Trial reportIntensive care medicine2026
Plasminogen supplementation reverses fibrinolytic insufficiency in sepsis-induced disseminated intravascular coagulation: a pilot study.
Trial report in Intensive care medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
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.
Who cites it
1 citing paper in PubMed.
- Reference Intervals for ROTEM-tPA: Whole-Blood Fibrinolysis Assessment in Healthy Adults.TH open : companion journal to thrombosis and haemostasis · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeSepsis-induced disseminated intravascular coagulation (DIC) is characterized by impaired fibrinolysis, partly due to neutrophil elastase-mediated plasminogen degradation. We aimed to evaluate whether plasminogen supplementation could restore fibrinolytic capacity in patients with sepsis-induced coagulopathy and in a murine model of septic DIC.
methods60 patients with sepsis-induced coagulopathy were randomized to receive 12 mL/kg of placebo (NaCl 0.9%) or OctaplasLG®, a pathogen-inactivated pooled human plasma containing 2 µM plasminogen. Pre- and post-infusion levels of functional plasminogen, plasmin generation, and fibrinolysis markers (plasmin-antiplasmin complexes, plasminogen activator inhibitor-1, and tissue-type plasminogen activator) were measured. In parallel, in a sepsis-induced DIC model, transgenic TM
resultsIn patients, baseline plasminogen and plasmin generation were significantly lower than in healthy controls. OctaplasLG® significantly increased functional plasminogen (+ 46 nM [-96; 118] vs. -84 [-180; 27] nM, p < 0.05) and improved plasmin generation (0.12 [-0.25; 1.27] vs. -0.36 [-1.58; 0.12] fmol, p < 0.05). No changes were observed in plasmin-antiplasmin, plasminogen activator inhibitor-1, or tissue-type plasminogen activator levels. A non-significant trend toward reduced mortality was noted in patients receiving OctaplasLG® (42.3% vs. 60.0%). Septic DIC-mice also exhibited reduced functional plasminogen (100 [66-126] vs. 295 [268-343] nM) and impaired plasmin generation (1.8 [1.4-2.1] vs. 3.0 [2.8-3.3] fmol, p < 0.05), which were restored after plasminogen supplementation (plasminogen: 346 [287; 360] nM; plasmin generation: 4.1 [3.7; 5.5] fmol).
conclusionPlasminogen supplementation restores fibrinolytic capacity, supporting its therapeutic potential in sepsis-induced DIC.
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Registered trials
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