Abstract
Nonsteroidal anti-inflammatory drugs (NSAIDs) are probably the main causes of drug hypersensitivity reactions, with NSAIDs-induced acute urticaria/angioedema (NIUA) being the most frequent clinical phenotype. The underlying mechanism of NSAID-hypersensitivity has been linked to COX-1 inhibition and the subsequent increase in cysteinyl-leukotrienes release from arachidonic acid, triggering a reaction in susceptible individuals. Different studies have highlighted the association between NIUA and the atopic status, especially with Dermatophagoides pteronyssinus (DP) sensitisation.
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