Nonsteroidal anti-inflammatory medication (NSAIDs) are the primary reason for drug hypersensitivity, being NSAID-induced urticaria/angioedema (NIUA) probably the most commun medical entity. NIUA has been related to an imbalance between prostaglandin and leukotriene (LT) biosynthesis within the arachidonic acid (AA) pathway resulting from COX-1 inhibition. LTB4 is an eicosanoid launched on this pathway by the LTA4 hydrolase/aminopeptidase (LTA4H). Though some research have reported associations between NIUA and single nucleotide polymorphisms (SNPs) in AA-related genes, there isn’t any data regarding SNPs within the LTA4H gene and this medical phenotype.
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