Peter L. Salgo, MD: All of asthma, we’re going to lump it into 1 big economic burden. Whatever the cause, whatever the dust mites, or the allergens, or whatever the phenotype, at some point it’s asthma, somebody has got to pay for it. How big a burden is that on the American economy?
Louis Christos, RPh: It’s a big burden. It comes up in discussions with employers, it comes up in discussions internally. And this is 1 of those disease areas where it’s more about the total cost of care. It’s the hospitalizations. It’s the medical side of the cost that’s the burden, not so much the primary cost.
Peter L. Salgo, MD: And do we understand the inflammatory process well enough to know what it is that’s costing us all this money?
Linda S. Cox, MD, FAAAAI, FACAAI, FACP: Cockroach. No, no, no, a New England Journal of Medicine paper.
Peter L. Salgo, MD: We went from dust mites to cockroaches.
Linda S. Cox, MD, FAAAAI, FACAAI, FACP: It was a very…
John J. Oppenheimer, MD: What it is, $81.9 billion, $81.9 billion.
Peter L. Salgo, MD: What is that?
John J. Oppenheimer, MD: $81.9 billion.
Peter L. Salgo, MD: Billion dollars.
John J. Oppenheimer, MD: That’s what they stated last year, and what’s intriguing is that’s including healthcare costs, pharmacy benefits, and absenteeism, as well as death. But what’s interesting is that presenteeism, Don, 1 of your interests, has never been calculated. So it’s mindboggling how expensive asthma is.
Don A. Bukstein, MD: And then we don’t calculate, we’re looking at asthma as just the airway disease. It really is because allergic precipitators and the Th2 [T-cell helper 2] allergic responses responsible, especially for most of the severe asthma, are well over 50%. We’re at a position where this inflammatory response is ongoing, and the cost may not just be in the lungs but it may be in the upper airway also. So, in other words, the comorbidities of this disease. And when you talk about absenteeism, we can also talk, if you’re an employer, you talk about presenteeism. How’s it going to affect the person when they’re actually working?
Peter L. Salgo, MD: You’re at the job but you really can’t work efficiently. Let me talk about the physiology. Actually, I’m going to ask you to talk about the physiology for a minute, and let’s talk about type 2 inflammation in asthma. What are the distinct roles of these type 2 cytokines? What are their effects? Let’s take it off from there.
Linda S. Cox, MD, FAAAAI, FACAAI, FACP: Boy, once you start tackling the immune system, it can get very complicated.
Peter L. Salgo, MD: That’s why you’re here.
Linda S. Cox, MD, FAAAAI, FACAAI, FACP: But let’s keep it simple. We generally think of 2 T cells, T-lymphocytes. There’s the Th1 [T-cell helper 1] and we lump them in with autoimmune disease, and then we have Th2, which is the allergic pathway that involves a number of cytokines like IL-4, IL-13 and ultimately the production of IgE [immunoglobulin E], which is the immunoglobulin that causes an allergic reaction. So that’s a very simplistic splitting up of the inflammatory…
Peter L. Salgo, MD: But there are phenotypes, right? There’s the high Th2 and the low Th2 phenotypes. What’s the difference? Is there a difference?
Linda S. Cox, MD, FAAAAI, FACAAI, FACP: I haven’t really heard of that grouping per se.
John J. Oppenheimer, MD: Well, T2 high and T2 low. So T2 high would be what we think classically of an asthmatic, an eosinophil upregulated phenomena, IL-4, or IL-13, IL-5, and IgE. And then T2 low would be either people that are paucicellular, so if you look…having no inflammatory or a dearth of inflammatory cells when doing bronchoalveolar lavage or neutrophil upregulation. So it’s a great way to stratify, and when we think about the rest of our conversation today, most of our therapy is directed towards T2 high. So one of the biggest problems we have is what do we do with these poor people that are T2 low?
Don A. Bukstein, MD: And T2 low may be associated with other cytokines, interleukin-17, others, interleukin-6. So there are other cytokines that may be, but we haven’t been as good about developing monoclonal antibodies to interrupt those pathways.
John J. Oppenheimer, MD: Well, the hope is if we hang out long enough, it will be there.
Louis Christos, RPh: Is the T high and T low, is that something measured routinely in physicians’ offices?
John J. Oppenheimer, MD: No, no, it is not.
Linda S. Cox, MD, FAAAAI, FACAAI, FACP: Not at all.
John J. Oppenheimer, MD: They’re not really stratifying….
Linda S. Cox, MD, FAAAAI, FACAAI, FACP: It’s more of a clinical picture.
Don A. Bukstein, MD: What we do is we measure things that give us an idea that it’s a T high or a T low. We don’t actually measure the cytokines. It would be great if we measured the interleukins, but we can’t do that efficiently at a clinical level. So what we do is we measure skin tests, we measure eosinophil counts, we measure IgE, we measure exhaled nitric oxide. It gives us the idea that it’s in that Th2 phenotype.
John J. Oppenheimer, MD: We have surrogates and that’s how we get approval for these biologics, which we’ll talk about in a few minutes. I mean, really we now have to think, instead of just using a big gun like a steroid, we now have to try to stratify, will people likely respond or not respond, based upon their phenotype.