AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsTechnology, Industry, AgricultureInformation ScienceNamed GroupsHealth CareGeographicals
AllelesHLA-DRB1 ChainsDrug-Induced Liver InjuryHLA-DQ beta-ChainsHLA-DR AntigensOligoclonal BandsHLA AntigensHLA-DQ AntigensHLA-DRB3 ChainsHLA-DQ alpha-ChainsGene FrequencyGenotypeLithuaniaGenetic Predisposition to DiseaseHaplotypesPolymorphism, GeneticPolymerase Chain ReactionEast TimorMolecular Sequence DataMultiple SclerosisMutationGenetic Association StudiesHLA-B AntigensBase SequenceDrug-Related Side Effects and Adverse ReactionsPhenotypeGenetic VariationAmino Acid SequenceHeterozygotePolymorphism, Single NucleotideDichlororibofuranosylbenzimidazoleGenes, MHC Class IIHomozygoteHistocompatibility TestingLinkage DisequilibriumLiverHLA-A AntigensModels, GeneticHLA-DP beta-ChainsChromosome MappingEvoked Potentials, VisualRisk FactorsCrosses, GeneticGenetic MarkersCase-Control StudiesHistocompatibility Antigens Class IGenetics, PopulationHLA-DRB4 ChainsGenes, MHC Class ISequence Analysis, DNASelection, GeneticGenetic LinkageDNA PrimersPolymorphism, Restriction Fragment LengthHLA-DRB5 ChainsGenes, LethalLiver Failure, AcuteAcetaminophenHLA-DR4 AntigenGenes, RecessiveImmunoglobulin Light ChainsHLA-DR Serological SubtypesAlanine TransaminaseImmunoglobulin Heavy ChainsMicrosatellite RepeatsDNAPedigreeHLA-C AntigensGenes, DominantRecombination, GeneticMajor Histocompatibility ComplexReverse Transcriptase Polymerase Chain ReactionHistocompatibility Antigens Class IIGenetic LociEpitopesLiver Function TestsExonsHLA-DP AntigensRNA, MessengerDNA Probes, HLAEuropean Continental Ancestry GroupTerminology as TopicCloning, MolecularHLA-D AntigensAsian Continental Ancestry GroupGenetic Complementation TestHLA-DR3 AntigenSuppression, GeneticMyosin Heavy ChainsEvolution, MolecularAntitubercular AgentsDrosophila melanogasterDNA Mutational AnalysisSequence Homology, Amino AcidMinisatellite RepeatsDisease SusceptibilityCell LinePoint MutationPhylogenyDiabetes Mellitus, Type 1
Human LeukocyDrug-induced liver injuryIdiosyncraticGenetic
Human Leukocy2
  • In addition, a relatively small number of human leukocyte antigen (HLA) alleles have overlapping associations with a variety of adverse reactions including DILI, cutaneous hypersensitivity and drug-induced pancreatitis. (medscape.com)
  • We performed a genetic analysis to identify possible human leukocyte antigen (HLA) associations with DILI in European Caucasian users of infliximab in a retrospective study of 16 infliximab-DILI patients and 60 matched controls. (nih.gov)
Drug-induced liver injury4
  • In contrast to the studies that have explored association of genetic variants with other complex traits, those investigating hepatotoxicity have identified risk alleles with substantially higher risk ratios for the susceptibility to drug-induced liver injury (DILI). (medscape.com)
  • these investigations in turn improved our understanding of pathogenic processes involved in the development of idiosyncratic drug-induced liver injury (DILI). (medscape.com)
  • Biomarkers that are able to identify patients at risk of drug-induced liver injury (DILI) after treatment with infliximab could be important in increasing the safety of infliximab use. (nih.gov)
  • Drug-induced liver injury (DILI), especially from antimicrobial agents, is an important cause of serious liver disease. (nih.gov)
Idiosyncratic1
  • Amoxicillin-clavulanate (AC) is a leading cause of idiosyncratic DILI, but little is understood about genetic susceptibility to this adverse reaction. (nih.gov)
Genetic4
  • A high negative predictive value of a genetic test can be used to identify the correct agent underlying DILI when the patient had been exposed to two concomitant medications with a potential to cause DILI. (medscape.com)
  • Inclusion of genetic tests in the causality assessment of an event, where DILI is suspected, may improve consistency and precision of causality assessment tools. (medscape.com)
  • In contrast to GWAS that have explored genetic variants in relation with complex traits, those investigating genetic susceptibility to hepatotoxicity have identified risk alleles with substantially stronger associations with DILI and higher risk ratios for susceptibility. (medscape.com)
  • We performed a genome-wide association study using 822,927 single nucleotide polymorphism (SNP) markers from 201 White European and US cases of DILI following AC administration (AC-DILI) and 532 population controls, matched for genetic background. (nih.gov)