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On chromosome 2 at about 64 cM (p = 0.002) evidence was found for a locus for severe asthma and for house dust mite sensitive asthma.
Forty-seven children aged 5 to 14 years with confirmed house dust mite sensitive asthma were randomised to receive six months treatment with either house dust mite barrier or placebo bedding.
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Aspirin-sensitivity triad or aspirin triad is also known as aspirin-intolerant asthma, aspirin-sensitive asthma (ASA-sensitive), Widal triad, Francis triad, Fernand-Widal triad, or aspirin-exacerbated respiratory disease (AERD).
To determine the prevalence of ibuprofen-sensitive asthma in school-aged children with mild or moderate persistent asthma.
On the other hand, there are many differences in phenotypes of childhood compared to adult asthma, for example, aspirin-sensitive asthma is a subset rather found in adults, and allergic or eosinophilic and non-allergic or non-eosinophilic asthma are not identical in children and adults.
Moreover, patients with aspirin-sensitive asthma seem to respond well to LTRAs.
This was true for tissue from non-aspirin-sensitive donors, as well as from patients with aspirin-sensitive asthma.
All subjects in the aspirin-sensitive asthma group had a history of aspirin-induced reaction, in that they developed a respiratory-type reaction following aspirin or NSAID ingestion.
Interestingly, after incubation with IL-1β, cells derived from patients with aspirin-sensitive asthma release higher levels of PGE2 than cells cultured from control donors.
These observations are consistent with others in the literature showing that both isoforms of COX are present in the airways of patients with aspirin-sensitive asthma (5).
Furthermore, in a subgroup of patients with asthma, aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) induce bronchoconstriction and acute asthma, resulting in the "aspirin-sensitive asthma" condition (3).
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