Breaking the cycle of AD

Alan D. Irvine, MD, DSC, was awarded the Marion B. Sulzberger, MD, Memorial Award and Lectureship for his work in atopic dermatitis (AD). Dr. Irvine, who practices in Dublin, Ireland, is known for his accomplishments in rare genetic skin disorders and vascular abnormalities.

At Sunday’s Plenary session (P151), Dr. Irvine provided an overview of the disease, including causes and cures in 2018. Underscoring the prevalence of AD, Dr. Irvine said it’s prevalent in up to 30% of children and up to 10% of adults.

“This is a condition that affects quality of life in multiple ways,” Dr. Irvine said. “Itching, visible lesions, sleep deprivation due to the discomfort, an inability to function during the day, and the direct and indirect costs associated with the condition can all take a toll on quality of life.”

Dr. Irvine reminded his colleagues that the comorbidities associated with AD included skin infections, neuropsychiatric issues (suicide and depression, both thought to be tied to sleep deprivation and poor self-esteem), and cardiovascular disease.

His primary research focuses on the pathogenesis of AD and three contributing factors. One of those factors — loss-of-function mutations in filaggrin (FLG) — is a major genetic risk for AD. Although the nature of this barrier defect is not fully understood, Dr. Irvine said patients with AD with filaggrin mutations are known to have more persistent disease, more severe disease, and a greater risk of food allergies, asthma, and eczema herpeticum. Two other factors impacting AD are staph aureus and Th2 cytokines.

“These three factors create a vicious cycle. If you don’t break this cycle, you’ll never get your patient cured,” he said.

Effective treatment, according to Dr. Irvine, requires blocking the pathways of these three factors. Certain drugs, such as dupilumab, can be effective, while a number others are in various stages of development and testing.

“It’s important to remember that AD is complex and multifactorial; all three factors play a part and targeted therapies are now emerging,” he said. “However, AD is unlikely to be solved by a single cytokine pathway.”


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