An Analysis of Biologic Therapies in Patients With Asthma and Chronic Rhinosinusitis.

Background Asthma, Allergic rhinitis (AR), Chronic Obstructive Pulmonary Disease (COPD), Eczema, and Chronic Rhinosinusitis with Sinonasal Polyposis (CRSwNP) are illnesses often characterized by type 2 (T2) inflammation, wherein T helper (Th) cells release pro-inflammatory cytokines such as IL (interleukin)-4, IL-5, IL-9, and IL-13. This response may also promote the production of IgE and an increase in/activation of serum eosinophils. In the aforementioned type 2 inflammatory diseases, this immune response can cause excess mucous production, inflammation of the airways, other atopic responses when patients are exposed to certain environmental allergic triggers. Relatively new biologic monoclonal antibody therapies such as dupilumab (blocks IL-4 and IL-13), benralizumab (blocks IL-5), mepolizumab (blocks IL-5), and omalizumab (blocks IgE Fc/fragment of crystallization region) offer novel therapeutic targets that more specifically and directly block type 2 inflammatory responses. Methods To examine the effect of monoclonal antibody biologic therapies on patient indicators of type 2 inflammation, a retrospective analysis of 193 patients on biologic therapy was conducted, and these patients were compared to 48 control patients with type 2 inflammatory diseases who did not initiate biologic therapy. Total Lund-MacKay radiographic score, FEV1 (forced expiratory volume in the first second), FEF25-75 (forced expiratory flow from 25-75% of the forced vital capacity curve), annualized pulmonary exacerbations, oral corticosteroid dose, and serum eosinophils were recorded at baseline (zero months), and at three, six, nine, and twelve months after initiation of biologic therapy. Least squares mean data and the percent change from the baseline of least squares mean for the biologic and control groups were compared. Results Omalizumab was the most common biologic therapy prescribed. Control patients were younger than patients who initiated biologic therapy. Patients on biologic therapy had statistically significant reductions in Lund-MacKay score, improvements in FEV1 and FEF25-75, reductions in serum IgE levels, and reductions in serum Eosinophils. Patients on biologic therapy also had statistically significant reductions in annualized pulmonary exacerbations and oral corticosteroid dose compared to controls. Conclusions Patients with a variety of type 2 inflammatory conditions appear to have significant improvements in lung function, radiographic sinusitis, and serum markers of type 2 inflammation after initiation of biologic therapy versus controls. These therapeutic medications appear to significantly improve type 2 inflammatory disease course in patients who can tolerate these medications.