Chronic inflammatory airway diseases, including asthma, chronic rhinosinusitis, eosinophilic COPD and allergic rhinitis are a global health concern. Despite the coexistence of these diseases and their common pathophysiology, they are often managed independently, resulting in poor asthma control, continued symptoms and poor quality of life. Understanding disease pathophysiology is important for best treatment practice, reduced disease burden and improved patient outcomes.The pathophysiology of type 2 inflammation is driven by both the innate immune system triggered by pollutants, viral or fungal infections involving type 2 innate lymphoid cells (ILC2) and the adaptive immune system, triggered by contact with an allergen involving type 2 T-helper (Th2) cells. Both ILC2 and Th2 cells produce the type-2 cytokines (interleukin (IL)-4, IL-5 and IL-13), each with several roles in the inflammation cascade. IL-4 and IL-13 cause B-cell class switching and IgE production, release of pro-inflammatory mediators, barrier disruption and tissue remodelling. In addition, IL-13 causes goblet-cell hyperplasia and mucus production. All three interleukins are involved in trafficking eosinophils to tissues, producing clinical symptoms characteristic of chronic inflammatory airway diseases.Asthma is a heterogenous disease; therefore, identification of biomarkers and early targeted treatment is critical for patients inadequately managed by inhaled corticosteroids and long-acting β-agonists alone. The Global Initiative for Asthma guidelines recommend add-on biological (anti IgE, IL-5/5R, IL-4R) treatments for those not responding to standard of care. Targeted therapies, including omalizumab, mepolizumab, reslizumab, benralizumab, dupilumab and tezepelumab, were developed on current understanding of the pathophysiology of type 2 inflammation. These therapies offer hope for improved management of type 2 inflammatory airway diseases.

Objective: The 2019 GINA guidance incorporates the presence of T2 inflammation in severe asthma patients to determine eligibility for add-on biologic therapy, though little data exists to characterize this population. The objective of this manuscript is to conduct a descriptive analysis to characterize patients with severe asthma in emerging countries based on disease severity, patient exacerbation history, and T2 phenotype. Methods: A cross-sectional survey of physicians treating asthma patients ages 12 years and older was conducted in eight countries. Physicians characterized their severe asthma patients and reported data from their patients' medical charts. Medical chart data was selected from the physicians' six most recent asthma patients taking prescription medication. Results: A total of 550 physicians completed the survey and filled out 3,300 patient record forms. A total of 876 patients have been characterized with uncontrolled severe asthma. Of the 420 patients with available EOS lab data, 40% are indicated with T2 inflammation (EOS ≥150/µL). Ninety-one percent of all patients with available IgE lab data (n = 498) had IgE 30 − 1500 IU/mL indicating allergy-driven asthma. Finally, chronic OCS use (as reported by physicians) was reported in 11% of patients. Conclusion:This research revealed that 65% of patients had at least one of three T2 inflammation comorbidities assessed: allergic rhinitis, chronic rhinosinusitis with nasal polyps, and atopic dermatitis. Discrepancies were observed between patients' treatment regimens and GINA step reported, suggesting there may be room to improve understanding of asthma severity as defined per GINA guidelines as well as asthma control assessment in clinical practice.supplemental data for this article can be accessed at publisher's website.

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