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    Poster Networking

    Fibrinolysis and Proteolysis

    Poster Networking Session

    PB1196 - In vitro comparisons of two fibrinogen concentrates on fibrin clot properties in dysfibrinogenemia

    Tuesday, June 27, 2023
    18:30 – 19:30 ET
    Room: Exhibition

      Presenting Author(s)

    • Rita Marchi

      PhD
      UNIGE
      Geneva, Geneve, Switzerland

      • Co-Author(s)

    • SD

      Stéphane Dural

      PhD
      UNIGE
      Geneva, Geneve, Switzerland

    • Tomas Simurda, MD, PhD.

      physician
      National Centre of Hemostasis and Thrombosis, Department of Hematology and Transfusiology, Comenius University in Bratislava, Jessenius Faculty of Medicine in Martin and University Hospital in Martin, Slovakia
      Martin, Zilina, Slovakia

    • MN

      Marguerite Neerman-Arbez

      Professor
      Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland
      Geneva, Geneve, Switzerland

    • Alessandro Casini, MD

      MD
      Division of Angiology and Hemostasis, Faculty of Medicine, Geneva University Hospitals, Geneva, Switzerland
      Geneva, Geneve, Switzerland

    Background: Fibrinogen concentrates (FgC) can be administered to treat or prevent the risk of bleeding in patients with hereditary fibrinogen disorders. However, the optimal fibrinogen concentration to target after FgC infusion in hereditary dysfibrinogenemia has not been explored yet.

    Aims: To compare the structural/functional changes in fibrin networks of dysfibrinogenemic plasma when fibrinogen activity is corrected with two different brands of FgC (A or B).

    Methods: Samples from a patient with hereditary dysfibrinogenemia (Aα p.Arg35His) with fibrinogen activity (Clauss) of 1.3 g/L was compared to a commercial plasma (CRYOcheck; 2.7g/L). Plasma samples were spiked with 2 g/L of FgC A or B. Thrombin time and fibrinogen activity were recorded in a Sysmex XN-9000. Fibrin structure was analyzed by turbidity at 405 nm, measuring the lag time (min), the slope (OD/s)x10-4, the MaxAbs (mOD) and the T50% (min). Area available for flow was measured by permeation (Ks, cm2) and fibrin network was visualized by scanning electron microscopy (SEM).

    Results: Based on our preliminary results showing that 2 g/L of FgC allows to obtain clot properties similar to those of healthy controls, we spiked plasmas with 2 g/L of FgC A or B. Table 1 summarizes the results. Overall, adding FgC in dysfibrinogenemic plasma shortened the thrombin time, enhanced fibrin polymerization, decreased fibrinolysis, and normalized the fibrin network structure. FgC B had a greater impact than FgC A for all parameters in both dysfibrinogenemic and normal plasma samples. By SEM it was observed that FgC A increased fibrin density more than FgC B.

    Conclusion(s): Our in vitro study shows that infusion of FgC B may lead to a better improvement of fibrin clot structure/function than infusion of FgC A. Future studies will analyze whether such differences are observed for other fibrinogen variants and will determine the impact of FgC purity on fibrin clot properties.