Although aspirin sensitive asthma has been recognized as a clinical entity since the beginning of this century, the mechanism for the production of this syndrome still remains obscure. Recent studies have indicated a higher than previously appreciated incidence of aspirin sensitive asthma, perhaps approaching 40% of steroid-dependent asthmatics. Challenge with both oral and bronchial instilled aspirin may be useful to identify aspirin-sensitive individuals. During aspirin-induced reactions, increased vascular permeability is noted. In addition, aspirin-sensitive individuals have altered levels of production of leukotriene E4 and enhanced sensitivity to inhaled leukotriene E4. However, nasal secretions of aspirin-sensitive individuals demonstrate enhanced leukotriene C4 concentration after aspirin challenge. It has also been noted that nonaspirin sensitive patients have enhanced leukotriene C4 concentration. Thus, the specific defect leading to the pathogenesis of aspirin-sensitive asthma and rhinosinusitis in selected individuals remains obscure. Eosinophil activation has been noted in aspirin-sensitive rhinosinusitis patients; however, other cell types, including platelets and monocytes, have also been noted to exhibit metabolic abnormalities in this syndrome. Aspirin desensitization may be a useful option in selected patients with significant aspirin sensitive rhinosinusitis and asthma.
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