ArticleClinical pharmacokinetics2017
A Joint Model for Vitamin K-Dependent Clotting Factors and Anticoagulation Proteins.
Article in Clinical pharmacokinetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Fever and reversible laboratory abnormalities associated with prolonged use of piperacillin/tazobactam: A case report.SAGE open medical case reports · 2024Article
- Piperacillin/tazobactam-induced coagulopathy in a patient through a vitamin K-dependent mechanism.European journal of hospital pharmacy : science and practice · 2021Article
- Evaluation of Assumptions Underpinning Pharmacometric Models.The AAPS journal · 2019Article
- A factor VII-based method for the prediction of anticoagulant response to warfarin.Scientific reports · 2018Article
- Response to R-warfarin anticoagulant effect.British journal of clinical pharmacology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundWarfarin acts by inhibiting the reduction of vitamin K (VK) to its active form, thereby decreasing the production of VK-dependent coagulation proteins. The aim of this research is to develop a joint model for the VK-dependent clotting factors II, VII, IX and X, and the anticoagulation proteins, proteins C and S, during warfarin initiation.
methodsData from 18 patients with atrial fibrillation who had warfarin therapy initiated were available for analysis. Nine blood samples were collected from each subject at baseline, and at 1-5, 8, 15 and 29 days after warfarin initiation and assayed for factors II, VII, IX and X, and proteins C and S. Warfarin concentration-time data were not available. The coagulation proteins data were modelled in a stepwise manner using NONMEM
resultsOne patient was administered VK and was excluded from the analysis. Each kinetic-pharmacodynamic model consisted of two parts: (1) a common one-compartment pharmacokinetic model with first-order absorption and elimination for warfarin; and (2) an inhibitory E
conclusionThe joint model represents the first work to quantify the influence of warfarin on all six VK-dependent coagulation proteins simultaneously. Future work will expand the model to predict the influence of exogenously administered VK on the time course of clotting factor concentrations after warfarin overdose and during perioperative warfarin reversal procedures.
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