Page 56 - ADULT-ONSET ASTHMA PREDICTORS OF CLINICAL COURSE AND SEVERITY

ADULT-ONSET ASTHMA – PREDICTORS OF CLINICAL COURSE AND SEVERITY
asthma a acks have also been noted for various biomarkers.7, 29, 30 These data suggest that discordance between biomarkers in di erent asthma phenotypes may point towards di erent underlying mechanisms.
There was no signi cant di erence in diagnos c accuracy of FeNO and blood eosinophils between atopic and non-atopic pa ents. One previous study showed lower diagnos c accuracy for FeNO in non-atopic pa ents than in atopic pa ents 8. The discrepancy between these results and ours could be due to di erences in pa ents’ characteris cs or the devices used to measure FeNO. The higher diagnos c accuracy of total IgE in non-atopic pa ents as compared to atopic pa ents might be related to di erent underlying mechanisms. While eosinophilia in classical atopic asthma is likely to be T-helper cell (TH)-2 driven and includes higher basal IgE produc on, in non-atopic asthma, there is accumula ng evidence that ac va on of eosinophils might be mediated by alterna ve pathways 14.
Pa ents with severe asthma o en show discrepancies between airway and blood eosinophilia, which is probably explained by their high doses of inhaled or oral cor costeroid treatment. We did not nd a di erence in the diagnos c accuracy of blood eosinophils or FeNO between mild-moderate and severe asthma pa ents, but previous studies have found con ic ng results. One study found and AUC of blood eosinophils of 0.55 in cor costeroid-treated pa ents, and of 0.73 in untreated pa ents 31, whereas these numbers were 0.75 and 0.62, respec vely, in another study 10. Three previous studies evaluated the accuracy of FeNO among severe/treated and mild/untreated asthma pa ents 8, 10, 32. None of them found considerable di erences in the di erences in the AUC’s. Remarkably, despite comparable AUC’s for FeNO and blood eosinophils in our study, the upper threshold range for blood eosinophils was rela vely wide due to the higher threshold in pa ents with severe asthma as compared to the other asthma phenotypes (Table 3 and E10). Apparently, a subset of pa ents with severe asthma shows elevated levels of blood eosinophils without evidence of airway eosinophilia, which con rms previous ndings12. Circula ng eosinophils might serve as a reservoir in these pa ents, thereby maintaining airway in amma on, which cannot be adequately suppressed by inhaled cor costeroids.
Smoking in asthma has o en been associated with neutrophilic airway in amma on 15, and
enhancement of T 2 mediated in amma on33, and has also been shown to be associated with H
reduced FeNO levels 34. Therefore, (ex)smoking could have had an e ect on the diagnos c accuracy of FeNO to detect sputum eosinophilia 8, 9. A previous study found a lower AUC for FeNO among smokers compared to non-smokers (0.63 vs. 0.77) 8, but this was obviously not the case in our study. This suggests that even in smokers and ex-smokers FeNO can be used as a biomarker for sputum eosinophilia.
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