QJM Advance Access originally published online on March 14, 2008
QJM 2008 101(5):419; doi:10.1093/qjmed/hcm144
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Risk factors for anticoagulation-related bleeding complications
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Assessment of anticoagulant-related bleeding risk, to which the authors have alluded,1 would be incomplete without mention of the role of genomic profiling, for polymorphisms of the enzyme responsible for metabolizing warfarin. In particular, a significant association has been documented between warfarin-related haemorrhagic risk and either CYP2C9#2 or CYP2C9#3 polymorphism,2 the hepatic microsomal enzyme CYP2C9 being the primary pathway for metabolizing S-warfarin. It has even been suggested that racial/ethnic differences in the risk of intracranial haemorrhages among patients with atrial fibrillation are attributable to polymorphisms of this enzyme.3 It is also worth profiling for the ApoE genotype, which is a marker for cerebral amyloid angiopathy, given the documentation of warfarin-associated haemorrhage and cerebral amyloid angiopathy.4
References
1. Hughes M, Lip GYH. Risk factors for anticoagulation-related bleeding complications in patients with atrial fibrillation; a systematic review. Q J Med (2007) 100:599–607.[Web of Science]
2. Higashi MK, Veenstra DL, Kondo LM, Wittowsky AN, Srinouanprachanh SL, Farin FM, et al. Association between CYP2C9 genetic variants and anticoagulant-related outcomes during warfarin therapy. JAMA (2002) 287:1690–8.
3. Shen AY-J, Yao JF, Brar SS, Jorgensen MB, Chen W. Racial/ethnic differences in the risk of intracranial hemorrhage among patients with atrial fibrillation. J Am Coll Cardiol (2007) 50:309–15.
4. Rosand J, Hylek EM, ODonnell HC, Greenberg SM. Warfarin-associated hemorrhage and cerbral amyloid angiopathy. Neurology (2000) 55:947–51.
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