Poster Presentations: Tuesday, October 25, 2011 |

Pathophysiological Features of Severe Asthma Patients With Frequent Exacerbations FREE TO VIEW

Akio Niimi, DSc; Makiko Jinnai, DSc; Hisako Matsumoto, DSc; Isao Ito, DSc; Tsuyoshi Oguma, MD; Michiaki Mishima, DSc
Chest. 2011;140(4_MeetingAbstracts):224A. doi:10.1378/chest.1118761
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PURPOSE: We aimed to clarify the detailed pathophysiological features including inflammatory profiles of sputum in severe asthma patients with frequent exacerbations (FE).

METHODS: Non-smoking outpatients with severe asthma who required high-dose inhaled corticosteroid (≥ 800 mcg/day of fluticasone or equivalent) and additional controller medication(s) for at least 1 year were divided into those with FE (≥ 2 exacerbations requiring oral corticosteroid in the previous year) and remainders as controls (≤ 1 such exacerbation). The two groups were compared for background characteristics and indices of spirometry, methacholine airway responsiveness, impulse oscillation, exhaled NO (eNO), sputum cells and mediators, and CT (airway wall thickness and air trapping) when their asthma was stable.

RESULTS: Eight patients with FE and 14 controls who successfully produced sputum were analyzed. Patients with FE had higher prevalence of familial history of asthma and higher eNO levels, and lower FEV1 (% predicted) and SpO2 as compared with controls, while the difference in sputum eosinophil count was marginal. Sputum levels of prostaglandin (PG) E2 was lower in FE than in controls, but levels of PGD2, PGF2α, thromboxane B2 , lipoxin A4, cysteinyl leukotrienes, and eosinophil cationic protein were similar between the two groups. Sputum neutrophil count and interleukin-8 and neutrophil elastase levels, IgE, atopy, airway responsiveness, impulse oscillation and CT indices did not also differ.

CONCLUSIONS: Patients with FE involve more severe airflow obstruction and airway inflammation as demonstrated by eNO levels, despite intensive treatment. Although this is a small pilot study, decrements in production of an “inhibitory” mediator PGE2 might likely be involved in the pathogenesis of FE. Larger studies are required to confirm these results.

CLINICAL IMPLICATIONS: Pathophysiological details of FE including roles of PGE2 need to be further explored in order to establish its treatment strategy, because FE is one of the most important phenotypes of severe asthma.

DISCLOSURE: The following authors have nothing to disclose: Akio Niimi, Makiko Jinnai, Hisako Matsumoto, Isao Ito, Tsuyoshi Oguma, Michiaki Mishima

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