Fixed versus variable dose of prothrombin complex concentrate for counteracting vitamin K antagonist therapy
Article first published online: 15 NOV 2010
© 2010 The Authors. Transfusion Medicine © 2010 British Blood Transfusion Society
Volume 21, Issue 2, pages 116–123, April 2011
How to Cite
Khorsand, N., Veeger, N. J. G. M., Muller, M., Overdiek, J. W. P. M., Huisman, W., van Hest, R. M. and Meijer, K. (2011), Fixed versus variable dose of prothrombin complex concentrate for counteracting vitamin K antagonist therapy. Transfusion Medicine, 21: 116–123. doi: 10.1111/j.1365-3148.2010.01050.x
- Issue published online: 17 FEB 2011
- Article first published online: 15 NOV 2010
- Received 14 June 2010; accepted for publication 14 October 2010
- prothrombin complex concentrate;
- vitamin K antagonist
Background: Although prothrombin complex concentrate (PCC) is often used to counteract vitamin K antagonist (VKA) therapy, evidence regarding the optimal dose for this indication is lacking. In Dutch hospitals, either a variable dose, based on body weight, target INR (international normalised ratio) and initial INR, or a fixed dose is used.
Aim/objectives: In this observational, pilot study, the efficacy and feasibility of the fixed dose strategy compared to the variable dosing regimen, is investigated.
Materials and Methods: Consecutive patients receiving PCC (Cofact®, Sanquin, Amsterdam) for VKA reversal because of a major non-cranial bleed or an invasive procedure were enrolled in two cohorts. Data were collected prospectively in the fixed dose group, cohort 1, and retrospectively in the variable dose regimen, cohort 2. Study endpoints were proportion of patients reaching target INR and successful clinical outcome.
Results: Cohort 1 consisted of 35 and cohort 2 of 32 patients. Target INR was reached in 70% of patients in cohort 1 versus 81% in cohort 2 (P = 0·37). Successful clinical outcome was seen in 91% of patients in cohort 1 versus 94% in cohort 2 (P = 1·00). Median INR decreased from 4·7 to 1·8 with a median dosage of 1040 IU factor IX (F IX) in cohort 1 and from 4·7 to 1·6 with a median dosage of 1580 IU F IX in cohort 2.
Conclusion: This study suggests that a fixed dose of 1040 IU of F IX may be an effective way to rapidly counteract VKA therapy in our patient population and provides a basis for future research.