ArticleBlood vessels, thrombosis & hemostasis2025
Multiomics reveal plasma constituents associated with thrombosis among trauma patients who do not respond to enoxaparin.
Article in Blood vessels, thrombosis & hemostasis, 2025. 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
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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
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Who cites it
2 citing papers in PubMed.
- Multiomic changes posthypovolemia in a lower body negative pressure model: unlocking new mechanisms or adding to the complexity?Physiological genomics · 2026Article
- Bridging practice and evidence: insights from the Scandinavian Society of Anaesthesiology and Intensive Care Medicine and Saudi Critical Care Society Guidelines on trauma-related VTE.Scandinavian journal of trauma, resuscitation and emergency medicine · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Venous thromboembolism (VTE) is among the most common complications affecting patients with severe injuries. Although enoxaparin resistance is common, predicting which patients among this subgroup will develop VTE remains a clinical challenge. The goal of this study was to use multiomics to identify plasma constituents associated with VTE development among trauma patients exhibiting poor responses to enoxaparin. We conducted a secondary analysis of trauma patients at high risk of VTE based on injury characteristics. Plasma was collected daily for the first 8 hospital days. Patients who never responded to enoxaparin were defined as not achieving an anti-factor Xa (FXa) level of ≥0.2 IU/mL during the sampling period. A total of 145 patients were included in the analysis, of whom 24 (16.6%) developed VTE. Proteomics analyses identified increased proteins involved in coagulation, complement activation, and immune response pathways among patients with VTE compared to those without VTE. A subset of patients (n = 26) never responded to enoxaparin; among them, 8 (30.8%) developed VTE. Partial least squares discriminant analysis on multiomics of never responders revealed clear separation based on VTE status. The top 25 differentially abundant proteins were involved in coagulation, fibrin cross-linking, inflammation, and acute phase responses. Differences were particularly robust on hospital day 5, at which we observed significant increases in FV, FXI, fibrinogen, complement, and C-reactive protein. In conclusion, proteomics signatures distinguish VTE development among trauma patients who do not respond to enoxaparin. These findings implicate novel pathways in postinjury VTE pathogenesis and new candidate proteins for future therapeutic intervention.
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Registered trials
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