Omalizumab lowers asthma exacerbations, oral corticosteroid intake and blood eosinophils: Results of a 5-YEAR single-centre observational study. (February 2019)

• Record Type: Journal Article
• Authors: Pelaia, Corrado; Calabrese, Cecilia; Barbuto, Sarah; Busceti, Maria Teresa; Preianò, Mariaimmacolata; Gallelli, Luca; Savino, Rocco; Vatrella, Alessandro; Pelaia, Girolamo
• Is Part Of: Pulmonary pharmacology & therapeutics. Volume 54(2019)
• Page Start: 25
• Page End: 30
• Publication Date: 2019-02
• Subjects: IgE -- Omalizumab -- Severe allergic asthma; Respiratory organs -- Diseases -- Chemotherapy -- Periodicals; 615.7205
• DOI: 10.1016/j.pupt.2018.11.002
• Languages: English
• ISSNs: 1094-5539

Abstract

Abstract: Omalizumab is a humanized monoclonal antibody which binds to human immunoglobulins E (IgE), thus preventing their interactions with both high affinity and low affinity IgE receptors. Therefore, omalizumab is currently recommended for add-on biological therapy of uncontrolled allergic asthma, mainly characterized by type 2 airway eosinophilic inflammation. Because omalizumab has been the first, and for a long time the only available monoclonal antibody for add-on treatment of type 2 asthma, some long-term studies have been published which provide a clear evidence of the therapeutic effectiveness of the anti-IgE pharmacological strategy. Within this context, the present single-centre observational study refers to 15 patients with severe allergic asthma, treated with omalizumab for at least 5 years at the Respiratory Unit of "Magna Græcia" University Hospital located in Catanzaro, Italy. In these asthmatic subjects we observed significant increases in asthma control test (ACT) score, with respect to baseline (14.60 ± 2.97), after 1 year (19.20 ± 2.98; p < 0.0001) and 5 years (21.67 ± 2.38; p < 0.0001) of add-on treatment with omalizumab. More importantly, omalizumab significantly lowered the number of annual asthma exacerbations (baseline: 3.66 ± 2.01) after 1 year (0.83 ± 1.14; p < 0.0001) and 5 years (0.63 ± 0.99; p < 0.0001), respectively. This excellent therapeutic outcome made it possible to drastically decrease the daily oral intake of prednisone (baseline: 22.50 ± 5.17 mg) after 1 year (1.83 ± 4.06 mg; p < 0.0001), as well as after 5 years (1.66 ± 3.61 mg; p < 0.0001). With regard to lung function, omalizumab significantly and persistently enhanced FEV1 (baseline: 1636 ± 628.4 mL) after 1 year (2000 ± 679.7 mL; p < 0.05) and 5 years (1929 ± 564.8 mL; p < 0.05), respectively. Such relevant clinical and functional improvements were associated with reductions of blood eosinophil counts (baseline: 646.0 ± 458.9 cells/μl), already detectable after 1 year (512.7 ± 327.8 cells/μl; not significant), which reached the threshold of statistical significance after 5 years (326.0 ± 171.8 cells/μl; p < 0.05). Therefore, these real-life data referring to our single-centre observational investigation further corroborate the long-term therapeutic ability of omalizumab to improve several clinical, functional and haematological signatures of severe type 2 asthma.