Exploring the causal association between fatty acid-binding proteins and anaphylactic shock due to adverse reactions to medications: A two-sample Mendelian randomization study
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Le résumé fourni par la source
Previous studies have identified a relationship between fatty acid-binding proteins (FABPs) and immune diseases. This study aimed to investigate whether a causal relationship exists between FABPs and anaphylactic shock resulting from adverse drug reactions. Single nucleotide polymorphisms associated with FABPs were utilized as instrumental variables, sourced from the National Human Genome Research Institute-European Bioinformatics Institute Catalog of human genome-wide association studies. Data on anaphylactic shock due to adverse effects of correctly administered drugs were obtained from the FinnGen database, which includes genomic and health data from 500,000 Finnish biobank donors. A two-sample Mendelian randomization analysis was conducted to explore the causality between FABPs and anaphylactic shock due to adverse drug reactions. The analysis revealed a negative causal relationship between FABP5 (odds ratio [OR] = 0.40; 95% confidence interval [CI] = 0.17-0.92; P = .032) and FABP12 (OR = 0.77; 95% CI = 0.63-0.94; P = .009) and anaphylactic shock due to adverse drug reactions. These findings were corroborated by Mendelian randomization-Egger, weighted median, and weighted mode methods. This study provides robust evidence supporting a protective relationship between FABP5 and FABP12 and anaphylactic shock due to adverse drug reactions. Further experimental studies are warranted to elucidate the causal mechanisms and associations between FABP5, FABP12, and anaphylactic shock in the context of adverse drug reactions.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Exploring the causal association between fatty acid-binding proteins and anaphylactic shock due to adverse reactions to medications: A two-sample Mendelian randomization study
- Date Crossref
- 02/05/2025
- Éditeur
- Ovid Technologies (Wolters Kluwer Health)
- Type
- journal-article
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