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Hemostatic changes in canger
Vol. 65, Suppl. 1
ABSTRACTS OF12THINTNAT'LCONGRESS
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S18 HEMOSTATIC CHANGES IN CANGER F.R. Rickles, M. Levine, R.L. Edwards Univ. CT. School of Medicine, Farmington, CT, USA McMaster University and The Hamilton Regional Cancer Center, Hamilton, ONT, CDN Nearly all patients with cancer manifest laboratory evidence of hypercoagulability and some develop clinical thromboembolic disease (TED). Routine laboratory studies of blood coagulation have been performed in several large, prospective cancer treatment trials. The results of these studies will be reviewed, as will data from several smaller studies of more sensitive tests of hypercoagulability [e.g. plasma levels of tibrinopeptide A (FPA); thrombinantithrombin (TAT); prothrombin fragment F1+2]. Although the levels of some clotting proteins parallel disease activity, they do not predict TED. Mechanisms in addition to tumor-related procoagulants may be involved in the pathogenesis of TED in some patients and special studies may be necessary to predict the risk of TED in individual patients (e.g. tumor cell cytokine production, tumor cell procoagulant activity, etc.). The cancer patient undergoing major surgery is at risk for thrombosis. Once thrombosis occurs in the cancer patient, the prevention of recurrence is important. All of these issues will be reviewed and recommendations will be made. Chemotherapy of cancer probably increases the liklihood of TED, particularly well-studied in patients with breast cancer treated with tamoxifen plus cytotoxic drugs. The mechanisms may bc complex but vascular injury is likely as a proximate cause of venous access catheter thrombosis and can be prevented with low dose coumadin therapy. The data regarding the risk for TED during breast cancer treatment will be reviewed and recommendations for additional studies will be discussed. The efficacy of prophylactic, low dose coumadin anticoagulation for patients with stage IV breast cancer is being studied. Single pulse dose heparin prior to intravenous chemotherapy should be considered for high risk patients.
s19 VENOUSTHROMBOSISAND CANCER: THE TROUSSEAUSYNDROHE J. Vermylen and R. Verhaeghe, Center for Thrombosis and Vas.cul!ar Research, University of Leuven, Belgium Armand Trousseau probably was the first to emphasize the link between venous thrombosis or superficial thrombophlebitis and cancer. Besides thronfbophlebitis migrans aut s,altansi,,nqnbacterial thrombotic endocarditis and digital microvascular thrombosis are specific manifestations of thromboembolism in cancer patients. The frequency of spontaneous venous thrombosis also is increased' in cancer patients; lung and gastrointestinal cancers are most frequently associated with thrombosis; the evidence that venous thrombosis is an early manifestation of an occult malignancy is discussed. The usefulness of screening patients with venous thrombosis for hidden cancer is reviewed critically. Pitfalls in the diagnosis of thrombosis in cancer patients are related to extrinsic venous compression or to tumor propagation within the lumen of the vein. The management of thrombosis in cancer patients in general is quite similar to that in patients without cancer, although attention is drawn to a number of specific characteristics; vitamin K antagonists sometimes are ineffective in cancer-related venous thrombosis, in particular thrombophlebitis migrans; peri-operative thrombosis prophylaxis requires high doses of subcutaneous heparin or low molecular weight heparin fractions.
ABSTRACTS OF12THINTNAT'LCONGRESS
Sll
S18 HEMOSTATIC CHANGES IN CANGER F.R. Rickles, M. Levine, R.L. Edwards Univ. CT. School of Medicine, Farmington, CT, USA McMaster University and The Hamilton Regional Cancer Center, Hamilton, ONT, CDN Nearly all patients with cancer manifest laboratory evidence of hypercoagulability and some develop clinical thromboembolic disease (TED). Routine laboratory studies of blood coagulation have been performed in several large, prospective cancer treatment trials. The results of these studies will be reviewed, as will data from several smaller studies of more sensitive tests of hypercoagulability [e.g. plasma levels of tibrinopeptide A (FPA); thrombinantithrombin (TAT); prothrombin fragment F1+2]. Although the levels of some clotting proteins parallel disease activity, they do not predict TED. Mechanisms in addition to tumor-related procoagulants may be involved in the pathogenesis of TED in some patients and special studies may be necessary to predict the risk of TED in individual patients (e.g. tumor cell cytokine production, tumor cell procoagulant activity, etc.). The cancer patient undergoing major surgery is at risk for thrombosis. Once thrombosis occurs in the cancer patient, the prevention of recurrence is important. All of these issues will be reviewed and recommendations will be made. Chemotherapy of cancer probably increases the liklihood of TED, particularly well-studied in patients with breast cancer treated with tamoxifen plus cytotoxic drugs. The mechanisms may bc complex but vascular injury is likely as a proximate cause of venous access catheter thrombosis and can be prevented with low dose coumadin therapy. The data regarding the risk for TED during breast cancer treatment will be reviewed and recommendations for additional studies will be discussed. The efficacy of prophylactic, low dose coumadin anticoagulation for patients with stage IV breast cancer is being studied. Single pulse dose heparin prior to intravenous chemotherapy should be considered for high risk patients.
s19 VENOUSTHROMBOSISAND CANCER: THE TROUSSEAUSYNDROHE J. Vermylen and R. Verhaeghe, Center for Thrombosis and Vas.cul!ar Research, University of Leuven, Belgium Armand Trousseau probably was the first to emphasize the link between venous thrombosis or superficial thrombophlebitis and cancer. Besides thronfbophlebitis migrans aut s,altansi,,nqnbacterial thrombotic endocarditis and digital microvascular thrombosis are specific manifestations of thromboembolism in cancer patients. The frequency of spontaneous venous thrombosis also is increased' in cancer patients; lung and gastrointestinal cancers are most frequently associated with thrombosis; the evidence that venous thrombosis is an early manifestation of an occult malignancy is discussed. The usefulness of screening patients with venous thrombosis for hidden cancer is reviewed critically. Pitfalls in the diagnosis of thrombosis in cancer patients are related to extrinsic venous compression or to tumor propagation within the lumen of the vein. The management of thrombosis in cancer patients in general is quite similar to that in patients without cancer, although attention is drawn to a number of specific characteristics; vitamin K antagonists sometimes are ineffective in cancer-related venous thrombosis, in particular thrombophlebitis migrans; peri-operative thrombosis prophylaxis requires high doses of subcutaneous heparin or low molecular weight heparin fractions.