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Pharmacogenomics of Heparin-Induced Thrombocytopenia (PHIT)
Pharmacogenomics of Warfarin in Hispanics and Latinos (Warfarin GWAS)
Warfarin Pharmacomicrobiomics
Pharmacogenomics of Heparin-Induced Thrombocytopenia (PHIT)
ClinicalTrials.gov Study Record
The pathogenesis of heparin-induced thrombocytopenia is characterized by gaps in our knowledge.
APC: Antigen-presenting cell; FcγRIIA: Platelet FcγRIIa receptor; HIPA: Heparin-induced platelet aggregation; HIT: Heparin-induced thrombocytopenia; IVIG: Intravenous immunoglobulin; NOAC: New oral anticoagulant; PF4: Platelet factor 4; SRA: Serotonin release assay.
STUDY SUMMARY:
Our research is aimed at understanding why people treated with the drug heparin get a severe, immune reaction called heparin-induced thrombocytopenia. In particular, we are trying to identify genetic factors that predispose people to this reaction. In addition, we are trying to determine genetic factors that can be used to quickly detect when a person will get heparin-induced thrombocytopenia.
Some people carry genetic factors from specific genes that predispose them to drug reactions. We have identified genetic factors in these genes that may predict whether a person will get heparin-induced thrombocytopenia. We are comparing differences in these genes in people that got heparin-induced thrombocytopenia to people that didn’t get heparin-induced thrombocytopenia. We are also testing whether a person’s immune response to heparin can be detected using genetic factors.
It is our goal to determine genetic factors that predispose people to heparin-induced thrombocytopenia, which can cause serious blood clots such as stroke. The genetic factors can then be tested, used to determine who will get the reaction, and heparin can be avoided in these people. These experiments will help us to prevent heparin-induced thrombocytopenia and the serious cardiovascular problems it causes. It is also our goal to use genetic factors to test for a person’s immune response to heparin. This will enable us to quickly determine if a person will get heparin-induced thrombocytopenia so that we can stop the heparin, start treatment, and prevent potentially devastating effects of the reaction.
Pharmacogenomics of Warfarin in Hispanics and Latinos (Warfarin GWAS)
ClinicalTrials.gov Study Record
Genes involved in warfarin metabolism and mechanism of action.
CALU = calumenin; CYP2C18 = cytochrome P450 family 2 subfamily C member 18; CYP2C9 = cytochrome P450 family 2 subfamily C member 9; CYP4F2 = cytochrome P450 family 4 subfamily F member 2; GGCX = gamma-glutamyl carboxylase; NAD = nicotinamide adenine dinucleotide; NQO1 = NAD(P)H quinone dehydrogenase 1; VKORC1 = vitamin K epoxide reductase.
STUDY SUMMARY:
Warfarin is a commonly used blood thinner to treat and prevent blood clots. It is important to take the right dose of warfarin because too much can increase the risk of bleeding and too little can increase the risk of blood clots. This is why patients are closely monitored especially when they begin warfarin therapy. When clinicians prescribe warfarin, they have to consider different factors such as patient’s age, body size, diet, and other medications that can interact with warfarin.
Certain genes have also been found to affect warfarin dose. Individuals have variations in these genes, which can help explain why some patients need higher dose and others require less. These factors have been used to better predict a patient’s warfarin dose requirement. However, these predictions were created based on Caucasian populations and they may not be accurate in predicting a safe warfarin dose if a patient is not Caucasian. This study aims to identify new genetic variation that affects warfarin dosing in Hispanic and Latino populations and try to better predict a Hispanic or Latino patient’s warfarin dose requirement.
Warfarin Pharmacomicrobiomics
Study Eligibility Survey
Microbial Gut Interactions with Medications
STUDY SUMMARY:
Warfarin is a commonly used blood thinner to treat and prevent blood clots. Correct warfarin dosing is important since over-dosing leads to bleeding and under-dosing leads to blood clots. In order to provide more accurate dosing, clinicians consider patient factors such as age, body size, diet, and other medications that interact with warfarin. In addition to these patient factors, genetic variation has been used to better predict a patient’s warfarin dose. However, these predictions still have room for improvement. Through collection of multiple stool samples, this study aims to explore the effect of human gut bacteria on warfarin dose. We predict that the addition of information regarding a patient’s gut bacteria will improve warfarin dose prediction.