Biologics have proven significantly beneficial among patients with more severe, uncontrolled, inflammation-driven forms of asthma. But they have not become or have been considered for overall asthma use. Is their potential limited to the worst-case scenarios of asthma progression?
In an interview with MD Magazine®, Thomas Casale, MD, professor of medicine at USF Health Morsani College of Medicine, explained where current understanding and expectation of biologic therapy stands in asthma research, and why their limitations are what they are.
MD Mag: Is the optimal use of biologics in asthma reserved for patients with severe forms of the disease?
Casale: At this point, I think so, with drugs that we have. And the reason I say that is obviously, the biggest driver of asthma cost is going to be asthma exacerbations, loss of work and productivity. So, we want to have drugs that would prevent you from going to the emergency room, losing work, and losing productivity. That's the only way that these things would be pharmaco-economically beneficial.
So, I think that's why in part, the answer to that is yes. But the other piece is that none of them have been shown to “cure the disease.” So, they work—but, by and large, they only work when you use them. If we had a biologic that you could say, ‘Look, if you take this for 3 years, you're going to have a much better outcome for the next 10 years,’ that's different. We're not there yet.
So it makes sense, really, to limit these to that patient population that is expending a lot on healthcare cost, because we don't have a cure.
MD Mag: Are their greatest benefits in reduced exacerbations and better chance of asthma control?
Casale: Correct. They’re not responding as well as they should to inhaled corticosteroids, and all of our other tools—long-acting beta agonists, anticholinergics, etc.
And they're still having symptoms, they're still having poor quality of life, exacerbations. But they have that “eosinophilic phenotype.”
Now, we do have drugs that are in development that may also improve patients that don't have that Th2-high or eosinophic-driven inflammation. But we have to see what happens in phase 3 trials, because we all know that sometimes they look good in early studies, but then when it gets down to it, you never know.
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