Aspirin-induced asthma, or Aspirin Exacerbated Respiratory Disease (AERD) is characterized clinically by the triad of asthma, recurrent nasal polyposis and hypersensitivity to aspirin and other cyclooxygenase 1 (COX-1) inhibitors such as ibuprofen.
Asthma symptoms translate to difficulty breathing after taking aspirin or other COX-1 inhibitors. COX-1 inhibitors are also present in food, vegetables and fruits. Low salicylate diets exist to alleviate asthma symptoms with AIA.
The AERD asthma subtype accounts for 5%–10% of adult asthmatics, yet represents a disproportionately high proportion of severe asthma cases and can be difficult to diagnose and treat. Desensitization to aspirin as performed by a trained Physician can reduce AERD symptoms. Aspirin is an inhibitor of COX-1 which is a key enzyme in the inflammatory response, starting from Arachidonic acid producing downstream prostaglandins mediators of inflammation.
For reasons yet to be clearly defined, leukotrienes are know to be augmented parallel to AERD. These include cysteinyl leukotrienes known to be overproduced in chronic sinusitis with nasal polyps and can perhaps explain or define chronic sinusitis with nasal polyps.
The eicosanoid inflammatory pathway is that of a response where arachidonic acid is converted to prostaglandin H2 via COX-1, COX-2 (the target of acetaminophen) or is converted to leukotrienes mediators of inflammatory response via lipoxygenase 5. The prostaglandins are involved in inflammation, fever, clotting, blood pressure, immune modulation, etc.
In aspirin-induced asthma, an increase in PGD-2 and a decrease in PGE-2 is observed, and a shift towards cysteinyl leukotrienes, tilting the balance towards inflammation and bronchoconstriction.
Also, FDA-approved drugs such as montelukast may help management of the disease.
Further, desensitization to aspirin as performed by trained Physicians in a clinical setting was demonstrated to improve asthma symptoms and sinus inflammation.