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An Explanation of the Asthma Paradox

1993; American Thoracic Society; Volume: 147; Issue: 6_pt_2 Linguagem: Inglês

10.1164/ajrccm/147.6_pt_2.s29

2376-3752

Clive P. Page,

Eosinophilic Esophagitis

The morbidity and mortality associated with asthma are rising, despite increased usage of anti-asthma medications. This report attempts to provide a plausible hypothesis for the “asthma paradox.” The hypothesis involves the role of mast cell degranulation as an endogenous anti-inflammatory mechanism to prevent antigens from entering the lower airways and to limit the extent of the subsequent repair process. By treating symptoms of asthma with drugs such as β2 agonists that inhibit mast cell degranulation, increased inflammation is allowed to occur, which may lead to the chronic appearance of excess repair tissue and the acceleration of the disease process.