SESSION TITLE: Allergy and Airway Poster Discussions
SESSION TYPE: Original Investigation Poster Discussion
PRESENTED ON: Wednesday, October 28, 2015 at 08:45 AM - 10:00 AM
PURPOSE: Severe asthma is a heterogenous disease. Current management of severe asthma is moving towards targeted treatment addressing the mechanism of disease including inflammation. This study aims to examine the sputum inflammatory phenotype of severe asthmatics who are exacerbation-prone.
METHODS: Cross sectional study of patients with severe treatment- resistant asthma (on a combination of high-dose inhaled corticosteroids and long-acting beta agonists) and frequent exacerbations (≥2 exacerbations requiring systemic corticosteroids in the past year) was performed. Sputum induction was performed using a validated protocol. Demographic data, sputum inflammatory cell counts, spirometry, methacholine challenge test results and blood eosinophil levels were obtained. Sputum cell counts were read by an investigator blinded to clinical phenotype of the patient. The cell counts were classified into 4 groups: eosinophilic (>3%), neutrophilic (>76%), paucigranulocytic (normal levels of both eosinophils and neutrophils) and mixed (more than 1 predominant cell type present).
RESULTS: 8 Patients were recruited. 3 patients could not expectorate any sputum despite induction. The results of 5 successful patients (3 males, 2 females) are presented. Mean age was 48 ±11.2 years and median number of controllers used was 2 (IQR: 2-4). They had an average of 4 ± 1.5 exacerbations in the past year and the mean post-bronchodilator FEV1 was 2.50 ± 0.65L (85.8±9.9% predicted). The median blood eosinophil count was 0.44 x 109/L (IQR: 0.37-0.67 x 109/L). 3 patients had a predominantly eosinophilic inflammatory phenotype, whilst 2 had a paucigranulocytic inflammatory phenotype. The median eosinophil count from induced sputum was 6.00% (IQR: 0.8- 15.7%) and median neutrophil count was 12.2% (IQR: 4.8-12.7%).
CONCLUSIONS: Preliminary results seem to suggest more eosinophilic inflammation in the sputum of frequent exacerbating severe treatment-resistant asthmatics. None of the patients examined had neutrophilic inflammation in their sputum.
CLINICAL IMPLICATIONS: Treatment targeting eosinophils and the Th2 pathway may be the key to reducing exacerbations amongst some of these patients with frequent exacerbations. Lack of sputum production and paucigranulocytic picture suggest airway inflammation may not be the main mechanism driving exacerbations in the other group of frequent exacerbators. Further studies are underway.
DISCLOSURE: The following authors have nothing to disclose: Shera Tan, Carrie Leong, Angela Takano, Therese Lapperre, Keng Leong Tan, Philine Chan, Kah Ling Lim, Mariko Koh
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