Aspirin intolerance syndrome is due to disturbances in the
arachidonic acid metabolism implicating both the
lipoxygenase and
cyclooxygenase pathways. This results in imbalances of
eicosanoid,
leukotriene and
prostaglandin synthesis. Thus, preinflammatory cysteinyl
leukotrienes increase and antiinflammatory
prostaglandins (PG) such as
PGE2 decrease. Clinically, intolerance reactions to nonsteroidal antiinflammatory drugs (
NSAIDs) can lead to different clinical manifestations; five phenotypes of the
aspirin intolerance syndrome are listed in the ENDA classification.
Aspirin-exacerbated respiratory disease (AERD) is the most common phenotype characterized by an eosinophil-dominated inflammatory disease of the airways that presents clinically with
nasal polyps, chronic
sinusitis and
bronchial asthma. About 34 % of patients with
aspirin-induced asthma and
rhinosinusitis are thought to have AERD. Important biochemical findings in many AERD patients are increased basal
leukotriene levels (at least in cell cultures) that excessively increase after intake of COX-1 inhibitors.
Aspirin desensitization uses the repetitive application of
aspirin to induce a tolerance to
NSAIDs, especially COX-1 inhibitors. After a dose-increase phase reaching a threshold dose, a dose-continuation phase is performed. For application, the nasal, bronchial, oral and intravenous routes have been described.
Aspirin desensitization has been proven to be efficacious and safe and was able to reduce the need for other medications in AERD patients.