Bilan biologique de la maladie thromboembolique veineuse - 01/01/00
J. Tapon-BretaudièreCorrespondance et tirés à part
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Mots clés : résistance à la protéine C activée ; syndrome des antiphospholipides ; thrombophilie héréditaire ; thrombose veineuse.
Abstract |
Evaluation of inherited thrombophilia in patients with venous thromboembolism includes testing for functional activity of antithrombin, protein C and protein S, and resistance to activated protein C (factor V Leiden), which can be assessed with plasma and DNA-based assays. The anti-phospholipid syndrome is an acquired disorder related to the development of antibodies against phospholipid-protein complexes. Testing for the antiphospholipid syndrome includes measurement of antibodies to phospholipid-protein complexes by immunoassay or by detecting interference of anti-phospholipid antibodies in sensitive phospholipid-based assays. Other genetic risk factors have been listed, including a common polymorphism in prothrombin gene (3'-untranslated region) related to an increase of prothrombin level (> 115%) and a common polymorphism in the methylene tetrahydrofolate reductase (enzyme involved in homocysteine metabolism) gene related to a mild increase of homocysteine blood level. More recently high plasmatic levels of factor VIII (> 150%) or factor XI (> 120%), not related so far to a molecular defect, have been identified as risk factors for deep vein thrombosis. As a candidate gene, factor XIII gene polymorphisms are under investigation. Beside the acquired or genetic risk factors involved in thrombophilia, the gene-environment interactions are of importance in the onset of thrombosis.
Mots clés : antiphospholipid syndrome ; inherited thrombophilia ; resistance to activated protein C ; venous thromboembolism.
Plan
Vol 7 - N° 6
P. 549-552 - décembre 2000 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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