NSAIDs are the most common cause of medication hypersensitivity responses. The whole genetic and molecular foundation of these processes, however, has yet to be discovered. In this article, researchers analyzed recent studies on the impact of genetic variations on the many clinical entities caused by NSAID hypersensitivity, with an emphasis on prostaglandin and leukotriene-related genes as well as those outsides of the arachidonic acid system. They discuss new contributions from high-throughput methods, such as genome-wide association studies, as well as data from epigenetics and next-generation sequencing. Finally, they discuss future possibilities in this discipline, including the potential for bioinformatics and systems biology, as well as the necessity for precise patient phenotyping.
The complete genetic and molecular foundation of clinical entities caused by NSAID hypersensitivity has yet to be discovered, and despite admirable efforts in recent years, no clinically validated genetic markers for these illnesses presently exist. It is sure that researchers will learn more about these reactions in the next years, as technology and experimental procedures develop and a precise description of distinct phenotypes become available.
