title: Prothrombin fragment F1+2 is not predictive for recurrent venous thromboembolism.
abstract: It would be important to estimate in advance the risk of recurrent thrombosis. Deficiencies of antithrombin, protein C or protein S, or resistance to activated protein C are associated with a biochemically detectable prethrombotic state. It is thus far unknown whether in patients with a history of thromboembolism but without a defined clotting abnormality a heightened coagulation activation is detectable. We investigated the value of prothrombin fragment F1+2 (F1+2) as a predictor of recurrent venous thromboembolism. Furthermore, we compared the F1+2 levels of thrombosis patients without a defined clotting defect to those of Factor V Leiden patients with a history of venous thrombosis and to those of healthy controls. 180 patients without a defined clotting abnormality and 73 patients with Factor V Leiden were prospectively followed after discontinuation of oral anticoagulants for venous thrombosis and F1+2 was measured at regular intervals. Recurrent venous thromboembolism occurred in 23 (9%) of the 253 patients. Before or at several time points after oral anticoagulants, no significant difference in F1+2 levels was found in patients with and without recurrent thrombosis. F1+2 levels at 3 weeks and prior to recurrence were not significantly different in both patient groups. Over a one-year observation period, F1+2 levels of both patients with and without Factor V Leiden were higher than those of the controls. No difference in F1+2 was seen between patients with and without Factor V Leiden. We conclude that monitoring of F1+2 is not suitable for identification of individuals at risk of recurrent venous thrombosis. Permanent hemostatic system activation is detectable both in patients with a defined abnormality of the clotting system and in patients in whom a particular defect has not (yet) been identified.
authors.affiliation: Department of Internal Medicine, University of Vienna, Austria.
authors.forename: P A
authors.initials: PA
authors.lastname: Kyrle
authors.forename: S
authors.initials: S
authors.lastname: Eichinger
authors.forename: I
authors.initials: I
authors.lastname: Pabinger
authors.forename: A
authors.initials: A
authors.lastname: Stümpflen
authors.forename: M
authors.initials: M
authors.lastname: Hirschl
authors.forename: C
authors.initials: C
authors.lastname: Bialonczyk
authors.forename: B
authors.initials: B
authors.lastname: Schneider
authors.forename: C
authors.initials: C
authors.lastname: Mannhalter
authors.forename: M
authors.initials: M
authors.lastname: Melichart
authors.forename: G
authors.initials: G
authors.lastname: Traxler
authors.forename: A
authors.initials: A
authors.lastname: Weltermann
authors.forename: W
authors.initials: W
authors.lastname: Speiser
authors.forename: K
authors.initials: K
authors.lastname: Lechner
mesh_terms: D000328:Adult; D000925:Anticoagulants / Q000627:therapeutic use; D005165:Factor V / Q000032:analysis; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000032:analysis*; D011237:Predictive Value of Tests; D011498:Protein Precursors / Q000032:analysis*; D011516:Prothrombin / Q000032:analysis*; D011655:Pulmonary Embolism / Q000097:blood / Q000453:epidemiology; D012008:Recurrence; D013923:Thromboembolism / Q000097:blood* / Q000175:diagnosis / Q000453:epidemiology*; D013997:Time Factors
chemical_list: D000925:Anticoagulants; D010446:Peptide Fragments; D011498:Protein Precursors; C095381:factor V Leiden; C029733:prothrombin fragment 1; C044183:prothrombin fragment 2; D005165:Factor V; D011516:Prothrombin