ArticleBlood advances2023
Impaired fibrinolysis and increased clot strength are potential risk factors for thrombosis in lymphoma.
Article in Blood advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Risk Assessment for Venous Thrombosis in Lymphoma and Emerging Biomarkers.International journal of molecular sciences · 2026Review
- Plasmin promotes hepatocellular carcinoma invasion and metastasis via CXCR4-mediated activation of PI3K/AKT/mTOR signaling.Oncogene · 2026Article
- Inflammatory Signaling and Endothelial Activation Drive Thrombosis in Hodgkin and Non-Hodgkin Lymphoma.Cells · 2026Article
- Fibrinogen Oxidation and Thrombosis: Shaping Structure and Function.Antioxidants (Basel, Switzerland) · 2025Review
- Hemorrhage in acute promyelocytic leukemia-fibrinolysis in focus.Research and practice in thrombosis and haemostasis · 2024Review
- Fibrinogen contribution to clot strength in patients with sepsis and hematologic malignancies and thrombocytopenia-a prospective, single-center, analytical, cross-sectional study.Research and practice in thrombosis and haemostasis · 2024Article
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4 authors at 1 institution in 1 country.
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Abstract
Thrombosis and bleeding are significant contributors to morbidity and mortality in patients with hematological cancer, and the impact of altered fibrinolysis on bleeding and thrombosis risk is poorly understood. In this prospective cohort study, we investigated the dynamics of fibrinolysis in patients with hematological cancer. Fibrinolysis was investigated before treatment and 3 months after treatment initiation. A dynamic clot formation and lysis assay was performed beyond the measurement of plasminogen activator inhibitor 1, tissue- and urokinase-type plasminogen activators (tPA and uPA), plasmin-antiplasmin complexes (PAP), α-2-antiplasmin activity, and plasminogen activity. Clot initiation, clot propagation, and clot strength were assessed using rotational thromboelastometry. A total of 79 patients were enrolled. Patients with lymphoma displayed impaired fibrinolysis with prolonged 50% clot lysis time compared with healthy controls (P = .048). They also displayed decreased clot strength at follow-up compared with at diagnosis (P = .001). A patient with amyloid light-chain amyloidosis having overt bleeding at diagnosis displayed hyperfibrinolysis, indicated by a reduced 50% clot lysis time, α-2-antiplasmin activity, and plasminogen activity, and elevated tPA and uPA. A patient with acute promyelocytic leukemia also displayed marked hyperfibrinolysis with very high PAP, indicating extreme plasmin generation, and clot formation was not measurable, probably because of the extremely fast fibrinolysis. Fibrinolysis returned to normal after treatment in both patients. In conclusion, patients with lymphoma showed signs of impaired fibrinolysis and increased clot strength, whereas hyperfibrinolysis was seen in patients with acute promyelocytic leukemia and light-chain amyloidosis. Thus, investigating fibrinolysis in patients with hematological cancer could have diagnostic value.
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