AI Article Synopsis
- Cefaclor is a common cause of drug-induced hypersensitivity reactions, particularly anaphylaxis, in Korea, but the genetic factors involved are not well understood.
- Researchers conducted whole exome sequencing and HLA genotyping on 43 patients to identify genetic biomarkers associated with cefaclor hypersensitivity.
- Results indicated significant associations with specific genes (LIMD1) and HLA types (HLA-DRB1∗04:03 and HLA-DRB1∗14:54), suggesting these may influence susceptibility to hypersensitivity, warranting further studies with larger groups.
Article Abstract
Background: Drug-induced hypersensitivity such as anaphylaxis is an important cause of drug-related morbidity and mortality. Cefaclor is a leading cause of drug induced type I hypersensitivity in Korea, but little is yet known about genetic biomarkers to predict this hypersensitivity reaction. We aimed to evaluate the possible involvement of genes in cefaclor induced type I hypersensitivity.
Methods: Whole exome sequencing (WES) and HLA genotyping were performed in 43 patients with cefaclor induced type I hypersensitivity. In addition, homology modeling was performed to identify the binding forms of cefaclor to HLA site.
Results: Anaphylaxis was the most common phenotype of cefaclor hypersensitivity (90.69%). WES results show that rs62242177 and rs62242178 located in LIMD1 region were genome-wide significant at the 5 × 10 significance level. Cefaclor induced type I hypersensitivity was significantly associated with HLA-DRB1∗04:03 (OR 4.61 [95% CI 1.51-14.09], P < 0.002) and HLA-DRB1∗14:54 (OR 3.86 [95% CI 1.09-13.67], P < 0.002).
Conclusion: LIMD1, HLA-DRB1∗04:03 and HLA-DRB1∗14:54 may affect susceptibility to cefaclor induced type I hypersensitivity. Further confirmative studies with a larger patient population should be performed to ascertain the role of HLA-DRB1 and LIMD1 in the development of cefaclor induced hypersensitivity.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11021981 | PMC |
| http://dx.doi.org/10.1016/j.waojou.2024.100901 | DOI Listing |
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