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En minut för att sprida ljus över nya möjligheter inom KOL

Författare : Sanofi
Redaktionsteam

Att förstå typ 2-inflammation* kan hjälpa till att belysa varför vissa patienter fortsätter att få exacerbationer. Titta på denna video för att lära dig hur.1

Tänk om du kunde identifiera patienter med högre risk?

En djupare titt på inflammationen bakom exacerbationer kan sprida ljus över nya möjligheter inom KOL. Mät blodeosinofiler, en biomarkör för KOL med typ 2-inflammation*, vilket kan hjälpa dig att identifiera de patienter som löper ökad risk för exacerbationer.1

Titta på videon nedan för att bättre förstå exacerbationer vid KOL och bättre identifiera patienter i riskzonen.1

Ignite new thinking in COPD - COPD, chronic obstructive pulmonary disease

In patients with COPD, exacerbations may :

  • Increase the risk of another1
  • Accelerate lung function decline2
  • Increase morbidity and mortality risk1,3-6

Different types of chronic inflammation have an important role in COPD7-15
Type 2 inflammation and beyond type 2 inflammation
Identifying COPD patients with type 2 inflammation may help determine those at increased risk of exacerbations16
Look for blood eosinophils, a biomarker of COPD with type 2 inflammation17,18,a,b
EOS ≥ 300 cells/ μL à 32% increased risk of COPD exacerbations16a,b
Understanding type 2 inflammation in COPD may shed light on why some patients continue to experience exacerbations

a Results from an observational analysis of 1553 patients with GOLD spirometry grade 2-4 COPD evaluating the relationship between blood eosinophil count and COPD exacerbation risk.
b Stratified analysis confirmed that increased exacerbation risk was driven by subjects with a history of frequent exacerbations, defined as ≥2 exacerbations per year.

  1. Suissa S, Dell’Anello S, Ernst P. Long-term natural history of chronic obstructive pulmonary disease: severe exacerbations and mortality. Thorax. 2012;67(11):957-963.

  2. Halpin DMG, Decramer M, Celli BR, Mueller A, Metzdorf N, Tashkin DP. Effect of a single exacerbation on decline in lung function in COPD. Respir Med. 2017;128:85-91.

  3. Hartl S, Lopez-Campos JL, Pozo-Rodriguez F, et al. Risk of death and readmission of hospital-admitted COPD exacerbations: European COPD Audit. Eur Respir J. 2016;47(1):113-121.

  4. Jones SE, Barker RE, Nolan CM, Patel S, Maddocks M, Man WDC. Pulmonary rehabilitation in patients with an acute exacerbation of chronic obstructive pulmonary disease. J Thorac Dis. 2018;10(suppl 12):S1390-S1399.

  5. Goërtz YMJ, Spruit MA, Van’t Hul AJ, et al. Fatigue is highly prevalent in patients with COPD and correlates poorly with the degree of airflow limitation. Ther Adv Respir Dis. 2019;13:1753466619878128. doi:10.1177/1753466619878128

  6. Miravitlles M, Worth H, Soler Cataluña JJ, et al. Observational study to characterise 24-hour COPD symptoms and their relationship with patient-reported outcomes: results from the ASSESS study. Respir Res. 2014;15(1):122. doi:10.1186/s12931-014-0122-1

  7. Cosio Piqueras MG, Cosio MG. Disease of the airways in chronic obstructive pulmonary disease. Eur Respir J. 2001;18(suppl 34):41s-49s.

  8. Tajti G, Gesztelyi R, Pak K, et al. Positive correlation of airway resistance and serum asymmetric dimethylarginine level in COPD patients with systemic markers of low-grade inflammation. Int J Chron Obstruct Pulmon Dis. 2017;12:873-884.

  9. Higham A, Quinn AM, Cançado JED, Singh D. The pathology of small airways disease in COPD: historical aspects and future directions. Respir Res. 2019;20(1):49. doi:10.1186/s12931-019-1017-y

  10. O’Donnell DE, Parker CM. COPD exacerbations. 3: Pathophysiology. Thorax. 2006;61(4):354-361.

  11. Calverley PMA. Respiratory failure in chronic obstructive pulmonary disease. Eur Respir J. 2003;22(suppl 47):26s-30s.

  12. Roussos C, Koutsoukou A. Respiratory failure. Eur Respir J. 2003;22(suppl 47):3s-14s.

  13. Aghapour M, Raee P, Moghaddam SJ, Hiemstra PS, Heijink IH. Airway epithelial barrier dysfunction in chronic obstructive pulmonary disease: role of cigarette smoke exposure. Am J Respir Cell Mol Biol. 2018;58(2):157-169.

  14. Brightling CE, Saha S, Hollins F. Interleukin-13: prospects for new treatment. Clin Exp Allergy. 2010;40(1):42-49.

  15. Barberá JA, Peinado VI, Santos S. Pulmonary hypertension in chronic obstructive pulmonary disease. Eur Respir J. 2003;21(5):892-905.

  16. Yun JH, Lamb A, Chase R, et al; for the COPDGene and ECLIPSE Investigators. Blood eosinophil count thresholds and exacerbations in patients with chronic obstructive pulmonary disease. J Allergy Clin Immunol. 2018;141(6):2037-2047.e10.

  17. Halpin DMG, Dransfield MT, Han MK, et al. The effect of exacerbation history on outcomes in the IMPACT trial. Eur Respir J. 2020;55:1901921. doi:10.1183/13993003.01921-2019

  18. Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (2023 report). Accessed [June 2, 2023]. https://goldcopd.org/2023-gold-report-2/

*Typ 2-inflammation definieras enligt förhöjda biomarkörer vid KOL (Blod-EOS ≥300 celler/µL eller ≥2%, eller Sputum-EOS ≥ 3%)

Referenser

  1. Yun JH, Lamb A, Chase R, et al; for the COPDGene and ECLIPSE Investigators. Blood eosinophil count thresholds and exacerbations in patients with chronic obstructive pulmonary disease. J Allergy Clin Immunol. 2018;141(6):2037-2047.e10.

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