The Whole Blood Coagulation Profile in Hyperhomocysteinemic Patients with Prior Thrombosis is Changed by Folic Acid Treatment as Evaluated by roTEG Thrombelastography
Abstract number: OR132
Ebbesen1,2 LS, Christiansen2 K, Ingerslev2 J
Hyperhomocysteinemia (HH) is an independent risk factor for thrombosis although the exact pathogenesis is still not elucidated. Previously, an animal model of HH was used to demonstrate that the whole blood coagulation profile (WBCP) in HH is changed in a thrombogenic direction characterized by a prolongation of the initiation phase, an increase of the velocity and of the maximal clot firmness. We hypothesized that the WBCP were changed similarly in patients suffering HH and that the WBCP could be normalized by folic acid treatment as demonstrated previously in our animal study.
Material and methods: Patients (n= 23), who previously had a thrombosis were admitted to our centre and were diagnosed with HH, were included in this study. All patients were treated with folic acid 5 mg/d for 2 weeks thereafter 5 mg/w. Pre- and post treatment tHcy and WBCP were recorded. Human recombinant TF was added to citrated whole blood, and coagulation was initiated by Ca++-addition. The WBCP were recorded by the roTEG Thrombelastograph (Pentapharm, Munich, Germany).
Results: Pre-treatment mean tHcy was 16.9 mmol/l and post-treatment mean tHcy was 9.9 mmol/l, P < 0.001. The initiation phase of coagulation was reduced by treatment; i.e. the mean pre-CT (clotting time) was 291.1 s and the mean post-CT was 262.5 s, P < 0.05. Furthermore, the mean pre-Tmax (time to max velocity) was 467.5 s and the mean post-Tmax was 434.5 s, P < 0.05. No change in velocity (0.185 and 0.199 mm/s) and maximal clot firmness (62.7 and 63.0 mm) were detected.
Discussion: The WBCP in HH patients is changed similarly to what has previously been detected in HH animals; a prolongation of the initiation phase during HH and the CT is reduced by treatment with folic acid. However, no change in velocity and maximal clot firmness were detected, which might be due to present effective antiplatelet-aggregation therapy.
To cite this abstract use the following format:
Journal of Thrombosis and Haemostasis 2005; Volume 3, Supplement 1: abstract number
|Session name:||XXIst ISTH Congress|
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