SERUM IgE
BLOOD EOSINOPHILS
COMORBIDITIES
LUNG FUNCTION
EXACERBATIONS
OCS USE

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SERUM lgE LEVEL
30 IU/mL
30 IU/mL
>800 IU/mL

Allergic asthma is mediated by the Type 2 immune response, and therefore cannot be fully characterized by serum IgE levels.1

BLOOD EOSINOPHIL LEVEL
75 cells/μL
75 cells/μL
>500 cells/μL

Blood eosinophil counts are highly variable and may fail to accurately characterize the broad spectrum of Type 2 inflammation
in asthma.2,3

COMORBIDITIES

—  Select all that applyType 2 inflammation may drive inflammatory
diseases of the upper and lower airways.4,5
 Nasal polyps
Nasal polyps are associated with severe asthma and present additional challenges for optimal patient management.6
 Chronic rhinosinusitis with nasal polyps
Patients with chronic rhinosinusitis with nasal polyps (CRSwNP) have a higher prevalence of premorbid and concurrent asthma.7
 Allergic rhinitis and rhinosinusitis
Patients with uncontrolled persistent asthma have a higher prevalence of comorbid allergic rhinitis and rhinosinusitis.8
LUNG FUNCTION
80% (FEV1 % predicted)
80%
50%

Reversible airway obstruction in uncontrolled asthma is caused by bronchoconstriction and mucus production, which contributes to the risk of severe exacerbations and poor
asthma control.9-14

ASTHMA EXACERBATIONS IN THE PRIOR YEAR
  1 exacerbation
  2 exacerbations
  3 exacerbations

Uncontrolled persistent asthma is strongly predictive of future asthma exacerbations.14

Asthma exacerbations were 3 times more likely to occur in patients with uncontrolled asthma than in those with better asthma control.14

DOES THIS PATIENT TAKE ORAL CORTICOSTEROIDS (OCS)?
  Short-term use (≤1 month)
  Intermittent use (>1 month – 6 months)
  Chronic use (>6 months)
  No use

Due to the potential for substantial side effects with long-term use of OCS, guidelines suggest not using OCS as maintenance therapy until all other pharmacologic options have been exhausted.15,16

THIS PATIENT MAY HAVE
TYPE 2 ASTHMAa

a For educational purposes only. This is not based on a real patient and is not intended as a diagnostic tool.

Type 2 inflammation IN ASTHMA encompasses both allergic AND eosinophilic phenotypes

Patients with uncontrolled persistent asthma driven by
Type 2 inflammation may present with1,4,14,17-21:

  • A broad range of symptoms
  • Higher exacerbation rates
  • Impaired lung function
  • Medication side effects
  • Poor quality of life
SERUM IgE LEVEL
BLOOD EOSINOPHIL LEVEL
COMORBIDITIES
LUNG FUNCTION
ASTHMA EXACERBATIONS
OCS USE

Asthma patients with Type 2 inflammation may present with a range of clinical characteristics

  • SERUM IgE LEVEL 100 IU/mL
  • COMORBIDITIES Chronic rhinosinusitis with nasal polyps
  • ASTHMA EXACERBATIONS 2 in the prior year
  • BLOOD EOSINOPHIL LEVEL 350 cells/μL
  • LUNG FUNCTION 70% FEV1 predicted
  • OCS USE Intermittent use (>1 month - 6 months)
  • SERUM IgE LEVEL 380 IU/mL
  • COMORBIDITIES Nasal polyps
  • ASTHMA EXACERBATIONS >3 in the prior year
  • BLOOD EOSINOPHIL LEVEL 215 cells/μL
  • LUNG FUNCTION 60% FEV1 predicted
  • OCS USE Chronic use (>6 months)
  • SERUM IgE LEVEL 450 IU/mL
  • COMORBIDITIES Allergic rhinitis
  • ASTHMA EXACERBATIONS 2 in the prior year
  • BLOOD EOSINOPHIL LEVEL 105 cells/μL
  • LUNG FUNCTION 65% FEV1 predicted
  • OCS USE Short term use (≤1 month)
  • SERUM IgE LEVEL 250 IU/mL
  • COMORBIDITIES Chronic rhinosinusitis with nasal polyps
  • ASTHMA EXACERBATIONS 1 in the prior year
  • BLOOD EOSINOPHIL LEVEL 480 cells/μL
  • LUNG FUNCTION 50% FEV1 predicted
  • OCS USE Chronic use (>6 months)
Identifying patients with uncontrolled asthma begins with an understanding of Type 2 inflammation

