit/hyperactivity disorder], some of the other comorbidities that have been linked.

Then finally, if you think about inflammation in general, we have learned a lot about psoriasis in the last few years, another chronic inflammatory skin condition. And we have learned that the inflammation in psoriasis—we've known for years there can be inflammation in the joints called psoriatic arthritis—and we've learned about the seeming increased risk of cardiovascular outcomes and morbidity in patients with psoriasis, presumably through that shared common inflammatory pathway.

So, those are some ways that you can link the pathophysiology of AD, to the extent that we know it, and it's comorbidities.