Allergy and intolerance to nonsteroidal anti-inflammatory agents.

Abstract

Intolerance to aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) usually includes severe bronchial asthma, nasal polyposis, and diverse systemic manifestations. These manifestations may be reproduced by challenge tests. Patients with aspirin and NSAID intolerance can be desensitized. Intolerance to aspirin and NSAIDs has been related to an alteration of arachidonic acid metabolism. Aspirin and NSAIDs inhibit the cycl-oxygenase (CO) enzyme which leads to the synthesis of prostaglandins and thromboxane. In intolerant patients, there is an up-regulation of the lip-oxygenase (LO) pathway, which leads to an overproduction of leukotrienes (LTs). LTs are potent spasmogens for nonvascular smooth muscles and exhibit chemotactic activity for neutrophils and proinflammatory properties. Moreover, it has been shown that intolerant asthmatics had a bronchial hypereactivity to LTE4. Based on these observations, it has recently been shown that administration of LT receptor antagonists and LO inhibitors might decrease or abolish adverse reactions to aspirin and NSAIDs in intolerant asthmatics. Like all analgesic drugs, NSAIDs can lead to various side effects, including IgE-dependent allergy and pharmacological intolerance owing to changes in metabolism of arachidonic acid (AA). Although the incidence of these adverse reactions is not precisely known, pharmacological intolerance appears to be far more common than allergy. The incidence of NSAID intolerance varies depending on the method of evaluation used. It is approx 4% when based on patient interviews, but there are numerous false positives and false negatives. When provocation tests are used, the reported incidence ranges from 10-20% (1).