Evidence map›Paper›PMID 19123042›Full record

ArticleMolecular biology reports2009

Impact of hemostatic gene single point mutations in patients with non-diabetic coronary artery disease.

Ahmet Var, Ozan Utük, Sinem Akçali, Tamer Sanlidağ, Bekir S Uyanik, Gönül Dinç

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 4 pooled it
1.1field-weighted citation impact, top 23% of its field
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

10 citing papers in PubMed, 4 syntheses or guidelines pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Article
  6. Association of FV G1691A Polymorphism but not A4070G With Coronary Artery Disease.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis · 2018
    Article
  7. PAI-1 4G/5G polymorphism and coronary artery disease risk: a meta-analysis.International journal of clinical and experimental medicine · 2015
    Article
  8. Article
  9. Article
  10. Review
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

6 authors at 1 institution in 1 country.

Ahmet VarDepartment of Biochemistry, Celal Bayar Medical University, Manisa, Turkey. ahmetvar@hotmail.com
Ozan Utük
Sinem Akçali
Tamer Sanlidağ
Bekir S Uyanik
Gönül Dinç
Manisa Celal Bayar University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Single point mutations in the genes coding for hemostatic factors were shown to be major inherited predisposing factors for venous thromboembolism. However, their contribution in the development of non-diabetic coronary artery disease [nDCAD] remains controversial. Angiographically demonstrated nDCAD patients (n = 86) and healthy controls (n = 90) were included in the study. Genotype analysis of hemostatic gene polymorphisms were assessed by using CVD strip assay, based on allele specific oligonucleotide probes. The carrier frequency of factor V (FV) H1299R, prothrombin G20210A, glycoprotein (Gp) IIIa L33P, plasminogen activator inhibitor-I (PAI-1) 4G/5G, 4G/4G, 5G/5G, methylenetetrahydrofolate reductase (MTHFR) A1298C and beta-fibrinogen -455 G > A were similar between patients and controls. In contrast, frequency of FV Leiden was significantly higher among patients (12.5%) than controls (5%, OR: 7.94; 95%CI: 1.9-49.6) and FXIII V34L was significantly lower among patients (23.7%) than controls (40%, OR: 0.24; 95%CI: 0.1-0.89). In addition, the frequency of the MTHFR C677T polymorphism was 32.5% among patients compared with 42.5% in controls, of which the T/T genotype was significantly lower among patients (5%) than controls (17.5%, OR: 0.06; 95%CI: 0.01-0.58). No difference was observed in prevalence of prothrombin G20210A, FV H1299R, Gp IIIa L33P, PAI-1 4G5G, MTHFR A1298C, beta fibrinogen 455 G > A mutations between patients and controls. However, lower frequency of FXIII Val34Leu and MTHFR C677T polymorphisms may decrease, while FV Leiden polymorphism may increase development of nDCAD.

Indexed as

Point MutationAdultAgedBlood Coagulation FactorsCoronary Artery DiseaseFemaleGenetic Predisposition to DiseaseHemostasisHumansLogistic ModelsMaleMethylenetetrahydrofolate Reductase (NADPH2)Middle AgedSignal TransductionBlood Coagulation FactorsMethylenetetrahydrofolate Reductase (NADPH2)

Identifiers

PMID19123042
OpenAlexW2028654766

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.