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HOW IT WORKS
OK GOT ITAllergic asthma is mediated by the Type 2 immune response, and therefore cannot be fully characterized by serum IgE levels.1
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 inflammatorydiseases of the upper and lower airways.4,5
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
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
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
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.