Pharmacogenetics to prevent heparin-induced thrombocytopenia: what do we know?
AuthorKarnes, Jason H
AffiliationUniv Arizona, Coll Pharm, Dept Pharm Practice & Sci
Univ Arizona, Coll Pharm, Dept Med, Sarver Heart Ctr
Univ Arizona, Coll Pharm, Dept Med, Ctr Appl Genet & Genom Med TCAG2M,Div Pharmacogen
genome-wide association study
low molecular weight heparin
MetadataShow full item record
PublisherFUTURE MEDICINE LTD
CitationKarnes, J. H. (2018). Pharmacogenetics to prevent heparin-induced thrombocytopenia: what do we know?. Pharmacogenomics, 19(18), 1413-1422.
Rights© 2018 Future Medicine Ltd
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at firstname.lastname@example.org.
AbstractHeparin-induced thrombocytopenia (HIT) is a life-threatening, immune-mediated adverse reaction to heparin anticoagulants. The inability to predict HIT represents a considerable liability associated with heparin administration. Genetic studies of HIT are challenging due to the scarcity of true HIT cases, potential for misclassification, and many environmental risk factors. Genetic studies have not consistently identified risk alleles for HIT, the production of platelet factor 4/heparin antibodies or the thromboembolic complications of HIT. Genes implicated in HIT and platelet factor 4/heparin antibody levels include FCGR2A, TDAG8, HLA-DR and others. Compelling evidence also suggests that the FCGR2A H131R polymorphism is associated with HIT-related thrombosis. There is a need for well-powered, multiethnic studies with laboratory confirmation of HIT, detailed patient- and drug-specific data, and inclusion of both serologic and thromboembolic outcomes. Genomic biomarkers identified from such studies offer the possibility of shifting current clinical practice paradigms from early detection and treatment to prevention.
Note12 month embargo; published online: 6 November 2018
VersionFinal accepted manuscript
SponsorsAmerican Heart Association [16SDG29090005]; American College of Clinical Pharmacy Research Institute (Futures Grant)