10.25376/hra.7999358.v1
Jason Karnes
Jason
Karnes
Genetics of HIT_8_30_18_clean.docx
Health Research Alliance
2019
Pharmacogenomics
heparin-induced thrombocytopenia
Heparin
Low molecular weight heparin
Anticoagulant
genome-wide association study
Genetics
Biomarker
Medicine
2019-04-16 15:19:50
Journal contribution
https://hra.figshare.com/articles/journal_contribution/Genetics_of_HIT_8_30_18_clean_docx/7999358
<p>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 (PF4)/heparin antibodies, nor the thromboembolic complications of HIT.
Genes implicated in HIT and PF4/heparin antibody levels include <i>FCGR2A</i>, <i>TDAG8</i>, <i>HLA-DR</i>, and
others. Compelling evidence also suggests that the <i>FCGR2A</i> 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.</p>