Altered Fibrinolysis in Hematological Malignances.

Semin Thromb Hemost

Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark.

Published: July 2021

AI Article Synopsis

  • The review focuses on how changes in fibrinolysis relate to bleeding and thrombosis in patients with hematological malignancies, excluding acute promyelocytic leukemia and disseminated intravascular coagulation.
  • After analyzing 32 studies, it was found that most of the research is outdated and incomplete, with no comprehensive examination of fibrinolysis markers.
  • Overall, the findings suggest hypofibrinolysis in myeloproliferative neoplasms and highlight the risk of hyperfibrinolysis and bleeding in conditions like AL-amyloidosis, indicating a need for more current investigation in this area.

Article Abstract

Bleeding and thrombosis are well-known complications to hematological malignancies, and changes in fibrinolysis impact both these issues. In the present systematic review, we provide an overview and discussion of the current literature in regards to clinical manifestations, diagnosis, and treatment of altered fibrinolysis in patients suffering from hematological malignancies, beyond acute promyelocytic leukemia. We performed a systematic literature search employing the databases Pubmed, Embase, and Web of Science to identify original studies investigating fibrinolysis in hematological malignancies. Studies investigating fibrinolysis in acute promyelocytic leukemia or disseminated intravascular coagulation were excluded. We identified 32 studies fulfilling the inclusion criteria. A majority of the studies were published more than two decades ago, and none of the studies examined all available markers of fibrinolysis or used dynamic clot lysis assays. In acute leukemia L-asparaginase treatment induced a hypofibrinolytic state, and prior to chemotherapy there seemed to be little to no change in fibrinolysis. In studies examining fibrinolysis during chemotherapy results were ambiguous. Two studies examining multiple myeloma indicated hypofibrinolysis prior to chemotherapy, and in another plasma cell disease, amyloid light chain-amyloidosis, clear signs of hyperfibrinolysis were demonstrated. In myeloproliferative neoplasms, the studies reported signs of hypofibrinolysis, in line with the increased risk of thrombosis in this disease. Only one study regarding lymphoma was identified, which indicated no alterations in fibrinolysis. In conclusion, this systematic review demonstrated that only sparse, and mainly old, evidence exists on fibrinolysis in hematological malignancy. However, the published studies showed a tendency toward hypofibrinolysis in myeloproliferative disorders, an increased risk of hyperfibrinolysis, and bleeding in patients with AL-amyloidosis, whereas studies regarding acute leukemias were inconclusive except with regard to L-asparaginase treatment, which induced a hypofibrinolytic state.

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Source
http://dx.doi.org/10.1055/s-0041-1725099DOI Listing

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