Findings from a new study could allow for safer dosing of the drug warfarin.
Researchers have found that variations in a single gene that regulates blood clotting may determine how people respond to the common blood-thinning drug warfarin.
The study by scientists at the University of Washington in Seattle and Washington University in St. Louis may eventually allow safer and more effective dosing of the drug taken by millions of people.
The drug is widely used to prevent clotting after a heart attack, stroke or major surgery. About 2 million people in the United States take the drug, most widely sold under the brand name Coumadin, on any particular day. Doctors find it difficult to manage patients on warfarin because individuals respond to it so differently.
"There is a narrow window between too much and too little effect," said Allan Rettie, a professor of medicinal chemistry at the University of Washington and senior author of the study appearing today in the New England Journal of Medicine. "A small change in dose can have quite a large effect on blood processes."
Scientists already know that variations in a gene that governs the enzyme that metabolizes warfarin accounts for about 10 percent of the differences in people's response to the drug, but tests for those variations are not routinely done.
Instead, doctors mainly rely on several months of office visits and needle-prick tests to find a patient's ideal dose.
Rettie and UW colleague Mark Rieder, a genome scientist, focused on another gene, called vitamin K epoxide reductase, which makes a protein that controls clotting and is the key target of warfarin.