Raffi Tachdjian, MD, MPH, FAAAAI, FACAAI: Hello, and thank you for joining this Peer Exchange titled “Biologics Treatment Selection in Patients With Moderate to Severe Asthma.” I’m Dr Raffi Tachdjian, an associate professor at the David Geffen School of Medicine at the University of California, Los Angeles. Joining me today is Dr Dareen Siri, an allergist and immunologist at Midwest Allergy Sinus Asthma in Central Illinois and an assistant professor at Southern Illinois University. I’m also joined by Dr Nicole Chase, an allergist and immunologist in Saint Paul, Minnesota, and an adjunct associate professor at the University of Minnesota. And lastly, Dr Andrew White, an allergist and immunologist at Scripps Health in San Diego, California, where he is a clinical professor.

In today’s discussion, we will discuss the role of type 2 inflammation in asthma, challenges with the long-term use of corticosteroids, and the emerging role of biologics in various mechanisms of action in the management of asthma. Thank you so much for joining us. Let’s begin.

The first question will go to Dr White. I’d like you to provide an overview of current classifications of endotypes and phenotypes in severe asthma.

Andrew White, MD: Thanks, Dr Tachdjian. It’s a very broad topic, and even a little bit complicated. You can think about this in a lot of different ways. The first way that I think about that is: What is a phenotype? What is an endotype? Phenotypes are ways that we can broadly classify the types of patients we see in our practice, because there are going to be certain characteristics that are unifying. And with asthma, it’s very common. There are a lot of different ways you can probably end up having asthma, and there are a lot of different types of inflammation. If you look at the [Global Initiative for Asthma] 2023 guidelines, they offer some examples of different phenotypes, such as allergic asthma or nonallergic asthma, adult-onset or asthma with airflow obstruction, or asthma associated with obesity. Those are some ways to think about phenotypes.

Then what’s an endotype? The best way to think about that is: What’s the root cause? What’s the inflammation that’s driving this? That’s probably the big question for a lot of our patients—whether we can drill down to what is really the process going on there. We’ll probably talk a lot about some of these other potential endotypes as we go through them. One of the big endotypes is type 2 inflammation, which I know we’re going to be discussing. When you think about type 2 endotypes, there are certain diseases that can cluster in there, like aspirin-exacerbated respiratory disease, which is a very classic disease process that’s driven by type 2 inflammation. You can also have other endotypes that aren’t driven by type 2 inflammation—maybe type 1 inflammation, type 17 inflammation, or endotypes associated with obesity or smoking. These are specific pathways of inflammation. That’s sort of a long answer. That’s how I think about that. I’m curious whether other panelists have ideas about that.

Raffi Tachdjian, MD, MPH, FAAAAI, FACAAI: Certainly, Dr White. Years ago, the emphasis was on genotyping and trying to find that Holy Grail, then we got into phenotyping to try to manage and define asthma. This newer endotype definition looks at the pathophysiological mechanisms that take certain individuals down certain routes and try to intervene. Are there any other comments from either of our other panelists on this broad overview?

Dareen D. Siri, MD, FAAAAI, FACAAI: Now that we have targeted therapies, it’s really important to endotype them and phenotype them so we can choose the right therapy for the patient. Great points, Dr White.

Andrew White, MD: The process has still been a bit elusive, too. Each layer we pull back, we find that there’s probably more we need to learn. So, this is a great road map for us, but we still clearly have a lot more to learn about asthma.

Transcript edited for clarity