AIM: Authors performed a Laboratory assessment for thrombophilia risk factors in a group of patients with previous deep venous thrombosis. METHODS: 123 consecutive patients were considered. The following parameters were investigated by using commercially available methods: PT, aPTT, TT, Fibrinogen, D-Dimer, Anti thrombin 3 (AT), Protein C (PC), Protein S (PS), activated C protein (APC) resistance, Lupus anticoagulant (LA), FV Leiden (G1691a mutation), Prothrombin G20210A mutation, MTHFR mutation (G677T mutation), anti Prothrombin auto-antibodies (PR) IgG and IgM, anti Beta 2 glycoprotein 1 (B2GP1) auto-antibodies IgG and IgM, anti Cardiolipin (CL) auto-antibodies IgG and IgM, homocysteine. RESULTS: In the 123 patients considered we observed: two AT deficiency, one PC deficiencies, one PS deficiency, 60 FV Leiden mutation (six homozygous), 1 Prothrombin gene mutations (heterozygous), 71 MTHFR mutations (15 homozygous). Study of anti phospholipid auto antibodies showed 10 patients positive for LA, 9 for anti CL antibodies (6IgG and 3IgM), 10 for anti B2GP1 antibody (5 IgG and 5IgM), 3 for anti PR antibody (IgG). Thirty nine patients showed hyper homocysteinemia. CONCLUSION: In our study only 19 patients were free of demonstrable thrombophilia risk factor. In 51 subjects a single risk factor was identified and in 53 multiple (from 2 to 5) risk factors were identified. In our opinion a Laboratory assessment of thrombophilia risk factors after a previous episode of deep venous thrombosis is a diagnostic tool of great importance. As a matter of fact, in our experience, by using a standard analytical panel, it was possible to highlight one or more risk factors in about 85% of the patients considered.
AIM: Authors performed a Laboratory assessment for thrombophilia risk factors in a group of patients with previous deep venous thrombosis. METHODS: 123 consecutive patients were considered. The following parameters were investigated by using commercially available methods: PT, aPTT, TT, Fibrinogen, D-Dimer, Anti thrombin 3 (AT), Protein C (PC), Protein S (PS), activated C protein (APC) resistance, Lupus anticoagulant (LA), FV Leiden (G1691a mutation), ProthrombinG20210A mutation, MTHFR mutation (G677T mutation), anti Prothrombin auto-antibodies (PR) IgG and IgM, anti Beta 2 glycoprotein 1 (B2GP1) auto-antibodies IgG and IgM, anti Cardiolipin (CL) auto-antibodies IgG and IgM, homocysteine. RESULTS: In the 123 patients considered we observed: two AT deficiency, one PC deficiencies, one PS deficiency, 60 FV Leiden mutation (six homozygous), 1 Prothrombin gene mutations (heterozygous), 71 MTHFR mutations (15 homozygous). Study of anti phospholipid auto antibodies showed 10 patients positive for LA, 9 for anti CL antibodies (6IgG and 3IgM), 10 for anti B2GP1 antibody (5 IgG and 5IgM), 3 for anti PR antibody (IgG). Thirty nine patients showed hyper homocysteinemia. CONCLUSION: In our study only 19 patients were free of demonstrable thrombophilia risk factor. In 51 subjects a single risk factor was identified and in 53 multiple (from 2 to 5) risk factors were identified. In our opinion a Laboratory assessment of thrombophilia risk factors after a previous episode of deep venous thrombosis is a diagnostic tool of great importance. As a matter of fact, in our experience, by using a standard analytical panel, it was possible to highlight one or more risk factors in about 85% of the patients considered.