TYPE 2 INFLAMMATION PLAYS A
MAJOR ROLE IN THE CLINICAL
MANIFESTATION OF ASTHMA1

Optimal asthma control goes beyond exacerbation reduction

Patients with uncontrolled persistent asthma may experience impact on their lungs and quality of life2-7

Higher
exacerbation
rates2
Impaired lung function
(resulting from
bronchoconstriction)8-11
Potential side
effects with OCS use7,12-14
Poor quality
of life5,6

Additionally, unaddressed Type 2 inflammation in children ages 6-11
often results in consequences lasting into adulthood13,15,16

Impairment of normal lung development
Children with severe asthma are more likely to have reduced lung function and more severe asthma in adulthood
Growth
suppression
High-dose ICS use is correlated with growth suppression and lower height in adulthood
Persistent airway inflammation
Airway inflammation leads to increased airway remodeling over time and may cause asthma to be more difficult to treat in adulthood

 
Up to 85% of children with asthma have Type 2 inflammation,
which includes elevation of IgE in response to allergen, viral, or
bacterial triggers1,17,18

Impaired lung function contributes to a cycle of
exacerbations and poor asthma control2,19

Lung function is critical to the assessment of future risk in patients with asthma13

  • Patients with frequent exacerbations and moderate-to-severe asthma experienced a significantly greater annual decline in FEV1 in a long-term study, compared with patients who had infrequent exacerbations20
  • Early and sustained improvements in lung function following therapy initiation reduced the rate and severity of future exacerbations3
There remains an unmet need to provide comprehensive care for
patients with uncontrolled persistent asthma2,13,21,22

GINA recommends considering the presence of Type 2 inflammation in patients
with severe asthma who are taking a high-dose ICS or daily OCS by identifying any
one of the below13,a,b:

Blood EOS
≥150 cells/µL
and/or
sputum EOS ≥2%

and/or

FeNO
≥20 ppb

and/or

Clinically allergen-
driven asthma

and/or

OCS dependence

Consider coexisting Type 2 inflammatory diseases

GINA recommends considering the presence of Type 2 inflammation
in children ages 6-11 by identifying the following characteristics13,b:

Elevated
EOS, IgE,
and/or FeNO

and/or

Multiple
aeroallergen
sensitization

and/or

Progressive loss
of lung function
and frequent
exacerbations

and/or

Coexisting Type 2
diseases, including
atopic dermatitis,
allergic rhinitis,
and food allergy
Biologic add-on therapy may be a viable option for treating
certain asthma patients with Type 2 inflammation13

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.

EOS, eosinophils; FeNO, fractional exhaled nitric oxide; FEV1, forced expiratory volume in 1 second; GINA, Global Initiative for Asthma; 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. Updated 2021. Accessed June 10, 2021. https://ginasthma.org/wp-content/uploads/2021/05/GINA-Main-Report-2021-V2-WMS.pdf 14. Rayos Prescribing Information. March 2021. 15. To M, Tsuzuki R, Katsube O, Yamawaki S, et al. Persistent asthma from childhood to adulthood presents a distinct phenotype of adult asthma. J Allergy Clin Immunol Pract. 2020;8(6):1921-1927.e2.16. Fahy JV. Type 2 inflammation in asthma—present in most, absent in many. Nat Rev Immunol. 2015;15(1):57-65. 17. Tran TN, Zeiger RS, Peters SP, et al. Overlap of atopic, eosinophilic, and TH2-high asthma phenotypes in a general population with current asthma. Ann Allergy Asthma Immunol. 2016;116(1):37-42. 18. Robinson D, Humbert M, Buhl R, et al. Revisiting type 2-high and type 2-low airway inflammation in asthma: current knowledge and therapeutic implications. Clin Exp Allergy. 2017;47(2):161-175. 19. 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. 20. 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. 21. Agache I, Akdis C, Jutel M, Virchow JC. Untangling asthma phenotypes and endotypes. Allergy. 2012;67(7):835-846. 22. 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.