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Pharmacogenomics. 2018 Nov 6. doi: 10.2217/pgs-2018-0147. [Epub ahead of print]

Pharmacogenetics to prevent heparin-induced thrombocytopenia: what do we know?

Karnes JH1,2,3.

Author information

1
Department of Pharmacy Practice & Science, University of Arizona College of Pharmacy, Tucson, AZ 85721, USA.
2
Sarver Heart Center, Department of Medicine, University of Arizona College of Medicine - Tucson, Tucson, AZ 85721, USA.
3
Division of Pharmacogenomics, Center for Applied Genetics & Genomic Medicine (TCAG2M), Department of Medicine, University of Arizona College of Medicine - Tucson, Tucson, AZ 85721, USA.

Abstract

Heparin-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.

KEYWORDS:

anticoagulant; biomarker; genetics; genome-wide association study; heparin; heparin-induced thrombocytopenia; low molecular weight heparin; pharmacogenomics

PMID:
30398086
DOI:
10.2217/pgs-2018-0147

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