Raj Chovatiya, MD, PhD: Type 2 Inflammation in Prurigo Nodularis, Chronic Spontaneous Urticaria, Eczema


In this interview segment, Dr. Chovatiya discussed the challenges of diagnosing Type 2 inflammation in several different dermatologic diseases.

In this segment of his interview with HCPLive, Raj Chovatiya, MD, PhD, spoke with the editorial team about the contents of his talk ‘Diving Below the Surface of Type 2 Inflammation in atopic dermatitis, prurigo nodularis, and chronic spontaneous urticaria: Implications for Clinical Practice.’

Chovatiya is director of the Center for Eczema and Itch at Northwestern, in addition to being assistant professor of dermatology at the Feinberg School of Medicine at Northwestern University.

Chovatiya’s talk was presented at the 2023 Fall Clinical Dermatology Conference in Las Vegas. During this interview, he was asked about the mechanisms of Type 2 inflammation in atopic dermatitis (AD), prurigo nodularis (PN), and chronic spontaneous urticaria (CSU).

“Type 2 inflammation is a pathway is an aspect of immunity we've learned a lot about through our studies of atopic dermatitis, particularly the role of cytokines like IL 4, 13, 31, 5 and others,” Chovatiya said. “And it's really come to our attention that, as we've learned more about other states like prurigo nodularis and, more recently, chronic spontaneous urticaria, there are some really interesting connections in terms of similar cytokines across all of these. That probably is the reason why all these diseases have some element of itch and really an interaction between the immune axis and the nervous system or nerve axis.”

He notes that this is probably because of the similar cytokine profile that has evolved across each of these diseases.

Later, Chovatiya was asked to elaborate on the diagnostic challenges and tools available for identifying Type 2 inflammation in these skin conditions.

“So for most of these diseases, there are clinical diagnoses,” he said. “So even though we have some limited understanding about what's happening below the surface, largely speaking, in the case of atopic dermatitis, we're making a clinical diagnosis based on usually itch, eczema lesions, and some other criteria in the case of prurigo nodularis.”

Chovatiya explained that this diagnosis is typically based upon primary lesions, itch being present for at least 6 weeks, and some of the other ancillary signs that you might see of picking, rubbing, and scratching.

“In the case of chronic spontaneous urticaria, again, chronic pruritus that's usually greater than 6 weeks plus, and lesions that come and go,” he said. “Hive-like or wheels, if you will, that have also been around for 6 weeks, too. So another interesting connective thread for clinical diagnosis across the states is that they all require a certain sense of understanding of patients symptoms, as well as skin signs. I think that that's a recurring theme throughout this talk, that you need the patient perspective and the clinician perspective to make appropriate diagnosis. Beyond that none of them have any really reliable molecular diagnostics that we use at this point in time.”

Chovatiya added that it is possible that clinicians’ understanding of Type 2 inflammation may unlock some of these types of diagnostics that allow the ability to parse through which individuals might be the best choice for a particular treatment in the future.

“One of the cool things about Type 2 inflammation is there's really only a small family of cytokines and pathways that seem to be at the core of a lot of these inflammatory programs,” he said. “And given that we've had a lot of therapeutic evolution in this space in terms of options for atopic dermatitis, prurigo nodularis, and other diseases, it really behooves us to understand the immunology and connect that to exactly what is being targeted or inhibited by our treatments and through that sort of rational thought.”

For further information from Chovatiya’s presentation at the conference, view the full video above.

The quotes contained in this description were edited for clarity.

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