Congenital antithrombin III deficiency: insights into the pathogenesis of the hypercoagulable state and its management using markers of hemostatic system activation
Key result
Congenital antithrombin III deficiency on warfarin is linked to higher plasma F1+2 levels.
Why the study?
Hereditary antithrombin III deficiency predisposes patients to venous thrombosis and the mechanisms of hypercoagulability and management strategies require further elucidation.
Does warfarin therapy adequately suppress hemostatic system activation in patients with congenital antithrombin III deficiency compared to anticoagulated patients without the disorder?
Population
Patients with hereditary antithrombin III deficiency
Comparison
Warfarin anticoagulation in ATIII deficiency vs anticoagulated persons without inherited thrombotic disorder
Design
Observational study using F1+2 radioimmunoassay to assess hemostatic activation
Authors
Discussion
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Member takes
Implication
May indicate incomplete suppression on warfarin in antithrombin III deficiency; hypothesis-generating, prospective trials needed before practice change.
Study Design
Type
Observational
Structured PICO
Does warfarin therapy adequately suppress hemostatic system activation in patients with congenital antithrombin III deficiency compared to anticoagulated patients without the disorder?
P
Population
Patients with hereditary antithrombin III (ATIII) deficiency
E
Exposure
Warfarin (oral anticoagulation)
C
Comparator
Anticoagulated persons without inherited thrombotic disorder
O
Outcome
Plasma factor Xa activity (measured by prothrombin fragment F1+2 radioimmunoassay)surrogate
Patients with congenital antithrombin III deficiency on warfarin have higher residual hemostatic system activation than anticoagulated patients without the disorder, suggesting standard anticoagulation may not fully suppress their hypercoagulable state.
Cite This Study
Bauer et al. (1989) conducted an observational in Congenital antithrombin III deficiency. Congenital antithrombin III deficiency vs. Persons without inherited thrombotic disorder was evaluated on Mean plasma F1+2 level. Patients with congenital antithrombin III deficiency on warfarin had significantly elevated mean plasma F1+2 levels compared to anticoagulated patients without the disorder.