An expert delves into the machinations of Type 2 asthma inflammation — a common condition in moderate-to-severe asthma patients.
Reynold A. Panettieri Jr., MD, emeritus professor of Medicine at the Perelman School of Medicine at the University of Pennsylvania, shared some telling numbers while presenting on type 2 ashtma at the 2017 Annual CHEST Meeting in Toronto, ON, CA.
From his most research, there are an estimated 25.7 million people with asthma in the US. About 5 to 10% of these patients (1.29 to 2.57 million) suffer from a severe form of the disease, and about 70% of moderate-to-severe patients suffer from the inflammatory characteristics of type 2 asthma (T2).
The characteristics include elevated sputum levels of Type 2 cytokines IL-4, IL-5, and IL-13, as well as elevated biomarkers of T2 inflammation such as blood eosinophils and fractional exhaled nitric oxide (FeNO).
T2 inflammation is common in asthma patients, Panettieri said, though the understanding of its characteristics are not far off from what he first learned years ago.
“In this day and age, despite fantastic medicines to treat asthma, we still have a major medical problem,” Panettieri said. “Since 1970, the rate of hospital visits and (emergency room visits linked to asthma) has been completely static. That’s astounding.”
Full asthma control is still unattainable in a majority of today’s patients, Panettieri noted. He referenced a study from colleague David Price, MB, MA, DRCOG, FRCGP, which analyzed 8,000 asthma patients undergoing treatment (REALISE).
The patients were divided into groups classified by their treatment (combination preventer inhaler plus oral pill; combination preventer inhaler; single-drug preventer inhaler; reliever). Only the reliever therapy group reported a higher percentage of patients to have partially controlled asthma, versus uncontrolled. None of the therapy groups reported a controlled asthma patient group of at least 30%.
Asthma patients with T2 inflammation similarly have issues in treatment limitation. Panettieri noted that in vitro evidence points to Type 2 cytokines IL-4, IL-5, and IL-13 promoting steroid resistance, stopping a subset of adult patients with uncontrolled asthma and T2 inflammation from having full corticosteroid response.
Asthma heterogeneity is astounding, Paneittieri said, adding to its difficult-to-treat nature. His resolve for at least addressing Type 2 asthma in patients is through better defining the pathobiology.
Its 2 forms — T2 and Non-Type 2 (Non-T2) Asthma — have stark characteristics. Eosinophils, FeNO, immunoglobulin E (IgE), and the protein periostin serve as biomarkers for T2. It’s also evident in patients with allergic asthma, eosinophilic asthma, and exercise-induced asthma.
Adversely, Non-T2 is evident in patients with obesity-associated asthma, smoking-association, or neutrophilic asthma, or smooth-muscle mediated asthma.
Overall, T2 comorbidities often include atopic dermatitis, chronic sinusitis with nasal polyps, and food and seasonal allergies — similarly to asthma, Panettieri said.
Asthma is an umbrella term for “many, many syndromes,” Panettieri said. A better grasp on its varied pathobiologies can only give patients a better chance to get it under control — whatever form of it they may have.
“Poor asthma control is common,” Panettieri said. “You see it, I see it. We’re in the trenches dealing with these patients.”
The presentation, “Type 2 Asthma: A Greater Understanding of Difficult-to-Control Asthma” was sponsored by Regeneron and Sanofi Genzyme.