The authors report a study on the
hemostatic status of a group of patients with
deep venous thrombosis in order to highlight the possible pathogenetic responsibility of blood coagulative disorders in the genesis of
thrombosis. The group consisted of 27 patients (14 males, 13 females, mean age 48 +/- 4 years) with
deep venous thrombosis of the lower limbs (clinical symptoms were primary in 21 cases, secondary in 6 cases) diagnosed on the basis of clinical data and ultrasonographic instrumental findings. Fourteen normal subjects were also examined as a control group (12 males, 2 females, mean age 28 +/- 5 years). Venous blood was collected on fasting from patients and controls to examine the following parameters:
fibrinogen (F), factor VII (F VII),
antithrombin III (AT III),
protein C (PC),
protein S (PS) using coagulometric methods (IL), and
tissue plasminogen activator (tPA),
plasminogen activator inhibitor (PAI-1),
fibrinopeptide A (FPA), betathromboglobulin (BTG) and dimer-
D (D-D) using ELISA methods (Boehringer). Patients with
deep venous thrombosis showed a significant increase in F, FVII, tPA and
D-D levels compared to controls, whereas a significant reduction was observed in
PAI-1. Nonsignificant variations were found for AT III, PC, PS and BTG. In the light of these results the authors affirm that: high
fibrinogen and
factor VII levels are highly prognostic for
thrombosis in patients with
deep venous thrombosis; the importance of the lack of inhibitory factors (AT III, PC, PS) is confined to individual genetically predisposed cases; there is an efficacious hyperfibrinolytic reactive response to the presence of
thrombus (increase in tPA and
D-D, reduction of PAI-1).