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Patients with uncontrolled persistent asthma may experience impacts on their lungs and quality of life2-7
Lung function is critical to the assessment of future risk in patients with asthma13
and/or
and/or
and/or
Consider coexisting Type 2 inflammatory diseases
a The below are not the criteria for eligibility for Type 2–targeted biologic therapy.
b Patients dependent on OCS may also have underlying Type 2 inflammation; however, biomarkers of Type 2 inflammation are often suppressed by OCS. If possible, therefore, these tests should be performed before starting OCS or on the lowest possible OCS dose.
CRSwNP, chronic rhinosinusitis with nasal polyposis; EOS, eosinophils; FeNO, fractional exhaled nitric oxide; FEV1, forced expiratory volume in 1 second; ICS, inhaled corticosteroid; OCS, oral corticosteroid.
References: 1. Gandhi NA, Bennett BL, Graham NMH, Pirozzi G, Stahl N, Yancopoulos GD. Targeting key proximal drivers of type 2 inflammation in disease. Nat Rev Drug Discov. 2016;15(1):35-50. 2. Haselkorn T, Fish JE, Zeiger RS, et al; TENOR Study Group. Consistently very poorly controlled asthma, as defined by the impairment domain of the Expert Panel Report 3 guidelines, increases risk for future severe asthma exacerbations in The Epidemiology and Natural History of Asthma: Outcomes and Treatment Regimens (TENOR) study. J Allergy Clin Immunol. 2009;124(5):895-902. 3. O’Byrne PM, Pedersen S, Lamm CJ, Tan WC, Busse WW; START Investigators Group. Severe exacerbations and decline in lung function in asthma. Am J Respir Crit Care Med. 2009;179(1):19-24. 4. Nguyen VQ, Ulrik CS. Measures to reduce maintenance therapy with oral corticosteroid in adults with severe asthma. Allergy Asthma Proc. 2016;37(6):125-139. 5. Haselkorn T, Chen H, Miller DP, et al. Asthma control and activity limitations: insights from the Real-world Evaluation of Asthma Control and Treatment (REACT) study. Ann Allergy Asthma Immunol. 2010;104(6):471-477. 6. Di Marco F, Verga M, Santus P, et al. Close correlation between anxiety, depression, and asthma control. Respir Med. 2010;104(1):22-28. 7. Sullivan PW, Ghushchyan VH, Globe G, Schatz M. Oral corticosteroid exposure and adverse effects in asthmatic patients. J Allergy Clin Immunol. 2018;141(1):110-116. 8. Elliot JG, Jones RL, Abramson MJ, et al. Distribution of airway smooth muscle remodelling in asthma: relation to airway inflammation. Respirology. 2015;20(1):66-72. 9. Mauad T, Bel EH, Sterk PJ. Asthma therapy and airway remodeling. J Allergy Clin Immunol. 2007;120(5):997-1009. 10. Fehrenbach H, Wagner C, Wegmann M. Airway remodeling in asthma: what really matters. Cell Tissue Res. 2017;367(3):551-569. 11. Holgate ST. The airway epithelium is central to the pathogenesis of asthma. Allergol Int. 2008;57(1):1-10. 12. National Heart, Lung, and Blood Institute, National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma—Full Report 2007. NHLBI Health Information Center; 2007. NIH publication 07-4051. 13. Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 2020. Accessed August 31, 2020. https://ginasthma.org/wp-content/uploads/2020/06/GINA-2020-report_20_06_04-1-wms.pdf 14. Rayos Prescribing Information. December 2019. 15. Patel M, Pilcher J, Reddel HK, et al; SMART Study Group. Predictors of severe exacerbations, poor asthma control, and β-agonist overuse for patients with asthma. J Allergy Clin Immunol Pract. 2014;2(6):751-758. 16. Bai TR, Vonk JM, Postma DS, Boezen HM. Severe exacerbations predict excess lung function decline in asthma. Eur Respir J. 2007;30(3):452-456. 17. Agache I, Akdis C, Jutel M, Virchow JC. Untangling asthma phenotypes and endotypes. Allergy. 2012;67(7):835-846. 18. Bjermer L. Time for a paradigm shift in asthma treatment: from relieving bronchospasm to controlling systemic inflammation. J Allergy Clin lmmunol. 2007;120(6):1269-1275.