Introduction & Physiology of an Asthmatic Episode

Peter L. Salgo, MD: Hello and thank you for joining this AJMC® Peer Exchange titled “The Use of Biologics for the Treatment of Asthma.”

Asthma has been thought of as a single disease for many years; however, there are new data to support the heterogeneity of the disease with multiple phenotypes and clinical characteristics. While we’re still learning the phenotypes, it is important to understand how the emerging therapies provide targeted and personal approaches to the treatment of asthma. So we’re going to look into these new therapies, we’re going to learn their effect on the treatment paradigm.

I am Dr Peter Salgo, professor of medicine and anesthesiology at Columbia University College of Physicians and Surgeons and associate director of surgical intensive care at New York-Presbyterian Hospital in New York.

Participating today on our distinguished panel are:

Dr Don Bukstein, physician at the Allergy, Asthma & Sinus Center in Greenfield, Wisconsin.

Dr Linda Cox, Associate Clinical Professor of Medicine at the University of Miami School of Medicine and the Nova Southeastern University School of Osteopathic Medicine in Fort Lauderdale, Florida.

Dr John Oppenheimer, clinical professor of medicine at the University of Medicine and Dentistry of New Jersey at Rutgers, and director of Clinical Research at Pulmonary and Allergy Associates in Summit, New Jersey.

And Mr Louis Christos, pharmacy director from a regional health plan in Trumbull, Connecticut.

I want to thank all of you for joining us. This is going to be great.

Let’s get some of the basics down first, shall we? What happens physiologically during an asthma attack?

John J. Oppenheimer, MD: Well, as you know, asthma is an inflammatory disease, so essentially the inflammation becomes worse. Triggers can be anything from cold air to having a viral infection, and the result is that with this inflammation, the lumen of the airway becomes tighter. Building upon that is the fact that there’s neurogenic stimulation, also, so the smooth muscles constricting. The bottom line is that the airway aperture is smaller.

Peter L. Salgo, MD: So the airway aperture is smaller, the resistance to breathing is higher. And, if there’s a neurogenic component, it occurs to me never having had asthma, check me on this, when it gets harder to breathe, the neurologic, the neurogenic, the psychiatric component becomes worse, too.

Don A. Bukstein, MD: Yeah, I think one of the most important concepts has always been that there’s an inflammatory response going on in the airway, and we’ve kind of separated that out from the bronchospastic response. But I think recent research is starting the merge of the 2, that the bronchospasm in and of itself can be proinflammatory. And certainly the inflammation makes the airway much twitchier and can add to that inflammatory component. So I think that it’s sometimes very difficult to separate those out, though oftentimes we like to say we’re pinpointing with our therapy, the bronchospastic component or we’re pinpointing the inflammatory component, they overlap.

Linda S. Cox, MD, FAAAI, FACAAI, FACP: But nobody has mentioned allergen. In fact, I think there is some, let’s talk about dust mites, the most prevalent allergen worldwide associated with allergic asthma.

Peter L. Salgo, MD: With.....

Linda S. Cox, MD, FAAAI, FACAAI, FACP: And we believe that most asthma has allergen, but I think there were some recent studies that the results showed that they found dust mites in the lumen of the bronchial wall.

Peter L. Salgo, MD: Really? Really?

Linda S. Cox, MD, FAAAI, FACAAI, FACP: You remember that?

Peter L. Salgo, MD: He’s, no, not me.

Linda S. Cox, MD, FAAAI, FACAAI, FACP: No, no, no, it’s true, and actually they’ve been implicated in inflammatory bowel disease. So there is evidence that allergens play a significant role in a majority of asthmatics.

Peter L. Salgo, MD: Well, whether it’s dust mites or not, why don’t we just agree there are triggers. They’re out there.


Peter L. Salgo, MD: I mean, there are triggers.

Linda S. Cox, MD, FAAAI, FACAAI, FACP: As long as we agree that allergen is important in inflammation.

Peter L. Salgo, MD: You think? Yes. Can we all agree? We can all vote.

Linda S. Cox, MD, FAAAI, FACAAI, FACP: Don, you’re not?

Peter L. Salgo, MD: Are you objecting to that?

Don A. Bukstein, MD: No.

Peter L. Salgo, MD: Oh, good.

Don A. Bukstein, MD: I think there’s no question. But the 1 thing we can’t do in asthma is a lump. And we’ve got this disease that is a syndrome. It’s not asthma, it’s asthmas. And we’ve got so many different, as you remarked in your opening remarks, different phenotypes, that it’s really important to understand that there are multiple triggers and there are different phenotypes where there are individual triggers or something starts this cascade. We’re going to be talking about cytokines, and these physiologically active substances that really cause a lot of the inflammatory response.

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