Purpose of review
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most frequent drugs involved in hypersensitivity drugs reactions. Both immunological and nonimmunological mechanisms can be involved. We describe the different phenotypes as well as analyze the genetic basis for NSAIDs hypersensitivity.
Five major clinical entities are currently accepted in the classification of hypersensitivity reactions to NSAIDs. Three are mediated by nonspecific immunological mechanisms: NSAIDs-exacerbated respiratory disease, NSAIDs-exacerbated cutaneous disease and NSAIDs-induced urticaria/angioedema. Two are mediated by specific immunological mechanisms: single-NSAID-induced urticaria/angioedema or anaphylaxis and single-NSAID-induced delayed hypersensitivity reactions. The classification becomes more complex if we consider that in an important number of cases skin and airway involvement can occur, as well as the participation of other organs.
Hypersensitivity reactions to NSAIDs are more complex than for other drugs like betalactams in terms of the number and types of reactions elicited, and mechanisms involved. As NSAIDs are the most frequent cause of drug hypersensitivity, it is feasible to gather a sufficient number of cases for undertaking pharmacogenetic studies.