References: 1. 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. 2. Albers FC, Müllerová H, Gunsoy NB, et al. Biologic treatment eligibility for real-world patients with severe asthma: the IDEAL study. J Asthma. 2018;55(2):152-160. 3. Korevaar DA, Westerhof GA, Wang J, et al. Diagnostic accuracy of minimally invasive markers for detection of airway eosinophilia in asthma: a systematic review and meta-analysis. Lancet Respir Med. 2015;3(4):290-300. 4. Wenzel SE. Emergence of biomolecular pathways to define novel asthma phenotypes: type-2 immunity and beyond. Am J Respir Cell Mol Biol. 2016;55(1):1-4. 5. Ray A, Raundhal M, Oriss TB, Ray P, Wenzel SE. Current concepts of severe asthma. J Clin Invest. 2016;126(7):2394-2403. 6. Ceylan E, Gencer M, San I. Nasal polyps and the severity of asthma. Respirology. 2007;12(2):272-276. 7. Tan BK, Chandra RK, Pollak J, et al. Incidence and associated premorbid diagnoses of patients with chronic rhinosinusitis. J Allergy Clin Immunol. 2013;131(5):1350-1360.
8. Marcus P, Arnold RJG, Ekins S, et al; CHARIOT Study Investigators. A retrospective randomized study of asthma control in the US: results of the CHARIOT study. Curr Med Res Opin. 2008;24(12):3443-3452. 9. 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. 10. Mauad T, Bel EH, Sterk PJ. Asthma therapy and airway remodeling. J Allergy Clin Immunol. 2007;120(5):997-1009.
11. Fehrenbach H, Wagner C, Wegmann M. Airway remodeling in asthma: what really matters. Cell Tissue Res. 2017;367(3):551-569. 12. Holgate ST. The airway epithelium is central to the pathogenesis of asthma. Allergol Int. 2008;57(1):1-10. 13. 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 lmmunol Pract. 2014;2(6):751-758. 14. 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. 15. 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. Bethesda, MD: NHLBI Health Information Center; 2007. NIH publication 07-4051. 16. Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 2018. http://ginasthma.org/2018-gina-report-global-strategy-for-asthma-management-and-prevention/. Accessed March 8, 2018. 17. 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. 18. 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. 19. 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. 20. Di Marco F, Verga M, Santus P, et al. Close correlation between anxiety, depression, and asthma control. Respir Med. 2010;104(1):22-28. 21. 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. 22. Seys SF, Scheers H, Van den Brande P, et al. Cluster analysis of sputum cytokine-high profiles reveals diversity in T(h)2-high asthma patients. Respir Res. 2017;18(1):39. doi:10.1186/s12931-017-0524-y 23. Peters MC, Mekonnen ZK, Yuan S, Bhakta NR, Woodruff PG, Fahy JV. Measures of gene expression in sputum cells can identify TH2-high and TH2-low subtypes of asthma. J Allergy Clin Immunol. 2014;133(2):388-394. 24. Agache I, Akdis C, Jutel M, Virchow JC. Untangling asthma phenotypes and endotypes. Allergy. 2012;67(7):835-846. 25. Bjermer L. Time for a paradigm shift in asthma treatment: From relieving bronchospasm to controlling systemic inflammation. J Allergy Clin Immunol. 2007;120(6):1269-1275.