http://purl.uniprot.org/citations/17994314 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/17994314 | http://www.w3.org/2000/01/rdf-schema#comment | "Oral anticoagulant treatment for secondary prevention after cerebral ischaemia of presumed arterial origin is associated with a higher bleeding rate than cardioembolic stroke. This discrepancy is only partly explained by known bleeding risk factors. Haemostatic genetic variants and AB0 blood group may be involved. We performed a nested casecontrol study in patients with cerebral ischaemia of presumed arterial origin on anticoagulant treatment (International Normalized Ratio between 3.0-4.5). All 34 cases with non-fatal haemorrhage (10 intracranial and 24 extracranial) and 68 control patients on anticoagulant treatment without such a bleeding were selected from the SPIRIT study. AB0 blood group and 11 haemostatic genetic variants were investigated. The Thr312Ala variant of the alpha fibrinogen gene was associated with a decreased bleeding risk (odds ratio (OR) 0.3 for Ala/Ala and Thr/Ala versus Thr/Thr genotype; 95% CI 0.1-0.8). Factor V Leiden was associated with an increased bleeding risk (OR 11.6; 95% CI 1.3-103). The APOE2 allele (OR 0.5; 95% CI 0.2-1.7) and the Tyr204Phe variant in the factor XIII subunit A (OR 2.1; 0.9-5) had nonsignificant relationships with bleeding risk. AB0 blood group and 7 other genetic variants in coagulation factors II and XIII, vitamin K epoxide reductase complex, beta fibrinogen and apolipoprotein E were not related with the risk of haemorrhage. The Ala312Thr variant in the alpha fibrinogen gene is associated with a decreased and factor V Leiden with an increased bleeding risk in patients on anticoagulant treatment after cerebral ischaemia of presumed arterial origin."xsd:string |
http://purl.uniprot.org/citations/17994314 | http://purl.org/dc/terms/identifier | "doi:10.1007/s00415-007-0609-5"xsd:string |
http://purl.uniprot.org/citations/17994314 | http://purl.uniprot.org/core/author | "Garcia A.A."xsd:string |
http://purl.uniprot.org/citations/17994314 | http://purl.uniprot.org/core/author | "Rosendaal F.R."xsd:string |
http://purl.uniprot.org/citations/17994314 | http://purl.uniprot.org/core/author | "Algra A."xsd:string |
http://purl.uniprot.org/citations/17994314 | http://purl.uniprot.org/core/author | "Kappelle L.J."xsd:string |
http://purl.uniprot.org/citations/17994314 | http://purl.uniprot.org/core/author | "Gorter J.W."xsd:string |
http://purl.uniprot.org/citations/17994314 | http://purl.uniprot.org/core/author | "Pruissen D.M."xsd:string |
http://purl.uniprot.org/citations/17994314 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
http://purl.uniprot.org/citations/17994314 | http://purl.uniprot.org/core/name | "J Neurol"xsd:string |
http://purl.uniprot.org/citations/17994314 | http://purl.uniprot.org/core/pages | "1660-1665"xsd:string |
http://purl.uniprot.org/citations/17994314 | http://purl.uniprot.org/core/title | "Haemostatic genetic variants, ABO blood group and bleeding risk during oral anticoagulant treatment after cerebral ischaemia of arterial origin."xsd:string |
http://purl.uniprot.org/citations/17994314 | http://purl.uniprot.org/core/volume | "254"xsd:string |
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