BACKGROUND: Cerebral venous thrombosis (CVT) is considered to be a relative unusual pathology, probably underdiagnosed. Many acquired and inherited hypercoagulability states (HS) have been described as cause of CVT. OBJECTIVE: [corrected] We evaluated the incidence of acquired and inherited thrombophilic risk factors in a population of CVT patients. METHODS: Hypercoagulability studies were to carried out for patients suffering from radiologically confirmed CVT during a 3 year period (1998-2000). Prothrombin time, aPTT, protein C, protein S and antithrombin III activities, screening and confirmatory tests for lupus anticoagulant (LA), and activated protein C resistance (APCR) were tested. Genetic tests for G1691A factor V (Factor V Leiden), G20210A prothrombin and C677T methylentetrahidrofolate reductase (MTHFR) were performed. Computer database was used for descriptive statistics. RESULTS: 16 patients with CVT (M/F, 6/10) were screened for inherited and acquired coagulation disorders. Mean age of 23.66 years with standard desviation of 19.74 years. Two older patients had antecedents of thrombosis (ischemic stroke and deep-vein thrombosis in leg). We found 1 heterocygosis factor V Leiden associated to LA, 2 heterocygosis G20210A prothrombin (one associated to LA), 2 homocygosis C677T MTHFR, 1 hereditary antithrombin III deficiency and 4 LA. COMMENTS: Although this is a small series, we found a high incidence of hereditary (37.5%) and acquired (37.5%) thrombophilia in patients with CVT.
BACKGROUND:Cerebral venous thrombosis (CVT) is considered to be a relative unusual pathology, probably underdiagnosed. Many acquired and inherited hypercoagulability states (HS) have been described as cause of CVT. OBJECTIVE: [corrected] We evaluated the incidence of acquired and inherited thrombophilic risk factors in a population of CVTpatients. METHODS: Hypercoagulability studies were to carried out for patients suffering from radiologically confirmed CVT during a 3 year period (1998-2000). Prothrombin time, aPTT, protein C, protein S and antithrombin III activities, screening and confirmatory tests for lupus anticoagulant (LA), and activated protein C resistance (APCR) were tested. Genetic tests for G1691A factor V (Factor V Leiden), G20210A prothrombin and C677T methylentetrahidrofolate reductase (MTHFR) were performed. Computer database was used for descriptive statistics. RESULTS: 16 patients with CVT (M/F, 6/10) were screened for inherited and acquired coagulation disorders. Mean age of 23.66 years with standard desviation of 19.74 years. Two older patients had antecedents of thrombosis (ischemic stroke and deep-vein thrombosis in leg). We found 1 heterocygosis factor V Leiden associated to LA, 2 heterocygosis G20210A prothrombin (one associated to LA), 2 homocygosis C677TMTHFR, 1 hereditary antithrombin III deficiency and 4 LA. COMMENTS: Although this is a small series, we found a high incidence of hereditary (37.5%) and acquired (37.5%) thrombophilia in patients with CVT.