ArticleResearch and practice in thrombosis and haemostasis2024
Traumatic bleeding and mortality in mice are intensified by iron deficiency anemia and can be rescued with tranexamic acid.
Article in Research and practice in thrombosis and haemostasis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Red Blood Cells and Tranexamic Acid in the Inhibition of Fibrinolysis.Seminars in thrombosis and hemostasis · 2026Review
- The effects of recombinant human activated factor VII and tranexamic acid on traumatic bleeding and mortality in mice.Research and practice in thrombosis and haemostasis · 2026Article
- Effect of a truncated mutant factor V on hemostatic function and embryonic development in mice.Scientific reports · 2026Article
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Authors and funding
7 authors.
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Abstract
Background: Clinical evidence suggests that anemia exacerbates traumatic bleeding and worsens outcomes. Objectives: To study the influence of iron deficiency anemia on traumatic bleeding, coagulopathy, and mortality. Methods: C57BL/6J mice received an iron-deficient diet (8 weeks; ±1 mg intraperitoneal iron dextran 2 weeks before trauma). Control mice received a normal diet. Iron deficiency anemia was confirmed by hematocrit, red cell indices, and liver iron. Mice received saline or tranexamic acid (TXA; 10 mg/kg) just before liver laceration. Blood loss, coagulopathy (activated partial thromboplastin time, factor [F]II, FV, FVIII, FX, and fibrinogen), D-dimer, thrombin-antithrombin complexes, and plasmin-alpha-2-antiplasmin complexes were analyzed at 15 and 60 minutes, and a cytokine panel was performed at 60 minutes and 6 hours after trauma. Survival was monitored for 7 days. Results: Compared with nonanemic mice, anemic mice had lower hematocrit and hepatic iron content. Anemic mice experienced higher blood loss compared with nonanemic mice, which was reduced by TXA. Both groups developed traumatic coagulopathy characterized by activated partial thromboplastin time prolongation, thrombin-antithrombin complex formation, and depletion of FV, FVIII, and fibrinogen. TXA corrected the coagulopathy. However, plasmin-alpha-2-antiplasmin complex formation and D-dimers, markers of fibrinolysis, were higher in anemic mice and were not corrected by TXA. Seven-day survival was low in anemic mice, and rescued by TXA, but high in nonanemic mice without additional improvement by TXA. Among cytokines, only interleukin-6 increased, which was prevented by TXA most notably in anemic mice. Conclusion: These observations provide first and critical proof-of-principle evidence that anemia accelerates traumatic bleeding and increases mortality, which could be rescued by anemia correction (parenteral iron) or periprocedural TXA.
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