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Related Concept Videos

Drug toxicity: Idiosyncratic Reactions01:16

Drug toxicity: Idiosyncratic Reactions

220
Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...
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Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

209
Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial...
209
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

81
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
81
Pharmacogenetics of Drug Metabolism: Overview01:27

Pharmacogenetics of Drug Metabolism: Overview

194
Genetic polymorphism in drug metabolism is crucial to the inter-individual variability observed in drug responses. Drug metabolism primarily involves the chemical modification of drugs and other xenobiotics to enhance their elimination by increasing their polarity. Two main classes of enzymes mediate this biotransformation process: Phase I enzymes, primarily cytochrome P450s, catalyze oxidation and reduction reactions, while other enzymes, such as esterases, mediate hydrolysis, and Phase II...
194
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

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Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
159
Principles of Pharmacogenetics: Types of Genetic Variants01:27

Principles of Pharmacogenetics: Types of Genetic Variants

138
The human genome is over 99.9% identical between individuals, yet genetic differences exist at millions of bases. The human genome contains approximately 3 million variant positions per individual, many of which are heterozygous, contributing to genetic diversity and individual traits. Genetic variations include single-nucleotide polymorphisms (SNPs), insertions, deletions, and copy number variations (CNVs).SNPs, the most common variation, involve single-base changes in DNA. These can be...
138

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Related Experiment Video

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Candidate Gene Testing in Clinical Cohort Studies with Multiplexed Genotyping and Mass Spectrometry
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Candidate Gene Testing in Clinical Cohort Studies with Multiplexed Genotyping and Mass Spectrometry

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Genotyping for severe drug hypersensitivity.

Eric Karlin1, Elizabeth Phillips

  • 1Vanderbilt University School of Medicine, 1161-21 St Avenue South, A-2200 Medical Center North, Nashville, TN, 37232-2582, USA.

Current Allergy and Asthma Reports
|January 17, 2014
PubMed
Summary

Severe adverse drug reactions are linked to specific HLA alleles. Genetic screening, like for HLA-B*57:01 and abacavir, shows promise for preventing hypersensitivity and improving drug safety.

Area of Science:

  • Immunology
  • Pharmacogenomics
  • Drug Safety

Background:

  • Significant advances in understanding severe immunologically-mediated adverse drug reactions (ADRs).
  • T-cell-mediated ADRs like Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) and drug-induced liver disease (DILI) are increasingly understood.
  • These reactions involve interactions with Human Leukocyte Antigen (HLA) alleles.

Purpose of the Study:

  • To review the immunopathogenesis and pharmacogenomics of severe ADRs.
  • To highlight the role of HLA alleles in T-cell-mediated drug hypersensitivity.
  • To discuss the translational roadmap from pharmacogenomic discovery to clinical implementation.

Main Methods:

  • Review of recent scientific literature on ADRs, immunopathogenesis, and pharmacogenomics.

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  • Analysis of key examples of HLA-drug associations.
  • Discussion of clinical implementation strategies.

    • Main Results:

    • Strong associations found between specific HLA alleles and severe ADRs.
    • Examples include HLA-B*15:02 with carbamazepine-induced SJS/TEN in Southeast Asians and HLA-B*57:01 with abacavir hypersensitivity.
    • HLA-B*57:01 screening demonstrates a successful model for preventing abacavir hypersensitivity.

    Conclusions:

    • Understanding drug-MHC interactions is crucial for improving drug safety.
    • Pharmacogenomic discoveries can inform drug design and pre-clinical toxicity testing.
    • Genetic screening strategies can prevent severe adverse drug reactions and guide clinical practice.