ArticleThe pharmacogenomics journal2019
Polymorphisms in CEP68 gene associated with risk of immediate selective reactions to non-steroidal anti-inflammatory drugs.
Article in The pharmacogenomics journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Centrosome linker protein CEP68 modulates cellular stress responses via nuclear condensate formation and HSP27 interaction.iScience · 2026Article
- Updating the classification and routine diagnosis of NSAID hypersensitivity reactions: A WAO Statement.The World Allergy Organization journal · 2025Review
- Towards a Multi-omics Understanding of Anaphylaxis: Insights into Pathogenesis and Biomarker Identification.Clinical reviews in allergy & immunology · 2025Review
- Host genetics and gut microbiota jointly regulate blood biochemical indicators in chickens.Applied microbiology and biotechnology · 2023Article
- Stress, pseudoallergens, autoimmunity, infection and inflammation in chronic spontaneous urticaria.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019Review
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
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Abstract
Non-steroidal anti-inflammatory drugs (NSAIDs) are the main triggers of drug hypersensitivity reactions. Such reactions can be pharmacologically or immunologically mediated, but in both cases individual susceptibility can be influenced by genetic factors. Polymorphisms in centrosomal protein of 68 kDa (CEP68) have been associated with pharmacologically mediated NSAIDs reactions. Here, we evaluated this gene in immunologically mediated single-NSAID-induced urticaria/angioedema or anaphylaxis (SNIUAA) by analyzing 52 single nucleotide polymorphisms in CEP68 in 176 patients and 363 NSAIDs-tolerant controls. Two intronic variants (rs2241160 and rs2241161) were significantly associated with an increased risk of SNIUAA, suggesting CEP68 to be a key player in both types of NSAIDs hypersensitivity. However, we found no overlap with genetic variants previously associated with pharmacologically mediated hypersensitivity, pointing to a complex role for this gene and its potential use in the development of biomarkers of clinical utility to diagnose patients at risk of these reactions and to differentiate entities.
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