Ischemic stroke is a multifactorial disorder whose incidence increases as a function of the number of risk factors, including hypertension, smoking, and diabetes mellitus. However, approximately half of stroke is not explained by these predisposing conditions. Evidence from twin, family-based, and animal studies suggests that genetic influences may account for some of this additional risk. Despite such evidence, the search for genes responsible for stroke has yielded inconsistent results to date. In recent years, an increasing number of largely inherited abnormalities of blood coagulation have been commonly associated with venous thromboembolism and sometimes arterial thrombosis. These conditions, that configure thrombophylia, include deficiencies of natural anticoagulant such as antithrombin III, protein S, and protein C and single point mutations in coagulation molecules such as factor V Leiden (1691G/A), or G20210A polymorphism of the prothrombin gene, and the C677T polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene, or other abnormalities such as hyperhomocisteinemia or the presence of antiphospholipid antibodies. The utility of laboratory testing for hypercoagulability in the setting of stroke is uncertain. Certain test, sue as homcysteine, antiphospholipid antibodies, may be useful in patients with a history of stroke or at high risk for stroke, as evidenced by prospective data, however factor V Leiden, prothrombin G20210A, protein C, protein S, and antithrombin are not recommended for routine testing but may be useful in certain populations, such as children or in patients with cerebral vein thrombosis.
|Translated title of the contribution||Hypercoagulable status and stroke in young adults|
|Number of pages||11|
|Journal||Rivista Italiana di Neurobiologia|
|Publication status||Published - 2008|
ASJC Scopus subject areas
- Clinical Neurology