Clinical Classification of Sensitivities to NSAIDs

The classic aspirin triad or NSAID sensitivity consists of asthma, rhinosinusitis, and nasal polyps. Symptoms may develop stepwise over a number of years. In some patients only two of the main symptoms may be present. It is one of two cross-reactive types of NSAID sensitivity. This state of intolerance, which occurs more often in women than men, is observed in patients with aspirin-induced asthma, but the recently suggested name, aspirin-exacerbated respiratory disease, is probably a more appropriate designation for the condition that is essentially not a hue drag hypersensitivity but an underlying chronic inflammatory respiratory disease occasionally exacerbated by aspirin or some other NSAID. Ingestion of aspirin or some NSAIDs by these patients provokes, within 3 h (usually 30 min to 2 h), an acute 

Respiratory reactions in aspirin-induced asthma are triggered by COX-1 and not COX-2 inhibitors. 

Airways symptoms tend to correlate with the potency of the inducing COX-1 NSAID. 

Leukotriene receptor antagonists and inhibitors of leukotriene synthesis prevent, or partially prevent, symptoms following aspirin challenge. 

Abnormalities in the lipoxygenase pathway may exist in patients hypersensitive to COX-1 inhibitors since they show higher levels of leukotrienes even before exposure to aspirin and other NSAIDs. Patients with aspirin-induced asthma may show increased baseline levels of urinary UK, that increase after challenge with aspirin and correlate with the severity of the induced reaction. 

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