Source: Annual Congress 2002 - Bronchial responsiveness in asthma and COPD
Disease area: Airway diseases

Abstract

Exercise-induced asthma (EIA) is a common phenomenon,its mechanism is undetermined.Inflammatory mediator release has been strongly implicated, but the triggering mechanism is uncertain. We tested the hypothesis that complement activation has a role in EIA through triggering mediator release.31 atopic asthmatic patients (20 are exercise responder, ER, and 11 are exercise non-responder,EN) and 14 normal subjects (C) were investigated by studying the serum level of complement activation (C4d for classical pathway, Bb for alternative pathway, SC5b-9 for terminal activation) both pre- and 15 min post-exercise challenge.Only In ER (the exercise - induced reduction in FEV1 as a percent of the baseline value is >=15%) the Bb rose significantly (from 3.45 ±] 1.83 mgr/ml, to 4.74 ±] 2.69, P<0.05 ) after exercise and not in EN or in normal subjects.C4d and SC5b did not change significantly in any group. Inhalation of fluticasone propionate (FP 250 mgr, bid, for 14 days) resulted in significant protection against the development of EIA in ER (the post-exercise % fall in FEV1= 29.61 ±] 13.88 without treatment and =8.43 ±] 3.08 with treatment,P<0.05). No significant change in the level of Bb, C4d, or SC5b-9 in response to exercise could be detected after treatment with FP. We conclude that the complement activation has a role in the pathogenesis of EIA and the protective effect of corticosteroid agaist EIA is related to its ability to inhibit complement activation.

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I. M. El-Akkary, E. M. Hassan, M. S. Ibrahim, I. A. Rashwan, L. M. Abou-Shamma, A. Mastino (Alexandria, Egypt; Rome, Italy). Complement activation and exercise-induced asthma. Eur Respir J 2002; 20: Suppl. 38, 1198

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