Hemostasis and Neoplasia

The incidence of clinical thrombotic or hemorrhagic complications associated with neoplasia is unknown. In one study of untreated dogs with cancer but no evidence of bleeding, abnormal coagulation results were obtained in 83% of patients, including thrombocytopenia, prolonged APTT, and hyper- and hypofibrinogenemia. One of the most common tumors associated with hemorrhagic tendencies is hemangiosarcoma in dogs. Most dogs with hemangiosarcoma have laboratory evidence of DIC. Abnormal hemostasis can be due to the maligancy itself, chemotherapy or metastatic disease (resulting in organ disease or failure) and can involve all pathways of hemostasis. Hemostatic abnormalities associated with chemotherapy are common in both human and animals, with thrombocytopenia due to myelosuppression being a frequent complication of chemotherapeutic protocols. Some antineoplastics produce thrombosis either due to direct toxic effects on the vasculature or because of effects on hemostasis, e.g. L-asparginase inhibits antithrombin production.
  • Primary hemostasis: Thrombocytopenia is a common finding in animals with neoplasia. This may be due to decreased production (myelophthisis, tumor release of suppressive cytokines or chemotherapy-related), immune-mediated destruction, blood loss, sequestration and increased consumption in DIC. As mentioned under the section on monoclonal gammopathies, animals with paraproteinemias have evidence of decreased platelet function. Acquired von Willebrand disease has been reported in human patients with multiple myeloma, lymphoma, Wilm's tumor and myeloproliferative disease. A similar phenomenon has not been reported in animals. In a recent study in dogs with lymphoma, platelets were shown to be hyperaggregable.

  • Secondary hemostasis: Isolated factor deficiencies have rarely been reported in animals with neoplasia, most factor deficiencies are due to DIC. Coagulation can be initiated by a variety of tumors, due to activation of factors directly (e.g. mucinous adenocarcinomas can activate factor X), tissue factor expression (e.g. hemangiosarcoma), and production of inhibitors (e.g. mast cell tumors, which release heparin).

  • Tertiary hemostasis: Excessive fibrinolysis is a feature of certain tumors in human patients, such as promyelocytic leukemia. This syndrome has not been recognized in animals.