1-4OAS Identification of Aspirin Exacerbated Respiratory Disease (AERD) Phenotypes Using Two Step Cluster Analysis

Wednesday, 14 October 2015: 11:45 - 12:00
Room R1 ABC (Floor 3) (Coex Convention Center)

Hyun Young Lee , Clinical Trial Center, Ajou University Medical Center, Suwon, South Korea

Young Min Ye, MD, PhD , Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, South Korea

Su Chin Kim , Clinical Trial Center, Ajou University Medical Center, Suwon, South Korea

Hae-Sim Park, MD, PhD , Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, South Korea

Background

Asthma is known a disease with many variations, and one of the subtypes is Aspirin Exacerbated Respiratory Disease (AERD). AERD patients experience severe bronchoconstriction to aspirin or other NSAIDs. AERD patients in general have relatively severe asthma with a high proportion requiring long-term oral corticosteroid (OCS). We aimed to classify AERD phenotype and its clusters.

Method

302 AERD patients who followed up at least 1 year in Ajou university hospital from Jan 1996 to Jul 2013 were enrolled. To fracture AERD phenotype using atopy, chronic rhinosinusitis (CRS) and urticaria, we performed two step cluster analysis. Severe exacerbation was defined as patients having taken intravenous steroid treatment or at least 2 burst of OCS in a year. The mean follow up duration was 7.2±5.2. Clinical characteristics among clusters were examined by Fisher’s exact test and ANOVA. The generalized estimating equation was applied for the possession rate of anti-asthmatics and severe exacerbation in a year.

Results

In the AERD, 4 clusters having good quality (0.7 silhouette) were obtained according to the urticarial, CRS and atopy: cluster 1 (AERD with CRS and atopy, and without urticaria), cluster 2 (AERD with only CRS), cluster 3 (AERD with only atopy) and cluster 4 (AERD with urticaria). There were significantly difference in severe asthma (27.3%, 14.8%, 19.7% and 7.7% in cluster 1, 2, 3 and 4, respectively, p=0.042), total IgE (564.3±732.5, 216.5±266.4, 352.0±398.7 and 345.5±440.7, p<0.001), sputum eosinophil (%)(31.5±37.8, 29.4±39.7, 13.4±27.3 and 18.7±30.9, p=0.024), and peripheral eosinophil count (485.0±374.8, 523.0±561.4, 349.3±379.3 and 245.1±242.5, p<0.001).

The occurrence of severe exacerbation was significant higher in cluster 1 than cluster 3 (OR: 2.121 (1.281-3.510), p=0.004). The patients of cluster 1 showed significantly higher possession rate of ICS+LABA than cluster 2, 3 and 4 (p<0.05), and of OCS than cluster 3 (p=0.010). The possession rate of LTRA was significantly higher in cluster 1 and 2 (vs. cluster 3 and 4, p<0.05). The possession rate of anti-histamines was significantly lower in cluster 3 (vs. 1,2 and 3, p<0.05).

Conclusion

Severe exacerbation rate and the possession rate of major anti-asthmatics were quite different among 4 clusters. Even AERD is recognized as a subtype of asthma, our results suggested that sophisticated therapeutic approach is needed for patients with AERD.