ArticleClinical pharmacokinetics2015
How to use warfarin assays in patient management: analysis of 437 warfarin measurements in a clinical setting.
Article in Clinical pharmacokinetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Warfarin and Flavonoids Do Not Share the Same Binding Region in Binding to the IIA Subdomain of Human Serum Albumin.Molecules (Basel, Switzerland) · 2017Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesApproximately 50% of inter-individual variation in warfarin dose requirements is attributed to the polymorphisms of cytochrome P450 (CYP) 2C9 (CYP2C9) and vitamin K epoxide reductase complex, subunit 1 (VKORC1) genotypes. What contributes to the remaining 50% of variation remains unclear. The aim of this study is to assess the clinical usefulness of monitoring plasma warfarin concentrations. We examined genotypic and clinical factors influencing high and low warfarin concentrations.
methodsWe included 325 Korean patients who received warfarin therapy for more than 7 days whose plasma warfarin concentrations were measured and whose genotypes for VKORC1 and CYP2C9 were determined. The plasma concentrations of total warfarin and 7-hydroxywarfarin were determined by high-performance liquid chromatography-tandem mass spectrometry.
resultsUsing 437 warfarin measurements obtained from 325 patients, we found a correlation between plasma warfarin concentration and warfarin dose (r (2) = 0.356; P < 0.001) and a significant difference in the warfarin/7-hydroxywarfarin ratios of the CYP2C9*1/*1 and CYP2C9*1/*3 genotypes combined with drugs that inhibited warfarin (P = 0.003). Insufficient warfarin dose and patient noncompliance were the most common causes of low warfarin concentrations (<0.54 µg/mL, <5th percentile). Genetic factors that cause pharmacodynamic resistance (e.g., VKORC1 genotype) and thus require high warfarin doses were the most common causes of high warfarin concentrations (>1.85 µg/mL, >95th percentile).
conclusionMonitoring warfarin concentrations along with the prothrombin time-international normalized ratio may be clinically useful for managing patients with long-term warfarin therapy and identifying factors contributing to inter- or intra-individual variability such as genetic polymorphisms, underlying diseases, drug interactions with warfarin, and patient compliance.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.