Evidence map›Paper›PMID 28550460›Full record

ArticleEuropean journal of clinical pharmacology2017

The impact of non-genetic and genetic factors on a stable warfarin dose in Thai patients.

Nitsupa Wattanachai, Sutthida Kaewmoongkun, Burabha Pussadhamma, Pattarapong Makarawate, Chaiyasith Wongvipaporn, Songsak Kiatchoosakun, Suda Vannaprasaht, Wichittra Tassaneeyakul

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Article in European journal of clinical pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Article
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  4. InnovativeFrontiers in genetics · 2022
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Nitsupa WattanachaiDepartment of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand. nitsupa@kku.ac.th.ORCID http://orcid.org/0000-0002-6300-3757
Sutthida KaewmoongkunDepartment of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.
Burabha PussadhammaDivision of Cardiology, Queen Sirikit Heart Center of the Northeast, Department of Medicine, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.
Pattarapong MakarawateDivision of Cardiology, Queen Sirikit Heart Center of the Northeast, Department of Medicine, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.
Chaiyasith WongvipapornDivision of Cardiology, Queen Sirikit Heart Center of the Northeast, Department of Medicine, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.
Songsak KiatchoosakunDivision of Cardiology, Queen Sirikit Heart Center of the Northeast, Department of Medicine, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.
Suda VannaprasahtDepartment of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.
Wichittra TassaneeyakulDepartment of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe aim of this study was to investigate the contributions of non-genetic and genetic factors on the variability of stable warfarin doses in Thai patients.

methodsA total of 250 Thai patients with stable warfarin doses were enrolled in the study. Demographics and clinical data, e.g., age, body mass index, indications for warfarin and concomitant medications, were documented. Four single nucleotide polymorphisms in the VKORC1 - 1639G > A, CYP2C9*3, CYP4F2 rs2108622, and UGT1A1 rs887829 genes were detected from gDNA using TaqMan allelic discrimination assays.

resultsThe patients with variant genotypes of VKORC1 - 1639G > A required significantly lower warfarin stable weekly doses (SWDs) than those with wild-type genotype (p < 0.001). Similarly, the patients with CYP2C9*3 variant allele required significantly lower warfarin SWDs than those with homozygous wild-type (p = 0.006). In contrast, there were no significant differences in the SWDs between the patients who carried variant alleles of CYP4F2 rs2108622 and UGT1A1 rs887829 as compared to wild-type allele carriers. Multivariate analysis, however, showed that CYP4F2 rs2108622 TT genotype accounted for a modest part of warfarin dose variability (1.2%). In contrast, VKORC1 - 1639G > A, CYP2C9*3, CYP4F2 rs2108622 genotypes and non-genetic factors accounted for 51.3% of dose variability.

conclusionsVKORC1 - 1639G > A, CYP2C9*3, and CYP4F2 rs2108622 polymorphisms together with age, body mass index, antiplatelet drug use, amiodarone use, and current smoker status explained 51.3% of individual variability in stable warfarin doses. In contrast, the UGT1A1 rs887829 polymorphism did not contribute to dose variability.

Indexed as

AdultAgedAged, 80 and overAnticoagulantsAsian PeopleCytochrome P-450 CYP2C9Cytochrome P450 Family 4Dose-Response Relationship, DrugFemaleGenotypeHumansMaleMiddle AgedSmokingThailandVitamin K Epoxide ReductasesAnticoagulantsCytochrome P-450 CYP2C9Cytochrome P450 Family 4Vitamin K Epoxide ReductasesVKORC1 protein, humanWarfarinCYP2C9CYP4F2Non-genetic factorsUGT1A1VKORC1Warfarin

Identifiers

PMID28550460
PMCPMC5508045

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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.