Evidence map›Paper›PMID 39941433›Full record

ReviewJournal of clinical medicine2025

Hypercoagulability in Tuberculosis: Pathophysiological Mechanisms, Associated Risks, and Advances in Management-A Narrative Review.

Denisa Maria Mitroi, Mara Amalia Balteanu, Ramona Cioboata, Silviu Gabriel Vlasceanu, Ovidiu Mircea Zlatian, Oana Maria Catana, Adina Andreea Mirea, Gabriel Florin Razvan Mogos, Ionela Rotaru, Viorel Biciusca

Abstract readReview
In one paragraph

Review in Journal of clinical medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

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  12. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
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  15. Observational
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  19. Lung epithelial injury impairs early host immune responses to Mycobacterium tuberculosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  20. Article
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

10 authors.

Denisa Maria MitroiDoctoral School, University of Medicine and Pharmacy, 200349 Craiova, Romania.
Mara Amalia BalteanuDepartment of Pulmonology, Faculty of Medicine, Titu Maiorescu University, 031593 Bucharest, Romania.ORCID 0009-0004-8409-5904
Ramona CioboataPneumology Department, University of Medicine and Pharmacy, 200349 Craiova, Romania.ORCID 0009-0006-6335-1627
Silviu Gabriel VlasceanuDepartment of Physiology, "Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania.ORCID 0009-0007-3856-7917
Ovidiu Mircea ZlatianMicrobiology Department, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania.ORCID 0000-0003-3510-3838
Oana Maria CatanaDoctoral School, University of Medicine and Pharmacy, 200349 Craiova, Romania.ORCID 0009-0000-9976-2256
Adina Andreea MireaDepartment of Oral-Dental Prevention, University of Medicine and Pharmacy, 200349 Craiova, Romania.ORCID 0009-0001-4039-0811
Gabriel Florin Razvan MogosDepartment of Surgery, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania.
Ionela RotaruDepartment of Hematology, Faculty of Medicine, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania.
Viorel BiciuscaPneumology Department, University of Medicine and Pharmacy, 200349 Craiova, Romania.ORCID 0000-0002-9451-6969

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tuberculosis (TB) induces a hypercoagulable state characterized by systemic inflammation, endothelial dysfunction, and alterations in the coagulation and fibrinolytic pathways. This review explores the pathophysiological mechanisms underlying hypercoagulability in TB, including increased pro-inflammatory cytokine release, endothelial damage, platelet activation, and reduced anticoagulant and fibrinolytic activity. These factors contribute to an elevated risk of venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE), which complicate TB prognosis and treatment. The potential role of adjunctive anti-inflammatory therapies, such as vitamin D, NSAIDs, corticosteroids, and anti-platelet agents, is highlighted as a strategy to mitigate systemic inflammation and reduce thrombotic risks in patients with TB. The challenges of anticoagulation therapy, particularly in managing the interactions between anti-TB medications and traditional anticoagulants, are discussed, along with the potential of novel oral anticoagulants (NOAs) as alternatives. We also address therapy of hypercoagulability in TB within resource-limited settings which requires low-cost diagnostics, accessible anticoagulation options, adjunctive therapies, and preventive strategies integrated into existing healthcare systems. Effective risk stratification and individualized management strategies are vital for reducing the morbidity and mortality associated with thrombotic complications in TB.

Indexed as

disease managementhypercoagulabilitytuberculosis

Identifiers

PMID39941433
PMCPMC11818899

What OpenQuestion holds

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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.