Purpose of review: NSAIDs are the main triggers of hypersensitivity reactions to drugs. However, the full genetic and molecular basis of these reactions has yet to be uncovered. In this article, we have summarized research from recent years into the effects of genetic variants on the different clinical entities induced by NSAID hypersensitivity, focusing on prostaglandin and leukotriene-related genes as well as others beyond the arachidonic acid pathway.
Recent findings: We introduce recent contributions of high-throughput approaches including genome-wide association studies as well as available information from epigenetics and next-generation sequencing. Finally, we give our thoughts on future directions in this field, including the scope for bioinformatics and systems biology and the need for clear patient phenotyping.
Summary: The full genetic and molecular basis of clinical entities induced by NSAIDs hypersensitivity has yet to be uncovered, and despite commendable efforts over recent years, no clinically proven genetic markers currently exist for these disorders. It is clear that we will continue to find more about these reactions in the coming years, concurrently with improvements in technology and experimental techniques, and a precise definition of different phenotypes.