Finding And Treating the Beats of the Atopic March

Jonathan Spergel, MD, PhD, and his team linked eosinophilic esophagitis to the condition-based theory. What others are part of the atopic march?

What makes the atopic march such an interesting theory is that it’s a very advanced theory. Its main points are well-evidenced, but not at a final conclusion.

Take, for example, the new data presented this week at the 2018 American Academy of Allergy, Asthma & Immunology (AAAAI) and World Allergy Joint Congress in Orlando, FL. Researchers from the Children’s Hospital of Philadelphia (CHOP), as led by Jonathan M. Spergel, MD, PhD, chief of the Allergy section, found a found a missing link to the theorized progression of pediatric immunologic diseases.

A 130,457-infant patient cohort study conducted by the team found that eosinophilic esophagitis (EoE) is a predictable condition in young children that have already been diagnosed with asthma, food allergy (FA), and atopic dermatitis (AD). The researchers also found that pediatric patients with EoE were more likely than the overall population to develop allergic rhinitis (AR) (95% CI; 1.4-2.7).

When regarding for these pediatric patients’ peak age of diagnosis, this is how Spergel and his team would map out the atopic march:

-Asthma (peak age 0.4 years)

-FA (peak age 1.0 year)

-AD (peak age 1.1 year)

-EoE (peak age 2.7 years)

-AR (peak age 4.1 years)

But in a separate interview with MD Magazine at AAAAI, Spergel suggested that nasal polyps or similar conditions could also be beats of the march. What may be missing to prove its place is analysis of adult patients.

“We’ve looked in a pediatric population, and those things are more adult-driven,” Spergel said. “I think if you looked at something called oral allergy syndrome, that would probably be in the same pathway, too.”

Though the march theoretically functions as a continuum of disease, it’s not a certain pattern in patients. Spergel reiterated that AD patients do not always develop asthma or FA, and vice versa. But the sensitization that develops in patients as a result of AD or another early disease is what increase the rate of risk.

This theory, and efforts in which to combat it, have progressed from animal models to patient studies in the past decade, Spergel said. But it’s also advanced from considering preventive measures, to realizing that treating it could stop the march in a patient altogether.

“If you treat someone for their allergies over time, they’re a little bit less likely to develop other allergies,” Spergel said. “So maybe, right now, that may be the best prevention: if we treat people aggressively, then maybe that makes a difference.”

Researchers are now onto clinical trials testing biologicals designed to specifically prevent the actions of the enabling pathways in these related conditions. In the following years, these therapies could become capable of treating not just one facet of atopic disease, but the whole gamut.

“It’s not going from (treating) A, to B, to C, then D,” Spergel said. “But, if we block A to B, then we could prevent C and D.”

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