Tissue Factor Pathway Inhibitor (TFPI) and Thrombin Activable Fibrinolysis Inhibitor (TAFI) in Juvenile Deep Vein Thrombosis

Abstract number: P1349

Rogolino A, Gori AM, Alessandrello LA, Blagojevich J, Marcucci R, Attanasio M, Ferrini S, Abbate R, Gensini GF, Prisco D

Low levels of tissue factor pathway inhibitor (TFPI) and elevated levels of thrombin activatable fibrinolysis inhibitor (TAFI) have been recently reported to be associated with an increased risk of deep venous thrombosis (DVT). Scarce data are available on the role of these parameters in juvenile DVT. We investigated 116 patients with a first episode of DVT before 50 years (median age 38, 17–50 years; 51 males/65 females) and 60 apparently health subjects comparable for age and sex. TFPI and TAFI plasma levels were measured by ELISAs (Asserachrom total- and free-TFPI, Diagnostica Stago; Asniere sur Seine, France; COALIZA TAFI, Chromogenix, IL, Milan, Italy). Venous blood samples were collected at least 6 months after the acute event. No patient was under anticoagulant treatment for at least three months. Free-TFPI plasma levels were not significantly different between patients and controls (10.7, 7–28.2 ng/ml vs 11.5, 5.6–48.7 ng/ml). Ten percent of healthy subjects had TFPI free antigen levels below 7.1 ng/ml (10^th percentile). A similar percentage (10.3%) of patients had free-TFPI below this cut-off. Total-TFPI plasma levels were not significantly different between patients and controls although a trend to higher levels was observed in patients (78.6, 42.7–190.9 ng/ml vs 69.8, 42.1–198.1 ng/ml). Ten percent of healthy subjects had TFPI total antigen levels below 51.2 ng/ml (10^th percentile). A similar percentage (7.5%) of patients had total-TFPI below this cut-off. As TAFI plasma levels are concerned, no significant differences were found between patients and controls (103, 47.6–262.9% vs 102, 57–233%). Ten out of 116 DVT patients (8.6%) had TAFI levels above 90^th percentile of control distribution (150.4%). These preliminary results do not support a relevant role for TFPI defect and TAFI excess in juvenile DVT. Further studies are needed on a larger number of patients and healthy controls to better assess the utility of their determination in the clinical management of patients with DVT.