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.