Evidence map›Paper›PMID 42260034›Full record

Observational studyBiochemical genetics2026

COVID-19 as a Modifier of Genetically Determined Coagulation Phenotype: Implications for Precision Risk Stratification After Infection.

Oleg Alexandrovich Perevezentsev, Ilgar Salekh Mamedov, Dmitry Vladimirovich Burtsev

Abstract readObservational Study
PubMed Publisher
In one paragraph

Observational study in Biochemical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Oleg Alexandrovich PerevezentsevDepartment of Personalized and Translational Medicine, Rostov State Medical University, Rostov-on-Don, Russia. PZPO@mail.ru.ORCID http://orcid.org/0000-0002-7070-3209
Ilgar Salekh MamedovLaboratory of Clinical Diagnostic and Genetic Research, Scientific and Practical Center for Specialized Medical Care for Children Named After V.F. Voyno-Yasenetsky Department of Health of the City of Mosсow, Aviatorov str., 38, Moscow, 199620, Russia.ORCID http://orcid.org/0000-0003-0783-2873
Dmitry Vladimirovich BurtsevDepartment of Personalized and Translational Medicine, Rostov State Medical University, Rostov-on-Don, Russia.ORCID http://orcid.org/0000-0002-4673-7003

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent endothelial dysfunction and coagulation abnormalities are increasingly recognized as central components of post-COVID syndrome. However, substantial interindividual variability in long-term coagulation biomarkers suggests the presence of genetically determined susceptibility factors capable of modulating post-infectious thromboinflammatory responses. To determine whether common prothrombotic genetic variants modify long-term D-dimer and INR levels after COVID-19 and to assess their value for precision risk stratification. A controlled observational cohort study included 504 adults aged 18-50 years examined more than two years after PCR-confirmed COVID-19 and 270 control individuals without clinically significant SARS-CoV-2 infection. Genotyping of F2 c.20210G > A, F5 c.1691G > A (Factor V Leiden), and MTHFR c.C677T was performed using real-time PCR. D-dimer and international normalized ratio (INR) were measured monthly for 12 months and averaged. Log-transformed D-dimer was analyzed using multivariable linear regression with interaction terms. All three variants were independent predictors of D-dimer. In adjusted models, F2 GA (+ 31%), F5 GA (+ 37%), MTHFR CT (+ 34%), and MTHFR TT (+ 67%) were associated with higher D-dimer levels (all p < 0.001). Significant amplification of genetic effects was observed in post-COVID individuals (Group × Genotype interaction p < 0.01). INR showed no genotype association. COVID-19 acts as a long-term modifier of inherited thrombophilia phenotypes. Incorporating genetic profiling into post-COVID evaluation may enable precision identification of individuals at risk for persistent hypercoagulability.

Indexed as

Blood CoagulationCOVID-19AdolescentAdultFactor VFemaleFibrin Fibrinogen Degradation ProductsGenetic Predisposition to DiseaseGenotypeHumansInternational Normalized RatioMaleMethylenetetrahydrofolate Reductase (NADPH2)Middle AgedPhenotypeProthrombinFactor Vfactor V LeidenFibrin Fibrinogen Degradation Productsfibrin fragment DMethylenetetrahydrofolate Reductase (NADPH2)MTHFR protein, humanProthrombinCOVID-19GeneticsHemostasis

Identifiers

PMID42260034

What Socratic 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 Socratic graph.